sulindac and Body-Weight

Topics: Anti-Inflammatory Agents, Non-Steroidal; Blood Pressure; Body Weight; Cross-Over Studies; Humans; Ibuprofen; Natriuresis; Piroxicam; Potassium; Renal Insufficiency; Sulindac

The effects of sulindac and indomethacin on the blood pressure response to labetalol were determined in well-controlled predominantly obese hypertensive patients (n = 26). A stabilized dose of labetalol alone was administered on weeks 1 and 3, and either indomethacin or sulindac was administered with labetalol on week 2, with cross-over to the other drug on week 4. Indomethacin and sulindac increased the sitting and standing systolic blood pressure (BP) to a statistically significant extent compared with placebo. The effects of indomethacin on systolic BP, diastolic BP, and weight were not significantly different from those with sulindac. Indomethacin but not sulindac produced minor increases in diastolic BP and weight compared with placebo.

Topics: Adult; Aged; Analysis of Variance; Blood Pressure; Body Weight; Chlorides; Drug Interactions; Humans; Hypertension; Indomethacin; Labetalol; Middle Aged; Obesity; Random Allocation; Sodium; Sulindac

Twenty-eight patients with mild to moderate essential hypertension well controlled by atenolol entered a five-week, double-blind, placebo-controlled trial of the effects of sulindac and naproxen on blood pressure (BP) control. Atenolol alone was administered during weeks 1, 3, and 5. Naproxen or sulindac was administered with atenolol during week 2, with crossover during week 4. Data were analyzed for 27 of the patients (one dropped out after developing a skin rash). Naproxen significantly increased the systolic BP compared with placebo (mean 4.0 mm Hg; 95 percent confidence interval, 1.1-7.0; p less than 0.05). There were no significant differences in systolic BP during sulindac administration compared with placebo or naproxen. No significant effects on diastolic BP were observed. Weight was increased by naproxen and sulindac compared with placebo (mean 0.6-0.8 kg, p less than 0.05), although not to a clinically significant extent. One-week therapy with naproxen has a greater potential than sulindac to increase systolic BP in well-controlled hypertensive patients receiving atenolol; however, the increase is minor and unlikely to be of clinical significance.

Topics: Adult; Aged; Atenolol; Blood Pressure; Body Weight; Double-Blind Method; Drug Interactions; Female; Humans; Hypertension; Male; Middle Aged; Naproxen; Sulindac

Seventeen patients with hypertension and osteoarthritis participated in a single-blind crossover study comparing the effects of sulindac 200 mg twice daily, naproxen 500 mg twice daily, and placebo on blood pressure. All patients were treated for hypertension with propranolol monotherapy. Blood pressures were back-titrated to achieve a baseline diastolic blood pressure of 90 to 100 mm Hg while taking naproxen. There were no significant differences in mean sitting or standing blood pressures among the patients receiving naproxen, sulindac, or placebo treatments. There was no change in pulse, weight, or any of the laboratory measurements at the end of each treatment phase. These results suggest that neither sulindac nor naproxen interferes with propranolol therapy for uncomplicated hypertension.

Topics: Blood Pressure; Blood Urea Nitrogen; Body Weight; Clinical Trials as Topic; Creatinine; Drug Interactions; Humans; Hypertension; Indenes; Middle Aged; Naproxen; Potassium; Propranolol; Pulse; Random Allocation; Renin; Sodium; Sulindac

We investigated the influence of two nonsteroidal anti-inflammatory drugs, indomethacin and sulindac, on the diuretic effect and kinetics of hydrochlorothiazide in healthy subjects. In an open, randomized, crossover study, eight healthy subjects were treated with hydrochlorothiazide, 50 mg a day, for 4 weeks. In the second and fourth weeks, indomethacin, 25 mg three times a day, or sulindac, 200 mg twice a day, were added. Blood pressure, body weight, plasma levels of potassium, creatinine, and albumin, the hematocrit, plasma renin activity (PRA), and the 24-hour urinary excretion of sodium and potassium were measured at the end of each week. Plasma concentrations of hydrochlorothiazide and its urinary excretion were also determined 0.5, 1, 2, 3, 4, 8, 10, and 24 hours after HCTZ dosing. When indomethacin was added to hydrochlorothiazide, body weight and plasma potassium levels increased and PRA decreased. Hydrochlorothiazide kinetics were not influenced. In contrast, sulindac decreased the renal clearance of hydrochlorothiazide and increased hydrochlorothiazide plasma levels in two subjects who had somewhat lower endogenous creatinine clearance values than the other subjects. Except for a decrease in PRA, there were no dynamic interactions. Our results suggest that an interaction between indomethacin and hydrochlorothiazide is caused by dynamic mechanisms such as inhibition of renal prostaglandin synthesis, whereas sulindac may alter the renal clearance of hydrochlorothiazide.

Topics: Adult; Blood Pressure; Body Weight; Clinical Trials as Topic; Drug Interactions; Female; Humans; Hydrochlorothiazide; Indenes; Indomethacin; Kinetics; Male; Random Allocation; Sulindac; Time Factors

Obesity is associated with an increased risk of colon cancer. Our current study examines whether weight loss and/or treatment with the NSAID sulindac suppresses the protumor effects of obesity in a mouse model of colon cancer. Azoxymethane-treated male FVB/N mice were fed a low-fat diet (LFD) or high-fat diet (HFD) for 15 weeks, then HFD mice were randomized to remain on HFD (obese) or switch to LFD [formerly obese (FOb-LFD)]. Within the control (LFD), obese, and FOb-LFD groups, half the mice started sulindac treatment (140 ppm in the diet). All mice were euthanized 7 weeks later. FOb-LFD mice had intermediate body weight levels, lower than obese but higher than control (P < 0.05). Sulindac did not affect body weight. Obese mice had greater tumor multiplicity and burden than all other groups (P < 0.05). Transcriptomic profiling indicated that weight loss and sulindac each modulate the expression of tumor genes related to invasion and may promote a more antitumor immune landscape. Furthermore, the fecal microbes Coprobacillus, Prevotella, and Akkermansia muciniphila were positively correlated with tumor multiplicity and reduced by sulindac in obese mice. Coprobacillus abundance was also decreased in FOb-LFD mice. In sum, weight loss and sulindac treatment, alone and in combination, reversed the effects of chronic obesity on colon tumor multiplicity and burden. Our findings suggest that an investigation regarding the effects of NSAID treatment on colon cancer risk and/or progression in obese individuals is warranted, particularly for those unable to achieve moderate weight loss.. Obesity is a colon cancer risk and/or progression factor, but the underlying mechanisms are incompletely understood. Herein we demonstrate that obesity enhances murine colon carcinogenesis and expression of numerous tumoral procancer and immunosuppressive pathways. Moreover, we establish that weight loss via LFD and/or the NSAID sulindac mitigate procancer effects of obesity.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Body Weight; Colonic Neoplasms; Diet, High-Fat; Disease Models, Animal; Male; Mice; Mice, Inbred C57BL; Mice, Obese; Microbiota; Obesity; Sulindac; Transcriptome; Weight Loss

The present study examined the protective effect of sulindac on bleomycin-induced lung fibrosis in rats. Animals were divided into saline group, bleomycin group (single intra-tracheal instillation of bleomycin) and bleomycin+sulindac (orally from day 1 to day 20). Bleomycin administration reduced the body weight, altered antioxidant status (such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione) while it increased the lung weight, hydroxyproline content, collagen deposition and lipid peroxidation. However, simultaneous administration of sulindac improved the body weight, antioxidant status and decreased the collagen deposition in lungs. Moreover, the levels of inflammatory cytokine tumour necrosis factor-α increased in bleomycin-induced group, whereas, on treatment with sulindac the levels of tumour necrosis factor-α were found reduced. Finally, histological evidence also supported the ability of sulindac to inhibit bleomycin-induced lung fibrosis. The results of the present study indicate that sulindac can be used as an agent against bleomycin-induced pulmonary fibrosis.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Antibiotics, Antineoplastic; Bleomycin; Body Weight; Bronchoalveolar Lavage Fluid; Catalase; Cell Count; Glutathione; Glutathione Peroxidase; Hydroxyproline; Lipid Peroxidation; Lung; Male; Organ Size; Pulmonary Fibrosis; Rats; Rats, Wistar; Sulindac; Superoxide Dismutase; Tumor Necrosis Factor-alpha

Treatment of cultured PANC-1, MIA PaCa-2, and BxPC-3 human pancreatic adenocarcinoma cells with 0.1 to 1.6 nM 12-O-tetradecanoylphorbol-13-acetate (TPA) for 96 h inhibited the proliferation of these cells in a dose-dependent manner, and PANC-1 and MIA PaCa-2 cells were more sensitive to TPA than BxPC-3 cells. Inhibition of proliferation by TPA in PANC-1 cells was associated with an increase in the level of p21, but this was not observed in MIA PaCa-2 or BxPC-3 cells. The TPA-induced increase of p21 in PANC-1 cells was blocked by bisindolylmaleimide or rottlerin (inhibitors of protein kinase C). Studies in NCr-immunodeficient mice with well established PANC-1 tumor xenografts indicated that daily i.p. injections of TPA strongly inhibited tumor growth, increased the percentage of caspase-3-positive cells, and decreased the ratio of mitotic cells to caspase-3-positive cells in the tumors. Studies with BxPC-3 tumors in NCr mice receiving daily i.p. injections of vehicle, TPA, all-trans retinoic acid (ATRA), or a TPA/ATRA combination showed that TPA had an inhibitory effect on tumor growth, but treatment of the animals with the TPA/ATRA combination had a greater inhibitory effect on tumor growth than TPA alone. Treatment with the TPA/ATRA combination resulted in a substantially decreased ratio of the percentage of mitotic cells to the percentage of caspase-3-positive cells in the tumors compared with tumors from the vehicle-treated control animals. The inhibitory effects of TPA on tumor growth occurred at clinically achievable blood levels.

Topics: Animals; Apoptosis; Body Weight; Cell Cycle; Cell Proliferation; Humans; Immunohistochemistry; Male; Mice; Neoplasm Transplantation; Paclitaxel; Pancreatic Neoplasms; Phosphorylation; Prostatic Neoplasms; Protein Kinase C; Retinoblastoma Protein; Sulindac; Tetradecanoylphorbol Acetate; Transplantation, Heterologous; Tretinoin; Tumor Cells, Cultured

The aim of the present study was to investigate the cardioprotective activity of sulindac as an aldose reductase inhibitor in the development of cardiomyopathy by non-invasive techniques; M-mode and Doppler echocardiography. Diabetes was induced by streptozotocin (45 mg/kg, iv) in the Sprague-Dawley rats. Echocardiography, biochemical and histological studies were carried out in normal control, diabetic untreated, diabetic vehicle (sodium carboxy methyl cellulose, 1%, po) and sulindac (6 mg/kg and 20 mg/kg, po) treated animals at varying time intervals. In the diabetic untreated and vehicle treated rats at 12 weeks after induction of diabetes, there was a significant decrease in the E-wave, an increase in the A-wave and corresponding decrease in the E/A ratio was observed. Significant decrease in the Eat was found after 12 weeks (P < 0.05). Whereas systolic function variables; ejection fraction and fractional shortening were significantly decreased (P < 0.05) after 12 weeks compared to their baseline data. In the sulindac treated animals, there were no significant alterations in the systolic and diastolic parameters were found throughout the study period. Myocardial fructose levels were significantly increased in the diabetic untreated animals compared to normal control rats (P < 0.05), whereas these were significantly decreased in the sulindac (6 mg/kg and 20 mg/kg) treated animals (301.11+/-37.98, 214.11+/-25.31, vs. 914.88+/-56.01 nmol/g) compared to diabetic vehicle treated group (P < 0.05). Extensive focal ischemic myocyte degeneration was observed in the diabetic untreated and vehicle treated rats, whereas in the sulindac (6 mg/kg) treated rats, minimal necrosis was found, with no evidence of necrosis in sulindac (20 mg/kg) group. Our results show for the first time that sulindac has a cardioprotective activity as this agent prevented the development of left ventricular dysfunction in STZ-induced diabetic rats in the 12-week chronic study.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Blood Glucose; Blood Proteins; Body Weight; Carboxymethylcellulose Sodium; Cardiomyopathy, Hypertrophic; Cholesterol; Diabetes Mellitus, Experimental; Echocardiography, Doppler; Fructose; Heart; Male; Myocardium; Rats; Rats, Sprague-Dawley; Sulindac; Triglycerides; Ventricular Dysfunction, Left

The present study examined the role of cyclooxygenase-synthetized prostanoids in the pathogenesis of angiotensin-II-induced inflammatory response and vascular injury in transgenic rats harboring mouse renin-2 gene (mREN2 rats). Five- to six-week-old, heterozygous mREN2 rats received the following drug regimens for 8 weeks: (1) controls; (2) cyclooxygenase-2 inhibitor (MF-tricyclic [3-(3,4-difluorophenyl)-4-(4-(methylsulfonyl) phenyl)-2(5H)-furanone], 14 mg kg(-1) p.o.); (3) cyclooxygenase-1/cyclooxygenase-2 inhibitor (sulindac, 14 mg kg(-1) p.o.); (4) angiotensin II receptor antagonist (losartan 40 mg kg(-1) p.o.); (5) MF-tricyclic + losartan; (6) sulindac + losartan. Normotensive Sprague-Dawley rats served as controls. mREN2 rats developed pronounced hypertension, cardiac hypertrophy, and albuminuria as compared to normotensive Sprague-Dawley controls. mREN2 rats showed pronounced perivascular inflammation and morphological damage in the kidneys and the heart. Both MF-tricyclic and sulindac further increased blood pressure and albuminuria in mREN2 rats. Neither MF-tricyclic nor sulindac were able to prevent angiotensin-II-induced perivascular inflammation and morphological changes in the heart or in the kidneys. Myocardial and renal cyclooxygenase-2 mRNA expressions were decreased in mREN2 rats, whereas no difference was found in cyclooxygenase-1 mRNA expressions. Sulindac increased both cyclooxygenase-1 and cyclooxygenase-2 gene expressions, whereas MF-tricyclic increased only cyclooxygenase-2 gene expressions. Losartan normalized blood pressure, cardiac hypertrophy, albuminuria, inflammatory response and morphological changes in mREN2 rats, both in the presence and absence of cyclooxygenase inhibitors. Our findings indicate that cyclooxygenase does not play a central role in the pathogenesis of angiotensin-II-induced inflammatory response and vascular injury in mREN2 rats.

Topics: Albuminuria; Angiotensin II; Animals; Animals, Genetically Modified; Antihypertensive Agents; Blood Pressure; Body Weight; Cardiomegaly; Cardiovascular System; Cyclooxygenase 1; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Eating; Furans; Gene Expression Regulation, Enzymologic; Isoenzymes; Kidney; Losartan; Male; Membrane Proteins; Mice; Prostaglandin-Endoperoxide Synthases; Rats; Rats, Sprague-Dawley; Renin; RNA, Messenger; Sulindac; Urination

No information is available on the interaction between cigarette smoke, the most important man-made carcinogen, and light, the most widespread natural carcinogen. In order to clarify this issue, SKH-1 hairless mice were exposed to environmental smoke and/or to the light emitted by sunlight-simulating halogen quartz bulbs. After 28 days, intermediate biomarkers were evaluated in skin, respiratory tract, bone marrow and peripheral blood. The results showed that, individually, the light produced extensive alterations not only in the skin but even at a systemic level, as shown by formation of bulky DNA adducts in both lung and bone marrow and induction of cytogenetic damage in bone marrow and peripheral blood erythrocytes. Smoke damaged the respiratory tract and produced significant alterations in the skin as well as an evident cytogenetic damage in both bone marrow and peripheral blood. Interestingly, as compared with exposure to smoke only, alternate daily cycles of exposure to both light and smoke significantly increased malondialdehyde concentrations and DNA adduct levels in lung and the frequency of micronuclei in pulmonary alveolar macrophages. The oral administration of sulindac, a non-steroidal anti-inflammatory drug, attenuated several biomarker alterations due to the combined exposure of mice to light and smoke. In conclusion, the light induces a systemic genotoxic damage, which is presumably due to the UV-mediated formation in the skin of long-lived derivatives, such as aldehydes. This damage may mechanistically be involved in light-related hematopoietic malignancies. In addition, the light displayed an insofar unsuspected synergism with smoke in the induction of DNA damage in the respiratory tract.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Biomarkers; Body Weight; Bone Marrow; DNA Adducts; DNA Damage; Female; Light; Mice; Mice, Hairless; Respiratory System; Skin; Sulindac; Tobacco Smoke Pollution; Ultraviolet Rays

Human esophageal adenocarcinoma (EAC) develops in a sequence from gastroesophageal reflux disease (GERD), columnar-lined esophagus (CLE), dysplasia, and eventually to EAC. We established a rat surgical EAC model with esophagogastroduodenal anastomosis (EGDA) to mimic the staged process of esophageal adenocarcinogenesis. Profiling of the AA metabolites with mass spectrometry showed that prostaglandin E2 (PGE2), leukotriene B4 (LTB4), 15-hydroeicosatetraenoic acid (HETE), 12-HETE, 8-HETE and 5-HETE all increased at the esophagoduodenal junction after EGDA as compared with the proximal esophagus, with PGE2 as the major metabolite. Consistent with this profile, cyclooxygenase 2 (Cox2) was overexpressed in the basal cell layer of esophageal squamous epithelium, CLE cells and EAC tumor cells of the EGDA rats, as compared with the normal esophageal epithelium. Sulindac (a Cox inhibitor), nordihydroguaiaretic acid (NDGA, a lipoxygenase inhibitor) and alpha-difluoromethylornithine (DFMO, an ornithine decarboxylase inhibitor) were tested for their possible inhibitory actions against the formation of EAC in the rat EGDA model. In a short-term study (for 4 weeks after surgery), dietary administration of both sulindac (300 and 600 p.p.m.) and NDGA (100 p.p.m.) effectively reduced the EGDA-induced inflammation. In a long-term chemoprevention study (for 40 weeks after surgery), 300 p.p.m. sulindac, alone or in combination with 100 p.p.m. NDGA or 0.5% DFMO, decreased the tumor incidence from 57.7 to 26.9%, or 16.7 or 20%, respectively (P < 0.05). NDGA alone (100 and 200 p.p.m.) slightly decreased the tumor incidence to 52.4 and 37%, respectively, although the difference was not statistically significant. DFMO alone did not show significant effects on tumor incidence. Inhibition of tumor formation by sulindac was correlated with lowered levels of PGE2. In conclusion, sulindac exerted its chemopreventive effect against the formation of EAC in the rat EGDA model possibly through its inhibition of Cox.

Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Animals; Arachidonic Acid; Body Weight; Cyclooxygenase 2; Dinoprostone; Eflornithine; Esophageal Neoplasms; Esophagus; Gas Chromatography-Mass Spectrometry; Hydroxyeicosatetraenoic Acids; Immunoenzyme Techniques; In Situ Hybridization; Inflammation; Isoenzymes; Leukotriene B4; Male; Masoprocol; Mass Spectrometry; Neoplasms; Prostaglandin-Endoperoxide Synthases; Rats; Rats, Sprague-Dawley; Sulindac; Time Factors

Epidemiologic and laboratory studies suggest a cancer protective effect and/or lack of a tumor promoting effect by dietary olive oil as compared with other types of non-marine oils. Squalene, a constituent of olive oil, and a key intermediate in cholesterol synthesis may be regarded as partially responsible for the beneficial effects of olive oil, which include decreased mortality rates among populations with high olive oil consumption. Thus, in this study we have assessed the chemopreventive efficacy of squalene on azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF). In addition, we measured the effect of squalene on serum cholesterol levels in the rats. Male F34 rats (5 weeks old) were fed the control diet (modified AIN-76A) or experimental diets containing 1% squalene or 320 p.p.m. sulindac. Two weeks later, all animals except those in vehicle (normal saline)-treated groups were s.c. injected with AOM (15 mg/kg body wt, once weekly for 2 weeks). At 16 weeks of age, all rats were killed, colons were evaluated for ACF and serum was assayed for the cholesterol levels. As expected, dietary administration of sulindac suppressed ACF development and reduced crypt multiplicity, i.e. number of aberrant crypts/focus. Administration of dietary squalene inhibited total ACF induction and crypt multiplicity by approximately >46% (P < 0.001). Further, squalene at a level of 1% did not show any significant effect on serum cholesterol levels. Our finding that squalene significantly suppresses colonic ACF formation and crypt multiplicity strengthens the hypothesis that squalene possesses chemopreventive activity against colon carcinogenesis.

Topics: Animals; Azoxymethane; Body Weight; Colonic Neoplasms; Male; Precancerous Conditions; Rats; Rats, Inbred F344; Squalene; Sulindac

Data from epidemiological studies suggest that isoflavones in soy may have a protective effect on the development of colon cancer in humans. Therefore, we have investigated whether soy isoflavones will inhibit intestinal tumour development in Apc(Min) mice. The mice were fed a Western-type high risk diet (high fat, low fibre and calcium) containing two different isolates of soy protein as a protein source. For the control and test groups this resulted in the administration of about 16 and 475 mg of total isoflavones per kg diet, respectively. As a positive control. a third group of mice was administered a low isoflavone diet supplemented with 300 ppm sulindac. No significant differences in the incidence, multiplicity, size and distribution of intestinal tumours were observed between Min mice fed low and high isoflavone-containing diets. However, a clear reduction in the number of small intestinal tumours was observed for the sulindac diet. Thus, in contrast to epidemiological studies, our results demonstrate that high amounts of soy isoflavones present in a Western-type high risk diet do not protect against intestinal tumour development in a relevant animal model such as the Min mice.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Body Weight; Calcium, Dietary; Colonic Neoplasms; Dietary Fats; Dietary Fiber; Drug Screening Assays, Antitumor; Female; Genistein; Isoflavones; Male; Mice; Soybean Proteins; Sulindac

The potential inhibitory effects of phenethyl isothiocyanate (PEITC), ellagic acid (EA), sulindac and supplemental dietary calcium (SDC) on N-nitrosomethylbenzylamine (NMBA)-induced esophageal carcinogenesis were evaluated in rats utilizing an abbreviated (5 week) NMBA treatment protocol which allowed administration of the putative inhibitors throughout the experiment (i.e. beginning 2 weeks prior to NMBA treatment) or following completion of NMBA dosing only. PEITC at 500 p.p.m. significantly inhibited tumor incidence and multiplicity when given before and during, but not following, NMBA treatment. Neither sulindac at 125 p.p.m. nor SDC (2% versus 0.5% in control diet) inhibited tumor development when given during or following NMBA treatment. EA, which was administered only following NMBA treatment, significantly reduced the incidence (66.7% versus 100% in NMBA controls), but not the multiplicity, of esophageal tumors at the high-dose (4000 p.p.m.) level. Together these findings indicate that: (i) PEITC selectively inhibits the induction but not the subsequent progression of NMBA-induced esophageal tumors; (ii) EA may repress esophageal tumor development when administered following NMBA treatment; (iii) at the doses administered, neither sulindac nor SDC possess significant inhibitory activity against NMBA-induced esophageal carcinogenesis in the rat.

Topics: Animals; Anticarcinogenic Agents; Body Weight; Calcium; Carcinogens; Diet; Dimethylnitrosamine; Ellagic Acid; Esophageal Neoplasms; Isothiocyanates; Male; Rats; Rats, Inbred F344; Sulindac; Time Factors

Topics: Adult; Anti-Inflammatory Agents, Non-Steroidal; Atrial Natriuretic Factor; Blood Pressure; Body Weight; Humans; Indomethacin; Male; Natriuresis; Sulindac; Time Factors

Indomethacin and sulindac were used as tools to study the role of renal and/or systemic prostaglandins in the pharmacological response to atenolol. Patients receiving chronic treatment with atenolol 100 mg received indomethacin 50 mg twice daily or sulindac 200 mg twice daily in a randomised crossover trial. Indomethacin significantly reduced the antihypertensive action of atenolol while sulindac had no effect. The role that systemic and/or renal prostaglandins may play in the antihypertensive action of atenolol is discussed with reference to renal PGI2 production and inhibition of platelet cyclo-oxygenase.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Atenolol; Blood Pressure; Body Weight; Drug Interactions; Female; Humans; Hypertension; Indenes; Indomethacin; Male; Middle Aged; Random Allocation; Renin; Sulindac; Thromboxane B2

A study of 690 osteoarthrosis (OA) patients with corresponding controls, and 475 soft-tissue rheumatism (STR) patients with the same number of controls was made in Finnish health centres. The aim of the study was to clarify certain etiological, social and therapeutical aspects. No clear differences were found in the working conditions of patients with OA, STR, or their controls, or in their occupational classes. OA patients were less satisfied with their working conditions than were the other. OA and STR patients had been more actively engaged in sports earlier in life, but during the study there were no differences; nor did the localisation of OA differ. The weight index qas slightly higher in OA, particularly when knee and ankle were affected, but not with arthrosis of the hip. There were no clear associations with other diseases. The maximum duration of a treatment period in this study was 1 month. The average sick leave in OA was 17.8 days, in STR 13.4 and in controls 15.4 days. After treatment, 31% of OA patients, and 56% of STR were recommended to resume work; 4% were recommended to change their occupation; 21% of OA and 7% of STR patients were recommended to retire on pension. Sulindac, indomethacin and many other drug combinations were used for medication. Certain side effects were found in about 5% of sulindac- and in 8-10% of indomethacin-treated patients. In 17% of OA and in 12% of STR patients, it was found necessary to consult a specialist for diagnosis or treatment.

Topics: Body Weight; Community Health Centers; Female; Finland; Humans; Indomethacin; Leisure Activities; Male; Middle Aged; Osteoarthritis; Rheumatic Diseases; Sulindac; Work