niacin has been researched along with Dyslipidemia in 232 studies
Niacin: A water-soluble vitamin of the B complex occurring in various animal and plant tissues. It is required by the body for the formation of coenzymes NAD and NADP. It has PELLAGRA-curative, vasodilating, and antilipemic properties.
vitamin B3 : Any member of a group of vitamers that belong to the chemical structural class called pyridines that exhibit biological activity against vitamin B3 deficiency. Vitamin B3 deficiency causes a condition known as pellagra whose symptoms include depression, dermatitis and diarrhea. The vitamers include nicotinic acid and nicotinamide (and their ionized and salt forms).
nicotinic acid : A pyridinemonocarboxylic acid that is pyridine in which the hydrogen at position 3 is replaced by a carboxy group.
| Excerpt | Relevance | Reference |
|---|---|---|
| "To assess the effects of anacetrapib added to statin ± other lipid-modifying therapies in patients with hypercholesterolemia and not at their low-density lipoprotein cholesterol (LDL-C) goal (as per National Cholesterol Education Program Adult Treatment Panel III [NCEP ATP III] guidelines) and in those with low high-density lipoprotein cholesterol (HDL-C)." | 9.24 | Lipid-Modifying Efficacy and Tolerability of Anacetrapib Added to Ongoing Statin Therapy in Patients with Hypercholesterolemia or Low High-Density Lipoprotein Cholesterol. ( Ashraf, TB; Ballantyne, CM; Cressman, MD; Gill, GG; Hunter, JA; Johnson-Levonas, AO; Kher, U; Mitchel, YB; Shah, S, 2017) |
| "Although the pharmacological effect of niacin in lowering blood cholesterol and triglyceride levels has been demonstrated in several clinical studies, information regarding the effect of dietary niacin intake is uncertain, and the longitudinal association between dietary niacin intake and the risk of dyslipidemia has not been adequately studied." | 9.22 | Dietary niacin intake and risk of dyslipidemia: A pooled analysis of three prospective cohort studies. ( Kim, C; Park, K, 2022) |
| "This study examined whether the increase of adiponectin associated with extended-release (ER) niacin/laropiprant combination attenuates the adverse effect of niacin on glucose and insulin resistance in Hong Kong Chinese patients with dyslipidaemia." | 9.20 | Effect of Extended-Release Niacin/Laropiprant Combination on Plasma Adiponectin and Insulin Resistance in Chinese Patients with Dyslipidaemia. ( Hu, M; Masuda, D; Tomlinson, B; Yamashita, S; Yang, YL, 2015) |
| " Patients (N = 100) with mixed dyslipidemia on a standard statin dose (10-40 mg simvastatin or 10-20 mg atorvastatin or 5-10 mg rosuvastatin) who had not achieved lipid targets were randomized to switch to the highest dose of rosuvastatin (40 mg/day) or to add-on-statin extended release nicotinic acid (ER-NA)/laropiprant (LRPT) (1000/20 mg/day for the first 4 weeks followed by 2000/40 mg/day for the next 8 weeks) or to add-on-statin micronized fenofibrate (200 mg/day) for a total of 3 months." | 9.19 | Effect of switch to the highest dose of rosuvastatin versus add-on-statin fenofibrate versus add-on-statin nicotinic acid/laropiprant on oxidative stress markers in patients with mixed dyslipidemia. ( Elisaf, M; Kei, A; Liberopoulos, E; Tellis, C; Tselepis, A, 2014) |
| "Extended-release niacin (ERN) improves multiple lipid parameters but is underused owing to niacin-induced flushing (NIF)." | 9.16 | Effectiveness and safety of laropiprant on niacin-induced flushing. ( Anderson, JW; Bays, HE; Chen, F; Kher, U; Maccubbin, DL; McCrary Sisk, C; Mitchel, YB; Olsson, AG; Sirah, W, 2012) |
| "To test the safety, tolerance, and efficacy of extended-release niacin monotherapy on dyslipidemia in persons with chronic tetraplegia." | 9.15 | Safety, tolerance, and efficacy of extended-release niacin monotherapy for treating dyslipidemia risks in persons with chronic tetraplegia: a randomized multicenter controlled trial. ( Bauman, WA; Dyson-Hudson, TA; Lewis, JE; Mendez, AJ; Nash, MS; Spungen, AM; Szlachcic, Y; Yee, F, 2011) |
| "A combination of fenofibrate and niacin with low-saturated-fat D/E is effective and safe in increasing HDL-C, decreasing non-HDL-C and hypertriglyceridemia, and ameliorating hypoadiponectinemia in patients with HIV/ART-associated dyslipidemia." | 9.15 | Combination of niacin and fenofibrate with lifestyle changes improves dyslipidemia and hypoadiponectinemia in HIV patients on antiretroviral therapy: results of "heart positive," a randomized, controlled trial. ( Balasubramanyam, A; Ballantyne, CM; Clark, P; Coraza, I; Cuevas-Sanchez, E; Giordano, TP; Iyer, D; Kamble, S; Patel, P; Pownall, HJ; Scott, LW; Sekhar, RV; Smith, EO; Taylor, AA, 2011) |
| "To assess the effect of niacin alone on erectile function in patients suffering from both ED and dyslipidemia." | 9.15 | Effect of niacin on erectile function in men suffering erectile dysfunction and dyslipidemia. ( Ho, AL; Lee, CP; Lee, VW; Ng, CF, 2011) |
| "A common adverse effect of niacin therapy is flushing, manifested by cutaneous warmth, redness, itching and/or tingling." | 9.14 | Flushing ASsessment Tool (FAST): psychometric properties of a new measure assessing flushing symptoms and clinical impact of niacin therapy. ( Davidson, MH; Jiang, P; Kawata, AK; Krause, S; Padley, RJ; Punzi, HA; Revicki, DA; Thakkar, R, 2009) |
| "Niacin extended-release (NER) is safe and effective for treatment of dyslipidemia." | 9.14 | Acetylsalicylic acid reduces niacin extended-release-induced flushing in patients with dyslipidemia. ( Jiang, P; Kashyap, ML; Krause, SL; Lewin, AJ; Padley, RJ; Thakkar, RB, 2009) |
| "Niacin has beneficial effects on a patient's lipid and lipoprotein profiles and cardiovascular risk, particularly at doses >2 g/day, but is underused due to flushing." | 9.14 | Flushing profile of extended-release niacin/laropiprant versus gradually titrated niacin extended-release in patients with dyslipidemia with and without ischemic cardiovascular disease. ( Davidson, M; Gavish, D; Koren, MJ; Maccubbin, D; Macdonell, G; Mallick, M; Mitchel, Y; Paolini, JF; Pasternak, RC; Sisk, CM, 2009) |
| "Niacin is underutilized due to flushing, which occurs in over 90% of niacin-treated patients." | 9.14 | Flushing profile of extended-release niacin/laropiprant at initiation of therapy in Asian lipid clinic patients. ( Chen, E; Hu, DY; Kim, HS; Kush, D; Maccubbin, D; McCrary Sisk, C; Paolini, JF; Sirah, W; Ye, P, 2009) |
| "The aim of this study was to evaluate the effects of low-dose niacin extended-release (niacin-ER) combined with simvastatin (SV) in the treatment of patients with mixed dyslipidemia who have not normalized their lipid profile with statin therapy alone." | 9.14 | Effects of low-dose of niacin associated to simvastatin in the treatment of mixed dyslipidemia Salgad. ( Casulari, LA; Dos Santos, AM; Salgado, BJ; Salgado, JV, 2010) |
| "The OCEANS study (Open-label evaluation of the safety and efficacy of a Combination of niacin ER and simvAstatin in patieNts with dySlipidemia; ClinicalTrials." | 9.13 | Long-term safety and efficacy of a combination of niacin extended release and simvastatin in patients with dyslipidemia: the OCEANS study. ( Bajorunas, DR; Davidson, MH; Karas, RH; Kashyap, ML; Keller, LH; Knopp, RH, 2008) |
| "Niacin was the first drug demonstrating lowered cholesterol prevents coronary heart disease (CHD) events, with two clinical CHD outcome studies establishing a cardioprotective niacin regimen: 1 g thrice daily with meals." | 8.93 | Niacin Alternatives for Dyslipidemia: Fool's Gold or Gold Mine? Part I: Alternative Niacin Regimens. ( Dunbar, RL; Goel, H, 2016) |
| "We report the case of a 63-year-old obese man with a rapid-onset of widespread acanthosis nigricans (AN) in the setting of having recently initiated treatment with niacin for dyslipidemia." | 8.87 | Acanthosis nigricans in the setting of niacin therapy. ( Defelice, T; Hartman, R; Meehan, S; Sanchez, M; Tzu, J, 2011) |
| "The triple combination therapy of simvastatin/ER niacin/laropiprant may reduce flushing side effects and facilitate a more comprehensive treatment for patients with mixed dyslipidemia." | 8.86 | A new paradigm for managing dyslipidemia with combination therapy: laropiprant + niacin + simvastatin. ( Cheung, BM; Tse, HF; Yiu, KH, 2010) |
| "Niacin is the most effective lipid-modifying agent for raising high-density lipoprotein cholesterol levels, but it also causes cutaneous vasodilation with flushing." | 8.86 | A "hot" topic in dyslipidemia management--"how to beat a flush": optimizing niacin tolerability to promote long-term treatment adherence and coronary disease prevention. ( Jacobson, TA, 2010) |
| "The reader will gain knowledge of the development of niacin as an antiatherosclerosis treatment and of the added value that laropiprant may offer this treatment principle; and also the present place of niacin/laropiprant in the armamentarium of cardiovascular preventive drugs." | 8.86 | Laropiprant plus niacin for dyslipidemia and prevention of cardiovascular disease. ( Olsson, AG, 2010) |
| "To summarise the metabolic responses to niacin that can lead to flushing and to critically evaluate flushing mitigation research." | 8.85 | The mechanism and mitigation of niacin-induced flushing. ( Ganji, SH; Kamanna, VS; Kashyap, ML, 2009) |
| "Niacin, or nicotinic acid, has established efficacy for the treatment of dyslipidemia, but the clinical use of niacin has been limited by cutaneous flushing, a well-recognized associated adverse effect." | 8.84 | Niacin use and cutaneous flushing: mechanisms and strategies for prevention. ( Davidson, MH, 2008) |
| "Niacin (nicotinic acid), the most effective available pharmacotherapy for increasing high-density lipoprotein cholesterol, also lowers triglycerides and hence may be useful, alone or in combination with hydroxymethylglutaryl coenzyme A reductase inhibitors (statins), to offset residual cardiovascular risk in patients with mixed or diabetic dyslipidemia." | 8.84 | Effects of niacin on glucose control in patients with dyslipidemia. ( Goldberg, RB; Jacobson, TA, 2008) |
| "Niacin has been widely used as an antihyperlipidemic drug, but the flushing effect restricted its clinical application." | 7.96 | Discovery of a novel niacin-lipoic acid dimer N2L attenuating atherosclerosis and dyslipidemia with non-flushing effects. ( Cai, W; Chen, J; Jiang, Y; Jin, M; Liu, P; Pi, R; Yan, J; Yao, M, 2020) |
| "Cutaneous flushing with niacin varies between individuals and is substantially reduced by concomitant laropiprant." | 7.81 | Pharmacogenetics of cutaneous flushing response to niacin/laropiprant combination in Hong Kong Chinese patients with dyslipidemia. ( Chan, P; Hu, M; Tomlinson, B; Yang, YL, 2015) |
| "Data were pooled from eight NER studies (administered as NER with a maximum dosage of 1000, 1500, and 2000 mg/day, either as monotherapy or in combination with simvastatin 20 or 40 mg/day [NER/S], or lovastatin 20 or 40 mg/day [NER/L]) to evaluate rates of study discontinuation due to flushing or any treatment-related adverse events." | 7.77 | Niacin extended-release therapy in phase III clinical trials is associated with relatively low rates of drug discontinuation due to flushing and treatment-related adverse events: a pooled analysis. ( Brinton, EA; Jiang, P; Kashyap, ML; Padley, RJ; Thakkar, RB; Vo, AN, 2011) |
| "The use of niacin to improve plasma lipid levels and reduce risk of myocardial infarction is limited by noxious skin effects that result from stimulation of G protein-coupled receptor 109A (GPR109A) in skin immune cells." | 7.76 | Seeing red: flushing out instigators of niacin-associated skin toxicity. ( Dunbar, RL; Gelfand, JM, 2010) |
| "The most common challenge during niacin treatment is flushing, although it typically decreases with ongoing use and can be ameliorated by pretreatment with aspirin and counseling by the prescriber." | 6.48 | Combination treatment with atorvastatin plus niacin provides effective control of complex dyslipidemias: a literature review. ( McKenney, JM, 2012) |
| "Treatment with niacin effectively improves multiple lipid parameters and cardiovascular outcomes." | 6.44 | Extended-release niacin/laropiprant: reducing niacin-induced flushing to better realize the benefit of niacin in improving cardiovascular risk factors. ( Ballantyne, CM; Bays, HE; Davidson, M; Kuznetsova, O; Lai, E; Maccubbin, D; Mitchel, YB; Norquist, JM; Paolini, JF; Pasternak, R; Sisk, CM; Waters, MG, 2008) |
| "Dyslipidemia is a major risk factor in the initiation and progression of cardiovascular diseases such as atherosclerosis." | 6.44 | Targeting multiple dyslipidemias with fixed combinations--focus on extended release niacin and simvastatin. ( Arora, A; Khan, BV; Pandian, A; Sperling, LS, 2008) |
| "Thus, the long-term treatment of dyslipidemias with these two agents may help to modify risk and reduce cardiovascular morbidity and mortality in these patients over and above benefits achieved by lowering blood pressure." | 6.43 | Niacin-ER/statin combination for the treatment of dyslipidemia: focus on low high-density lipoprotein cholesterol. ( Chrysant, SG; Ibrahim, M, 2006) |
| "We assumed that adding the niacin to the medication in patients with type 2 diabetes would reduce dyslipidemia and achieve target lipid levels." | 5.41 | The efficacy of niacin supplementation in type 2 diabetes patients: Study protocol of a randomized controlled trial. ( Wang, S; Yan, X, 2021) |
| "Niacin has profound and unique effects on lipid metabolism." | 5.36 | Niacin as potential treatment for dyslipidemia and hyperphosphatemia associated with chronic renal failure: the need for clinical trials. ( Ahmed, MH, 2010) |
| "Niacin is an effective drug for raising HDL cholesterol and reducing coronary risks, but patients show low compliance with treatment due to severe facial flushing upon taking the drug." | 5.35 | Pyrazole acids as niacin receptor agonists for the treatment of dyslipidemia. ( Blom, D; Carballo-Jane, E; Cheng, K; Ciecko, T; Colletti, S; Gerard Waters, M; Holt, TG; Krsmanovic, M; Lubell, S; McCann, PE; Raghavan, S; Ren, N; Schmidt, D; Smenton, A; Taggart, A; Tata, J; Wilsie, L; Wolff, M, 2009) |
| "GPR109A (HM74A), a G-protein-coupled receptor, is hypothesized to mediate lipid and lipoprotein changes and dermal flushing associated with niacin administration." | 5.30 | A Randomized, Placebo-Controlled Trial to Assess the Effects of 8 Weeks of Administration of GSK256073, a Selective GPR109A Agonist, on High-Density Lipoprotein Cholesterol in Subjects With Dyslipidemia. ( de Gouville, AC; Fossler, MJ; Gao, F; Haws, TF; Lepore, JJ; Mahar, KM; Olson, EJ; Sprecher, DL, 2019) |
| "To assess the effects of anacetrapib added to statin ± other lipid-modifying therapies in patients with hypercholesterolemia and not at their low-density lipoprotein cholesterol (LDL-C) goal (as per National Cholesterol Education Program Adult Treatment Panel III [NCEP ATP III] guidelines) and in those with low high-density lipoprotein cholesterol (HDL-C)." | 5.24 | Lipid-Modifying Efficacy and Tolerability of Anacetrapib Added to Ongoing Statin Therapy in Patients with Hypercholesterolemia or Low High-Density Lipoprotein Cholesterol. ( Ashraf, TB; Ballantyne, CM; Cressman, MD; Gill, GG; Hunter, JA; Johnson-Levonas, AO; Kher, U; Mitchel, YB; Shah, S, 2017) |
| "Although the pharmacological effect of niacin in lowering blood cholesterol and triglyceride levels has been demonstrated in several clinical studies, information regarding the effect of dietary niacin intake is uncertain, and the longitudinal association between dietary niacin intake and the risk of dyslipidemia has not been adequately studied." | 5.22 | Dietary niacin intake and risk of dyslipidemia: A pooled analysis of three prospective cohort studies. ( Kim, C; Park, K, 2022) |
| "This study examined whether the increase of adiponectin associated with extended-release (ER) niacin/laropiprant combination attenuates the adverse effect of niacin on glucose and insulin resistance in Hong Kong Chinese patients with dyslipidaemia." | 5.20 | Effect of Extended-Release Niacin/Laropiprant Combination on Plasma Adiponectin and Insulin Resistance in Chinese Patients with Dyslipidaemia. ( Hu, M; Masuda, D; Tomlinson, B; Yamashita, S; Yang, YL, 2015) |
| " Patients (N = 100) with mixed dyslipidemia on a standard statin dose (10-40 mg simvastatin or 10-20 mg atorvastatin or 5-10 mg rosuvastatin) who had not achieved lipid targets were randomized to switch to the highest dose of rosuvastatin (40 mg/day) or to add-on-statin extended release nicotinic acid (ER-NA)/laropiprant (LRPT) (1000/20 mg/day for the first 4 weeks followed by 2000/40 mg/day for the next 8 weeks) or to add-on-statin micronized fenofibrate (200 mg/day) for a total of 3 months." | 5.19 | Effect of switch to the highest dose of rosuvastatin versus add-on-statin fenofibrate versus add-on-statin nicotinic acid/laropiprant on oxidative stress markers in patients with mixed dyslipidemia. ( Elisaf, M; Kei, A; Liberopoulos, E; Tellis, C; Tselepis, A, 2014) |
| " In a randomized controlled trial of patients with dyslipidemia assigned to either extended release niacin (ERN) alone, ERN combined with the selective prostaglandin D2 receptor subtype 1 inhibitor laropiprant (ERN-L) or placebo, niacin lowered serum phosphorus; however, it is not known if it lowers FGF23 concentrations." | 5.19 | Effect of niacin on FGF23 concentration in chronic kidney disease. ( Bostom, A; Ix, JH; Rao, M; Steffes, M, 2014) |
| " In this study, mixed dyslipidemia patients (n = 100) inadequately controlled with a standard statin dose were randomized to switch to 40 mg of rosuvastatin or add-on extended release nicotinic acid/laropiprant (ER-NA/LRPT) or add-on fenofibrate." | 5.17 | Lipid-modulating treatments for mixed dyslipidemia increase HDL-associated phospholipase A2 activity with differential effects on HDL subfractions. ( Elisaf, M; Kei, A; Liberopoulos, E; Tellis, C; Tselepis, A, 2013) |
| "The purpose of this research was to compare the effects of niacin extended-release in combination with simvastatin (NER/S) versus atorvastatin monotherapy on high-density lipoprotein (HDL) particle number and size in patients with hyperlipidemia or dyslipidemia from the SUPREME study." | 5.16 | Niacin extended-release/simvastatin combination therapy produces larger favorable changes in high-density lipoprotein particles than atorvastatin monotherapy. ( Jiang, P; Padley, RJ; Thakker, KM; Toth, PP, 2012) |
| "Extended-release niacin (ERN) improves multiple lipid parameters but is underused owing to niacin-induced flushing (NIF)." | 5.16 | Effectiveness and safety of laropiprant on niacin-induced flushing. ( Anderson, JW; Bays, HE; Chen, F; Kher, U; Maccubbin, DL; McCrary Sisk, C; Mitchel, YB; Olsson, AG; Sirah, W, 2012) |
| " We studied lean (n = 6) and overweight and obese (n = 5) subjects during continuous feeding on two occasions: during intravenous infusion of niacin (2." | 5.16 | Intravenous niacin acutely improves the efficiency of dietary fat storage in lean and obese humans. ( Miles, JM; Nelson, RH; Smailovic, A; Vlazny, D, 2012) |
| "To test the safety, tolerance, and efficacy of extended-release niacin monotherapy on dyslipidemia in persons with chronic tetraplegia." | 5.15 | Safety, tolerance, and efficacy of extended-release niacin monotherapy for treating dyslipidemia risks in persons with chronic tetraplegia: a randomized multicenter controlled trial. ( Bauman, WA; Dyson-Hudson, TA; Lewis, JE; Mendez, AJ; Nash, MS; Spungen, AM; Szlachcic, Y; Yee, F, 2011) |
| "In patients with primary hypercholesterolemia or mixed dyslipidemia, extended-release niacin/laropiprant (ERN/LRPT) improves key lipid parameters associated with increased atherosclerotic coronary heart disease (CHD) risk." | 5.15 | Extended-release niacin/laropiprant lipid-altering consistency across patient subgroups. ( Bays, H; Dong, Q; Maccubbin, D; McCrary Sisk, C; Shah, A, 2011) |
| "A combination of fenofibrate and niacin with low-saturated-fat D/E is effective and safe in increasing HDL-C, decreasing non-HDL-C and hypertriglyceridemia, and ameliorating hypoadiponectinemia in patients with HIV/ART-associated dyslipidemia." | 5.15 | Combination of niacin and fenofibrate with lifestyle changes improves dyslipidemia and hypoadiponectinemia in HIV patients on antiretroviral therapy: results of "heart positive," a randomized, controlled trial. ( Balasubramanyam, A; Ballantyne, CM; Clark, P; Coraza, I; Cuevas-Sanchez, E; Giordano, TP; Iyer, D; Kamble, S; Patel, P; Pownall, HJ; Scott, LW; Sekhar, RV; Smith, EO; Taylor, AA, 2011) |
| "To assess the effect of niacin alone on erectile function in patients suffering from both ED and dyslipidemia." | 5.15 | Effect of niacin on erectile function in men suffering erectile dysfunction and dyslipidemia. ( Ho, AL; Lee, CP; Lee, VW; Ng, CF, 2011) |
| "A common adverse effect of niacin therapy is flushing, manifested by cutaneous warmth, redness, itching and/or tingling." | 5.14 | Flushing ASsessment Tool (FAST): psychometric properties of a new measure assessing flushing symptoms and clinical impact of niacin therapy. ( Davidson, MH; Jiang, P; Kawata, AK; Krause, S; Padley, RJ; Punzi, HA; Revicki, DA; Thakkar, R, 2009) |
| "Niacin extended-release (NER) is safe and effective for treatment of dyslipidemia." | 5.14 | Acetylsalicylic acid reduces niacin extended-release-induced flushing in patients with dyslipidemia. ( Jiang, P; Kashyap, ML; Krause, SL; Lewin, AJ; Padley, RJ; Thakkar, RB, 2009) |
| "Niacin has beneficial effects on a patient's lipid and lipoprotein profiles and cardiovascular risk, particularly at doses >2 g/day, but is underused due to flushing." | 5.14 | Flushing profile of extended-release niacin/laropiprant versus gradually titrated niacin extended-release in patients with dyslipidemia with and without ischemic cardiovascular disease. ( Davidson, M; Gavish, D; Koren, MJ; Maccubbin, D; Macdonell, G; Mallick, M; Mitchel, Y; Paolini, JF; Pasternak, RC; Sisk, CM, 2009) |
| "Niacin is underutilized due to flushing, which occurs in over 90% of niacin-treated patients." | 5.14 | Flushing profile of extended-release niacin/laropiprant at initiation of therapy in Asian lipid clinic patients. ( Chen, E; Hu, DY; Kim, HS; Kush, D; Maccubbin, D; McCrary Sisk, C; Paolini, JF; Sirah, W; Ye, P, 2009) |
| "We performed a post hoc data analysis of serum phosphorus concentrations that had been determined serially (at baseline and weeks 4, 8, 12, 18, and 24) among 1547 patients who had dyslipidemia and were randomly assigned in a 3:2:1 ratio to treatment with extended release niacin (ERN; 1 g/d for 4 weeks and dose advanced to 2 g/d for 20 weeks) combined with the selective prostaglandin D2 receptor subtype 1 inhibitor laropiprant (L; n = 761), ERN alone (n = 518), or placebo (n = 268)." | 5.14 | Hypophosphatemic effect of niacin in patients without renal failure: a randomized trial. ( Bostom, AG; Hanlon, WA; Kuznetsova, O; Maccubbin, D; Tipping, D, 2010) |
| "The aim of this study was to evaluate the effects of low-dose niacin extended-release (niacin-ER) combined with simvastatin (SV) in the treatment of patients with mixed dyslipidemia who have not normalized their lipid profile with statin therapy alone." | 5.14 | Effects of low-dose of niacin associated to simvastatin in the treatment of mixed dyslipidemia Salgad. ( Casulari, LA; Dos Santos, AM; Salgado, BJ; Salgado, JV, 2010) |
| "To compare the effects of combination niacin extended-release + simvastatin (NER/S) versus atorvastatin alone on apolipoproteins and lipid fractions in a post hoc analysis from SUPREME, a study which compared the lipid effects of niacin extended-release + simvastatin and atorvastatin in patients with hyperlipidemia or mixed dyslipidemia." | 5.14 | Combination of niacin extended-release and simvastatin results in a less atherogenic lipid profile than atorvastatin monotherapy. ( Insull, W; Jiang, P; Krause, S; Padley, RJ; Parreno, RA; Superko, HR; Thakkar, RB; Toth, PP, 2010) |
| "Niacin (nicotinic acid) is not optimally used mainly because of flushing, a process mediated primarily by prostaglandin D(2), which leads to poor patient compliance and suboptimal dosing." | 5.13 | Effects of laropiprant on nicotinic acid-induced flushing in patients with dyslipidemia. ( Ballantyne, CM; Bays, HE; Davidson, M; Kher, U; Lai, E; Meehan, AG; Mitchel, YB; Norquist, JM; Paolini, JF; Reyes, R; Watson, DJ, 2008) |
| "The OCEANS study (Open-label evaluation of the safety and efficacy of a Combination of niacin ER and simvAstatin in patieNts with dySlipidemia; ClinicalTrials." | 5.13 | Long-term safety and efficacy of a combination of niacin extended release and simvastatin in patients with dyslipidemia: the OCEANS study. ( Bajorunas, DR; Davidson, MH; Karas, RH; Kashyap, ML; Keller, LH; Knopp, RH, 2008) |
| "Niacin was the first drug demonstrating lowered cholesterol prevents coronary heart disease (CHD) events, with two clinical CHD outcome studies establishing a cardioprotective niacin regimen: 1 g thrice daily with meals." | 4.93 | Niacin Alternatives for Dyslipidemia: Fool's Gold or Gold Mine? Part I: Alternative Niacin Regimens. ( Dunbar, RL; Goel, H, 2016) |
| "The use of FDA-approved niacin (nicotinic acid or vitamin B3) formulations at therapeutic doses, alone or in combination with statins or other lipid therapies, is safe, improves multiple lipid parameters, and reduces atherosclerosis progression." | 4.88 | Niacin: the evidence, clinical use, and future directions. ( Gore, RS; Kim, AS; Taylor, AJ; Villines, TC, 2012) |
| "Niacin is one of the oldest drugs used in the treatment of dyslipidemia." | 4.88 | Safety and tolerability of extended-release niacin with laropiprant. ( Ammori, BJ; Issa, B; Kwok, S; Soran, H; Yadav, R, 2012) |
| " This article focuses on optimizing treatment of atherogenic dyslipidemias involving this lipid triad, emphasizing niacin-based or fibrate-based therapies." | 4.87 | Optimal pharmacotherapy to combat the atherogenic lipid triad. ( Chapman, MJ; Giral, P; McGovern, ME; Redfern, JS, 2011) |
| "We report the case of a 63-year-old obese man with a rapid-onset of widespread acanthosis nigricans (AN) in the setting of having recently initiated treatment with niacin for dyslipidemia." | 4.87 | Acanthosis nigricans in the setting of niacin therapy. ( Defelice, T; Hartman, R; Meehan, S; Sanchez, M; Tzu, J, 2011) |
| "The triple combination therapy of simvastatin/ER niacin/laropiprant may reduce flushing side effects and facilitate a more comprehensive treatment for patients with mixed dyslipidemia." | 4.86 | A new paradigm for managing dyslipidemia with combination therapy: laropiprant + niacin + simvastatin. ( Cheung, BM; Tse, HF; Yiu, KH, 2010) |
| "Niacin is the most effective lipid-modifying agent for raising high-density lipoprotein cholesterol levels, but it also causes cutaneous vasodilation with flushing." | 4.86 | A "hot" topic in dyslipidemia management--"how to beat a flush": optimizing niacin tolerability to promote long-term treatment adherence and coronary disease prevention. ( Jacobson, TA, 2010) |
| "The reader will gain knowledge of the development of niacin as an antiatherosclerosis treatment and of the added value that laropiprant may offer this treatment principle; and also the present place of niacin/laropiprant in the armamentarium of cardiovascular preventive drugs." | 4.86 | Laropiprant plus niacin for dyslipidemia and prevention of cardiovascular disease. ( Olsson, AG, 2010) |
| "Oral fixed-dose niacin extended release/simvastatin is associated with clinically relevant improvements in plasma lipid profiles, including lowering of non-high-density lipoprotein cholesterol levels, relative to simvastatin monotherapy in patients with mixed dyslipidemias who had not responded fully to simvastatin monotherapy, and is generally well tolerated." | 4.86 | Niacin extended release (ER)/simvastatin (Simcor®): a guide to its use in lipid regulation. ( Lyseng-Williamson, KA, 2010) |
| "Niacin has long been used in the treatment of dyslipidemia and cardiovascular disease." | 4.85 | Niacin: an old drug rejuvenated. ( Ganji, SH; Kamanna, VS; Kashyap, ML, 2009) |
| "To summarise the metabolic responses to niacin that can lead to flushing and to critically evaluate flushing mitigation research." | 4.85 | The mechanism and mitigation of niacin-induced flushing. ( Ganji, SH; Kamanna, VS; Kashyap, ML, 2009) |
| " As a result of new data, guidelines have begun to focus on non-HDL-cholesterol, HDL-cholesterol and triglycerides as treatment targets, with the end result being a recommendation for combination therapy, such as niacin plus statin for the treatment of dyslipidemia." | 4.84 | Fixed-dose combination of extended-release niacin plus simvastatin for lipid disorders. ( Kashyap, ML; Vo, AN, 2008) |
| "Niacin, or nicotinic acid, has established efficacy for the treatment of dyslipidemia, but the clinical use of niacin has been limited by cutaneous flushing, a well-recognized associated adverse effect." | 4.84 | Niacin use and cutaneous flushing: mechanisms and strategies for prevention. ( Davidson, MH, 2008) |
| "Niacin (nicotinic acid), the most effective available pharmacotherapy for increasing high-density lipoprotein cholesterol, also lowers triglycerides and hence may be useful, alone or in combination with hydroxymethylglutaryl coenzyme A reductase inhibitors (statins), to offset residual cardiovascular risk in patients with mixed or diabetic dyslipidemia." | 4.84 | Effects of niacin on glucose control in patients with dyslipidemia. ( Goldberg, RB; Jacobson, TA, 2008) |
| "Niacin has been widely used as an antihyperlipidemic drug, but the flushing effect restricted its clinical application." | 3.96 | Discovery of a novel niacin-lipoic acid dimer N2L attenuating atherosclerosis and dyslipidemia with non-flushing effects. ( Cai, W; Chen, J; Jiang, Y; Jin, M; Liu, P; Pi, R; Yan, J; Yao, M, 2020) |
| "Cutaneous flushing with niacin varies between individuals and is substantially reduced by concomitant laropiprant." | 3.81 | Pharmacogenetics of cutaneous flushing response to niacin/laropiprant combination in Hong Kong Chinese patients with dyslipidemia. ( Chan, P; Hu, M; Tomlinson, B; Yang, YL, 2015) |
| "Data were pooled from eight NER studies (administered as NER with a maximum dosage of 1000, 1500, and 2000 mg/day, either as monotherapy or in combination with simvastatin 20 or 40 mg/day [NER/S], or lovastatin 20 or 40 mg/day [NER/L]) to evaluate rates of study discontinuation due to flushing or any treatment-related adverse events." | 3.77 | Niacin extended-release therapy in phase III clinical trials is associated with relatively low rates of drug discontinuation due to flushing and treatment-related adverse events: a pooled analysis. ( Brinton, EA; Jiang, P; Kashyap, ML; Padley, RJ; Thakkar, RB; Vo, AN, 2011) |
| "To examine the effects of treatments with niacin or anacetrapib (an inhibitor of cholesteryl ester transfer protein) on the ability of high-density lipoprotein (HDL) to promote net cholesterol efflux and reduce toll-like receptor-mediated inflammation in macrophages." | 3.76 | Cholesterol efflux potential and antiinflammatory properties of high-density lipoprotein after treatment with niacin or anacetrapib. ( Fisher, T; Hubbard, B; Kling, J; Li, H; Pagler, T; Sparrow, CP; Taggart, AK; Tall, AR; Yvan-Charvet, L, 2010) |
| "Statin treatment (and possibly niacin when given alone or in combination with statins) appears to be associated with a slightly increased risk of new onset diabetes mellitus (NODM)." | 3.76 | Lipid-lowering agents and new onset diabetes mellitus. ( Athyros, VG; Karagiannis, A; Mikhailidis, DP; Tziomalos, K, 2010) |
| "The use of niacin to improve plasma lipid levels and reduce risk of myocardial infarction is limited by noxious skin effects that result from stimulation of G protein-coupled receptor 109A (GPR109A) in skin immune cells." | 3.76 | Seeing red: flushing out instigators of niacin-associated skin toxicity. ( Dunbar, RL; Gelfand, JM, 2010) |
| "Combination of statins with niacin appears to be an attractive association, in the presence of mixed dyslipidemia with low HDL-c levels, when monotherapy is insufficient to achieve target lipid levels." | 3.73 | [Drug combinations: statins and niacin]. ( Borges, JL, 2005) |
| " The statins can be used alone, or in combination with a bile acid sequestrant, ezetimibe, or niacin in patients with mixed dyslipidemias." | 3.72 | Achieving cholesterol goals. Current and future drug therapies. ( Jones, PH, 2003) |
| " However, the trial also identified previously unrecognized serious adverse effects (including new-onset diabetes, bleeding, and infection)." | 2.90 | Serious Adverse Effects of Extended-release Niacin/Laropiprant: Results From the Heart Protection Study 2-Treatment of HDL to Reduce the Incidence of Vascular Events (HPS2-THRIVE) Trial. ( Armitage, J; Chen, F; Haynes, R; Hopewell, JC; Landray, MJ; Li, J; Parish, S; Valdes-Marquez, E, 2019) |
| "Extended-release niacin with laropiprant did not significantly reduce the risk of major vascular events and increased the risk of serious adverse events in Heart Protection Study 2-Treatment of HDL to Reduce the Incidence of Vascular Events (HPS2-THRIVE), but its net effects on health and healthcare costs are unknown." | 2.82 | Effects of Vascular and Nonvascular Adverse Events and of Extended-Release Niacin With Laropiprant on Health and Healthcare Costs. ( Armitage, J; Collins, R; Gray, A; Haynes, R; Hopewell, JC; Kent, S; Landray, MJ; Mihaylova, B; Parish, S, 2016) |
| "In statin-treated men with type 2 diabetes mellitus, ERN decreased plasma Lp(a) concentrations by decreasing the production of apo(a) and Lp(a)-apoB-100." | 2.80 | Effects of extended-release niacin on the postprandial metabolism of Lp(a) and ApoB-100-containing lipoproteins in statin-treated men with type 2 diabetes mellitus. ( Barrett, PH; Chan, DC; Hamilton, SJ; Marcovina, SM; McCormick, SP; Ooi, EM; Pang, J; Tenneti, VS; Watts, GF, 2015) |
| "Twelve men with type 2 diabetes mellitus were recruited for a randomized, crossover design trial." | 2.79 | Effect of niacin on high-density lipoprotein apolipoprotein A-I kinetics in statin-treated patients with type 2 diabetes mellitus. ( Barrett, PH; Chan, DC; Hamilton, SJ; Pang, J; Tenneti, VS; Watts, GF, 2014) |
| "Nicotinic acid (NA) is used for treatment of dyslipidemias, and the lowering effect of NA on Lp(a) has been previously reported." | 2.79 | Effect of Nicotinic acid/Laropiprant in the lipoprotein(a) concentration with regard to baseline lipoprotein(a) concentration and LPA genotype. ( Bea, AM; Calmarza, P; Cenarro, A; Civeira, F; Ferrando, J; Jarauta, E; Mateo-Gallego, R; Puzo, J, 2014) |
| "placebo on the incidence of new onset type 2 diabetes mellitus (T2DM) and cardiovascular event rates in patients with normal and impaired fasting glucose (IFG)." | 2.78 | Effects of niacin on the incidence of new onset diabetes and cardiovascular events in patients with normoglycaemia and impaired fasting glucose. ( Canner, PL; Maccubbin, D; Sazonov, V; Sisk, CM, 2013) |
| "Nicotinic acid is an effective treatment for dyslipidemia." | 2.76 | Efficacy and tolerability of a new extended-release formulation of nicotinic acid in Korean adults with mixed dyslipidemia: an 8-week, multicenter, prospective, randomized, double-blind, and placebo-controlled trial. ( Kang, HJ; Kim, HS; Kim, MK; Kim, SH; Kim, YJ; Lee, HY; Park, BJ, 2011) |
| " Treatment-related adverse experiences (AEs) related to flushing, pruritis, rash, gastrointestinal upset and elevations in liver transaminases and fasting serum glucose occurred more frequently with ERN/LRPT added to statin vs." | 2.75 | Efficacy and safety of extended-release niacin/laropiprant plus statin vs. doubling the dose of statin in patients with primary hypercholesterolaemia or mixed dyslipidaemia. ( Ceska, R; Giezek, H; Gil-Extremera, B; Maccubbin, D; Mao, A; McCrary Sisk, C; Paolini, JF; Shah, S; Vandormael, K, 2010) |
| "Niacin has complementary lipid-modifying efficacy to statins and cardiovascular benefit, but is underutilised because of flushing, mediated primarily by prostaglandin D(2) (PGD(2))." | 2.73 | Lipid-modifying efficacy and tolerability of extended-release niacin/laropiprant in patients with primary hypercholesterolaemia or mixed dyslipidaemia. ( Bays, HE; Betteridge, A; Elinoff, V; Elis, A; Kuznetsova, O; Maccubbin, D; Mitchel, Y; Olsson, AG; Paolini, JF; Pasternak, RC; Reyes, R; Sirah, W; Sisk, CM; Yu, Q, 2008) |
| "The main objective was to evaluate the safety and tolerability of prolonged-release nicotinic acid [incidence of adverse events (AE) and serious AE] in the overall population (the safety population)." | 2.72 | Evaluation of the safety and tolerability of prolonged-release nicotinic acid in a usual care setting: the NAUTILUS study. ( Hostalek, U; Kassner, U; Steinhagen-Thiessen, E; Vogt, A, 2006) |
| " Blood samples for pharmacokinetic analysis were obtained immediately before and up to 72 hours after administration during each of the 4 treatment periods." | 2.72 | An open-label, crossover study of the pharmacokinetics of Insoluble Drug Delivery-MicroParticle fenofibrate in combination with atorvastatin, simvastatin, and extended-release niacin in healthy volunteers. ( Braun, SL; Guha-Ray, DK; Penn, R; Rains, KT; Sawyers, WG; Williams, RX, 2006) |
| "Niacin was well-tolerated." | 2.72 | Safety and efficacy of extended-release niacin for the treatment of dyslipidaemia in patients with HIV infection: AIDS Clinical Trials Group Study A5148. ( Aberg, JA; Alston-Smith, BL; Deeg, MA; Dubé, MP; Greenwald, M; Lee, D; Martinez, AI; McGovern, ME; Shriver, SL; Stein, JH; Wu, JW, 2006) |
| " Thirteen patients (10%) were lost to follow-up and 4 (3%) withdrew because of dermatological adverse effects: flushing, pruritus, and rash." | 2.72 | Evaluation of efficacy and safety of fixed dose lovastatin and niacin(ER) combination in asian Indian dyslipidemic patients: a multicentric study. ( Gupta, R; Hira, HS; Kumar, N; Mohan, B; Panwar, RB; Sharma, DR; Sharma, M; Sharma, SK; Singh, V, 2006) |
| "Nephrotic syndrome is a highly prevalent disease that is associated with high morbidity despite notable advances in its treatment." | 2.58 | Dyslipidaemia in nephrotic syndrome: mechanisms and treatment. ( Agrawal, S; Fornoni, A; Smoyer, WE; Zaritsky, JJ, 2018) |
| "The armamentarium for the treatment of dyslipidemia today comprises six different modes of action with overall around 24 different drugs." | 2.53 | Antilipidemic Drug Therapy Today and in the Future. ( Kramer, W, 2016) |
| "Niacin therapy was associated with a RR of 1." | 2.53 | Niacin therapy and the risk of new-onset diabetes: a meta-analysis of randomised controlled trials. ( Goldie, C; McCoy, C; Nguyen, P; Preiss, D; Taylor, AJ; Zhao, XQ, 2016) |
| "Niacin is an important vitamin (B3) that can be used in gram doses to positively modify pathogenetically relevant lipid disorders: elevated LDL cholesterol, elevated non-HDL cholesterol, elevated triglycerides, elevated lipoprotein(a), and reduced HDL cholesterol." | 2.52 | Niacin as antidyslipidemic drug. ( Julius, U, 2015) |
| "Niacin also has been found to reduce inflammatory markers like C-reactive protein (CRP) and lipoprotein-associated phospholipase-A2 (Lp-PLA2) and to decrease small-dense LDL and increase large-particle LDL, all potentially anti-atherosclerotic properties." | 2.49 | The role of niacin in lipid-lowering treatment: are we aiming too high? ( Berthold, HK; Gouni-Berthold, I, 2013) |
| "Niacin has been used for more than 50 years in the treatment of cardiovascular disease, although its use has largely been superseded by better-tolerated lipid-modulating interventions." | 2.48 | Niacin in cardiovascular disease: recent preclinical and clinical developments. ( Choudhury, RP; Digby, JE; Ruparelia, N, 2012) |
| "The most common challenge during niacin treatment is flushing, although it typically decreases with ongoing use and can be ameliorated by pretreatment with aspirin and counseling by the prescriber." | 2.48 | Combination treatment with atorvastatin plus niacin provides effective control of complex dyslipidemias: a literature review. ( McKenney, JM, 2012) |
| "Niacin has been shown to prevent CV events, reduce mortality and has beneficial effects on vascular endothelial function." | 2.48 | Extended-release niacin with laropiprant : a review on efficacy, clinical effectiveness and safety. ( Ammori, BJ; France, M; Hama, S; Kwok, S; Soran, H; Yadav, R; Younis, N, 2012) |
| "In the metabolic syndrome and type 2 diabetes, excess energy intake on the background of genetic predisposition and lifestyle factors leads to the dysregulation of fatty acid metabolism and acquired insulin resistance." | 2.48 | Management of dyslipidemias in the presence of the metabolic syndrome or type 2 diabetes. ( Matikainen, N; Taskinen, MR, 2012) |
| "Niacin has a profound ability to reduce low-density lipoprotein-C, very low-density lipoprotein-C and triglycerides and is the most effective pharmacological agent to increase high-density lipoprotein-C." | 2.47 | Future of GPR109A agonists in the treatment of dyslipidaemia. ( Judd, RL; Wanders, D, 2011) |
| "Niacin is a water-soluble B vitamin (B3) known to have favorable effects on multiple lipid parameters, including raising high-density lipoprotein cholesterol (HDL-C) levels and lowering triglycerides (TGs), lipoprotein(a), and low-density lipoprotein cholesterol (LDL-C)." | 2.47 | Important considerations for treatment with dietary supplement versus prescription niacin products. ( Backes, JM; Moriarty, PM; Padley, RJ, 2011) |
| "Atherosclerosis is a chronic inflammatory disease affecting medium and large arteries resulting from a complex interaction between genetic and environmental risk factors that include dyslipidemia, hypertension, diabetes mellitus, and smoking." | 2.47 | Progress in HDL-based therapies for atherosclerosis. ( Chyu, KY; Peter, A; Shah, PK, 2011) |
| "Dyslipidemia is an important risk factor for cardiovascular complications in persons with diabetes." | 2.47 | Treatment approaches for diabetes and dyslipidemia. ( Lyons, TJ; Wu, M, 2011) |
| "Niacin is a lipid-altering drug that has been used to lower cholesterol since the 1950s." | 2.47 | The facts behind niacin. ( Berg, DD; Giugliano, RP; Hochholzer, W, 2011) |
| "Dyslipidemia is a well established risk factor for cardiovascular disease and is estimated to account for more than half of the global cases of coronary artery disease." | 2.46 | Dyslipidemia in the elderly: should it be treated? ( Alpert, JS; Rough, SJ; Shanmugasundaram, M, 2010) |
| "Low HDL-C levels are common in type 2 diabetes but are not currently recommended as a target for treatment because of the lack of definitive cardiovascular outcome studies supporting this goal, and because of the difficulty in raising HDL-C." | 2.46 | Management of dyslipidemia in people with type 2 diabetes mellitus. ( Dunn, FL, 2010) |
| "The lipid profile of type 2 diabetes mellitus is characterized by increased triglycerides (TGs), decreased high-density lipoprotein cholesterol (HDL-C), increased very low density lipoproteins (VLDLs), and small, dense low-density lipoprotein particles, the combination of which is highly atherogenic." | 2.45 | Managing diabetic dyslipidemia: beyond statin therapy. ( Gadi, R; Neeli, H; Rader, DJ, 2009) |
| "Dyslipidemia is central to the process of atherosclerosis." | 2.45 | Nicotinic acid: a new look at an old drug. ( Farmer, JA, 2009) |
| " There is a need for further research in order to come to a clear conclusion regarding combined therapies of aspirin and laropiprant pretreatment, as well as exact dosage requirements." | 2.45 | Mechanisms of flushing due to niacin and abolition of these effects. ( Arora, R; Sood, A, 2009) |
| "The evidence to support treating dyslipidemia in hemodialysis patients, however, has been mixed, with several outcome trials pending." | 2.44 | Managing dyslipidemia in chronic kidney disease. ( Harper, CR; Jacobson, TA, 2008) |
| "Treatment with niacin effectively improves multiple lipid parameters and cardiovascular outcomes." | 2.44 | Extended-release niacin/laropiprant: reducing niacin-induced flushing to better realize the benefit of niacin in improving cardiovascular risk factors. ( Ballantyne, CM; Bays, HE; Davidson, M; Kuznetsova, O; Lai, E; Maccubbin, D; Mitchel, YB; Norquist, JM; Paolini, JF; Pasternak, R; Sisk, CM; Waters, MG, 2008) |
| "Dyslipidemia is a major risk factor in the initiation and progression of cardiovascular diseases such as atherosclerosis." | 2.44 | Targeting multiple dyslipidemias with fixed combinations--focus on extended release niacin and simvastatin. ( Arora, A; Khan, BV; Pandian, A; Sperling, LS, 2008) |
| "Hydroxychloroquine, a common treatment for SLE, can improve lipid profiles and should be considered for all patients with SLE." | 2.44 | Management of dyslipidemia in children and adolescents with systemic lupus erythematosus. ( Ardoin, SP; Sandborg, C; Schanberg, LE, 2007) |
| "Niacin may also increase glucose levels, liver enzymes, and uric acid levels and cause other AEs that may have clinical relevance in selected patients." | 2.44 | Safety of niacin and simvastatin combination therapy. ( Bays, H, 2008) |
| "Niacin has been shown to regress atherosclerosis when used as monotherapy, in combination with a statin, and in combination with nonstatin therapies (including cholesterol-binding resins) and fibrates." | 2.44 | Evidence to support aggressive management of high-density lipoprotein cholesterol: implications of recent imaging trials. ( Taylor, AJ, 2008) |
| "Fifth, combined hyperlipidemia is the most common lipid disorder, has the strongest risk for CVD, and combines elevated LDL, hypertriglyceridemia, and low HDL." | 2.44 | Comprehensive lipid management versus aggressive low-density lipoprotein lowering to reduce cardiovascular risk. ( Atkinson, B; Dowdy, A; Knopp, RH; Paramsothy, P, 2008) |
| " The US Food and Drug Administration's (FDA) Adverse Event Reporting System provides 1 mechanism to evaluate the safety of niacin as it is used in common clinical practice." | 2.44 | The safety of niacin in the US Food and Drug Administration adverse event reporting database. ( Alsheikh-Ali, AA; Karas, RH, 2008) |
| "The metabolic syndrome and type 2 diabetes mellitus are both becoming more prevalent, and both increase the risk of cardiovascular disease." | 2.43 | Beyond low-density lipoprotein: addressing the atherogenic lipid triad in type 2 diabetes mellitus and the metabolic syndrome. ( Nesto, RW, 2005) |
| "Thus, the long-term treatment of dyslipidemias with these two agents may help to modify risk and reduce cardiovascular morbidity and mortality in these patients over and above benefits achieved by lowering blood pressure." | 2.43 | Niacin-ER/statin combination for the treatment of dyslipidemia: focus on low high-density lipoprotein cholesterol. ( Chrysant, SG; Ibrahim, M, 2006) |
| "Stroke is an uncommon disease in childhood with an estimated incidence of 1 to 6 per 100,000 and stenoocclusive arteriopathy is the main risk factor of recurrent pediatric arterial ischemic stroke (AIS)." | 1.46 | Elevated serum lipoprotein(a) as a risk factor for combined intracranial and extracranial artery stenosis in a child with arterial ischemic stroke: A case report. ( Han, JY; Kim, HJ; Lee, IG; Park, J; Shin, S, 2017) |
| "Hyperphosphatemia is thought to be a central-risk factor for CKD-MBD." | 1.42 | Niacin and Chronic Kidney Disease. ( Masuda, M; Miyamoto, K; Segawa, H; Takeda, E; Taketani, Y; Tatsumi, S; Yamamoto, H; Yamanaka-Okumura, H, 2015) |
| "Dyslipidemia is frequently found in association with obesity." | 1.37 | Obesity and dyslipidemia. ( Repas, T, 2011) |
| "Niacin has profound and unique effects on lipid metabolism." | 1.36 | Niacin as potential treatment for dyslipidemia and hyperphosphatemia associated with chronic renal failure: the need for clinical trials. ( Ahmed, MH, 2010) |
| " Subjects who took =2000 mg of Niaspan were automatically converted to Slo-Niacin in a 1:1 dosing ratio conversion." | 1.36 | Lipid and transaminase concentrations after formulary conversion of Niaspan to Slo-Niacin. ( Byrd, C; Mowrey, KA, 2010) |
| "Niacin is an effective drug for raising HDL cholesterol and reducing coronary risks, but patients show low compliance with treatment due to severe facial flushing upon taking the drug." | 1.35 | Pyrazole acids as niacin receptor agonists for the treatment of dyslipidemia. ( Blom, D; Carballo-Jane, E; Cheng, K; Ciecko, T; Colletti, S; Gerard Waters, M; Holt, TG; Krsmanovic, M; Lubell, S; McCann, PE; Raghavan, S; Ren, N; Schmidt, D; Smenton, A; Taggart, A; Tata, J; Wilsie, L; Wolff, M, 2009) |
| "Niacin is an effective lipid-altering agent that has been reported to reduce the risk of cardiovascular disease." | 1.35 | Blood pressure-lowering effects of extended-release niacin alone and extended-release niacin/laropiprant combination: a post hoc analysis of a 24-week, placebo-controlled trial in dyslipidemic patients. ( Bays, HE; Kuznetsova, O; Maccubbin, D; Meehan, AG; Mitchel, YB; Paolini, JF, 2009) |
| "Average daily dosage (ADD) and titration patterns of ER niacin therapy at defined time points after the index prescription, and the incidence and timing of continuous gaps of >/=30 days in ER niacin therapy." | 1.35 | Dosage, titration, and gaps in treatment with extended release niacin in clinical practice. ( Burke, TA; Kamal-Bahl, SJ; Watson, DJ; Wentworth, CE, 2008) |
| " Current drug labeling warns of an increased risk of adverse events with statin and niacin combinations." | 1.34 | Safety of lovastatin/extended release niacin compared with lovastatin alone, atorvastatin alone, pravastatin alone, and simvastatin alone (from the United States Food and Drug Administration adverse event reporting system). ( Alsheikh-Ali, AA; Karas, RH, 2007) |
| "Likewise, the metabolic syndrome is a secondary target of treatment." | 1.32 | CHD risk equivalents and the metabolic syndrome. Trial evidence supports aggressive management. ( Thompson, PD, 2003) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 103 (44.40) | 29.6817 |
| 2010's | 125 (53.88) | 24.3611 |
| 2020's | 4 (1.72) | 2.80 |
| Authors | Studies |
|---|---|
| Boatman, PD | 1 |
| Richman, JG | 2 |
| Semple, G | 2 |
| Skinner, PJ | 1 |
| Webb, PJ | 1 |
| Sage, CR | 1 |
| Dang, TH | 1 |
| Pride, CC | 1 |
| Chen, R | 1 |
| Tamura, SY | 1 |
| Connolly, DT | 1 |
| Schmidt, D | 1 |
| Smenton, A | 1 |
| Raghavan, S | 1 |
| Carballo-Jane, E | 1 |
| Lubell, S | 1 |
| Ciecko, T | 1 |
| Holt, TG | 1 |
| Wolff, M | 1 |
| Taggart, A | 1 |
| Wilsie, L | 1 |
| Krsmanovic, M | 1 |
| Ren, N | 1 |
| Blom, D | 1 |
| Cheng, K | 1 |
| McCann, PE | 1 |
| Gerard Waters, M | 1 |
| Tata, J | 1 |
| Colletti, S | 1 |
| Kim, C | 1 |
| Park, K | 1 |
| Haynes, R | 2 |
| Valdes-Marquez, E | 1 |
| Hopewell, JC | 2 |
| Chen, F | 2 |
| Li, J | 1 |
| Parish, S | 2 |
| Landray, MJ | 2 |
| Armitage, J | 2 |
| Jiang, Y | 1 |
| Jin, M | 1 |
| Chen, J | 2 |
| Yan, J | 1 |
| Liu, P | 1 |
| Yao, M | 1 |
| Cai, W | 1 |
| Pi, R | 1 |
| Kothawade, PB | 1 |
| Thomas, AB | 1 |
| Chitlange, SS | 1 |
| Yan, X | 1 |
| Wang, S | 1 |
| Agrawal, S | 1 |
| Zaritsky, JJ | 1 |
| Fornoni, A | 1 |
| Smoyer, WE | 1 |
| Han, JY | 1 |
| Kim, HJ | 1 |
| Shin, S | 1 |
| Park, J | 1 |
| Lee, IG | 1 |
| Streja, E | 1 |
| Streja, DA | 1 |
| Soohoo, M | 1 |
| Kleine, CE | 1 |
| Hsiung, JT | 1 |
| Park, C | 1 |
| Moradi, H | 1 |
| Tuteja, S | 2 |
| Qu, L | 1 |
| Vujkovic, M | 1 |
| Dunbar, RL | 5 |
| DerOhannessian, S | 1 |
| Rader, DJ | 4 |
| Riaz, H | 1 |
| Khan, SU | 1 |
| Rahman, H | 1 |
| Shah, NP | 1 |
| Kaluski, E | 1 |
| Lincoff, AM | 1 |
| Nissen, SE | 1 |
| Gebhardt, A | 1 |
| Fichtenbaum, CJ | 2 |
| Olson, EJ | 1 |
| Mahar, KM | 1 |
| Haws, TF | 1 |
| Fossler, MJ | 1 |
| Gao, F | 1 |
| de Gouville, AC | 1 |
| Sprecher, DL | 1 |
| Lepore, JJ | 1 |
| Steinhagen-Thiessen, E | 4 |
| Dänschel, W | 1 |
| Buffleben, C | 1 |
| Smolka, W | 1 |
| Pittrow, D | 1 |
| Hildemann, SK | 1 |
| Khoueiry, G | 1 |
| Abdallah, M | 1 |
| Saiful, F | 1 |
| Abi Rafeh, N | 1 |
| Raza, M | 1 |
| Bhat, T | 1 |
| El-Sayegh, S | 1 |
| Kalantar-Zadeh, K | 1 |
| Lafferty, J | 1 |
| Kei, A | 4 |
| Liberopoulos, EN | 1 |
| Mikhailidis, DP | 3 |
| Elisaf, M | 4 |
| Sazonov, V | 1 |
| Maccubbin, D | 11 |
| Sisk, CM | 5 |
| Canner, PL | 1 |
| Wierzbicki, AS | 3 |
| Liberopoulos, E | 3 |
| Tellis, K | 1 |
| Rizzo, M | 2 |
| Tselepis, A | 3 |
| Reiner, Z | 2 |
| Song, WL | 1 |
| FitzGerald, GA | 1 |
| Tellis, C | 2 |
| Niesor, EJ | 1 |
| Gauthamadasa, K | 1 |
| Silva, RA | 1 |
| Suchankova, G | 1 |
| Kallend, D | 1 |
| Gylling, H | 1 |
| Asztalos, B | 1 |
| Damonte, E | 1 |
| Rossomanno, S | 1 |
| Abt, M | 1 |
| Davidson, WS | 1 |
| Benghozi, R | 1 |
| Pang, J | 2 |
| Chan, DC | 2 |
| Hamilton, SJ | 2 |
| Tenneti, VS | 2 |
| Watts, GF | 3 |
| Barrett, PH | 2 |
| Cenarro, A | 1 |
| Puzo, J | 1 |
| Ferrando, J | 1 |
| Mateo-Gallego, R | 1 |
| Bea, AM | 1 |
| Calmarza, P | 1 |
| Jarauta, E | 1 |
| Civeira, F | 1 |
| Boden, WE | 1 |
| Sidhu, MS | 1 |
| Toth, PP | 6 |
| Bajnok, L | 1 |
| Manoria, PC | 1 |
| Chopra, HK | 1 |
| Parashar, SK | 1 |
| Dutta, AL | 1 |
| Pinto, B | 1 |
| Mullasari, A | 1 |
| Prajapati, S | 1 |
| Mayor, S | 1 |
| Nasser Figueiredo, V | 1 |
| Vendrame, F | 1 |
| Colontoni, BA | 1 |
| Quinaglia, T | 1 |
| Roberto Matos-Souza, J | 1 |
| Azevedo Moura, F | 1 |
| Coelho, OR | 1 |
| de Faria, EC | 1 |
| Sposito, AC | 1 |
| Barylski, M | 1 |
| Nikolic, D | 1 |
| Montalto, G | 1 |
| Banach, M | 1 |
| Rao, M | 1 |
| Steffes, M | 1 |
| Bostom, A | 1 |
| Ix, JH | 2 |
| Farnier, M | 2 |
| Chen, E | 3 |
| Johnson-Levonas, AO | 3 |
| McCrary Sisk, C | 5 |
| Mitchel, YB | 7 |
| Catapano, AL | 2 |
| Foody, JM | 1 |
| Tomassini, JE | 1 |
| Brudi, P | 1 |
| Tershakovec, AM | 2 |
| Khera, AV | 1 |
| Qamar, A | 1 |
| Reilly, MP | 1 |
| Pisaniello, AD | 1 |
| Scherer, DJ | 1 |
| Kataoka, Y | 1 |
| Nicholls, SJ | 2 |
| Masana, L | 2 |
| Cabré, A | 1 |
| Heras, M | 1 |
| Amigó, N | 1 |
| Correig, X | 1 |
| Martínez-Hervás, S | 1 |
| Real, JT | 1 |
| Ascaso, JF | 2 |
| Quesada, H | 1 |
| Julve, J | 1 |
| Palomer, X | 1 |
| Vázquez-Carrera, M | 1 |
| Girona, J | 1 |
| Plana, N | 1 |
| Blanco-Vaca, F | 1 |
| Flink, L | 1 |
| Underberg, JA | 1 |
| Newman, JD | 1 |
| Gianos, E | 1 |
| Sekhar, RV | 2 |
| Bays, HE | 9 |
| Brinton, EA | 2 |
| Triscari, J | 1 |
| MacLean, AA | 1 |
| Gibson, KL | 1 |
| Ruck, RA | 1 |
| O'Neill, EA | 1 |
| Savinova, OV | 1 |
| Fillaus, K | 1 |
| Harris, WS | 2 |
| Shearer, GC | 2 |
| Dubé, MP | 2 |
| Komarow, L | 1 |
| Cadden, JJ | 1 |
| Overton, ET | 1 |
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| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Randomized Trial of the Long-term Clinical Effects of Raising HDL Cholesterol With Extended Release Niacin/Laropiprant[NCT00461630] | Phase 3 | 25,673 participants (Actual) | Interventional | 2007-01-31 | Completed | ||
| AIM HIGH: Niacin Plus Statin to Prevent Vascular Events[NCT00120289] | Phase 3 | 3,414 participants (Actual) | Interventional | 2005-09-30 | Terminated (stopped due to AIM-HIGH was stopped on the recommendation of the DSMB because of lack of efficacy of niacin in preventing primary outcome events.) | ||
| A Two Part, Multicenter Phase IIa, Placebo Controlled Study, to Examine the Safety, Tolerability, and Effects of GSK256073 on Lipids in Subjects With Dyslipidemia[NCT00903617] | Phase 2 | 80 participants (Actual) | Interventional | 2009-06-15 | Completed | ||
| Comparison of High-Dose Rosuvastatin Versus Low Statin Dose Plus Fenofibrate Versus Low Statin Dose Plus Niacin in the Treatment of Mixed Hyperlipidemia[NCT01010516] | Phase 4 | 120 participants (Anticipated) | Interventional | 2009-10-31 | Recruiting | ||
| Short-term Effect of Extended-release Niacin With and Without the Addition of Laropiprant on Endothelial Function[NCT01942291] | Phase 4 | 18 participants (Actual) | Interventional | 2012-03-31 | Completed | ||
| A Worldwide, Multicenter, Double-Blind, Randomized, Parallel, Placebo-Controlled Study to Evaluate the Lipid-Altering Efficacy, Safety and Tolerability of MK0524A in Patients With Primary Hypercholesterolemia or Mixed Hyperlipidemia[NCT00269204] | Phase 3 | 1,620 participants (Actual) | Interventional | 2005-12-31 | Completed | ||
| "A Multicenter, Randomized, Double-Blind, Factorial Design Study to Evaluate the Lipid-Altering Efficacy and Safety of Coadministered MK0524B Tablets in Patients With Primary Hypercholesterolemia or Mixed Hyperlipidemia"[NCT00269217] | Phase 3 | 1,400 participants (Actual) | Interventional | 2006-01-31 | Completed | ||
| Estudio clínico Fase III Para Evaluar la Eficacia terapéutica en Pacientes Mexicanos Con Dislipidemia Mediante el Uso vía Oral de L-Carnitina + Atorvastatina Comparado Con Atorvastatina[NCT03696940] | Phase 3 | 120 participants (Actual) | Interventional | 2018-05-28 | Active, not recruiting | ||
| Hypertension Management and Outcomes in a Family Practice Setting[NCT03579108] | 200 participants (Anticipated) | Observational | 2018-02-24 | Recruiting | |||
| A Multicenter, Randomized, Double-Blind, Placebo Controlled 36 Week Study to Evaluate the Efficacy and Safety of Extended Release (ER) Niacin/Laropiprant in Patients With Type 2 Diabetes[NCT00485758] | Phase 3 | 796 participants (Actual) | Interventional | 2007-07-31 | Completed | ||
| Niacin, N-3 Fatty Acids and Insulin Resistance[NCT00286234] | Phase 4 | 68 participants (Actual) | Interventional | 2007-10-31 | Completed | ||
| Effect of HDL-Raising Therapies on Endothelial Function, Lipoproteins, and Inflammation in HIV-infected Subjects With Low HDL Cholesterol: A Phase II Randomized Trial of Extended Release Niacin vs. Fenofibrate[NCT01426438] | Phase 2 | 99 participants (Actual) | Interventional | 2011-11-30 | Completed | ||
| Effect of Tredaptive on Serum Lipoproteins, Lipoproteins Metabolism, Oxidative Stress and HDL Antioxidant Function[NCT01054508] | Phase 4 | 38 participants (Actual) | Interventional | 2010-06-30 | Completed | ||
| Carotid Plaque Composition by Magnetic Resonance Imaging During Lipid Lowering Therapy[NCT00715273] | Phase 4 | 217 participants (Actual) | Interventional | 2001-05-01 | Completed | ||
| A 24-Week, Worldwide, Multicenter, Double-Blind, Randomized, Parallel, Placebo-Controlled Study to Assess the Efficacy and Tolerability of Anacetrapib When Added to Ongoing Statin Therapy With or Without Other Lipid Modifying Medication(s) in Patients Wit[NCT01717300] | Phase 3 | 459 participants (Actual) | Interventional | 2012-11-06 | Completed | ||
| Obesity in Pediatric Sickle Cell Disease: A New Phenomenon[NCT04676113] | 100 participants (Actual) | Observational | 2021-03-01 | Completed | |||
| Establishment of the Pediatric Obesity Weight Evaluation Registry (POWER): A Prospective Pilot Project of Children and Adolescents Presenting for Weight Management[NCT02121132] | 10,000 participants (Anticipated) | Observational [Patient Registry] | 2014-05-31 | Recruiting | |||
| ER Niacin/Laropiprant Impact on Cardiovascular Markers and Atheroprogression in HIV-infected Individuals on cART[NCT01683656] | Phase 4 | 4 participants (Actual) | Interventional | 2012-08-31 | Terminated (stopped due to Withdrawal of IMP from the market. Data on risk-benefit ratio pending.) | ||
| A Randomized, Double-blind, Parallel, Multicenter, Placebo-controlled, Prospective Study to Evaluate the Functionality of the Flushing ASsessment Tool (FAST) in Subjects Administered Niaspan® Plus Acetylsalicylic Acid (ASA), Niaspan® Plus ASA Placebo or N[NCT00630877] | Phase 3 | 276 participants (Actual) | Interventional | 2008-02-29 | Completed | ||
| Multicenter, Randomized, Double-Blind, Parallel, Acetylsalicylic Acid (ASA) Run-In Study to Evaluate the EFFECTS of Acetylsalicylic Acid on Niaspan®-Induced Flushing in Subjects With Dyslipidemia[NCT00626392] | Phase 3 | 277 participants (Actual) | Interventional | 2008-02-29 | Completed | ||
| A Worldwide, Multicenter, Double-Blind, Parallel Study to Evaluate the Tolerability of MK0524A Versus Niacin Extended-Release[NCT00378833] | Phase 3 | 1,300 participants (Actual) | Interventional | 2006-07-31 | Completed | ||
| A Multicenter, Randomized, Double-Blind, Placebo-Controlled Study to Evaluate the Tolerability and Effect of MK0524A on Niacin-Induced Acute Flushing in Lipid Clinic Patients[NCT00533611] | Phase 3 | 330 participants | Interventional | 2007-04-30 | Completed | ||
| The Effect of Niacin Supplementation on Systemic Nicotinamide Adenine Dinucleotide (NAD+) Metabolism, Physiology and Muscle Performance in Healthy Controls and Mitochondrial Myopathy Patients[NCT03973203] | 15 participants (Actual) | Interventional | 2014-06-01 | Completed | |||
| NiaMIT (NiaMIT_0001) Continuation for Early-stage Mitochondrial Myopathy Patients to Investigate the Effect of Niacin Supplementation on Systemic Nicotinamide Adenine Dinucleotide (NAD+) Metabolism, Physiology and Muscle Performance[NCT04538521] | 3 participants (Actual) | Interventional | 2019-02-11 | Completed | |||
| Post-prandial Effects of Extra Virgin Olive Oil on Endothelial Function in Adults at Risk for Type 2 Diabetes: A Randomized Crossover Controlled Trial[NCT04025281] | 20 participants (Actual) | Interventional | 2019-07-09 | Completed | |||
| The Impact of Consumption of Eggs in the Context of Plant-Based Diets on[NCT04316429] | 35 participants (Actual) | Interventional | 2020-06-09 | Completed | |||
| A Multicenter, Randomized, Double-Blind, Parallel Group, 12 Week Study to Evaluate the Efficacy and Safety of Extended-release (ER) Niacin/Laropiprant in Patients With Primary Hypercholesterolemia or Mixed Dyslipidemia.[NCT00479388] | Phase 3 | 1,216 participants (Actual) | Interventional | 2007-07-31 | Completed | ||
| Diet/Exercise, Niacin, Fenofibrate for HIV Lipodystrophy[NCT00246376] | 221 participants (Actual) | Interventional | 2004-01-31 | Completed | |||
| A Worldwide, Multicenter, Double-Blind, Randomized, Parallel, Placebo-Controlled Study to Evaluate the Long-term Efficacy, Safety and Tolerability of ERN/LRPT in Patients With Dyslipidemia[NCT00961636] | Phase 3 | 1,152 participants (Actual) | Interventional | 2009-10-31 | Completed | ||
| Treatment Study for Severe High-Density Lipoprotein Deficiency[NCT00458055] | 19 participants (Actual) | Interventional | 2006-11-30 | Completed | |||
| Effect of Tomato Consumption on Serum High Density Lipoprotein-cholesterol Levels. A Randomized, Open-label, Single Blind, Clinical Trial[NCT01342666] | 50 participants (Actual) | Interventional | 2009-03-31 | Completed | |||
| Efficacy Of An Education Plan And Adherence Follow-Up To The Exercise In Patients With Angioplasty And Implantation Of Coronary Stent, Measured With Hdl And Met In A Cardiac Rehabilitation Unit - Random Triple Blind Clinical Trial[NCT03231631] | 71 participants (Actual) | Interventional | 2017-01-10 | Completed | |||
| Part A: A Randomized, Double-Blind, Placebo-Controlled Study to Assess the Effects of MK0524 Compared to Placebo Part B: A Dose-Ranging Study to Evaluate the Tolerability of MK0524 and Its Effects on Niacin-Induced Flushing in Lipid Clinic Patients[NCT00536237] | Phase 2 | 154 participants (Actual) | Interventional | 2004-08-31 | Completed | ||
| An Open-Label Evaluation of the Safety and Efficacy of a Combination of Niacin ER and Simvastatin in Patients With Dyslipidemia (OCEANS)[NCT00080275] | Phase 3 | 600 participants | Interventional | 2004-03-31 | Completed | ||
| Validation of an Enzymatic Assay for Quantification of Nicotinamide Adenine Dinucleotide in Blood Plasma After Ingestion of the Vitamin B3 Variant Nicotinamide Riboside: a Randomized Controlled Trial[NCT06005350] | 54 participants (Anticipated) | Interventional | 2023-11-01 | Recruiting | |||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
(NCT00461630)
Timeframe: During scheduled treatment period (median duration 3.9 years)
| Intervention | participants (Number) |
|---|---|
| ER Niacin/Laropiprant | 807 |
| Placebo | 897 |
Non-fatal myocardial infarction (MI) or coronary death (NCT00461630)
Timeframe: During scheduled treatment period (median duration 3.9 years)
| Intervention | participants (Number) |
|---|---|
| ER Niacin/Laropiprant | 668 |
| Placebo | 694 |
Non-fatal myocardial infarction or coronary death, non-fatal or fatal stroke, or revascularisation (NCT00461630)
Timeframe: During scheduled treatment period (median duration 3.9 years)
| Intervention | participants (Number) |
|---|---|
| ER Niacin/Laropiprant | 1696 |
| Placebo | 1758 |
All-cause mortality (NCT00461630)
Timeframe: During scheduled treatment period (median duration 3.9 years)
| Intervention | participants (Number) |
|---|---|
| ER Niacin/Laropiprant | 798 |
| Placebo | 732 |
Fatal or non-fatal (NCT00461630)
Timeframe: During scheduled treatment period (median duration 3.9 years)
| Intervention | participants (Number) |
|---|---|
| ER Niacin/Laropiprant | 498 |
| Placebo | 499 |
(NCT00120289)
Timeframe: Time to first event measured from date of randomization through last follow-up visit (common termination), for an average of 36 months follow-up, maximum 66 months.
| Intervention | participants (Number) |
|---|---|
| ERN + Simvastatin | 45 |
| Placebo + Simvastatin | 38 |
(NCT00120289)
Timeframe: Time to first event measured from date of randomization through last follow-up visit (common termination) for an average of 36 months follow-up, maximum 66 months.
| Intervention | participants (Number) |
|---|---|
| ERN + Simvastatin | 282 |
| Placebo + Simvastatin | 274 |
(NCT00120289)
Timeframe: Time to first event measured from date of randomization through last follow-up visit (common termination) for an average of 36 months follow-up, maximum 66 months
| Intervention | participants (Number) |
|---|---|
| ERN + Simvastatin | 171 |
| Placebo + Simvastatin | 158 |
(NCT00120289)
Timeframe: Time to first event measured from date of randomization through last follow-up visit (common termination) for an average of 36 months follow-up, maximum 66 months
| Intervention | participants (Number) |
|---|---|
| ERN + Simvastatin | 156 |
| Placebo + Simvastatin | 138 |
Flushing assessment was captured by participants in individual diaries provided to each study participant. Participants were instructed to return their diaries after each study visit (Week 2, Week 4, Week 6 and Week 8) where they were given a new diary for the time between visits. The time to the onset of the first flushing (if more than one happens to occur on each day) was analyzed. (NCT00903617)
Timeframe: Up to Week 8
| Intervention | Hours (Median) |
|---|---|
| GSK256073 5 mg | 9.1 |
| GSK256073 50 mg | 3.6 |
| GSK256073 150 mg | 1.0 |
| Placebo | 4.1 |
Flushing assessment was captured by participants in individual diaries provided to each study participant. Participants were instructed to return their diaries after each study visit (Week 2, Week 4, Week 6 and Week 8) where they were given a new diary for the time between visits. Participants self-assessed intensity of flushing using a 100 mm VAS once daily at the first flushing episode. The left hand side of the scale (0) represented 'No Flushing Sensation' and the right hand side of the scale (100) represented 'Unbearable Flushing Sensation'. The intensity of flushing of each episode was measured in centimeters (to the nearest 1/100) from the 0 point of the scale. Data is reported for average VAS scores over 8 weeks of treatment. (NCT00903617)
Timeframe: Up to Week 8
| Intervention | Scores on a scale (Mean) |
|---|---|
| GSK256073 5 mg | 9.0 |
| GSK256073 50 mg | 31.8 |
| GSK256073 150 mg | 24.9 |
| Placebo | 17.1 |
Flushing assessment was captured by participants in individual diaries provided to each study participant. Participants were instructed to return their diaries after each study visit (Week 2, Week 4, Week 6 and Week 8) where they were given a new diary for the time between visits. (NCT00903617)
Timeframe: Up to follow up (14 days from last dose)
| Intervention | Participants (Count of Participants) |
|---|---|
| GSK256073 5 mg | 0 |
| GSK256073 50 mg | 0 |
| GSK256073 150 mg | 0 |
| Placebo | 0 |
Blood samples for assessment of hematology parameters of platelet count, red blood cell count, white blood cell count, hemoglobin, haptoglobin, reticulocyte count, hematocrit, mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, neutrophils, lymphocytes, monocytes, eosinophils and basophils was collected at Baseline and at Weeks 2, 4, 6 and 8. (NCT00903617)
Timeframe: Baseline (Week 0) up to Week 8
| Intervention | Participants (Count of Participants) |
|---|---|
| GSK256073 5 mg | 0 |
| GSK256073 50 mg | 0 |
| GSK256073 150 mg | 0 |
| Placebo | 0 |
Flushing assessment was captured by participants in individual diaries provided to each study participant. Participants were instructed to return their diaries after each study visit (Week 2, Week 4, Week 6 and Week 8) where they were given a new diary for the time between visits. Participant's average duration of flushing was analyzed. (NCT00903617)
Timeframe: Up to Week 8
| Intervention | Minutes (Median) |
|---|---|
| GSK256073 5 mg | 36.7 |
| GSK256073 50 mg | 151.7 |
| GSK256073 150 mg | 60.0 |
| Placebo | 72.1 |
All participants treated with GSK256073 or placebo participated in PK sampling. Blood samples for PK analysis of GSK256073 to determine AUC(0-t) was collected at Week 2, 4, 6 and 8. For samples obtained during time windows, every attempt was made to collect three samples during each time window: pre-dose to 2 hours after dosing, 2 hours to 4.5 hours after dose, and 6 hours to 12 hours after dose. During each window, 3 samples spaced at least 30 minutes apart were collected (i.e., avoid collection from all participants at the same time within a window or only at the extremes of a time window). The AUC 0-t was determined using the linear trapezoidal rule for increasing concentrations and the logarithmic trapezoidal rule for decreasing concentrations. (NCT00903617)
Timeframe: 0-2 hours after dosing (pre-dose plus 3 samples spaced at least 30 minutes apart), 2 to 4.5 hours after dose (3 samples spaced at least 30 minutes apart) and 6-12 hours post dose (3 samples spaced at least 30 minutes apart) on Week 2, 4, 6 and 8
| Intervention | Hour nanogram per milliliter (h*ng/mL) (Geometric Mean) |
|---|---|
| GSK256073 5 mg | 8352.281 |
| GSK256073 50 mg | 75587.96 |
| GSK256073 150 mg | 340551.4 |
All participants treated with GSK256073 or placebo participated in PK sampling. Blood samples for PK analysis of GSK256073 to determine Cmax was collected at Week 2, 4, 6 and 8. For samples obtained during time windows, every attempt was made to collect three samples during each time window: pre-dose to 2 hours after dosing, 2 hours to 4.5 hours after dose, and 6 hours to 12 hours after dose. During each window, 3 samples spaced at least 30 minutes apart were collected (i.e., avoid collection from all participants at the same time within a window or only at the extremes of a time window). The first occurrence of the Cmax was determined directly from the raw concentration-time data. (NCT00903617)
Timeframe: 0-2 hours after dosing (pre-dose plus 3 samples spaced at least 30 minutes apart), 2 to 4.5 hours after dose (3 samples spaced at least 30 minutes apart) and 6-12 hours post dose (3 samples spaced at least 30 minutes apart) on Week 2, 4, 6 and 8
| Intervention | Nanograms per mililiter (ng/mL) (Geometric Mean) |
|---|---|
| GSK256073 5 mg | 923.709 |
| GSK256073 50 mg | 7223.709 |
| GSK256073 150 mg | 22961.25 |
All participants treated with GSK256073 or placebo participated in PK sampling. Blood samples for PK analysis of GSK256073 to determine Tmax was collected at Week 2, 4, 6 and 8. For samples obtained during time windows, every attempt was made to collect three samples during each time window: pre-dose to 2 hours after dosing, 2 hours to 4.5 hours after dose, and 6 hours to 12 hours after dose. During each window, 3 samples spaced at least 30 minutes apart were collected (i.e., avoid collection from all participants at the same time within a window or only at the extremes of a time window). The time at which Cmax was observed was determined directly from the raw concentration-time data. (NCT00903617)
Timeframe: 0-2 hours after dosing (pre-dose plus 3 samples spaced at least 30 minutes apart), 2 to 4.5 hours after dose (3 samples spaced at least 30 minutes apart) and 6-12 hours post dose (3 samples spaced at least 30 minutes apart) on Week 2, 4, 6 and 8
| Intervention | Hours (Median) |
|---|---|
| GSK256073 5 mg | 2.417 |
| GSK256073 50 mg | 1.350 |
| GSK256073 150 mg | 2.500 |
Flushing assessment was captured by participants in individual diaries provided to each study participant. Participants were instructed to return their diaries after each study visit (Week 2, Week 4, Week 6 and Week 8) where they were given a new diary for the time between visits. Flushing symptom questionnaire (FSQ) was used to measure participant reported feelings of severity associated with different types of flushing symptoms. The FSQ comprised of 11 items. The response scale combined verbal descriptors as well as a 0-10 numerical rating scale. Items 1, 2, 4 and 10 had verbal descriptors. The items 3, 5, 6, 7, 8, 9 and 11 were rated on a 0 to 10 scale (none=0, mild=1-3, moderate=4-6, severe=7-9 and extreme=10). The total score for these items ranged from 0 (not at all) to 70 (extreme). Higher score indicated more severe flushing symptoms and 0 indicated no flushing symptoms. (NCT00903617)
Timeframe: Up to Week 8
| Intervention | Participants (Count of Participants) | |||
|---|---|---|---|---|
| None | Mild | Moderate | Severe | |
| GSK256073 150 mg | 8 | 8 | 4 | 0 |
| GSK256073 5 mg | 15 | 2 | 1 | 0 |
| GSK256073 50 mg | 16 | 2 | 2 | 0 |
| Placebo | 15 | 4 | 0 | 1 |
"Flushing assessment was captured by participants in individual diaries provided to each study participant. Participants were instructed to return their diaries after each study visit (Week 2, Week 4, Week 6 and Week 8) where they were given a new diary for the time between visits. Participants with average number of flushing episodes was reported as did not have flushing episode, 1 flushing episode, 2 flushing episode and 3 or more flushing episode." (NCT00903617)
Timeframe: Up to Week 8
| Intervention | Participants (Count of Participants) | |||
|---|---|---|---|---|
| Did not have flushing episodes | 1 flushing episode | 2 flushing episode | 3 or more flushing episode | |
| GSK256073 150 mg | 8 | 9 | 3 | 0 |
| GSK256073 5 mg | 15 | 3 | 0 | 0 |
| GSK256073 50 mg | 16 | 1 | 2 | 1 |
| Placebo | 15 | 1 | 3 | 1 |
Heart rate was assessed at Baseline (Week 0), Week 2, 4, 6 and 8. Baseline was defined at Week 0. Change from Baseline was calculated by subtracting the post-Baseline value from the Baseline value. (NCT00903617)
Timeframe: Baseline (Week 0) up to Week 8
| Intervention | Beats per minute (Mean) | |||
|---|---|---|---|---|
| Week 2, 0 hour | Week 4, 0 hour | Week 6, 0 hour | Week 8, 0 hour | |
| GSK256073 150 mg | 1.9 | 3.6 | 2.8 | 4.6 |
| GSK256073 5 mg | 1.4 | -1.2 | -1.4 | 0.0 |
| GSK256073 50 mg | -0.5 | -1.9 | -0.2 | 3.5 |
| Placebo | 1.1 | 1.9 | 3.6 | 2.2 |
SBP and DBP was assessed at Baseline (Week 0), Week 2, 4, 6 and 8. Baseline was defined at Week 0. Change from Baseline was calculated by subtracting the post-Baseline value from the Baseline value. (NCT00903617)
Timeframe: Baseline (Week 0) up to Week 8
| Intervention | Millimeters of mercury (mmHg) (Mean) | |||||||
|---|---|---|---|---|---|---|---|---|
| DBP, Week 2, 0 hour | DBP, Week 4, 0 hour | DBP, Week 6, 0 hour | DBP, Week 8, 0 hour | SBP, Week 2, 0 hour | SBP, Week 4, 0 hour | SBP, Week 6, 0 hour | SBP, Week 8, 0 hour | |
| GSK256073 150 mg | -1.0 | 0.8 | 1.6 | 2.0 | -2.7 | -3.2 | -0.1 | -1.3 |
| GSK256073 5 mg | -2.1 | -2.6 | -0.6 | 0.8 | -3.0 | -4.5 | 3.7 | 1.8 |
| GSK256073 50 mg | -0.1 | 0.8 | -1.3 | -1.7 | 2.7 | 6.1 | 0.9 | 1.0 |
| Placebo | 1.1 | 1.6 | 1.4 | 1.9 | 2.1 | 4.2 | 0.2 | 0.8 |
Blood samples for assessment of clinical chemistry parameters of blood urea nitrogen, creatinine, glucose (fasting), sodium, creatine phosphokinase, potassium, chloride, total carbon dioxide, calcium, total lactose dehydrogenase (LDH), aspartate aminotransferase (AST), alanine amino transferase (ALT), gamma glutamyl transferase (GGT), alkaline phosphatase, phosphate, total and direct bilirubin, uric acid, albumin and total protein was collected at Baseline and at Weeks 2, 4, 6 and 8. (NCT00903617)
Timeframe: Up to Week 8
| Intervention | Participants (Count of Participants) | |
|---|---|---|
| Creatine kinase, Week 6, High | Phosphorous, inorganic, Week 8, low | |
| GSK256073 150 mg | 0 | 0 |
| GSK256073 5 mg | 0 | 1 |
| GSK256073 50 mg | 1 | 0 |
| Placebo | 0 | 0 |
Urinalysis assessment was done for urine occult blood, urine glucose, urine ketones and urine protein over eight weeks treatment period. (NCT00903617)
Timeframe: Up to Week 8
| Intervention | Participants (Count of Participants) | ||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Urine Occult Blood, Baseline, Predose, 1+ | Urine Occult Blood, Baseline, Predose, Trace | Urine Occult Blood, Week 2, Predose, 1+ | Urine Occult Blood, Week 2, Predose, Trace | Urine Occult Blood, Week 4, Predose, 1+ | Urine Occult Blood, Week 4, Predose, Trace | Urine Occult Blood, Week 6, Predose, 3+ | Urine Occult Blood, Week 6, Predose, Trace | Urine Occult Blood, Week 8, 0 hour, 1+ | Urine Occult Blood, Week 8, 0 hour, Trace | Urine Ketones, Baseline, Predose, Trace | Urine Ketones, Week 2, Predose, Trace | Urine Ketones, Week 4, Predose, 2+ | Urine Ketones, Week 6, Predose, Trace | Urine Ketones, Week 8, 0 hour, 1+ | Urine Protein, Baseline, Predose, Trace | Urine Protein, Week 2, Predose, Trace | Urine Protein, Week 4, Predose, 1+ | Urine Protein, Week 4, Predose, Trace | Urine Protein, Week 6, Predose, 1+ | Urine Protein, Week 6, Predose, Trace | Urine Protein, Week 8, 0 hour, 1+ | Urine Protein, Week 8, 0 hour, Trace | |
| GSK256073 150 mg | 1 | 0 | 1 | 0 | 0 | 1 | 1 | 0 | 0 | 2 | 0 | 1 | 1 | 0 | 1 | 1 | 0 | 1 | 2 | 1 | 1 | 0 | 3 |
| GSK256073 5 mg | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 1 | 0 | 0 | 0 | 1 | 0 | 1 |
| GSK256073 50 mg | 0 | 1 | 0 | 2 | 0 | 1 | 0 | 2 | 0 | 0 | 1 | 0 | 0 | 1 | 0 | 1 | 1 | 0 | 1 | 0 | 1 | 0 | 0 |
| Placebo | 0 | 1 | 0 | 2 | 1 | 0 | 0 | 0 | 1 | 0 | 0 | 0 | 0 | 0 | 0 | 2 | 1 | 0 | 0 | 0 | 1 | 1 | 2 |
An AE is any untoward medical occurrence in a participant, temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. An SAE is any untoward medical occurrence that, at any dose results in death, is life-threatening, requires hospitalization or prolongation of existing hospitalization, results in disability/incapacity or is a congenital anomaly/birth defect, medically significant or it is associated with liver injury and impaired liver function. (NCT00903617)
Timeframe: Up to follow up (14 days from last dose)
| Intervention | Participants (Count of Participants) | |
|---|---|---|
| Any AEs | Any SAEs | |
| GSK256073 150 mg | 17 | 0 |
| GSK256073 5 mg | 8 | 0 |
| GSK256073 50 mg | 12 | 0 |
| Placebo | 14 | 0 |
Single 12-lead ECGs was obtained at each time point during the study using an ECG machine that automatically calculated the heart rate and measured PR, QRS, QT, and QTc intervals. Participants with normal, abnormal- clinically significant (CS) and abnormal- not clinically significant (NCS) ECG values were reported. (NCT00903617)
Timeframe: Up to Week 8
| Intervention | Participants (Count of Participants) | ||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Baseline, Predose, Normal | Baseline, Predose, Abnormal-NCS | Baseline, Predose, Abnormal-CS | Week 2, Predose, Normal | Week 2, Predose, Abnormal-NCS | Week 2, Predose, Abnormal-CS | Week 4, Predose, Normal | Week 4, Predose, Abnormal-NCS | Week 4, Predose, Abnormal-CS | Week 6, Predose, Normal | Week 6, Predose, Abnormal-CS | Week 6, Predose, Abnormal-NCS | Week 8, 0 hour, Normal | Week 8, 0 hour, Abnormal-NCS | Week 8, 0 hour, Abnormal-CS | |
| GSK256073 150 mg | 8 | 12 | 0 | 9 | 10 | 0 | 10 | 8 | 0 | 10 | 6 | 0 | 9 | 6 | 0 |
| GSK256073 5 mg | 9 | 10 | 0 | 10 | 8 | 0 | 8 | 9 | 0 | 9 | 7 | 0 | 10 | 6 | 0 |
| GSK256073 50 mg | 5 | 15 | 0 | 10 | 9 | 0 | 5 | 12 | 0 | 4 | 12 | 0 | 5 | 10 | 0 |
| Placebo | 13 | 8 | 0 | 13 | 7 | 0 | 16 | 4 | 0 | 15 | 5 | 0 | 13 | 7 | 0 |
Flushing assessment was captured by participants in individual diaries provided to each study participant. Participants were instructed to return their diaries after each study visit (Week 2, Week 4, Week 6 and Week 8) where they were given a new diary for the time between visits. Participants were asked to perform an assessment of their perceived flushing intensity after their completion of VAS assessment once daily after their first flushing episode (if more than one happens to occur). The scale was from 0 to 3, where 0 represents no flushing, 1 represents mild flushing, 2 represents moderate flushing, and 3 represents severe flushing. (NCT00903617)
Timeframe: Up to Week 8
| Intervention | Participants (Count of Participants) | |||||||||
|---|---|---|---|---|---|---|---|---|---|---|
| Baseline, No flushing | Week 2, No flushing | Week 4, No flushing | Week 6, No flushing | Baseline, Mild flushing | Week 2, Mild flushing | Week 4, Mild flushing | Week 6, Mild flushing | Baseline, Moderate flushing | Baseline, Severe flushing | |
| GSK256073 150 mg | 9 | 18 | 15 | 14 | 6 | 1 | 1 | 1 | 1 | 2 |
| GSK256073 5 mg | 17 | 15 | 12 | 14 | 1 | 1 | 1 | 0 | 0 | 0 |
| GSK256073 50 mg | 14 | 17 | 17 | 14 | 1 | 1 | 0 | 0 | 1 | 0 |
| Placebo | 18 | 19 | 20 | 20 | 0 | 0 | 0 | 0 | 0 | 0 |
Blood samples for analysis of fasting levels of TC, TG, glucose, LDLc, ApoAII and ApoB was collected at Baseline (Week 0) and Week 2, 4, 6 and 8. Baseline was defined at Week 0. Change from Baseline was calculated by subtracting the post-Baseline value from the Baseline value. Percent change from Baseline was calculated by multiplying change from baseline value with 100. (NCT00903617)
Timeframe: Baseline (Week 0) up to Week 8
| Intervention | Percent change (Mean) | |||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| ApoAII, Week 2 | ApoAII, Week 4 | ApoAII, Week 6 | ApoAII, Week 8 | ApoB, Week 2 | ApoB, Week 4 | ApoB, Week 6 | ApoB, Week 8 | Glucose, Week 2 | Glucose, Week 4 | Glucose, Week 6 | Glucose, Week 8 | LDLc, Week 2 | LDLc, Week 4 | LDLc, Week 6 | LDLc, Week 8 | TC, Week 2 | TC, Week 4 | TC, Week 6 | TC, Week 8 | TG, Week 2 | TG, Week 4 | TG, Week 6 | TG, Week 8 | |
| GSK256073 150 mg | -4.7 | -3.8 | -5.3 | 3.3 | -2.2 | 2.0 | 5.9 | 6.5 | 0.6 | -2.2 | -2.6 | -6.1 | 2.1 | 7.6 | 7.7 | 8.4 | -3.3 | -0.8 | -0.5 | 1.3 | 8.9 | 3.0 | 8.4 | 21.0 |
| GSK256073 5 mg | -9.9 | 7.2 | 5.9 | 7.9 | -8.1 | -3.4 | -3.8 | -2.8 | 0.1 | -0.3 | 0.7 | -1.0 | -2.7 | -6.7 | -4.3 | -1.8 | -4.0 | -4.8 | -2.9 | -0.5 | 2.2 | 6.1 | 7.5 | 6.6 |
| GSK256073 50 mg | -6.9 | 3.4 | -7.0 | 5.2 | -9.8 | -6.1 | -6.5 | -5.1 | 7.0 | 1.2 | 2.3 | 2.6 | -10.0 | -7.4 | -7.9 | -6.5 | -9.3 | -5.9 | -6.2 | -5.7 | 16.9 | 10.1 | 0.9 | 5.6 |
| Placebo | 0.1 | -1.6 | 2.0 | 2.1 | -2.6 | -0.8 | -1.8 | -0.8 | 2.8 | 0.9 | 1.0 | -0.0 | -2.9 | -3.0 | 0.6 | -3.0 | -2.4 | -2.5 | -1.3 | -2.1 | 6.6 | 3.5 | -4.6 | -4.0 |
Blood samples for analysis of fasting levels of HDLc and ApoA1 was collected at Baseline (Week 0) and Week 2, 4, 6 and 8. Baseline was defined at Week 0. Change from Baseline was calculated by subtracting the post-Baseline value from the Baseline value. Percent change from Baseline was calculated by multiplying change from baseline value with 100. (NCT00903617)
Timeframe: Baseline (Week 0) up to Week 8
| Intervention | Percent change (Mean) | |||||||
|---|---|---|---|---|---|---|---|---|
| ApoA1, Week 2 | ApoA1, Week 4 | ApoA1, Week 6 | ApoA1, Week 8 | HDLc, Week 2 | HDLc, Week 4 | HDLc, Week 6 | HDLc, Week 8 | |
| GSK256073 150 mg | -5.9 | -6.5 | -1.1 | -2.0 | -9.4 | -7.0 | -7.9 | -9.1 |
| GSK256073 5 mg | -2.7 | 1.4 | 0.6 | 4.2 | -2.2 | -1.2 | -2.0 | 4.2 |
| GSK256073 50 mg | -5.7 | -1.8 | -3.1 | -0.2 | -8.4 | -4.6 | -4.9 | -1.9 |
| Placebo | -2.2 | 1.3 | -1.3 | 0.3 | -2.8 | -1.3 | 0.2 | 1.1 |
Blood samples for analysis of insulin was collected at Baseline (Week 0) and Week 2, 4, 6 and 8. Baseline was defined at Week 0. Change from Baseline was calculated by subtracting the post-Baseline value from the Baseline value. Percent change from Baseline was calculated by multiplying change from Baseline value with 100. (NCT00903617)
Timeframe: Baseline (Week 0) up to Week 8
| Intervention | Percent change (Mean) | |||
|---|---|---|---|---|
| Week 2 | Week 4 | Week 6 | Week 8 | |
| GSK256073 150 mg | 25.3 | 13.2 | 4.2 | 13.7 |
| GSK256073 5 mg | 23.1 | 9.1 | 16.6 | 2.8 |
| GSK256073 50 mg | 21.2 | 16.3 | 17.8 | 18.3 |
| Placebo | -2.8 | -3.8 | -3.4 | -0.2 |
Blood samples for analysis of Lp[a] was collected at Baseline (Week 0) and Week 2, 4, 6 and 8. Baseline was defined at Week 0. Change from Baseline was calculated by subtracting the post-Baseline value from the Baseline value. Percent change from Baseline was calculated by multiplying change from Baseline value with 100. (NCT00903617)
Timeframe: Baseline (Week 0) up to Week 8
| Intervention | Percent change (Mean) | |||
|---|---|---|---|---|
| Week 2 | Week 4 | Week 6 | Week 8 | |
| GSK256073 150 mg | 4.5 | 1.6 | 6.5 | 6.4 |
| GSK256073 5 mg | 1.8 | -6.6 | 2.7 | 4.0 |
| GSK256073 50 mg | -10.3 | -11.3 | -7.3 | -15.8 |
| Placebo | -4.6 | -1.7 | -1.7 | -5.6 |
Blood samples for analysis of NEFA was collected at Baseline (Week 0) and Week 2, 4, 6 and 8. Baseline was defined at Week 0. Change from Baseline was calculated by subtracting the post-Baseline value from the Baseline value. Percent change from Baseline was calculated by multiplying change from Baseline value with 100. (NCT00903617)
Timeframe: Baseline (Week 0) up to Week 8
| Intervention | Percent change (Mean) | |||
|---|---|---|---|---|
| Week 2 | Week 4 | Week 6 | Week 8 | |
| GSK256073 150 mg | 29.1 | 26.2 | 8.0 | 19.3 |
| GSK256073 5 mg | 32.1 | 38.8 | 47.8 | 56.6 |
| GSK256073 50 mg | 16.8 | 37.4 | 29.1 | 59.4 |
| Placebo | 24.4 | 7.0 | -1.1 | 10.4 |
After 12 weeks of treatment, to assess the increase of high-density lipoprotein cholesterol in patients with Type 2 diabetes when compared to placebo (NCT00485758)
Timeframe: Baseline and 12 Weeks
| Intervention | Percent change at Wk 12 compared to Bl (Least Squares Mean) |
|---|---|
| Extended Release Niacin/Laropiprant | 25.4 |
| Placebo | 2.2 |
After 12 Weeks of treatment, to assess the reduction of low-density lipoprotein cholesterol in patients with Type 2 diabetes when compared to placebo (NCT00485758)
Timeframe: Baseline and 12 Weeks
| Intervention | Percent change at Wk 12 compared to Bl (Least Squares Mean) |
|---|---|
| Extended Release Niacin/Laropiprant | -15.8 |
| Placebo | 2.1 |
after 12 weeks of treatment, to assess the reduction of triglycerides in patients with Type 2 diabetes when compared to placebo (NCT00485758)
Timeframe: Baseline and 12 Weeks
| Intervention | Percent change at Wk 12 compared to Bl (Median) |
|---|---|
| Extended Release Niacin/Laropiprant | -22.2 |
| Placebo | 2.3 |
Change From Baseline to 4 Months in Serum Non-HDL cholesterol (NCT00286234)
Timeframe: baseline and 4 months
| Intervention | mg/dl (Mean) |
|---|---|
| Dual Placebo | 145 |
| Niaspan | 155 |
| Lovaza | 133 |
| Combined Therapy | 170 |
Change From Baseline to 4 Months in Serum Triglycerides (NCT00286234)
Timeframe: 4 months
| Intervention | mg/dl (Mean) |
|---|---|
| Dual Placebo | 233 |
| Niaspan | 157 |
| Lovaza | 176 |
| Combined Therapy | 156 |
The absolute change in maximum relative flow mediated dilation (FMD) (%) of the brachial artery from baseline to week 24. (NCT01426438)
Timeframe: 0 and 24 weeks
| Intervention | % FMD (Median) |
|---|---|
| Arm A: Extended-release Niacin With Aspirin | 0.60 |
| Arm B: Fenofibrate | 0.50 |
Change in C-reactive protein from week 0 to week 24. (NCT01426438)
Timeframe: 0 and 24 weeks
| Intervention | ug/ml (Median) |
|---|---|
| Arm A: Extended-release Niacin With Aspirin | -0.6 |
| Arm B: Fenofibrate | 0.7 |
Absolute change in total cholesterol from week 0 to week 24. (NCT01426438)
Timeframe: 0 and 24 weeks
| Intervention | mg/dL (Median) |
|---|---|
| Arm A: Extended-release Niacin With Aspirin | -9 |
| Arm B: Fenofibrate | -2 |
Change in D-Dimer from week 0 to week 24 (NCT01426438)
Timeframe: 0 and 24 weeks
| Intervention | ug/ml (Median) |
|---|---|
| Arm A: Extended-release Niacin With Aspirin | 0.06 |
| Arm B: Fenofibrate | 0.06 |
Change in total HDL particles from week 0 to week 24 (NCT01426438)
Timeframe: 0 and 24 weeks
| Intervention | nmol/L (Median) |
|---|---|
| Arm A: Extended-release Niacin With Aspirin | -1.7 |
| Arm B: Fenofibrate | 4.3 |
Absolute change from week 0 to week 24 in insulin resistance as estimated by HOMA-IR (NCT01426438)
Timeframe: 0 and 24 weeks
| Intervention | HOMA IR Score (Median) |
|---|---|
| Arm A: Extended-release Niacin With Aspirin | 1.3 |
| Arm B: Fenofibrate | 0.3 |
Change in IL-6 from week 0 to week 24 (NCT01426438)
Timeframe: 0 and 24 weeks
| Intervention | pg/ml (Median) |
|---|---|
| Arm A: Extended-release Niacin With Aspirin | 0.1 |
| Arm B: Fenofibrate | 0.2 |
Change in Large HDL Particles from week 0 to week 24 (NCT01426438)
Timeframe: 0 and 24 weeks
| Intervention | nmol/L (Median) |
|---|---|
| Arm A: Extended-release Niacin With Aspirin | 0.9 |
| Arm B: Fenofibrate | -0.3 |
Change in LDL cholesterol (mg/dL) from week 0 to week 24. (NCT01426438)
Timeframe: 0 and 24 weeks
| Intervention | mg/dL (Median) |
|---|---|
| Arm A: Extended-release Niacin With Aspirin | -1 |
| Arm B: Fenofibrate | 7 |
Change in non-HDL Cholesterol (mg/dL) from week 0 to week 24. (NCT01426438)
Timeframe: 0 and 24 weeks
| Intervention | mg/dL (Median) |
|---|---|
| Arm A: Extended-release Niacin With Aspirin | -17 |
| Arm B: Fenofibrate | -4 |
Change in Small LDL particles from week 0 to week 24. (NCT01426438)
Timeframe: 0 and 24 weeks
| Intervention | nmol/L (Median) |
|---|---|
| Arm A: Extended-release Niacin With Aspirin | -176 |
| Arm B: Fenofibrate | -119 |
Change in Triglycerides (mg/dL) from week 0 to week 24. (NCT01426438)
Timeframe: 0 and 24 weeks
| Intervention | mg/dL (Median) |
|---|---|
| Arm A: Extended-release Niacin With Aspirin | -65 |
| Arm B: Fenofibrate | -54 |
Among men, change in HDL Cholesterol (mg/dL) from week 0 to week 24. (NCT01426438)
Timeframe: 0 and 24 weeks
| Intervention | mg/dL (Median) |
|---|---|
| Arm A: Extended-release Niacin With Aspirin | 3 |
| Arm B: Fenofibrate | 6.5 |
Among women, change in HDL cholesterol (mg/dL) from week 0 to week 24. (NCT01426438)
Timeframe: 0 and 24 weeks
| Intervention | mg/dL (Median) |
|---|---|
| Arm A: Extended-release Niacin With Aspirin | 16 |
| Arm B: Fenofibrate | 8 |
"The primary endpoint of this study is carotid plaque lipid composition identified by MRI. The determination of plaque lipid content for each carotid artery will be performed using the automated interactive system. These measurements will be performed from the MRI scans at four time points blinded to time sequence of MRI examinations, patient treatment, lipid levels and clinical course.~Volume Measurements: Contours were placed around the lumen, outer-wall boundaries, and plaque features of carotid artery. (Arterial wall area) = (outer-wall area) - (lumen area). Volume calculated as: area x 2 mm (slice thickness). Tissue volume/wall volume x (100%) is presented as percentage. Annualized change presented mm^3/year (for volume) and as percentage change/year." (NCT00715273)
Timeframe: Measured at Years 1, 2, and 3
| Intervention | mm^3/year (Mean) |
|---|---|
| 1 - Single Therapy Group | -4.6 |
| 2 - Double Therapy Group | -15.1 |
| 3 - Triple Therapy Group | -9.4 |
"The primary endpoint of this study is carotid plaque lipid composition identified by MRI. The determination of plaque lipid content for each carotid artery will be performed using the automated interactive system. These measurements will be performed from the MRI scans at four time points blinded to time sequence of MRI examinations, patient treatment, lipid levels and clinical course.~Volume Measurements: Contours were placed around the lumen, outer-wall boundaries, and plaque features of carotid artery. (Arterial wall area) = (outer-wall area) - (lumen area). Volume calculated as: area x 2 mm (slice thickness). Tissue volume/wall volume x (100%) is presented as percentage. Annualized change presented mm^3/year (for volume) and as percentage change/year." (NCT00715273)
Timeframe: Measured at Years 1, 2, and 3
| Intervention | percentage change/year (Mean) | |
|---|---|---|
| LRNC change | Wall Volume change | |
| 1 - Single Therapy Group | -1.6 | -0.6 |
| 2 - Double Therapy Group | -3.6 | -1.4 |
| 3 - Triple Therapy Group | -2.8 | -1.2 |
Any cardiovascular events such as death from any cause, nonfatal myocardial infarction, stroke, and revascularization procedures (PCI or CABG) due to unstable ischemia will be recorded and verified. (NCT00715273)
Timeframe: Measured at Years 3, 4, and 5
| Intervention | Participants (Count of Participants) | ||
|---|---|---|---|
| Composite Measured at Year 3 | Composite Measured at Year 4 (cumulative) | Composite Measured at Year 5 (cumulative) | |
| 1 - Single Therapy Group | 6 | 7 | 9 |
| 2 - Double Therapy Group | 6 | 11 | 11 |
| 3 - Triple Therapy Group | 7 | 9 | 9 |
The relationship between maximum flushing severity and overall flushing troublesomeness was evaluated by examining the Spearman rank-order correlation. Flushing severity was assessed using the FAST on a scale of 1 to 10, with 10 being the most severe. Overall flushing troublesomeness was assessed using the FAST on a scale of 1 to 10, with 10 being the most troublesome. (NCT00630877)
Timeframe: Week 1
| Intervention | Spearman correlation coefficient (Number) |
|---|---|
| Modified Intent-to-Treat (m-ITT) Population | 0.66 |
The relationship between mean flushing severity and overall flushing troublesomeness was evaluated by examining the Spearman rank-order correlation. Flushing severity was assessed using the FAST on a scale of 1 to 10, with 10 being the most severe. Overall flushing troublesomeness was assessed using the FAST on a scale of 1 to 10, with 10 being the most troublesome. (NCT00630877)
Timeframe: Week 1
| Intervention | Spearman correlation coefficient (Number) |
|---|---|
| Modified Intent-to-Treat (m-ITT) Population | 0.64 |
The relationship between the change in maximum flushing severity scores from Week 1 to Week 2, and the subject-rated overall treatment effect scale administered at Week 2, was assessed by examining the Spearman rank-order correlation. Flushing severity was assessed using the FAST on a scale of 1 to 10, with 10 being the most severe. The overall treatment effect was assessed on a scale of 1 (symptoms are worse since study start), 2 (symptoms are about the same since study start), or 3 (symptoms are better since study start). (NCT00630877)
Timeframe: Week 1 to Week 2
| Intervention | Spearman correlation coefficient (Number) |
|---|---|
| Modified Intent-to-Treat (m-ITT) Population | -0.42 |
The relationship between the change in mean flushing severity scores from Week 1 to Week 2, and the subject-rated overall treatment effect scale administered at Week 2, was assessed by examining the Spearman rank-order correlation. Flushing severity was assessed using the FAST on a scale of 1 to 10, with 10 being the most severe. The overall treatment effect was assessed on a scale of 1 (symptoms are worse since study start), 2 (symptoms are about the same since study start), or 3 (symptoms are better since study start). (NCT00630877)
Timeframe: Week 1 to Week 2
| Intervention | Spearman correlation coefficient (Number) |
|---|---|
| Modified Intent-to-Treat (m-ITT) Population | -0.44 |
The change in maximum flushing severity scores from study start to Day 43 was compared in subjects classified as responders vs. nonresponders. Flushing severity was assessed using the FAST on a scale of 1 to 10, with 10 being the most severe. Changes in maximum flushing severity scores were negative if flushing symptoms improved and positive if flushing symptoms worsened. (NCT00630877)
Timeframe: Study start to Day 43
| Intervention | Units on a scale (Number) |
|---|---|
| Responders | -1.85 |
| Nonresponders | -0.18 |
The change in mean flushing severity scores from study start to Day 43 was compared in subjects classified as responders vs. nonresponders. Flushing severity was assessed using the FAST on a scale of 1 to 10, with 10 being the most severe. Changes in mean flushing severity scores were negative if flushing symptoms improved and positive if flushing symptoms worsened. (NCT00630877)
Timeframe: Study start to Day 43
| Intervention | Units on a scale (Number) |
|---|---|
| Responders | -0.51 |
| Nonresponders | 0.15 |
Test-retest reliability of the maximum flushing severity score was evaluated. The intraclass correlation coefficient comparing flushing severity scores for Week 1 and Week 2 was examined to determine test-retest reliability. Flushing severity was assessed using the FAST on a scale of 1 to 10, with 10 being the most severe. (NCT00630877)
Timeframe: Week 1 to Week 2
| Intervention | Intraclass correlation coefficient (Number) |
|---|---|
| Subjects With Stable Flushing Symptoms | 0.40 |
Test-retest reliability of the mean flushing severity score was evaluated. The intraclass correlation coefficient comparing flushing severity scores for Week 1 and Week 2 was examined to determine test-retest reliability. Flushing severity was assessed using the FAST on a scale of 1 to 10, with 10 being the most severe. (NCT00630877)
Timeframe: Week 1 to Week 2
| Intervention | Intraclass correlation coefficient (Number) |
|---|---|
| Subjects With Stable Flushing Symptoms | 0.75 |
The severity of flushing events was assessed as none, mild, moderate, severe, or very severe using the FAST. The maximum severity of flushing events overall during the study was compared among treatment groups. (NCT00630877)
Timeframe: Week 1 to Week 6
| Intervention | Percentage of subjects (Number) | |||||
|---|---|---|---|---|---|---|
| None | Mild | None/Mild | Moderate | Severe | Very Severe | |
| NER Placebo/ASA Placebo | 37 | 38 | 75 | 22 | 2 | 0 |
| NER/ASA | 26 | 23 | 49 | 34 | 17 | 0 |
| NER/ASA Placebo | 14 | 16 | 30 | 31 | 32 | 7 |
Flushing was assessed daily using the Flushing Assessment Tool via an e-diary and the mean number of flushing events per subject per week considered moderate or greater in severity was calculated. Flushing events were rated by the subject using a categorical scale of mild, moderate, severe, or very severe. (NCT00626392)
Timeframe: 4 weeks
| Intervention | Number of Events per Subject per Week (Mean) |
|---|---|
| Any Acetylsalicylic Acid | 0.3 |
| No Acetylsalicylic Acid | 0.8 |
Subjects assessed the severity of flushing events on a 10-point numeric rating scale of 1-3 (mild), 4-6 (moderate), 7-9 (severe), and 10 (very severe) using the Flushing Assessment Tool via an e-diary. For subjects who did not experience flushing, a score of 0 was assigned. Flushing was assessed daily. (NCT00626392)
Timeframe: 4 weeks
| Intervention | Scores on a Scale (Mean) |
|---|---|
| Any Acetylsalicylic Acid | 3.1 |
| No Acetylsalicylic Acid | 5.1 |
The maximum severity of flushing events subjects experienced during Week 1 of NER treatment was categorized as none, mild, moderate, severe, or very severe using the Flushing Assessment Tool via an e-diary. Flushing was assessed daily and the percentage of subjects with maximum flushing severity in each category was calculated. (NCT00626392)
Timeframe: From Baseline to end of Week 1
| Intervention | Percentage of Subjects (Number) | |||||
|---|---|---|---|---|---|---|
| None | Mild | None/mild | Moderate | Severe | Very severe | |
| Any Acetylsalicylic Acid | 57 | 28 | 85 | 11 | 4 | 1 |
| No Acetylsalicylic Acid | 48 | 24 | 71 | 17 | 8 | 4 |
The maximum severity of flushing events subjects experienced during 4 weeks of NER treatment was categorized as none, mild, moderate, severe, or very severe using the Flushing Assessment Tool via an e-diary. Flushing was assessed daily and the percentage of subjects with maximum flushing severity in each category was calculated. (NCT00626392)
Timeframe: 4 weeks
| Intervention | Percentage of Subjects (Number) | |||||
|---|---|---|---|---|---|---|
| None | Mild | None/Mild | Moderate | Severe | Very severe | |
| Any Acetylsalicylic Acid | 30 | 28 | 58 | 28 | 11 | 4 |
| No Acetylsalicylic Acid | 15 | 14 | 30 | 35 | 23 | 13 |
(NCT00479388)
Timeframe: Baseline and 12 Weeks
| Intervention | Percent (Least Squares Mean) |
|---|---|
| ER Niacin/Laropiprant + Run-in Statin | 15.8 |
| Run-in Statin Dose Doubled | 0.2 |
(NCT00479388)
Timeframe: Baseline and 12 Weeks
| Intervention | Percent (Least Squares Mean) |
|---|---|
| ER Niacin/Laropiprant + Run-in Statin | -10.0 |
| Run-in Statin Dose Doubled | -5.5 |
(NCT00479388)
Timeframe: Baseline and 12 Weeks
| Intervention | Percent (Median) |
|---|---|
| ER Niacin/Laropiprant + Run-in Statin | -17.6 |
| Run-in Statin Dose Doubled | -4.0 |
HDL-C (mg/dL): Fasting lipid levels (NCT00246376)
Timeframe: Measured at 24 weeks
| Intervention | mg/dl (Mean) |
|---|---|
| Group 1 - Usual Care | 37.1 |
| Group 2 - Diet/Exercise Only | 38.7 |
| Group 3 - Diet/Exercise + Fenofibrate | 40.7 |
| Group 4 - Diet/Exercise + Niacin | 41.8 |
| Group 5 - Diet/Exercise + Fenofibrate + Niacin | 44.8 |
non-HDL-C (mg/dL): Fasting lipid levels (NCT00246376)
Timeframe: Measured at 24 weeks
| Intervention | mg/dl (Mean) |
|---|---|
| Group 1 - Usual Care | 162.2 |
| Group 2 - Diet/Exercise Only | 165.4 |
| Group 3 - Diet/Exercise + Fenofibrate | 145.8 |
| Group 4 - Diet/Exercise + Niacin | 154 |
| Group 5 - Diet/Exercise + Fenofibrate + Niacin | 137.1 |
Total cholesterol (mg/dL): Fasting lipid levels (NCT00246376)
Timeframe: Measured at 24 weeks
| Intervention | mg/dL (Mean) |
|---|---|
| Group 1 - Usual Care | 195.6 |
| Group 2 - Diet/Exercise Only | 200.1 |
| Group 3 - Diet/Exercise + Fenofibrate | 184 |
| Group 4 - Diet/Exercise + Niacin | 190.8 |
| Group 5 - Diet/Exercise + Fenofibrate + Niacin | 178.4 |
Total cholesterol : HDL-C ratio: Fasting lipid levels (NCT00246376)
Timeframe: Measured at 24 weeks
| Intervention | ratio (Mean) |
|---|---|
| Group 1 - Usual Care | 5.2 |
| Group 2 - Diet/Exercise Only | 5.1 |
| Group 3 - Diet/Exercise + Fenofibrate | 4.5 |
| Group 4 - Diet/Exercise + Niacin | 4.6 |
| Group 5 - Diet/Exercise + Fenofibrate + Niacin | 4 |
Triglycerides (mg/dL): Fasting lipid levels (NCT00246376)
Timeframe: Measured at 24 weeks
| Intervention | mg/dL (Mean) |
|---|---|
| Group 1 - Usual Care | 199 |
| Group 2 - Diet/Exercise Only | 216.9 |
| Group 3 - Diet/Exercise + Fenofibrate | 155.1 |
| Group 4 - Diet/Exercise + Niacin | 177.6 |
| Group 5 - Diet/Exercise + Fenofibrate + Niacin | 135.6 |
"Body cell mass (kg)~Fat mass (kg)" (NCT00246376)
Timeframe: Measured at 24 weeks
| Intervention | kg (Mean) | |
|---|---|---|
| Body cell mass | Fat mass | |
| Group 1 - Usual Care | 59.6 | 36.8 |
| Group 2 - Diet/Exercise | 67.3 | 37.5 |
| Group 3 - Diet/Exercise + Fenofibrate | 66.6 | 35.8 |
| Group 4 - Diet/Exercise + Niacin | 67.1 | 37.7 |
| Group 5 - Diet/Exercise + Fenofibrate + Niacin | 68.2 | 36.2 |
Adiponectin (micrograms/ml) (NCT00246376)
Timeframe: Measured at 24 weeks
| Intervention | micrograms/ml (Mean) | |||
|---|---|---|---|---|
| Fasting insulin | HOMA-IR | Insulin sensitvity index | Adiponectin | |
| Group 1 - Usual Care | 8.7 | 1.92 | 3.54 | 7.12 |
| Group 2 - Diet/Exercise Only | 6.7 | 1.38 | 4.95 | 6.04 |
| Group 3 - Diet/Exercise + Fenofibrate | 9.5 | 2.02 | 3.81 | 5.24 |
| Group 4 - Diet/Exercise + Niacin | 11.9 | 2.76 | 2.88 | 11.01 |
| Group 5 - Diet/Exercise + Fenofibrate + Niacin | 10.3 | 2.38 | 2.38 | 10.34 |
Flushing symptoms were recorded using participant's response to the Global Flushing Severity Score (GFSS), which assesses the overall severity of the flushing experience (including redness, warmth, tingling, or itching) using a scale with response categories of None, Mild, Moderate, Severe, and Extreme. The categories were supplemented with numbers 0 to 10 to allow for greater precision within each category (None=0, Mild=1-3, Moderate=4-6, Severe=7-9, Extreme=10). The daily response was recorded in the morning, and reflected the symptoms experienced during the previous 24 hours. (NCT00961636)
Timeframe: Week 21 to Week 32
| Intervention | Participants (Number) |
|---|---|
| ERN/LRPT | 71 |
| ERN/LRPT Then ERN | 173 |
| Placebo | 19 |
Flushing symptoms were recorded using participant's response to the Global Flushing Severity Score (GFSS), which assessed the overall severity of the flushing experience, using a scale of 0 (no symptom) to 10 (extreme). The number of days/week was derived as: 7*(total number of days with GFSS ≥4 across Weeks 21-32 divided by the total number of days with nonmissing GFSS across the same period). The number of days/week with a GFSS ≥4 for each participant was listed in 1 of the following 6 categories: 0, >0 to 0.5, >0.5 to 1, >1 to 2, >2 to 3, and >3 days per week. (NCT00961636)
Timeframe: Week 21 to Week 32
| Intervention | Participants (Number) | |||||
|---|---|---|---|---|---|---|
| 0 Days per week | >0 to ≤ 0.5 Days per week | >0.5 to ≤1 Days per week | >1.0 to ≤2 Days per week | >2 to ≤3 Days per week | >3 Days per week | |
| ERN/LRPT | 291 | 43 | 3 | 8 | 1 | 16 |
| ERN/LRPT Then ERN | 181 | 74 | 32 | 30 | 17 | 20 |
| Placebo | 188 | 7 | 4 | 3 | 1 | 4 |
To evaluate the effect of two daily tomatoes consumption on HDL-c levels. (NCT01342666)
Timeframe: Baseline and after one month
| Intervention | mg/dL (Mean) | |
|---|---|---|
| Baseline HDL-c | Final HDL-c | |
| Cucumber Consumption | 36.8 | 35.8 |
| Tomato Consumption | 36.5 | 41.6 |
121 reviews available for niacin and Dyslipidemia
| Article | Year |
|---|---|
Nicotinic acid receptor agonists.
Topics: Animals; Chemistry, Pharmaceutical; Drug Design; Dyslipidemias; Humans; Kinetics; Ligands; Mice; Mod | 2008 |
Dietary niacin intake and risk of dyslipidemia: A pooled analysis of three prospective cohort studies.
Topics: Cohort Studies; Diet; Dyslipidemias; Humans; Niacin; Prospective Studies | 2022 |
Novel Niacin Receptor Agonists: A Promising Strategy for the Treatment of Dyslipidemia.
Topics: Dyslipidemias; Humans; Niacin; Pyrazoles; Receptors, G-Protein-Coupled | 2021 |
Dyslipidaemia in nephrotic syndrome: mechanisms and treatment.
Topics: Anticholesteremic Agents; Cholesterol; Cholesterol, HDL; Cholesterol, VLDL; Dyslipidemias; Ezetimibe | 2018 |
Precision Medicine and Personalized Management of Lipoprotein and Lipid Disorders in Chronic and End-Stage Kidney Disease.
Topics: Anticholesteremic Agents; Cardiovascular Diseases; Dyslipidemias; Ezetimibe; Fenofibrate; Humans; Hy | 2018 |
Effects of high-density lipoprotein targeting treatments on cardiovascular outcomes: A systematic review and meta-analysis.
Topics: Adult; Aged; Biomarkers; Cardiovascular Diseases; Cholesterol Ester Transfer Proteins; Cholesterol, | 2019 |
Current pharmacotherapy for the treatment of dyslipidemia associated with HIV infection.
Topics: Anti-Retroviral Agents; Drug Interactions; Dyslipidemias; Ezetimibe; HIV Infections; Humans; Hydroxy | 2019 |
High-density lipoprotein in uremic patients: metabolism, impairment, and therapy.
Topics: Acetamides; Acetates; Acetyl-CoA C-Acetyltransferase; Anti-Inflammatory Agents; Anticholesteremic Ag | 2014 |
Managing the residual cardiovascular disease risk associated with HDL-cholesterol and triglycerides in statin-treated patients: a clinical update.
Topics: Antibodies, Monoclonal; Anticholesteremic Agents; Apolipoprotein A-I; Benzimidazoles; Cardiovascular | 2013 |
Niacin, an old drug with a new twist.
Topics: Animals; Dyslipidemias; Humans; Hypolipidemic Agents; Lipoproteins, HDL; Lipoproteins, LDL; Niacin; | 2013 |
The therapeutic role of niacin in dyslipidemia management.
Topics: Animals; Cholesterol; Disease Management; Dyslipidemias; Humans; Hypolipidemic Agents; Lipoproteins; | 2014 |
[HDL, or non-HDL: that is the question. Possibilities of pharmacological treatment in residual dyslipidaemia].
Topics: Anticholesteremic Agents; Azetidines; Cholesterol Ester Transfer Proteins; Cholesterol, HDL; Cholest | 2014 |
The nuances of atherogenic dyslipidemia in diabetes: focus on triglycerides and current management strategies.
Topics: Atherosclerosis; Comorbidity; Diabetes Mellitus, Type 2; Diabetic Angiopathies; Disease Management; | 2013 |
Should low high-density lipoprotein cholesterol (HDL-C) be treated?
Topics: Cardiovascular Diseases; Cholesterol, HDL; Dyslipidemias; Female; Fibric Acids; Humans; Hydroxymethy | 2014 |
Combination therapy in dyslipidemia: where are we now?
Topics: Azetidines; Bile Acids and Salts; Cardiovascular Diseases; Cholesterol; Cholesterol, LDL; Clinical T | 2014 |
Ongoing challenges for pharmacotherapy for dyslipidemia.
Topics: Cardiovascular Diseases; Cholesterol Ester Transfer Proteins; Clinical Trials as Topic; Dyslipidemia | 2015 |
The recent national lipid association recommendations: how do they compare to other established dyslipidemia guidelines?
Topics: Anticholesteremic Agents; Disease Management; Dyslipidemias; Fatty Acids, Omega-3; Fibric Acids; Hum | 2015 |
Treatment of dyslipidemia in HIV.
Topics: Anti-HIV Agents; Anticholesteremic Agents; Azetidines; Cholesterol, HDL; Cholesterol, LDL; Diet Ther | 2015 |
Antilipidemic Drug Therapy Today and in the Future.
Topics: Cholesterol, HDL; Cholesterol, LDL; Dyslipidemias; Ezetimibe; Humans; Hydroxymethylglutaryl-CoA Redu | 2016 |
Niacin therapy and the risk of new-onset diabetes: a meta-analysis of randomised controlled trials.
Topics: Diabetes Mellitus; Drug Therapy, Combination; Dyslipidemias; Humans; Hydroxymethylglutaryl-CoA Reduc | 2016 |
Niacin as antidyslipidemic drug.
Topics: Cholesterol, HDL; Cholesterol, LDL; Dyslipidemias; Humans; Hypolipidemic Agents; Male; Niacin; Trigl | 2015 |
Nonstatin therapies for management of dyslipidemia: a review.
Topics: Anticholesteremic Agents; Cardiovascular Diseases; Cholesterol Ester Transfer Proteins; Cholesterol, | 2015 |
Niacin Alternatives for Dyslipidemia: Fool's Gold or Gold Mine? Part I: Alternative Niacin Regimens.
Topics: Clinical Trials as Topic; Coronary Disease; Dyslipidemias; Humans; Hydroxymethylglutaryl-CoA Reducta | 2016 |
Niacin Alternatives for Dyslipidemia: Fool's Gold or Gold Mine? Part II: Novel Niacin Mimetics.
Topics: Animals; Biomimetic Materials; Cardiovascular Diseases; Cholesterol; Dyslipidemias; Humans; Hypolipi | 2016 |
Translational and Therapeutic Approaches to the Understanding and Treatment of Dyslipidemia.
Topics: Biological Transport; Cholesterol; Cholesterol Ester Transfer Proteins; Cholesterol, HDL; Cholestero | 2016 |
Nicotinic acid: recent developments.
Topics: Animals; Coronary Disease; Dyslipidemias; Humans; Lipid Metabolism; Niacin; Receptors, G-Protein-Cou | 2008 |
Managing dyslipidemia in chronic kidney disease.
Topics: Algorithms; Anticholesteremic Agents; Cardiovascular Diseases; Clofibric Acid; Dyslipidemias; Fatty | 2008 |
Lipid screening and cardiovascular health in childhood.
Topics: Anion Exchange Resins; Anticholesteremic Agents; Atherosclerosis; Cardiovascular Diseases; Child; Di | 2008 |
Lipid screening and cardiovascular health in childhood.
Topics: Anion Exchange Resins; Anticholesteremic Agents; Atherosclerosis; Cardiovascular Diseases; Child; Di | 2008 |
Lipid screening and cardiovascular health in childhood.
Topics: Anion Exchange Resins; Anticholesteremic Agents; Atherosclerosis; Cardiovascular Diseases; Child; Di | 2008 |
Lipid screening and cardiovascular health in childhood.
Topics: Anion Exchange Resins; Anticholesteremic Agents; Atherosclerosis; Cardiovascular Diseases; Child; Di | 2008 |
Strategies for reducing cardiovascular risk in patients with hypertriglyceridemia.
Topics: Aged; Anticholesteremic Agents; Cardiovascular Diseases; Clofibric Acid; Dyslipidemias; Exercise; Fa | 2007 |
When high is low: raising low levels of high-density lipoprotein cholesterol.
Topics: Anticholesteremic Agents; Cardiovascular Diseases; Cholesterol, HDL; Clofibric Acid; Dyslipidemias; | 2008 |
Fixed-dose combination of extended-release niacin plus simvastatin for lipid disorders.
Topics: Animals; Cholesterol; Clinical Trials as Topic; Coronary Disease; Delayed-Action Preparations; Drug | 2008 |
Extended-release niacin/laropiprant: reducing niacin-induced flushing to better realize the benefit of niacin in improving cardiovascular risk factors.
Topics: Animals; Delayed-Action Preparations; Drug Combinations; Dyslipidemias; Flushing; Humans; Hypolipide | 2008 |
Niacin: an old drug rejuvenated.
Topics: Adipocytes; Anti-Inflammatory Agents; Antioxidants; Apolipoprotein A-I; Cardiovascular Diseases; Cho | 2009 |
A review of the current status of the management of mixed dyslipidemia associated with diabetes mellitus and metabolic syndrome.
Topics: Anticholesteremic Agents; Cholesterol, LDL; Clofibric Acid; Diabetes Mellitus, Type 2; Drug Therapy, | 2008 |
The importance of recognizing and treating low levels of high-density lipoprotein cholesterol: a new era in atherosclerosis management.
Topics: Apolipoprotein A-I; Atherosclerosis; Cardiovascular Diseases; Cholesterol Ester Transfer Proteins; C | 2008 |
Targeting multiple dyslipidemias with fixed combinations--focus on extended release niacin and simvastatin.
Topics: Cardiovascular Diseases; Delayed-Action Preparations; Drug Combinations; Dyslipidemias; Humans; Hydr | 2008 |
Managing diabetic dyslipidemia: beyond statin therapy.
Topics: Cholesterol, HDL; Cholesterol, LDL; Diabetes Complications; Diabetes Mellitus, Type 2; Diabetic Angi | 2009 |
Lipid management in the geriatric patient.
Topics: Aged; Anticholesteremic Agents; Cardiovascular Diseases; Cholesterol; Clofibric Acid; Coronary Disea | 2009 |
Nicotinic acid: a new look at an old drug.
Topics: Dyslipidemias; Humans; Lipoproteins; Lipoproteins, IDL; Lipoproteins, VLDL; Niacin | 2009 |
The use of lipid-lowering drug therapy in children and adolescents.
Topics: Adolescent; Atherosclerosis; Azetidines; Bile Acids and Salts; Cardiovascular Diseases; Child; Chole | 2009 |
[Diabetic dyslipoproteinemia: beyond LDL].
Topics: Atherosclerosis; Cardiovascular Diseases; Cholesterol, HDL; Cholesterol, LDL; Cholesterol, VLDL; Chy | 2009 |
Fibrates in the treatment of cardiovascular risk and atherogenic dyslipidaemia.
Topics: Cardiovascular Diseases; Cholesterol, HDL; Cholesterol, LDL; Clofibric Acid; Creatinine; Diabetes Me | 2009 |
Management of complex lipid abnormalities with a fixed dose combination of simvastatin and extended release niacin.
Topics: Aged; Cardiovascular Diseases; Delayed-Action Preparations; Drug Combinations; Dyslipidemias; Female | 2009 |
Niacin: a re-emerging pharmaceutical for the treatment of dyslipidaemia.
Topics: Animals; Atherosclerosis; Drug Design; Dyslipidemias; Humans; Hypolipidemic Agents; Medication Adher | 2009 |
Niacin: a re-emerging pharmaceutical for the treatment of dyslipidaemia.
Topics: Animals; Atherosclerosis; Drug Design; Dyslipidemias; Humans; Hypolipidemic Agents; Medication Adher | 2009 |
Niacin: a re-emerging pharmaceutical for the treatment of dyslipidaemia.
Topics: Animals; Atherosclerosis; Drug Design; Dyslipidemias; Humans; Hypolipidemic Agents; Medication Adher | 2009 |
Niacin: a re-emerging pharmaceutical for the treatment of dyslipidaemia.
Topics: Animals; Atherosclerosis; Drug Design; Dyslipidemias; Humans; Hypolipidemic Agents; Medication Adher | 2009 |
The mechanism and mitigation of niacin-induced flushing.
Topics: Arachidonic Acid; Delayed-Action Preparations; Dyslipidemias; Flushing; Humans; Hypolipidemic Agents | 2009 |
The obesity, metabolic syndrome, and type 2 diabetes mellitus pandemic: II. Therapeutic management of atherogenic dyslipidemia.
Topics: Cardiovascular Diseases; Clofibric Acid; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Dysli | 2009 |
Thinking beyond low-density lipoprotein cholesterol: strategies to further reduce cardiovascular risk.
Topics: Biomarkers; Cardiovascular Diseases; Cholesterol, HDL; Cholesterol, LDL; Clofibric Acid; Drug Therap | 2009 |
[Combination pharmacotherapy therapy in the management of atherogenic dyslipidemia].
Topics: Adult; Anticholesteremic Agents; Atherosclerosis; Clofibric Acid; Drug Therapy, Combination; Dyslipi | 2005 |
Triglycerides and HDL cholesterol: stars or second leads in diabetes?
Topics: Atherosclerosis; Cardiovascular Diseases; Cholesterol, HDL; Coronary Disease; Diabetes Complications | 2009 |
Triglycerides and HDL cholesterol: stars or second leads in diabetes?
Topics: Atherosclerosis; Cardiovascular Diseases; Cholesterol, HDL; Coronary Disease; Diabetes Complications | 2009 |
Triglycerides and HDL cholesterol: stars or second leads in diabetes?
Topics: Atherosclerosis; Cardiovascular Diseases; Cholesterol, HDL; Coronary Disease; Diabetes Complications | 2009 |
Triglycerides and HDL cholesterol: stars or second leads in diabetes?
Topics: Atherosclerosis; Cardiovascular Diseases; Cholesterol, HDL; Coronary Disease; Diabetes Complications | 2009 |
Mechanisms of flushing due to niacin and abolition of these effects.
Topics: Aspirin; Dose-Response Relationship, Drug; Dyslipidemias; Humans; Hypolipidemic Agents; Indoles; Nia | 2009 |
Prediction of cardiovascular event risk reduction from lipid changes associated with high potency dyslipidemia therapy.
Topics: Algorithms; Azetidines; Cardiovascular Diseases; Dyslipidemias; Ezetimibe; Female; Humans; Hypolipid | 2010 |
Review of extended-release niacin/laropiprant fixed combination in the treatment of mixed dyslipidemia and primary hypercholesterolemia.
Topics: Biomarkers; Cholesterol, HDL; Cholesterol, LDL; Drug Combinations; Dyslipidemias; Flushing; Humans; | 2009 |
[Global therapy of diabetic dyslipidemia: benefits and new therapeutic approaches].
Topics: Clofibric Acid; Diabetes Complications; Drug Therapy, Combination; Dyslipidemias; Humans; Hydroxymet | 2010 |
Dyslipidemia in the elderly: should it be treated?
Topics: Age Factors; Aged; Aged, 80 and over; Aging; Dyslipidemias; Fibric Acids; Health Services Needs and | 2010 |
A new paradigm for managing dyslipidemia with combination therapy: laropiprant + niacin + simvastatin.
Topics: Delayed-Action Preparations; Drug Therapy, Combination; Dyslipidemias; Humans; Hydroxymethylglutaryl | 2010 |
Niacin and fibrates in atherogenic dyslipidemia: pharmacotherapy to reduce cardiovascular risk.
Topics: Animals; Atherosclerosis; Cardiovascular Diseases; Clinical Trials as Topic; Drug Therapy, Combinati | 2010 |
Management of dyslipidemia in people with type 2 diabetes mellitus.
Topics: Azetidines; Cholesterol, LDL; Clinical Trials as Topic; Diabetes Mellitus, Type 2; Dyslipidemias; Ez | 2010 |
A "hot" topic in dyslipidemia management--"how to beat a flush": optimizing niacin tolerability to promote long-term treatment adherence and coronary disease prevention.
Topics: Aspirin; Attitude to Health; Coronary Disease; Delayed-Action Preparations; Dose-Response Relationsh | 2010 |
Laropiprant plus niacin for dyslipidemia and prevention of cardiovascular disease.
Topics: Atherosclerosis; Cardiovascular Diseases; Cholesterol, HDL; Cholesterol, LDL; Drug Therapy, Combinat | 2010 |
Niacin's role in the statin era.
Topics: Cholesterol, HDL; Cholesterol, LDL; Drug Therapy, Combination; Dyslipidemias; Humans; Hydroxymethylg | 2010 |
Beyond statin therapy: a review of the management of residual risk in diabetes mellitus.
Topics: Atherosclerosis; Clofibric Acid; Diabetes Complications; Diabetes Mellitus; Drug Therapy, Combinatio | 2010 |
Genetic determinants of plasma triglycerides.
Topics: Adaptor Proteins, Signal Transducing; Angiopoietin-Like Protein 3; Angiopoietin-like Proteins; Angio | 2011 |
'Trig-onometry': non-high-density lipoprotein cholesterol as a therapeutic target in dyslipidaemia.
Topics: Adult; Azetidines; Cardiovascular Diseases; Cholesterol, HDL; Dyslipidemias; Ezetimibe; Fatty Acids, | 2011 |
Niacin extended release (ER)/simvastatin (Simcor®): a guide to its use in lipid regulation.
Topics: Clinical Trials as Topic; Delayed-Action Preparations; Drug Combinations; Dyslipidemias; Humans; Hyp | 2010 |
Future of GPR109A agonists in the treatment of dyslipidaemia.
Topics: Adipocytes; Cardiovascular Diseases; Dyslipidemias; Hepatocytes; Humans; Niacin; Nicotinic Agonists; | 2011 |
Important considerations for treatment with dietary supplement versus prescription niacin products.
Topics: Cardiovascular Diseases; Cholesterol, HDL; Delayed-Action Preparations; Dietary Supplements; Dyslipi | 2011 |
Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management.
Topics: Cardiovascular Diseases; Cholesterol, HDL; Clinical Trials as Topic; Dyslipidemias; Fatty Acids, Ome | 2011 |
Optimal pharmacotherapy to combat the atherogenic lipid triad.
Topics: Atherosclerosis; Dyslipidemias; Fibric Acids; Humans; Hypolipidemic Agents; Niacin; Treatment Outcom | 2011 |
Progress in HDL-based therapies for atherosclerosis.
Topics: Animals; Apolipoproteins; Atherosclerosis; Dyslipidemias; Endothelium, Vascular; Fibric Acids; Fibri | 2011 |
Treatment approaches for diabetes and dyslipidemia.
Topics: Apolipoprotein B-100; Cholesterol, HDL; Cholesterol, LDL; Diabetes Complications; Diabetes Mellitus; | 2011 |
Combination therapy for dyslipidemia.
Topics: Anticholesteremic Agents; Azetidines; Drug Therapy, Combination; Dyslipidemias; Ezetimibe; Fibric Ac | 2011 |
The facts behind niacin.
Topics: Biomarkers; Cardiovascular Diseases; Cholesterol, HDL; Cholesterol, LDL; Drug Therapy, Combination; | 2011 |
Acanthosis nigricans in the setting of niacin therapy.
Topics: Acanthosis Nigricans; Cardiovascular Diseases; Diagnosis, Differential; Dyslipidemias; Epidermal Gro | 2011 |
Niacin: the evidence, clinical use, and future directions.
Topics: Atherosclerosis; Disease Progression; Dyslipidemias; Humans; Hypolipidemic Agents; Lipids; Niacin | 2012 |
Niacin: vitamin and antidyslipidemic drug.
Topics: Animals; Clinical Trials as Topic; Dyslipidemias; Humans; Hypolipidemic Agents; Lipid Metabolism; Li | 2012 |
Safety and tolerability of extended-release niacin with laropiprant.
Topics: Animals; Delayed-Action Preparations; Drug Combinations; Dyslipidemias; Flushing; Humans; Hypolipide | 2012 |
Niacin in cardiovascular disease: recent preclinical and clinical developments.
Topics: Animals; Anti-Inflammatory Agents; Biomarkers; Cardiovascular Diseases; Cholesterol, HDL; Dyslipidem | 2012 |
Combination treatment with atorvastatin plus niacin provides effective control of complex dyslipidemias: a literature review.
Topics: Atorvastatin; Coronary Disease; Drug Therapy, Combination; Dyslipidemias; Flushing; Heptanoic Acids; | 2012 |
[Multimodal therapy of dyslipidemia].
Topics: Animals; Biomarkers; Drug Therapy, Combination; Dyslipidemias; Fatty Acids, Omega-3; Fibric Acids; H | 2011 |
Extended-release niacin with laropiprant : a review on efficacy, clinical effectiveness and safety.
Topics: Animals; Cardiovascular Diseases; Delayed-Action Preparations; Dyslipidemias; Evidence-Based Medicin | 2012 |
Niacin: chemical forms, bioavailability, and health effects.
Topics: Biological Availability; Cardiovascular Diseases; Cholesterol, HDL; Cholesterol, LDL; Dose-Response | 2012 |
Management of dyslipidemias in the presence of the metabolic syndrome or type 2 diabetes.
Topics: Atherosclerosis; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Dyslipidemias; Fibric Acids; | 2012 |
The role of niacin in lipid-lowering treatment: are we aiming too high?
Topics: Animals; Atherosclerosis; Cardiovascular Diseases; Diabetes Complications; Drug Therapy, Combination | 2013 |
Extended-release niacin/lovastatin: the first combination product for dyslipidemia.
Topics: Delayed-Action Preparations; Drug Combinations; Dyslipidemias; Humans; Lovastatin; Niacin | 2004 |
Management of dyslipidemia in women in the post-hormone therapy era.
Topics: Anticholesteremic Agents; Azetidines; Cardiovascular Diseases; Cholesterol, HDL; Clofibric Acid; Die | 2005 |
What is the most effective strategy for managing diabetic dyslipidaemia?
Topics: Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Diabetes Mellitus; Diabetic Angiopathies; Drug | 2005 |
The potential role of HDL- and LDL-cholesterol modulation in atheromatous plaque development.
Topics: Atherosclerosis; Cholesterol, HDL; Cholesterol, LDL; Dyslipidemias; Humans; Hydroxymethylglutaryl-Co | 2005 |
Clinical practice. Low HDL cholesterol levels.
Topics: Adult; Alcohol Drinking; Cholesterol; Cholesterol, HDL; Clofibric Acid; Diet, Fat-Restricted; Drug T | 2005 |
Clinical practice. Low HDL cholesterol levels.
Topics: Adult; Alcohol Drinking; Cholesterol; Cholesterol, HDL; Clofibric Acid; Diet, Fat-Restricted; Drug T | 2005 |
Clinical practice. Low HDL cholesterol levels.
Topics: Adult; Alcohol Drinking; Cholesterol; Cholesterol, HDL; Clofibric Acid; Diet, Fat-Restricted; Drug T | 2005 |
Clinical practice. Low HDL cholesterol levels.
Topics: Adult; Alcohol Drinking; Cholesterol; Cholesterol, HDL; Clofibric Acid; Diet, Fat-Restricted; Drug T | 2005 |
Beyond low-density lipoprotein: addressing the atherogenic lipid triad in type 2 diabetes mellitus and the metabolic syndrome.
Topics: Cholesterol, HDL; Cholesterol, LDL; Coronary Artery Disease; Diabetes Mellitus, Type 2; Diet; Drug T | 2005 |
Prolonged-release nicotinic acid: a review of its use in the treatment of dyslipidaemia.
Topics: Delayed-Action Preparations; Dose-Response Relationship, Drug; Drug Therapy, Combination; Dyslipidem | 2005 |
Strategies for modifying high-density lipoprotein cholesterol: a role for nicotinic acid.
Topics: Cardiovascular Diseases; Cholesterol, HDL; Cholesterol, LDL; Dyslipidemias; Humans; Hydroxymethylglu | 2005 |
[Treatment of dyslipidemia: how and when to combine lipid lowering drugs].
Topics: Anticholesteremic Agents; Azetidines; Cholesterol, HDL; Clofibric Acid; Drug Therapy, Combination; D | 2006 |
Clinical evidence for use of acetyl salicylic acid in control of flushing related to nicotinic acid treatment.
Topics: Aspirin; Dose-Response Relationship, Drug; Dyslipidemias; Flushing; Humans; Hypolipidemic Agents; Ni | 2006 |
Niacin-ER/statin combination for the treatment of dyslipidemia: focus on low high-density lipoprotein cholesterol.
Topics: Cholesterol, HDL; Cholesterol, LDL; Clinical Trials as Topic; Coronary Disease; Drug Combinations; D | 2006 |
Dyslipidaemia in diabetes.
Topics: Azetidines; Bezafibrate; Diabetes Complications; Diabetic Angiopathies; Drug Therapy, Combination; D | 2006 |
Atherogenic dyslipidemia in metabolic syndrome and type 2 diabetes: therapeutic options beyond statins.
Topics: Clofibric Acid; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Dyslipidemias; Humans; Hydroxy | 2006 |
Optimal lipid modification: the rationale for combination therapy.
Topics: Anticholesteremic Agents; Azetidines; Cardiovascular Diseases; Cholesterol, LDL; Clinical Trials as | 2005 |
Lipoprotein metabolism and lipid management in chronic kidney disease.
Topics: Antioxidants; Cardiovascular Diseases; Chronic Disease; Dyslipidemias; Humans; Hydroxymethylglutaryl | 2007 |
Cardiovascular metabolic syndrome - an interplay of, obesity, inflammation, diabetes and coronary heart disease.
Topics: Cardiovascular Diseases; Coronary Disease; Diabetes Mellitus, Type 2; Dyslipidemias; Endothelium, Va | 2007 |
The significance of low HDL-cholesterol levels in an ageing society at increased risk for cardiovascular disease.
Topics: Age Factors; Aged; Aging; Cardiovascular Diseases; Cholesterol, HDL; Cholesterol, LDL; Drug Therapy, | 2007 |
Management of dyslipidemia in children and adolescents with systemic lupus erythematosus.
Topics: Adolescent; Bile Acids and Salts; Child; Complementary Therapies; Dyslipidemias; Humans; Hydroxychlo | 2007 |
Do we need a statin-nicotinic acid-aspirin mini-polypill to treat combined hyperlipidaemia?
Topics: Aspirin; Drug Combinations; Dyslipidemias; Health Services Needs and Demand; Humans; Hydroxymethylgl | 2007 |
Correction of low HDL cholesterol to reduce cardiovascular risk: practical considerations relating to the therapeutic use of prolonged-release nicotinic acid (Niaspan).
Topics: Cardiovascular Diseases; Cholesterol, HDL; Delayed-Action Preparations; Dyslipidemias; Flushing; Hum | 2007 |
Treatment of dyslipidemia to reduce cardiovascular risk in patients with multiple risk factors.
Topics: Cardiovascular Diseases; Clofibric Acid; Dyslipidemias; Fatty Acids, Omega-3; Humans; Hydroxymethylg | 2007 |
Prolonged-release nicotinic acid for the management of dyslipidemia: an update including results from the NAUTILUS study.
Topics: Atorvastatin; Azetidines; Cholesterol, HDL; Delayed-Action Preparations; Drug Therapy, Combination; | 2007 |
Targeting high-density lipoprotein cholesterol in the management of cardiovascular disease.
Topics: Cardiovascular Diseases; Cholesterol, HDL; Clofibric Acid; Dyslipidemias; Humans; Hydroxymethylgluta | 2007 |
Nicotinic acid: an old drug with a promising future.
Topics: Animals; Dyslipidemias; Flushing; Humans; Hypolipidemic Agents; Lipid Metabolism; Niacin; Receptors, | 2008 |
Cardiovascular disease risk of type 2 diabetes mellitus and metabolic syndrome: focus on aggressive management of dyslipidemia.
Topics: Anticholesteremic Agents; Atorvastatin; Cardiovascular Diseases; Cholesterol, HDL; Cholesterol, LDL; | 2005 |
Combination therapy in the management of mixed dyslipidaemia.
Topics: Cardiovascular Diseases; Cholesterol, LDL; Diabetes Mellitus, Type 2; Drug Administration Routes; Dr | 2008 |
Do statins reduce events in patients with metabolic syndrome?
Topics: C-Reactive Protein; Cholesterol, LDL; Dyslipidemias; Humans; Hydroxymethylglutaryl-CoA Reductase Inh | 2008 |
Niacin use and cutaneous flushing: mechanisms and strategies for prevention.
Topics: Anticholesteremic Agents; Dyslipidemias; Flushing; Humans; Hypolipidemic Agents; Niacin; Risk Factor | 2008 |
Mechanism of action of niacin.
Topics: Anticholesteremic Agents; Apolipoproteins; Cholesterol, HDL; Cholesterol, LDL; Cholesterol, VLDL; Dy | 2008 |
Reducing the residual risk of 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibitor therapy with combination therapy.
Topics: Anticholesteremic Agents; C-Reactive Protein; Cholesterol, HDL; Coronary Artery Disease; Drug Therap | 2008 |
Safety of niacin and simvastatin combination therapy.
Topics: Anticholesteremic Agents; Drug Therapy, Combination; Dyslipidemias; Humans; Hypolipidemic Agents; Ni | 2008 |
Evidence to support aggressive management of high-density lipoprotein cholesterol: implications of recent imaging trials.
Topics: Anticholesteremic Agents; Cholesterol, HDL; Clofibric Acid; Coronary Artery Disease; Disease Progres | 2008 |
Niacin and lipoprotein(a): facts, uncertainties, and clinical considerations.
Topics: Anticholesteremic Agents; Cholesterol, HDL; Cholesterol, LDL; Dyslipidemias; Humans; Hypertriglyceri | 2008 |
Comprehensive lipid management versus aggressive low-density lipoprotein lowering to reduce cardiovascular risk.
Topics: Anticholesteremic Agents; Apolipoprotein A-I; Cardiovascular Diseases; Cholesterol, HDL; Cholesterol | 2008 |
Nicotinic acid, alone and in combinations, for reduction of cardiovascular risk.
Topics: Anticholesteremic Agents; Cardiovascular Diseases; Cholesterol, HDL; Cholesterol, LDL; Clofibric Aci | 2008 |
The safety of niacin in the US Food and Drug Administration adverse event reporting database.
Topics: Adverse Drug Reaction Reporting Systems; Anticholesteremic Agents; Delayed-Action Preparations; Drug | 2008 |
Effects of niacin on glucose control in patients with dyslipidemia.
Topics: Blood Glucose; Dyslipidemias; Humans; Hypolipidemic Agents; Lipids; Niacin; Practice Guidelines as T | 2008 |
Nicotinic acid, nicotinamide, and nicotinamide riboside: a molecular evaluation of NAD+ precursor vitamins in human nutrition.
Topics: Animals; Caloric Restriction; Candida glabrata; Dietary Supplements; Dyslipidemias; Humans; NAD; Nia | 2008 |
53 trials available for niacin and Dyslipidemia
| Article | Year |
|---|---|
Serious Adverse Effects of Extended-release Niacin/Laropiprant: Results From the Heart Protection Study 2-Treatment of HDL to Reduce the Incidence of Vascular Events (HPS2-THRIVE) Trial.
Topics: Cardiovascular Diseases; Delayed-Action Preparations; Diabetes Mellitus; Double-Blind Method; Drug T | 2019 |
The efficacy of niacin supplementation in type 2 diabetes patients: Study protocol of a randomized controlled trial.
Topics: Adult; Delayed-Action Preparations; Diabetes Mellitus, Type 2; Dietary Supplements; Double-Blind Met | 2021 |
Genetic Variants Associated With Plasma Lipids Are Associated With the Lipid Response to Niacin.
Topics: Biomarkers; Drug Therapy, Combination; Dyslipidemias; Female; Genetic Variation; Genome-Wide Associa | 2018 |
A Randomized, Placebo-Controlled Trial to Assess the Effects of 8 Weeks of Administration of GSK256073, a Selective GPR109A Agonist, on High-Density Lipoprotein Cholesterol in Subjects With Dyslipidemia.
Topics: Aged; Cholesterol, HDL; Drug Administration Routes; Dyslipidemias; Female; Flushing; Humans; Male; M | 2019 |
Comparison of switch to the highest dose of rosuvastatin vs. add-on nicotinic acid vs. add-on fenofibrate for mixed dyslipidaemia.
Topics: Cholesterol, HDL; Delayed-Action Preparations; Double-Blind Method; Drug Therapy, Combination; Dysli | 2013 |
Effects of niacin on the incidence of new onset diabetes and cardiovascular events in patients with normoglycaemia and impaired fasting glucose.
Topics: Blood Glucose; Coronary Disease; Diabetes Mellitus, Type 2; Diabetic Angiopathies; Double-Blind Meth | 2013 |
Effect of hypolipidemic treatment on emerging risk factors in mixed dyslipidemia: a randomized pilot trial.
Topics: 1-Alkyl-2-acetylglycerophosphocholine Esterase; Adult; Aged; Apolipoproteins B; Atherosclerosis; C-R | 2013 |
Lipid-modulating treatments for mixed dyslipidemia increase HDL-associated phospholipase A2 activity with differential effects on HDL subfractions.
Topics: Aged; Blood Chemical Analysis; Delayed-Action Preparations; Dose-Response Relationship, Drug; Dyslip | 2013 |
Xanthophylls, phytosterols and pre-β1-HDL are differentially affected by fenofibrate and niacin HDL-raising in a cross-over study.
Topics: Apolipoprotein A-II; Cross-Over Studies; Dyslipidemias; Female; Fenofibrate; High-Density Lipoprotei | 2013 |
Effect of niacin on high-density lipoprotein apolipoprotein A-I kinetics in statin-treated patients with type 2 diabetes mellitus.
Topics: Aged; Apolipoprotein A-I; Apolipoproteins B; Biomarkers; Cholesterol, HDL; Cholesterol, LDL; Cross-O | 2014 |
Effect of Nicotinic acid/Laropiprant in the lipoprotein(a) concentration with regard to baseline lipoprotein(a) concentration and LPA genotype.
Topics: Apolipoproteins B; Cholesterol; Cholesterol, HDL; Cholesterol, LDL; Dyslipidemias; Female; Genotype; | 2014 |
Effect of switch to the highest dose of rosuvastatin versus add-on-statin fenofibrate versus add-on-statin nicotinic acid/laropiprant on oxidative stress markers in patients with mixed dyslipidemia.
Topics: Aged; Apolipoprotein B-100; Atorvastatin; Bilirubin; Biomarkers; Dinoprost; Drug Therapy, Combinatio | 2014 |
Short-term effects of extended-release niacin with and without the addition of laropiprant on endothelial function in individuals with low HDL-C: a randomized, controlled crossover trial.
Topics: Aged; Cholesterol, HDL; Cross-Over Studies; Delayed-Action Preparations; Double-Blind Method; Dyslip | 2014 |
Effect of niacin on FGF23 concentration in chronic kidney disease.
Topics: Aged; Calcium; Delayed-Action Preparations; Double-Blind Method; Drug Therapy, Combination; Dyslipid | 2014 |
Effects of extended-release niacin/laropiprant, simvastatin, and the combination on correlations between apolipoprotein B, LDL cholesterol, and non-HDL cholesterol in patients with dyslipidemia.
Topics: Adult; Aged; Apolipoproteins B; Biomarkers; Cardiovascular Diseases; Cholesterol, HDL; Cholesterol, | 2014 |
Effects of niacin, statin, and fenofibrate on circulating proprotein convertase subtilisin/kexin type 9 levels in patients with dyslipidemia.
Topics: Aged; Apoptosis; Biomarkers; Dose-Response Relationship, Drug; Drug Therapy, Combination; Dyslipidem | 2015 |
Remarkable quantitative and qualitative differences in HDL after niacin or fenofibrate therapy in type 2 diabetic patients.
Topics: Adult; Aged; Antioxidants; Biomarkers; Cholesterol, HDL; Cross-Sectional Studies; Diabetes Mellitus, | 2015 |
Extended-release niacin/laropiprant significantly improves lipid levels in type 2 diabetes mellitus irrespective of baseline glycemic control.
Topics: Aged; Biomarkers; Blood Glucose; Delayed-Action Preparations; Diabetes Mellitus, Type 2; Double-Blin | 2015 |
Effects of niacin and omega-3 fatty acids on the apolipoproteins in overweight patients with elevated triglycerides and reduced HDL cholesterol.
Topics: Adult; Apolipoproteins; Biomarkers; Cholesterol, HDL; Delayed-Action Preparations; Double-Blind Meth | 2015 |
Extended-Release Niacin Versus Fenofibrate in HIV-Infected Participants With Low High-Density Lipoprotein Cholesterol: Effects on Endothelial Function, Lipoproteins, and Inflammation.
Topics: Adult; Brachial Artery; C-Reactive Protein; Cholesterol, HDL; Delayed-Action Preparations; Dyslipide | 2015 |
Effect of Extended-Release Niacin/Laropiprant Combination on Plasma Adiponectin and Insulin Resistance in Chinese Patients with Dyslipidaemia.
Topics: Adiponectin; Adolescent; Adult; Aged; Aged, 80 and over; Blood Glucose; China; Dyslipidemias; Female | 2015 |
Effect of Extended-Release Niacin on High-Density Lipoprotein (HDL) Functionality, Lipoprotein Metabolism, and Mediators of Vascular Inflammation in Statin-Treated Patients.
Topics: Adult; Aged; Apolipoprotein B-100; Biomarkers; Cholesterol, HDL; Cholesterol, LDL; Cross-Over Studie | 2015 |
Effects of extended-release niacin on the postprandial metabolism of Lp(a) and ApoB-100-containing lipoproteins in statin-treated men with type 2 diabetes mellitus.
Topics: Aged; Apolipoprotein B-100; Apolipoproteins A; Biomarkers; Cross-Over Studies; Delayed-Action Prepar | 2015 |
Niacin Therapy Increases High-Density Lipoprotein Particles and Total Cholesterol Efflux Capacity But Not ABCA1-Specific Cholesterol Efflux in Statin-Treated Subjects.
Topics: Animals; Atorvastatin; ATP Binding Cassette Transporter 1; Biological Transport; Carotid Artery Dise | 2016 |
Extended-Release Niacin/Laropiprant Improves Overall Efficacy of Postprandial Reverse Cholesterol Transport.
Topics: Aged; Animals; Anticholesteremic Agents; Apolipoprotein B-100; Biological Transport; Cell Line, Tumo | 2016 |
Effects of Vascular and Nonvascular Adverse Events and of Extended-Release Niacin With Laropiprant on Health and Healthcare Costs.
Topics: Aged; Aged, 80 and over; Biomarkers; Cardiovascular Diseases; China; Cost-Benefit Analysis; Delayed- | 2016 |
Lipid-Modifying Efficacy and Tolerability of Anacetrapib Added to Ongoing Statin Therapy in Patients with Hypercholesterolemia or Low High-Density Lipoprotein Cholesterol.
Topics: Aged; Anticholesteremic Agents; Cholesterol Ester Transfer Proteins; Cholesterol, HDL; Cholesterol, | 2017 |
Lipid-modifying efficacy and tolerability of extended-release niacin/laropiprant in patients with primary hypercholesterolaemia or mixed dyslipidaemia.
Topics: Adolescent; Adult; Aged; Aged, 80 and over; Delayed-Action Preparations; Double-Blind Method; Drug C | 2008 |
Flushing ASsessment Tool (FAST): psychometric properties of a new measure assessing flushing symptoms and clinical impact of niacin therapy.
Topics: Adult; Aged; Aged, 80 and over; Computers, Handheld; Delayed-Action Preparations; Double-Blind Metho | 2009 |
Acetylsalicylic acid reduces niacin extended-release-induced flushing in patients with dyslipidemia.
Topics: Administration, Oral; Adult; Aged; Aspirin; Delayed-Action Preparations; Dose-Response Relationship, | 2009 |
Flushing profile of extended-release niacin/laropiprant versus gradually titrated niacin extended-release in patients with dyslipidemia with and without ischemic cardiovascular disease.
Topics: Adolescent; Adult; Aged; Aged, 80 and over; Confidence Intervals; Delayed-Action Preparations; Doubl | 2009 |
Flushing profile of extended-release niacin/laropiprant at initiation of therapy in Asian lipid clinic patients.
Topics: Adult; Aged; Asian People; Double-Blind Method; Drug Combinations; Dyslipidemias; Female; Flushing; | 2009 |
Flushing profile of extended-release niacin/laropiprant at initiation of therapy in Asian lipid clinic patients.
Topics: Adult; Aged; Asian People; Double-Blind Method; Drug Combinations; Dyslipidemias; Female; Flushing; | 2009 |
Flushing profile of extended-release niacin/laropiprant at initiation of therapy in Asian lipid clinic patients.
Topics: Adult; Aged; Asian People; Double-Blind Method; Drug Combinations; Dyslipidemias; Female; Flushing; | 2009 |
Flushing profile of extended-release niacin/laropiprant at initiation of therapy in Asian lipid clinic patients.
Topics: Adult; Aged; Asian People; Double-Blind Method; Drug Combinations; Dyslipidemias; Female; Flushing; | 2009 |
Hypophosphatemic effect of niacin in patients without renal failure: a randomized trial.
Topics: Aged; Biomarkers; Calcium; Chronic Disease; Delayed-Action Preparations; Double-Blind Method; Drug T | 2010 |
Efficacy and safety of extended-release niacin/laropiprant plus statin vs. doubling the dose of statin in patients with primary hypercholesterolaemia or mixed dyslipidaemia.
Topics: Adult; Aged; Aged, 80 and over; Cholesterol, HDL; Cholesterol, LDL; Delayed-Action Preparations; Dos | 2010 |
Once-daily extended-release niacin lowers serum phosphorus concentrations in patients with metabolic syndrome dyslipidemia.
Topics: Calcium; Delayed-Action Preparations; Drug Administration Schedule; Dyslipidemias; Glomerular Filtra | 2011 |
Effects of low-dose of niacin associated to simvastatin in the treatment of mixed dyslipidemia Salgad.
Topics: Aged; Aspirin; Delayed-Action Preparations; Diabetes Mellitus, Type 2; Drug Combinations; Dyslipidem | 2010 |
Combination of niacin extended-release and simvastatin results in a less atherogenic lipid profile than atorvastatin monotherapy.
Topics: Adult; Aged; Aged, 80 and over; Anticholesteremic Agents; Atherosclerosis; Atorvastatin; Delayed-Act | 2010 |
Safety, tolerance, and efficacy of extended-release niacin monotherapy for treating dyslipidemia risks in persons with chronic tetraplegia: a randomized multicenter controlled trial.
Topics: Adolescent; Adult; Aged; Cholesterol; Chronic Disease; Delayed-Action Preparations; Double-Blind Met | 2011 |
Extended-release niacin/laropiprant lipid-altering consistency across patient subgroups.
Topics: Adult; Aged; Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Delayed-Action Preparations; Doub | 2011 |
Extended-release niacin/laropiprant lipid-altering consistency across patient subgroups.
Topics: Adult; Aged; Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Delayed-Action Preparations; Doub | 2011 |
Extended-release niacin/laropiprant lipid-altering consistency across patient subgroups.
Topics: Adult; Aged; Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Delayed-Action Preparations; Doub | 2011 |
Extended-release niacin/laropiprant lipid-altering consistency across patient subgroups.
Topics: Adult; Aged; Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Delayed-Action Preparations; Doub | 2011 |
Extended-release niacin/laropiprant lipid-altering consistency across patient subgroups.
Topics: Adult; Aged; Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Delayed-Action Preparations; Doub | 2011 |
Extended-release niacin/laropiprant lipid-altering consistency across patient subgroups.
Topics: Adult; Aged; Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Delayed-Action Preparations; Doub | 2011 |
Extended-release niacin/laropiprant lipid-altering consistency across patient subgroups.
Topics: Adult; Aged; Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Delayed-Action Preparations; Doub | 2011 |
Extended-release niacin/laropiprant lipid-altering consistency across patient subgroups.
Topics: Adult; Aged; Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Delayed-Action Preparations; Doub | 2011 |
Extended-release niacin/laropiprant lipid-altering consistency across patient subgroups.
Topics: Adult; Aged; Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Delayed-Action Preparations; Doub | 2011 |
Extended-release niacin/laropiprant lipid-altering consistency across patient subgroups.
Topics: Adult; Aged; Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Delayed-Action Preparations; Doub | 2011 |
Extended-release niacin/laropiprant lipid-altering consistency across patient subgroups.
Topics: Adult; Aged; Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Delayed-Action Preparations; Doub | 2011 |
Extended-release niacin/laropiprant lipid-altering consistency across patient subgroups.
Topics: Adult; Aged; Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Delayed-Action Preparations; Doub | 2011 |
Extended-release niacin/laropiprant lipid-altering consistency across patient subgroups.
Topics: Adult; Aged; Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Delayed-Action Preparations; Doub | 2011 |
Extended-release niacin/laropiprant lipid-altering consistency across patient subgroups.
Topics: Adult; Aged; Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Delayed-Action Preparations; Doub | 2011 |
Extended-release niacin/laropiprant lipid-altering consistency across patient subgroups.
Topics: Adult; Aged; Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Delayed-Action Preparations; Doub | 2011 |
Extended-release niacin/laropiprant lipid-altering consistency across patient subgroups.
Topics: Adult; Aged; Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Delayed-Action Preparations; Doub | 2011 |
Combination of niacin and fenofibrate with lifestyle changes improves dyslipidemia and hypoadiponectinemia in HIV patients on antiretroviral therapy: results of "heart positive," a randomized, controlled trial.
Topics: Adiponectin; Adult; Aged; Anti-Retroviral Agents; Double-Blind Method; Dyslipidemias; Exercise; Fema | 2011 |
Effect of niacin on erectile function in men suffering erectile dysfunction and dyslipidemia.
Topics: Dyslipidemias; Erectile Dysfunction; Humans; Hypolipidemic Agents; Male; Middle Aged; Niacin; Severi | 2011 |
Efficacy and tolerability of a new extended-release formulation of nicotinic acid in Korean adults with mixed dyslipidemia: an 8-week, multicenter, prospective, randomized, double-blind, and placebo-controlled trial.
Topics: Blood Pressure; Body Weight; Cholesterol, HDL; Cholesterol, LDL; Delayed-Action Preparations; Double | 2011 |
Niacin extended-release/simvastatin combination therapy produces larger favorable changes in high-density lipoprotein particles than atorvastatin monotherapy.
Topics: Atorvastatin; Biomarkers; Delayed-Action Preparations; Drug Combinations; Dyslipidemias; Female; Hep | 2012 |
Effectiveness and safety of laropiprant on niacin-induced flushing.
Topics: Adolescent; Adult; Aged; Double-Blind Method; Dyslipidemias; Female; Flushing; Humans; Hypolipidemic | 2012 |
Laropiprant attenuates EP3 and TP prostanoid receptor-mediated thrombus formation.
Topics: Blood Coagulation; Blood Platelets; Calcium; Dyslipidemias; Female; Gene Expression Regulation; Huma | 2012 |
Intravenous niacin acutely improves the efficiency of dietary fat storage in lean and obese humans.
Topics: Administration, Intravenous; Adult; Dietary Fats; Dyslipidemias; Female; Humans; Intra-Abdominal Fat | 2012 |
Evaluation of the safety and tolerability of prolonged-release nicotinic acid in a usual care setting: the NAUTILUS study.
Topics: Adult; Aged; Aged, 80 and over; Delayed-Action Preparations; Drug Evaluation; Drug-Related Side Effe | 2006 |
An open-label, crossover study of the pharmacokinetics of Insoluble Drug Delivery-MicroParticle fenofibrate in combination with atorvastatin, simvastatin, and extended-release niacin in healthy volunteers.
Topics: Administration, Oral; Adolescent; Adult; Atorvastatin; Cross-Over Studies; Delayed-Action Preparatio | 2006 |
Genetically determined apo B levels and peak LDL density predict angiographic response to intensive lipid-lowering therapy.
Topics: Adult; Analysis of Variance; Apolipoproteins B; Colestipol; Coronary Angiography; Coronary Stenosis; | 2006 |
Safety and efficacy of extended-release niacin for the treatment of dyslipidaemia in patients with HIV infection: AIDS Clinical Trials Group Study A5148.
Topics: Adult; Blood Glucose; Delayed-Action Preparations; Dyslipidemias; HIV Infections; Humans; Hypolipide | 2006 |
Evaluation of efficacy and safety of fixed dose lovastatin and niacin(ER) combination in asian Indian dyslipidemic patients: a multicentric study.
Topics: Apolipoprotein A-I; Apolipoproteins B; Asian People; Cholesterol; Cholesterol, HDL; Cholesterol, LDL | 2006 |
Effects of laropiprant on nicotinic acid-induced flushing in patients with dyslipidemia.
Topics: Adolescent; Adult; Aged; Creatine Kinase; Cross-Over Studies; Delayed-Action Preparations; Dose-Resp | 2008 |
Long-term safety and efficacy of a combination of niacin extended release and simvastatin in patients with dyslipidemia: the OCEANS study.
Topics: Adult; Aged; Aged, 80 and over; Cholesterol; Cholesterol, HDL; Delayed-Action Preparations; Drug Com | 2008 |
58 other studies available for niacin and Dyslipidemia
| Article | Year |
|---|---|
5-N,N-Disubstituted 5-aminopyrazole-3-carboxylic acids are highly potent agonists of GPR109b.
Topics: Animals; Atherosclerosis; Carboxylic Acids; Chemistry, Pharmaceutical; CHO Cells; Cricetinae; Cricet | 2009 |
Pyrazole acids as niacin receptor agonists for the treatment of dyslipidemia.
Topics: Animals; Cholesterol, HDL; Dyslipidemias; Fatty Acids, Nonesterified; Hypolipidemic Agents; Mice; Ni | 2009 |
Discovery of a novel niacin-lipoic acid dimer N2L attenuating atherosclerosis and dyslipidemia with non-flushing effects.
Topics: Animals; Atherosclerosis; Cell Line; Cricetulus; Dimerization; Disease Models, Animal; Drug Design; | 2020 |
Elevated serum lipoprotein(a) as a risk factor for combined intracranial and extracranial artery stenosis in a child with arterial ischemic stroke: A case report.
Topics: Child; Dyslipidemias; Humans; Intracranial Arteriosclerosis; Lipoprotein(a); Male; Niacin; Risk Fact | 2017 |
Extended-release niacin/laropiprant for lipid management: observational study in clinical practice.
Topics: Adult; Aged; Aged, 80 and over; Cholesterol, HDL; Cholesterol, LDL; Delayed-Action Preparations; Dru | 2013 |
Dyslipidaemia: Failure to THRIVE: the end for niacin?
Topics: Biomarkers; Drug Combinations; Drug Therapy, Combination; Dyslipidemias; Humans; Hydroxymethylglutar | 2013 |
Nicotinic acid plus laropiprant suspended for dyslipidaemia.
Topics: Cholesterol, HDL; Drug Combinations; Dyslipidemias; Humans; Hydroxymethylglutaryl-CoA Reductase Inhi | 2013 |
Dyslipidaemia: cardiovascular prevention--end of the road for niacin?
Topics: Cardiovascular Diseases; Cholesterol, HDL; Cholesterol, LDL; Drug Therapy, Combination; Dyslipidemia | 2014 |
New thinking on niacin use. Using niacin to raise "good" cholesterol doesn't lower your risk of having a heart attack or stroke.
Topics: Cholesterol, HDL; Dyslipidemias; Humans; Hypolipidemic Agents; Niacin | 2014 |
(8) Cardiovascular disease and risk management.
Topics: Antihypertensive Agents; Cardiovascular Diseases; Coronary Disease; Diabetes Complications; Diabetes | 2015 |
(8) Cardiovascular disease and risk management.
Topics: Antihypertensive Agents; Cardiovascular Diseases; Coronary Disease; Diabetes Complications; Diabetes | 2015 |
(8) Cardiovascular disease and risk management.
Topics: Antihypertensive Agents; Cardiovascular Diseases; Coronary Disease; Diabetes Complications; Diabetes | 2015 |
(8) Cardiovascular disease and risk management.
Topics: Antihypertensive Agents; Cardiovascular Diseases; Coronary Disease; Diabetes Complications; Diabetes | 2015 |
Effects of phenotypic and genotypic factors on the lipid responses to niacin in Chinese patients with dyslipidemia.
Topics: Apolipoprotein A-I; Apolipoproteins B; Asian People; Cholesterol, LDL; Diacylglycerol O-Acyltransfer | 2015 |
Placing HPS2-THRIVE in context using Bayesian analysis.
Topics: Bayes Theorem; Cardiovascular Diseases; Delayed-Action Preparations; Dyslipidemias; Flushing; Humans | 2015 |
Pharmacogenetics of cutaneous flushing response to niacin/laropiprant combination in Hong Kong Chinese patients with dyslipidemia.
Topics: Asian People; Body Mass Index; Drug Therapy, Combination; Dyslipidemias; Female; Flushing; Hong Kong | 2015 |
Niacin and Chronic Kidney Disease.
Topics: Biological Transport; Bone Diseases; Cardiovascular Diseases; Dyslipidemias; Humans; Hyperphosphatem | 2015 |
Diabetic dyslipidemia: a practical guide to therapy.
Topics: Clofibric Acid; Coronary Disease; Diabetes Complications; Drug Therapy, Combination; Dyslipidemias; | 2008 |
Molecule of the Month. TREDAPTIVE (nicotinic acid/laropiprant): a new lipid-modifying therapy for the treatment of LDL-C, HDL-C and triglycerides.
Topics: Animals; Cholesterol, HDL; Cholesterol, LDL; Dyslipidemias; Humans; Hypercholesterolemia; Indoles; N | 2008 |
On the road to better dyslipidemia outcomes.
Topics: Azetidines; Cardiovascular Diseases; Clofibric Acid; Dyslipidemias; Ezetimibe; Fish Oils; Humans; Hy | 2009 |
Blood pressure-lowering effects of extended-release niacin alone and extended-release niacin/laropiprant combination: a post hoc analysis of a 24-week, placebo-controlled trial in dyslipidemic patients.
Topics: Adult; Aged; Aged, 80 and over; Blood Pressure; Clinical Trials, Phase III as Topic; Delayed-Action | 2009 |
Dyslipidemia and cardiovascular diseases.
Topics: Benzimidazoles; Cardiovascular Diseases; Dyslipidemias; Humans; Lipoproteins, HDL; Niacin; Propionat | 2009 |
Dyslipidemia and cardiovascular risk: the importance of early prevention.
Topics: Cardiovascular Diseases; Clofibric Acid; Drug Combinations; Dyslipidemias; Fatty Acids, Omega-3; Hum | 2009 |
Reshaping the dyslipidemia management paradigm.
Topics: Adult; Aged; Cholesterol, HDL; Cholesterol, LDL; Clofibric Acid; Coronary Disease; Dyslipidemias; Fe | 2003 |
Achieving cholesterol goals. Current and future drug therapies.
Topics: Aged; Anticholesteremic Agents; Azetidines; Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Dy | 2003 |
CHD risk equivalents and the metabolic syndrome. Trial evidence supports aggressive management.
Topics: Adult; Cholesterol, LDL; Clofibric Acid; Coronary Disease; Diabetes Complications; Dyslipidemias; Fe | 2003 |
Cholesterol efflux potential and antiinflammatory properties of high-density lipoprotein after treatment with niacin or anacetrapib.
Topics: Animals; Anti-Inflammatory Agents; ATP Binding Cassette Transporter 1; ATP Binding Cassette Transpor | 2010 |
Lipid-lowering agents and new onset diabetes mellitus.
Topics: Cardiovascular Diseases; Clofibric Acid; Diabetes Mellitus; Dyslipidemias; Evidence-Based Medicine; | 2010 |
Niacin as potential treatment for dyslipidemia and hyperphosphatemia associated with chronic renal failure: the need for clinical trials.
Topics: Clinical Trials as Topic; Dyslipidemias; Humans; Hyperphosphatemia; Hypolipidemic Agents; Kidney Fai | 2010 |
Lipoprotein-associated phospholipase A2 mass is significantly reduced in dyslipidemic patients treated with lifestyle modification and combination lipid-modifying drug therapy.
Topics: 1-Alkyl-2-acetylglycerophosphocholine Esterase; Allylamine; Anticholesteremic Agents; Azetidines; Bi | 2010 |
Seeing red: flushing out instigators of niacin-associated skin toxicity.
Topics: Cyclooxygenase 2; Dyslipidemias; Flushing; Fumarates; Humans; Myocardial Infarction; Niacin; Recepto | 2010 |
Lipid and transaminase concentrations after formulary conversion of Niaspan to Slo-Niacin.
Topics: Alanine Transaminase; Aspartate Aminotransferases; Cholesterol, HDL; Cholesterol, LDL; Delayed-Actio | 2010 |
Adherence to single-pill combination versus multiple-pill combination lipid-modifying therapy among patients with mixed dyslipidemia in a managed care population.
Topics: Aged; Anticholesteremic Agents; Azetidines; Databases, Factual; Dyslipidemias; Ezetimibe; Female; Fo | 2011 |
A promising codrug of nicotinic acid and ibuprofen for managing dyslipidemia. I: synthesis and in vitro evaluation.
Topics: Animals; Cyclooxygenase Inhibitors; Drug Combinations; Drug Design; Dyslipidemias; Half-Life; Humans | 2011 |
Cost-effectiveness of extended-release niacin/laropiprant added to a stable simvastatin dose in secondary prevention patients not at cholesterol goal in Germany.
Topics: Aged; Aged, 80 and over; Anticholesteremic Agents; Cost-Benefit Analysis; Drug Therapy, Combination; | 2012 |
Sustained hypophosphatemic effect of once-daily niacin/laropiprant in dyslipidemic CKD stage 3 patients.
Topics: Dose-Response Relationship, Drug; Drug Administration Schedule; Drug Therapy, Combination; Dyslipide | 2011 |
Niacin extended-release therapy in phase III clinical trials is associated with relatively low rates of drug discontinuation due to flushing and treatment-related adverse events: a pooled analysis.
Topics: Clinical Trials, Phase III as Topic; Delayed-Action Preparations; Dose-Response Relationship, Drug; | 2011 |
Therapy: HIV-associated dyslipidemia: the heart positive study.
Topics: Drug Therapy, Combination; Dyslipidemias; Exercise Therapy; Fenofibrate; Heart Diseases; HIV Infecti | 2011 |
Efficacy and safety of sustained-release niacins.
Topics: Dyslipidemias; Humans; Hypolipidemic Agents; Niacin | 2011 |
Obesity and dyslipidemia.
Topics: Anti-Obesity Agents; Cholesterol, HDL; Cholesterol, LDL; Cholesterol, VLDL; Dyslipidemias; Humans; H | 2011 |
HDL: who needs it?
Topics: Biomarkers; Cholesterol, HDL; Clinical Trials as Topic; Dyslipidemias; Humans; Hypolipidemic Agents; | 2011 |
[Alternative drugs to statins].
Topics: Dyslipidemias; Fibric Acids; Humans; Hypolipidemic Agents; Niacin | 2011 |
Is niacin ineffective? Or did AIM-HIGH miss its target?
Topics: Brain Ischemia; Cholesterol, HDL; Cholesterol, LDL; Coronary Artery Disease; Dyslipidemias; Female; | 2012 |
Managing dyslipidaemia: evolving role of combination therapy.
Topics: Atorvastatin; Azetidines; Drug Therapy, Combination; Dyslipidemias; Ezetimibe; Fenofibrate; Heptanoi | 2011 |
Consistency of extended-release niacin/laropiprant effects on Lp(a), ApoB, non-HDL-C, Apo A1, and ApoB/ApoA1 ratio across patient subgroups.
Topics: Aged; Apolipoprotein A-I; Apolipoproteins B; Cardiovascular Diseases; Clinical Trials, Phase III as | 2012 |
Consistency of extended-release niacin/laropiprant effects on Lp(a), ApoB, non-HDL-C, Apo A1, and ApoB/ApoA1 ratio across patient subgroups.
Topics: Aged; Apolipoprotein A-I; Apolipoproteins B; Cardiovascular Diseases; Clinical Trials, Phase III as | 2012 |
Consistency of extended-release niacin/laropiprant effects on Lp(a), ApoB, non-HDL-C, Apo A1, and ApoB/ApoA1 ratio across patient subgroups.
Topics: Aged; Apolipoprotein A-I; Apolipoproteins B; Cardiovascular Diseases; Clinical Trials, Phase III as | 2012 |
Consistency of extended-release niacin/laropiprant effects on Lp(a), ApoB, non-HDL-C, Apo A1, and ApoB/ApoA1 ratio across patient subgroups.
Topics: Aged; Apolipoprotein A-I; Apolipoproteins B; Cardiovascular Diseases; Clinical Trials, Phase III as | 2012 |
Consistency of extended-release niacin/laropiprant effects on Lp(a), ApoB, non-HDL-C, Apo A1, and ApoB/ApoA1 ratio across patient subgroups.
Topics: Aged; Apolipoprotein A-I; Apolipoproteins B; Cardiovascular Diseases; Clinical Trials, Phase III as | 2012 |
Consistency of extended-release niacin/laropiprant effects on Lp(a), ApoB, non-HDL-C, Apo A1, and ApoB/ApoA1 ratio across patient subgroups.
Topics: Aged; Apolipoprotein A-I; Apolipoproteins B; Cardiovascular Diseases; Clinical Trials, Phase III as | 2012 |
Consistency of extended-release niacin/laropiprant effects on Lp(a), ApoB, non-HDL-C, Apo A1, and ApoB/ApoA1 ratio across patient subgroups.
Topics: Aged; Apolipoprotein A-I; Apolipoproteins B; Cardiovascular Diseases; Clinical Trials, Phase III as | 2012 |
Consistency of extended-release niacin/laropiprant effects on Lp(a), ApoB, non-HDL-C, Apo A1, and ApoB/ApoA1 ratio across patient subgroups.
Topics: Aged; Apolipoprotein A-I; Apolipoproteins B; Cardiovascular Diseases; Clinical Trials, Phase III as | 2012 |
Consistency of extended-release niacin/laropiprant effects on Lp(a), ApoB, non-HDL-C, Apo A1, and ApoB/ApoA1 ratio across patient subgroups.
Topics: Aged; Apolipoprotein A-I; Apolipoproteins B; Cardiovascular Diseases; Clinical Trials, Phase III as | 2012 |
Consistency of extended-release niacin/laropiprant effects on Lp(a), ApoB, non-HDL-C, Apo A1, and ApoB/ApoA1 ratio across patient subgroups.
Topics: Aged; Apolipoprotein A-I; Apolipoproteins B; Cardiovascular Diseases; Clinical Trials, Phase III as | 2012 |
Consistency of extended-release niacin/laropiprant effects on Lp(a), ApoB, non-HDL-C, Apo A1, and ApoB/ApoA1 ratio across patient subgroups.
Topics: Aged; Apolipoprotein A-I; Apolipoproteins B; Cardiovascular Diseases; Clinical Trials, Phase III as | 2012 |
Consistency of extended-release niacin/laropiprant effects on Lp(a), ApoB, non-HDL-C, Apo A1, and ApoB/ApoA1 ratio across patient subgroups.
Topics: Aged; Apolipoprotein A-I; Apolipoproteins B; Cardiovascular Diseases; Clinical Trials, Phase III as | 2012 |
Consistency of extended-release niacin/laropiprant effects on Lp(a), ApoB, non-HDL-C, Apo A1, and ApoB/ApoA1 ratio across patient subgroups.
Topics: Aged; Apolipoprotein A-I; Apolipoproteins B; Cardiovascular Diseases; Clinical Trials, Phase III as | 2012 |
Consistency of extended-release niacin/laropiprant effects on Lp(a), ApoB, non-HDL-C, Apo A1, and ApoB/ApoA1 ratio across patient subgroups.
Topics: Aged; Apolipoprotein A-I; Apolipoproteins B; Cardiovascular Diseases; Clinical Trials, Phase III as | 2012 |
Consistency of extended-release niacin/laropiprant effects on Lp(a), ApoB, non-HDL-C, Apo A1, and ApoB/ApoA1 ratio across patient subgroups.
Topics: Aged; Apolipoprotein A-I; Apolipoproteins B; Cardiovascular Diseases; Clinical Trials, Phase III as | 2012 |
Consistency of extended-release niacin/laropiprant effects on Lp(a), ApoB, non-HDL-C, Apo A1, and ApoB/ApoA1 ratio across patient subgroups.
Topics: Aged; Apolipoprotein A-I; Apolipoproteins B; Cardiovascular Diseases; Clinical Trials, Phase III as | 2012 |
HDL cholesterol--how do I raise my patients good cholesterol?
Topics: Cholesterol, HDL; Clinical Trials as Topic; Drug Therapy, Combination; Dyslipidemias; Evidence-Based | 2012 |
Time as a variable with niacin extended-release/lovastatin vs. atorvastatin and simvastatin.
Topics: Atorvastatin; Cholesterol, HDL; Cholesterol, LDL; Delayed-Action Preparations; Drug Therapy, Combina | 2005 |
Modifying plasma low-density lipoprotein and high-density lipoprotein cholesterol: what combinations are available in the future?
Topics: Carrier Proteins; Cholesterol Ester Transfer Proteins; Cholesterol, HDL; Cholesterol, LDL; Clofibric | 2005 |
The importance of low serum levels of high-density lipoprotein cholesterol (HDL-C) as a cardiovascular risk factor.
Topics: Biomarkers; Cardiovascular Diseases; Cholesterol, HDL; Combined Modality Therapy; Diabetes Complicat | 2005 |
[Pharmacology of niacin or nicotinic acid].
Topics: Delayed-Action Preparations; Dyslipidemias; Flushing; Humans; Hypolipidemic Agents; Niacin | 2005 |
[Drug combinations: statins and niacin].
Topics: Age Distribution; Atherosclerosis; Atorvastatin; Cholesterol, HDL; Cholesterol, LDL; Drug Interactio | 2005 |
Low HDL cholesterol levels.
Topics: Blood Glucose; Cholesterol, HDL; Diabetes Complications; Dyslipidemias; Humans; Niacin | 2006 |
Low HDL cholesterol levels.
Topics: Adult; Cholesterol, HDL; Dyslipidemias; Humans; Macular Edema; Male; Middle Aged; Niacin; Vision Dis | 2006 |
Report from the 7th International Lipodystrophy Meeting.
Topics: Anti-HIV Agents; Dyslipidemias; HIV Infections; Humans; Lipodystrophy; Niacin | 2006 |
The appropriateness of nicotinic acid derivative use in patients with the metabolic syndrome: insights from the ARBITER 2 study.
Topics: Dyslipidemias; Humans; Hypolipidemic Agents; Insulin; Lipids; Metabolic Syndrome; Niacin; Randomized | 2006 |
Treating dyslipidaemia in the setting of diabetes mellitus and cardiovascular disease: another focus.
Topics: Diabetes Mellitus, Type 2; Diabetic Angiopathies; Dyslipidemias; Humans; Hydroxymethylglutaryl-CoA R | 2006 |
Safety of lovastatin/extended release niacin compared with lovastatin alone, atorvastatin alone, pravastatin alone, and simvastatin alone (from the United States Food and Drug Administration adverse event reporting system).
Topics: Adverse Drug Reaction Reporting Systems; Atorvastatin; Chemical and Drug Induced Liver Injury; Drug | 2007 |
Reaching target lipid levels in patients at high risk of cardiovascular event: the experience of a Canadian tertiary care lipid clinic.
Topics: Body Mass Index; Canada; Cardiovascular Diseases; Cohort Studies; Diabetes Complications; Dyslipidem | 2007 |
Niacin therapy: an evolving paradigm for the management of mixed dyslipidemia and low high-density lipoprotein cholesterol. Introduction.
Topics: Cholesterol, HDL; Cholesterol, LDL; Coronary Artery Disease; Dyslipidemias; Humans; Hypolipidemic Ag | 2008 |
Simcor: a niacin/simvastatin combination.
Topics: Cholesterol, HDL; Cholesterol, LDL; Costs and Cost Analysis; Drug Combinations; Drug Interactions; D | 2008 |
Dosage, titration, and gaps in treatment with extended release niacin in clinical practice.
Topics: Adult; Cohort Studies; Delayed-Action Preparations; Dyslipidemias; Female; Humans; Hypolipidemic Age | 2008 |