cholecalciferol and Hyperparathyroidism--Secondary

Vitamin D deficiency (<20 ng/mL) and insufficiency (20-29 ng/mL) are common among patients with chronic kidney disease (CKD) or undergoing dialysis. In addition to nutritional and sunlight exposure deficits, factors that affect vitamin D deficiency include race, sex, age, obesity and impaired vitamin D synthesis and metabolism. Serum 1,25(OH)₂D levels also decrease progressively because of 25(OH)D deficiency, together with impaired availability of 25(OH)D by renal proximal tubular cells, high fibroblast growth factor (FGF)-23 and decreased functional renal tissue. As in the general population, this condition is associated with increased morbidity and poor outcomes. Together with the progressive decline of serum calcitriol, vitamin D deficiency leads to secondary hyperparathyroidism (SHPT) and its complications, tertiary hyperparathyroidism and hypercalcemia, which require surgical parathyroidectomy or calcimimetics. Kidney Disease Outcomes Quality Initiative (KDOQI) and Kidney Disease Improving Global Outcomes (KDIGO) experts have recognized that vitamin D insufficiency and deficiency should be avoided in CKD and dialysis patients by using supplementation to prevent SHPT. Many vitamin D supplementation regimens using either ergocalciferol or cholecalciferol daily, weekly or monthly have been reported. The benefit of native vitamin D supplementation remains debatable because observational studies suggest that vitamin D receptor activator (VDRA) use is associated with better outcomes and it is more efficient for decreasing the serum parathormone (PTH) levels. Vitamin D has pleiotropic effects on the immune, cardiovascular and neurological systems and on antineoplastic activity. Extra-renal organs possess the enzymatic capacity to convert 25(OH)D to 1,25(OH)₂D. Despite many unanswered questions, much data support vitamin D use in renal patients. This article emphasizes the role of native vitamin D replacement during all-phases of CKD together with VDRA when SHPT persists.

Topics: Cholecalciferol; Dialysis; Dietary Supplements; Ergocalciferols; Fibroblast Growth Factor-23; Humans; Hypercalcemia; Hyperparathyroidism, Secondary; Parathyroid Hormone; Randomized Controlled Trials as Topic; Renal Insufficiency, Chronic; Vitamin D Deficiency

Deranged vitamin D metabolism represents an active trigger of secondary hyperparathyroidism (SHPT) in CKD. Correction of 25(OH)D deficiency by nutritional Vitamin D administration is suggested by KDIGO guidelines, to prevent and treat SHPT in CKD stage G3-G5 and G1T-G5T patients, although with a still inconsistent background. Nutritional vitamin D is available as cholecalciferol, ergocalciferol, or calcifediol. Superiority of calcifediol in increasing 25(OH)D levels has been suggested due to its better bioavailability. The safer pharmacokinetic of the recent modified-release (MR) formulation of calcifediol was effective in replenishing 25(OH)D levels with minimal impact on vitamin D catabolism and fibroblast-growth factor-23 (FGF-23) activation. Areas covered: the review discusses utility of calcifediol for treating SHPT in different CKD stages under physiology driven approach, focusing on vitamin D metabolism, guidelines suggestions and comparison between clinical effects on SHPT elicited by calcifediol, cholecalciferol and ergocalciferol. Expert commentary: although optimal targets of 25(OH)D and parathormone remain uncertain, calcifediol, especially in its newer MR formulation, may represent an intriguing option to combine an efficacious correction of 25(OH)D deficit and SHPT, with a limited impact on vitamin D catabolism and FGF-23 activation. Newer data are required to better explore the role of MR calcifediol in treating SHPT.

Topics: Animals; Biological Availability; Calcifediol; Cholecalciferol; Delayed-Action Preparations; Ergocalciferols; Fibroblast Growth Factor-23; Humans; Hyperparathyroidism, Secondary; Practice Guidelines as Topic; Renal Insufficiency, Chronic; Vitamin D; Vitamins

Nutritional disorders of captive reptiles remain very common despite the increasing knowledge about reptile husbandry and nutrition. Many nutritional disorders are diagnosed late in the disease process; often secondary complications, such as pathologic fractures in reptiles suffering from nutritional secondary hyperparathyroidism have occurred. Therefore, every attempt should be made to educate reptile owners and keepers about the proper care and dietary needs of reptiles under their care because all nutritional disorders seen in captive reptiles are preventable.

Topics: Animal Husbandry; Animals; Animals, Zoo; Calcium; Cholecalciferol; Diet; Hyperparathyroidism, Secondary; Hypothyroidism; Nutrition Disorders; Nutritional Status; Reptiles

Vitamin D deficiency is widespread in both the pediatric and adult chronic kidney disease (CKD) population. CKD is characterized by dysregulation of vitamin D and mineral metabolism. Secondary hyperparathyroidism and its management puts patients with CKD at increased cardiovascular risk. Emergence of experimental and some clinical data suggesting beneficial effects of vitamin D on proteinuria, blood pressure, inflammation and cardiovascular outcomes has pushed it to the center stage of CKD research. Pediatric data on vitamin D dysregulation and its consequences are still in its infancy. Ongoing prospective studies such as Chronic Kidney disease in Children (CKiD) and the Cardiovascular Comorbidity in Children with CKD (4 C) should help to delineate the evolution of disturbances in mineral metabolism and its adverse effects on growth, CKD progression and cardiovascular outcomes.

Topics: Child; Cholecalciferol; Dietary Supplements; Ergocalciferols; Growth Disorders; Humans; Hyperparathyroidism, Secondary; Kidney; Renal Insufficiency, Chronic; Vitamin D; Vitamin D Deficiency; Vitamins

Serum parathyroid hormone concentrations decrease progressively during the first 3 to 6 month after successful renal transplantation. However 1 year after transplantation, persistent hyperparathyroidism is common. Hypercalcemia due to persistent hyperparathyroidism cause graft dysfunction and cardiovascular calcification. Renal transplant recipients with persistent hyperparathyroidism need treatment with vitamin D and calcium, in some cases parathyroidectomy has to be considered.

Topics: Calcinosis; Calcium; Cardiovascular Diseases; Cholecalciferol; Humans; Hypercalcemia; Hyperparathyroidism, Secondary; Kidney Transplantation; Parathyroidectomy

Serum calcium levels are regulated by the action of parathyroid hormone (PTH). Major drivers of PTH hypersecretion and parathyroid cell proliferation are the hypocalcemia and hyperphosphatemia that develop in chronic kidney disease patients with secondary hyperparathyroidism (SHPT) as a result of low calcitriol levels and decreased kidney function. Increased PTH production in response to systemic hypocalcemia is mediated by the calcium-sensing receptor (CaR). Furthermore, as SHPT progresses, reduced expression of CaRs and vitamin D receptors (VDRs) in hyperplastic parathyroid glands may limit the ability of calcium and calcitriol to regulate PTH secretion. Current treatment for SHPT includes the administration of vitamin D sterols and phosphate binders. Treatment with vitamin D is initially effective, but efficacy often wanes with further disease progression. The actions of vitamin D sterols are undermined by reduced expression of VDRs in the parathyroid gland. Furthermore, the calcemic and phosphatemic actions of vitamin D mean that it has the potential to exacerbate abnormal mineral metabolism, resulting in the formation of vascular calcifications. Effective new treatments for SHPT that have a positive impact on mineral metabolism are clearly needed. Recent research shows that drugs that selectively target the CaR, calcimimetics, have the potential to meet these requirements.

Topics: Calcium; Cholecalciferol; Chronic Disease; Homeostasis; Humans; Hyperparathyroidism, Secondary; Kidney Diseases; Receptors, Calcitriol; Receptors, Calcium-Sensing

Topics: Biomarkers; Calcium; Cholecalciferol; Dementia; Humans; Hypercalcemia; Hyperparathyroidism; Hyperparathyroidism, Secondary; Hypocalcemia; Hypothyroidism; Parathyroid Hormone; Parathyroidectomy; Phosphorus

Topics: Calcitriol; Cholecalciferol; Drug Design; Ergocalciferols; Humans; Hydroxycholecalciferols; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Vitamin D

Oral Vitamin D(3) is usually administered to children with chronic renal failure in the morning. Is there enough evidence that evening dosing is more beneficial with respect to suppression of parathyroid hormone and reduction of side effects such as hypercalcemia?

Topics: Child; Cholecalciferol; Chronotherapy; Humans; Hyperparathyroidism, Secondary

Chronic renal failure is characterized by diminished synthesis of, and resistance to, the active vitamin D metabolite 1,25-dihydroxy-vitamin D3 (1,25(OH)2D3, calcitriol). Calcitriol results from the biotransformation of the precursor 25-hydroxy-vitamin D3 (25(OH)D3) to 1,25(OH)2D3. 25(OH)D3 is synthesized in the liver, and 1alpha-hydroxylase, the rate-limiting enzyme for its biotransformation into the most active metabolite, 1,25(OH)2D3, is located in the kidney. The regulation of 1alpha-hydroxylase in renal failure is not well known. Recent work indicates that, in contrast to previous opinion, 1alpha-hydroxylase is predominantly expressed not in the proximal tubule but in the distal tubule [1]. In vivo, the main stimulatory signal is presumably parathyroid hormone (PTH) and the main inhibitory signal hyperphosphataemia. Both signals are altered in renal failure. There is also evidence that the renal 1alpha-hydroxylase becomes substrate-dependent in patients with renal failure. This means that a higher concentration of the precursor 25(OH)2D3 will result in a higher rate of transformation into the active metabolite 1,25(OH)2D3 in renal patients. Calcitriol is not exclusively synthesized in the kidney, but may also be synthesized in extra-renal tissues, e.g. activated monocytes/macrophages [2], particularly in granuloma [3] as shown by anephric uraemic patients who develop hypercalcaemia and elevated calcitriol concentrations when sarcoidosis [4] or tuberculosis [5] supervenes. On the other hand, calcitriol is less effective in uraemia. This may be to some extent due to diminished expression of vitamin D receptors [6], particularly in parathyroid glands when they undergo nodular transformation [7], but there may also be resistance to calcitriol at the post-receptor level [8]. In a series of elegant experiments [9,10], calcitriol resistance has been related to disturbed genomic effects of active vitamin D because the interaction of the vitamin D receptor ligand complex with vitamin D-responsive elements (VDREs) upstream of vitamin D-regulated genes was disturbed by the action of low molecular weight substances in uraemia, which have not been completely characterized. The role of genetically determined polymorphisms of the vitamin D receptor in the genesis of disturbed calcium metabolism of renal failure is currently unclear.

Topics: Animals; Biomarkers; Calcitriol; Calcium; Calcium Channel Agonists; Cholecalciferol; Humans; Hypercalcemia; Hyperparathyroidism, Secondary; Hypocalcemia; Parathyroid Hormone; Uremia

Calcitriol, the most active metabolite of vitamin D, controls parathyroid gland growth and suppresses the synthesis and secretion of parathyroid hormone (PTH). However, because of its potent effects on intestinal calcium absorption and bone mobilization, calcitriol treatment can induce hypercalcemia, often precluding its use at therapeutic doses. Hyperphosphatemia is also a persistent problem among patients undergoing chronic hemodialysis and can be aggravated by therapeutic doses of calcitriol. Several pharmaceutical companies were able to modify the side-chain of the 1,25(OH)2D3, allowing some of these new analogs to retain the action on the parathyroid glands while decreasing their hypercalcemic and hyperphosphatemic effects. The structure-activity relationship for ligand-mediated transcriptional regulation has been studied in detail. In some analogs the serum binding protein (DBP) plays a key role in determining the pharmacokinetics of the vitamin D compound. The affinity to DBP for 22-oxacalcitriol (OCT), an analog of calcitriol for the treatment of secondary hyperparathryoidism, is approximately 300-400 times lower than that of calcitriol and the analog is rapidly cleared from the circulation. The mechanisms for the selectivity of 19-nor-1,25(OH)2D2 (paricalcitol) (Zemplar) another analog of calcitriol, is clearly different from OCT. Although the mechanisms of action is not completely known, it does appear that paricalcitol down-regulates the VDR in the intestine. It is likely that the unique biological profiles of vitamin D analogs in vivo are due to multiple mechanisms. Understanding the molecular basis of the analog selectivity will not only provide an explanation for their unique actions but allow intelligent design of more effective analogs in the future.

Topics: Animals; Calcitriol; Cholecalciferol; Humans; Hyperparathyroidism, Secondary; Parathyroid Hormone; Structure-Activity Relationship

Topics: Aged; Calcium, Dietary; Cholecalciferol; Female; Food, Fortified; Hip Fractures; Humans; Hyperparathyroidism, Secondary; Osteoporosis; Risk Factors

The two main determinants of hip fractures are falls and bone loss leading to an intrinsic femoral fragility. Substantial femoral bone loss continues throughout old age, with a continuous and exponential increase in the risk of hip fracture; thus any reduction or arrest of this loss will induce an important reduction in the incidence of hip fracture. Preventive measures may be achieved during childhood by increasing peak bone mass with calcium and exercise, by using long-term estrogen replacement therapy after menopause, but also by using vitamin D and calcium supplements for late prevention in the elderly. Vitamin D insufficiency and a deficit in calcium intake are very common in the elderly living either in institutions or at home and the cumulative response to these deficits is a negative calcium balance which stimulates parathyroid hormone secretion. This senile secondary hyperparathyroidism is one of the determinants of femoral bone loss and can be reversed by calcium and vitamin D supplements. We have shown in a 3-year controlled prospective study that the daily use of supplements (1.2 g calcium and 800 IU vitamin D3) given in a large population of 3270 elderly ambulatory women living in nursing homes reduced the number of hip fractures by 23% (intention-to-treat analysis). In parallel, serum parathyroid hormone concentrations were reduced by 28% and low baseline serum 25-hydroxyvitamin D concentration returned to normal values. After 18 months of treatment the bone density of the total proximal femoral region had increased by 2.7% in the vitamin D3-calcium group and decreased by 4.6% in the placebo group (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Accidental Falls; Aged; Bone Density; Bone Resorption; Calcium Compounds; Cholecalciferol; Female; Hip Fractures; Humans; Hyperparathyroidism, Secondary; Osteoporosis; Prospective Studies; Risk Factors

Topics: Animals; Bone Resorption; Calcitonin; Calcium; Cat Diseases; Cats; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dog Diseases; Dogs; Female; Hyperparathyroidism; Hyperparathyroidism, Secondary; Hypoparathyroidism; Kidney; Liver; Male; Parathyroid Diseases; Parathyroid Glands; Parathyroid Hormone; Parathyroid Neoplasms; Pregnancy; Tetany

Current status of our understanding of the metabolism of vitamin D and its implications in metabolic bone disease is reviewed. The details of metabolism of vitamin D3 to 25-hydroxyvitamin D3 in the liver and its further conversion in the kidneys to either 1,25-dihydroxyvitamin D3 or 24,25-dihydroxyvitamin D3 are presented. The latter conversions are regulated by the vitamin D status, serum calcium through the parathyroid gland system, and serum inorganic phosphorus concentration. The 1,25-dihydroxyvitamin D3 can now be regarded as a calcium- and a phosphate-mobilizing hormone and must be considered as one of the most important serum calcium-regulating hormones. Disruption of the vitamin D metabolic sequence or the signal system for 1,25-dihydroxyvitamin D3 results in several bone and calcium metabolism disorders such as renal osteodystrophy, hypoparathyroidism, pseudohypoparathyroidism, and vitamin D-dependency rickets. The use of the synthetic analogs of 1,25-dihydroxyvitamin D3 as well as 1,25-dihydroxyvitamin D3 itself in the management of these disease states is discussed.

Topics: Animals; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Endocrine Glands; Ergocalciferols; Homeostasis; Humans; Hyperparathyroidism, Secondary; Intestinal Absorption; Kidney; Phosphates; Vitamin D

Topics: Aluminum Hydroxide; Animals; Calcium; Child; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Hyperparathyroidism, Secondary; Intestinal Absorption; Kidney; Kidney Failure, Chronic; Magnesium; Parathyroid Hormone; Vitamin D

Topics: Amino Acid Sequence; Animals; Calcium; Cholecalciferol; Chronic Disease; Humans; Hydroxycholecalciferols; Hydroxylation; Hyperparathyroidism, Secondary; Kidney Diseases; Metabolic Clearance Rate; Molecular Weight; Parathyroid Hormone; Vitamin D

Topics: Biological Transport, Active; Bone and Bones; Calcium; Cell Membrane Permeability; Cholecalciferol; Endoplasmic Reticulum; Homeostasis; Humans; Hyperparathyroidism, Secondary; Intestinal Absorption; Intestinal Mucosa; Kidney; Kidney Failure, Chronic; Kidney Transplantation; Kidney Tubules; Liver; Magnesium; Muscle Contraction; Phosphates; Postoperative Complications; Sodium

Topics: Animals; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Hydroxycholecalciferols; Hyperparathyroidism, Secondary; Kidney; Kidney Failure, Chronic; Liver; Parathyroid Hormone; Rats; Uremia; Vitamin D

Topics: Bicarbonates; Bone Resorption; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Diet Therapy; Dihydroxycholecalciferols; Humans; Hyperparathyroidism, Secondary; Hypocalcemia; Kidney Failure, Chronic; Kidney Tubules; Magnesium; Parathyroid Glands; Parathyroid Hormone; Phosphorus; Renal Dialysis; Structure-Activity Relationship

Topics: Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Hyperparathyroidism, Secondary; Hypocalcemia; Intestinal Absorption; Kidney Failure, Chronic; Kidney Transplantation; Osteoporosis; Osteosclerosis; Phosphates; Transplantation, Homologous; Vitamin D

In India, there is a lack of information about the adequate daily dose of vitamin D3 supplementation in school children. Hence, we undertook this study to evaluate the adequacy and efficacy of different doses of vitamin D3 in schoolchildren. A total of 1008 vitamin D-deficient (VDD) children, aged 6-16 years with serum 25-hydroxyvitamin D (25(OH)D) levels <50nmol/l, were cluster randomised into three groups (A-344, B-341 and C-232) for supplementation (600, 1000 and 2000 IU daily) of vitamin D3 under supervision for 6 months. Of the 1008 subjects who completed the study, 938 (93 %) were compliant. Baseline and post-supplementation fasting blood and urine samples were evaluated for Ca, phosphates, alkaline phosphatase, 25(OH)D and parathormone and urine Ca:creatinine ratio. The mean age of the subjects was 11·7 (sd 2·4) years, and the overall mean baseline serum 25(OH)D level was 24·3 (SD 9·5)nmol/l. Post-supplementation rise in serum 25(OH)D in compliant group was maximum with 2000 IU (70·0 (SD 30·0)nmol/l), followed by 1000 IU (46·8 (SD 22·5)nmol/l) and 600 IU (36·5 (SD 18·5)nmol/l), and serum 25(OH)D levels of ≥50nmol/l were achieved in 71·5, 81·8 and 92·9 % by groups A, B and C, respectively. Secondary hyperparathyroidism decreased from 31·7 to 8·4 % post-supplementation. Two participants developed hypercalciuria, but none developed hypercalcaemia. Children with VDD benefit maximum with the daily supplementation of 2000 IU of vitamin D3. Whether recommendations of 400 IU/d by Indian Council of Medical Research or 600 IU by Indian Academy of Pediatrics or Institute of Medicine would suffice to achieve vitamin D sufficiency in children with VDD remains debatable.

Topics: Adolescent; Alkaline Phosphatase; Calcium; Child; Cholecalciferol; Creatinine; Dietary Supplements; Female; Humans; Hyperparathyroidism, Secondary; India; Male; Parathyroid Hormone; Phosphates; Prospective Studies; Single-Blind Method; Students; Vitamin D; Vitamin D Deficiency; Vitamins

Calcidiol insufficiency may accelerate the development of secondary hyperparathyroidism (SHPT). We tested the effect of a substantial increase in calcidiol on mineral metabolism in patients with chronic kidney disease (CKD).. Ninety-five patients with CKD Stages 3-4, parathyroid hormone (PTH) above 6.8 pmol/L and calcidiol below 75 nmol/L were randomized to receive either cholecalciferol 8000 IU/day or placebo for 12 weeks. The primary endpoint was difference in the mean change in iPTH after 12 weeks. The proportion of participants having a 30% reduction in PTH and the effect on hand grip strength, fatigue and different biochemical variables were also investigated.. Baseline calcidiol was 57.5 ± 22 and 56.8 ± 22 nmol/L in the cholecalciferol and placebo groups, respectively. The corresponding concentrations of PTH were 10.9 ± 5 and 13.1 ± 9 pmol/L. Calcidiol increased to 162 ± 49 nmol/L in patients receiving cholecalciferol, and PTH levels remained constant at 10.5 ± 5 pmol/L. In the placebo group, calcidiol remained stable and PTH increased to 15.2 ± 11 pmol/L. The mean change in PTH differed significantly between the two groups (P < 0.01). The proportion of subjects reaching a 30% decrease in PTH did not differ. No effect on grip strength, fatigue, phosphate or fibroblast growth factor 23 was observed. Cholecalciferol treatment resulted in stable calcium concentrations and a substantial increase in calcitriol.. Treatment with high daily doses of cholecalciferol in patients with CKD Stages 3-4 halts the progression of SHPT and does not cause hypercalcaemia or other side effects.

Topics: Aged; Calcium; Calcium-Regulating Hormones and Agents; Cholecalciferol; Disease Progression; Double-Blind Method; Female; Fibroblast Growth Factor-23; Fibroblast Growth Factors; Humans; Hyperparathyroidism, Secondary; Male; Middle Aged; Prognosis; Renal Insufficiency, Chronic

We evaluated the improvement of intact parathyroid hormone (iPTH) levels and bone parameters by supplementing nutritional vitamin D (cholecalciferol) to combined calcimimetic (cinacalcet) and active vitamin D analog (calcitriol) among severe secondary hyperparathyroidism (SHPT) hemodialysis (HD) patients. A randomized, controlled open-label study was undertaken in 60 HD patients with serum iPTH > 1000 pg/mL or persistently high iPTH ≥ 600 pg/mL even after >3 months of calcitriol (3 μg/week). The study group received oral cholecalciferol (5000 IU/ day) and the control group received a placebo. All patients received fixed dose cinacalcet (30 mg/day, orally) and calcitriol. Calcitriol was reduced if iPTH ≤ 300 pg/mL and cinacalcet was withdrawn if serum iPTH was persistently low (iPTH ≤ 300 pg/mL) for 4 weeks after the reduction of calcitriol. A significantly lower iPTH level was noted from the 20th week in the study group compared to the placebo group, and the target iPTH ≤ 300 pg/mL was achieved at the 24th week in the study group. Most patients achieved serum 25-(OH)D₃ ≥ 30 ng/mL in the study group. Nearly 40% of study patients gained >10% improvement in femoral neck (FN) bone mineral density (BMD). We conclude that cholecalciferol additively reduced serum iPTH levels, improved 25-(OH)D₃ levels and improved FN BMD when used together with cinacalcet/calcitriol in severe SHPT HD patients.

Topics: Aged; Bone Density; Calcifediol; Calcimimetic Agents; Calcitriol; Cholecalciferol; Cinacalcet; Dietary Supplements; Female; Femur Neck; Humans; Hyperparathyroidism, Secondary; Male; Middle Aged; Parathyroid Hormone; Renal Dialysis; Severity of Illness Index; Vitamins

Bariatric patients often suffer from vitamin D deficiency (VDD), and both, morbid obesity and VDD, are related to non-alcoholic fatty liver disease. However, limited data are available regarding best strategies for treating VDD, particularly, in bariatric patients undergoing omega-loop gastric bypass (OLGB). Therefore, we examined the efficacy and safety of a forced vitamin D dosing regimen and intervention effects in liver fibrotic patients.. Compared with control group, higher increase of 25(OH)D (67.9 (21.1) vs. 55.7 nmol/L (21.1); p = 0.049) with lower prevalence of secondary hyperparathyroidism (10 vs. 24 %; p = 0.045) was observed in intervention group. No (serious) adverse events related to study medication were found. The loading dose regimen was more effective in increasing 25(OH)D in patients with significant liver fibrosis while this was not the case for conventional supplementation (placebo with maintenance dose) (71.5 (20.5) vs. 22.5 nmol/L (13.8); p = 0.022; n = 14).. Our findings indicate that a high vitamin D

Topics: Adult; Cholecalciferol; Dietary Supplements; Double-Blind Method; Female; Gastric Bypass; Humans; Hyperparathyroidism, Secondary; Liver Cirrhosis; Male; Middle Aged; Non-alcoholic Fatty Liver Disease; Obesity, Morbid; Postoperative Period; Prevalence; Vitamin D; Vitamin D Deficiency; Vitamins; Weight Loss

Active Vitamin D analogues are used clinically for prevention and treatment of secondary hyperparathyroidism (SHPT) in hemodialysis (HD) patients. Nutritional vitamin D supplementation is used for additional local parathyroid (PTH) suppression, with lower incidence of hypercalcemia and hyperphosphatemia. This study evaluates the possible beneficial effects of combined vitamin D treatment (paricalcitol and cholecalciferol).. Sixty HD patients with serum parathyroid hormone (iPTH) >300 pg/mL were enrolled. All patients administered 2 mcg/day of paricalcitol and were randomly allocated into control group (placebo) or study group (cholecalciferol) for 16 weeks. Serum 25(OH)D₃, iPTH and human cathelicidin (hCAP-18) were measured at baseline and during follow-up.. iPTH levels decreased in the study group appropriately and were more significantly decreased at 16 weeks. Study group had significantly increased 25(OH)D₃ levels. In addition, the study group had significantly increased serum hCAP-18 levels compared with control group. Correlation analysis showed a significant correlation between the percentage increase in serum hCAP-18 and 25(OH)D₃ levels.. Cholecalciferol, in combination with paricalcitol, additively lowers the iPTH levels in a significant number of patients after 16 weeks of supplementation. A dose of 5000 IU/week of cholecalciferol could maintain serum 25(OH)D₃ levels above 30 ng/dL as early as 8 weeks after beginning supplementation. Doubling of serum cathelicidin levels were noted after 16 weeks of cholecalciferol supplementation in 40% of study patients.

Topics: Aged; Antimicrobial Cationic Peptides; Calcifediol; Cathelicidins; Cholecalciferol; Drug Interactions; Drug Therapy, Combination; Ergocalciferols; Female; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Placebos; Renal Dialysis; Treatment Outcome; Vitamin D

To study the effect of Vitamin D3 supplementation on metabolic control in an obese type 2 diabetes Emirati population.. This randomized double-blind clinical trial was conducted with 87 vitamin D-deficient obese, type 2 diabetic participants. The vitamin D-group (n=45) and the placebo group (n=42) were matched for gender, age, HbA1c and 25-hydroxy vitamin D (25(OH) D) at the baseline. The study was divided into two phases of 3 months each; in phase 1, the vitamin D-group received 6000 IU vitamin D3/day followed by 3000 IU vitamin D3/day in phase 2, whereas the placebo group (n=42) received matching placebo.. After supplementation, serum 25(OH) D peaked in the vitamin D-group in phase 1 (77.2±30.1 nmol/l, P=0.003) followed by a decrease in the phase 2 (61.4±18.8 nmol/l, P=0.006), although this was higher compared with baseline. In the placebo group, no difference was observed in the serum 25(OH) D levels throughout the intervention. Relative to baseline serum, parathyroid hormone decreased 24% (P=0.003) in the vitamin D-group in phase 2, but remained unchanged in the placebo group. No significant changes were observed in blood pressure, fasting blood glucose, HbA1c, C-peptide, creatinine, phosphorous, alkaline phosphatase, lipids, C-reactive protein or thyroid stimulating hormone concentrations compared with baseline in either group.. Six months of vitamin D3 supplementation to vitamin D-deficient obese type 2 diabetes patients in the UAE normalized the vitamin D status and reduced the incidence of eucalcemic parathyroid hormone elevation but showed no effect on the metabolic control.

Topics: Adult; Body Mass Index; Calcifediol; Cholecalciferol; Diabetes Mellitus, Type 2; Dietary Supplements; Double-Blind Method; Female; Glycated Hemoglobin; Humans; Hyperparathyroidism, Secondary; Incidence; Lost to Follow-Up; Male; Middle Aged; Obesity; Parathyroid Hormone; Patient Dropouts; United Arab Emirates; Vitamin D Deficiency

To evaluate whether fortification of yogurts with vitamin D and calcium exerts an additional lowering effect on serum parathyroid hormone (PTH) and bone resorption markers (BRM) as compared to iso-caloric and iso-protein dairy products in aged white women at risk of fragility fractures.. A randomized double-blind controlled trial.. A community dwelling home.. Forty-eight women over 60 years (mean age 73.4).. Consumption during 84 days of two 125 g servings of either vitamin D and calcium-fortified yogurts (FY) at supplemental levels of 10 µg vitamin D3/d and 520 mg/d of calcium (total=800 mg/d), or non fortified control yogurts (CY) providing 280 mg/d of calcium.. Serum changes from baseline (D0) to D28, D56 and D84 in 25OHD, PTH and in two BRM: Tartrate-resistant-acid-phosphatase-isoform-5b (TRAP5b) and carboxy-terminal-cross-linked-telopeptide of type-I-collagen (CTX).. The 10 years risk of major and hip fractures were 13.1 and 5.0%, and 12.9 and 4.2 %, in FY and CY groups, respectively. From D0 to D84, serum 25OHD increased (mean±SE) from 34.3±2.4 to 56.3±2.4 nmol/L in FY (n=24) and from 35.0±2.5 to 41.3±3.0 nmol/L in CY (n=24), (P=0.00001). The corresponding changes in PTH were from 64.1±5.1 to 47.4±3.8 ng/L in FY and from 63.5±4.6 to 60.7±4.2 ng/L in CY (P=0.0011). After D84, TRAP5b was reduced significantly (P=0.0228) and CTX fell though not significantly (P=0.0773) in FY compared to CY.. This trial in aged white women living in a community dwelling home at risk for osteoporotic fractures confirms that fortification of dairy products with vitamin D3 and calcium should provide a greater prevention of secondary hyperparathyroidism and accelerated bone resorption as compared to non-fortified equivalent foods.

Topics: Acid Phosphatase; Aged; Aged, 80 and over; Biomarkers; Bone Resorption; Calcium, Dietary; Cholecalciferol; Collagen Type I; Double-Blind Method; Female; Food, Fortified; Hip Fractures; Humans; Hyperparathyroidism, Secondary; Isoenzymes; Middle Aged; Nursing Homes; Osteoporotic Fractures; Parathyroid Hormone; Risk; Tartrate-Resistant Acid Phosphatase; White People; Yogurt

There are several published reports on the prevalence of low vitamin D levels in otherwise healthy Indian population. Vitamin D deficiency has shown variable effect on muscle performance and strength but there is paucity of data on the effect of vitamin D deficiency on muscle energy metabolism. The present study was proposed to investigate the influence of severe vitamin D deficiency on high-energy metabolite levels in resting skeletal muscle and thereafter, monitor the response after vitamin D supplementation using ³¹P magnetic resonance spectroscopy (MRS). Study was conducted on 19 otherwise healthy subjects but with low serum 25(OH)D levels (<5 ng/ml). Subjects were supplemented with cholecalciferol at a dose of 60,000 IU/week for 12 weeks. MRS measurements of inorganic phosphate (Pi), phosphocreatine (PCr), phosphodiester (PDE) and ATP of the calf muscle were taken pre- and post-vitamin D supplementation. The study revealed significantly increased PCr/Pi ratio and decreased [Pi] and PDE/ATP ratio with raised serum 25(OH)D levels after 12 weeks of supplementation. The study indicates that serum 25(OH)D level plays an important role in improving the skeletal muscle energy metabolism and vitamin D deficiency might be one of the primary reasons for prevalence of low PCr/Pi ratio and high PDE values in normal Indian population as reported earlier. The findings of this preliminary study are highly encouraging and warrant further in-depth research, involving larger number of subjects of different age groups, regions and socio-economic sections of the society to further strengthen a correlation between vitamin D levels and muscle energy metabolism.

Topics: Adenosine Triphosphate; Adolescent; Adult; Calcifediol; Cholecalciferol; Dietary Supplements; Energy Metabolism; Female; Humans; Hyperparathyroidism, Secondary; India; Magnetic Resonance Imaging; Male; Muscle, Skeletal; Phosphocreatine; Phosphoric Diester Hydrolases; Phosphorus Isotopes; Pilot Projects; Severity of Illness Index; Vitamin D Deficiency; Whole Body Imaging; Young Adult

Nutritional prevention of bone deterioration with fortified foods seems particularly suitable in institutionalized elderly women at risk of vitamin D deficiency, secondary hyperparathyroidism, increased bone resorption, and osteoporotic fracture.. The objective was to evaluate whether fortification of yogurts with vitamin D and calcium exerts an additional lowering effect on serum PTH and bone resorption markers as compared with isocaloric and isoprotein dairy products in elderly women.. A randomized double-blind controlled-trial, 56-day intervention was conducted in institutionalized women (mean age 85.5 years) consuming 2 125-g servings of either vitamin D- and calcium-fortified yogurt (FY) at supplemental levels of 10 μg/d vitamin D₃ and 800 mg/d calcium or nonfortified control yogurt (CY) providing 280 mg/d calcium.. The endpoints were serum changes from baseline (day 0) to day 28 and day 56 in 25-hydroxyvitamin-D (25OHD), PTH, and bone resorption markers tartrate-resistant acid phosphatase isoform-5b (TRAP5b), the primary outcome, and carboxyl-terminal cross-linked telopeptide of type I collagen (CTX).. At day 56, serum 25OHD increased (mean ± SEM) by 25.3 ± 1.8 vs 5.2 ± 2.5 nmol/L in FY (n = 29) and CY (n = 27), respectively (P < .0001). The corresponding changes in PTH were -28.6% ± 7.2% vs -8.0% ± 4.3% (P = .0003); in TRAP5b, -21.9% ± 4.3% vs 3.0% ± 3.2% (P < .0001); and in CTX, -11.0% ± 9.7% vs -3.0% ± 4.1% (P = .0146), in FY and CY, respectively. At day 28, these differences were less pronounced but already significant for 25OHD, PTH, and TRAP5b.. This study in institutionalized elderly at high risk for osteoporotic fracture suggests that fortification of dairy products with vitamin D₃ and calcium provides a greater prevention of accelerated bone resorption as compared with nonfortified equivalent foods.

Topics: Acid Phosphatase; Aged, 80 and over; Biomarkers; Bone Density Conservation Agents; Bone Resorption; Calcium, Dietary; Cholecalciferol; Collagen Type I; Double-Blind Method; Female; Food, Fortified; France; Homes for the Aged; Humans; Hyperparathyroidism, Secondary; Isoenzymes; Nursing Homes; Osteoporosis, Postmenopausal; Osteoporotic Fractures; Parathyroid Hormone; Peptides; Risk; Tartrate-Resistant Acid Phosphatase; Vitamin D Deficiency; Yogurt

Vitamin D deficiency contributes to secondary hyperparathyroidism, which occurs early in chronic kidney disease (CKD).. We aimed to determine whether high-dose cholecalciferol supplementation for 1 y in early CKD is sufficient to maintain optimal vitamin D status (serum 25-hydroxyvitamin D [25(OH)D] concentration ≥30 ng/mL) and decrease serum parathyroid hormone (PTH). A secondary aim was to determine the effect of cholecalciferol on blood pressure and serum fibroblast growth factor-23 (FGF23).. This was a double-blind, randomized, placebo-controlled trial. Forty-six subjects with early CKD (stages 2-3) were supplemented with oral cholecalciferol (vitamin D group; 50,000 IU/wk for 12 wk followed by 50,000 IU every other week for 40 wk) or a matching placebo for 1 y.. By 12 wk, serum 25(OH)D increased in the vitamin D group only [baseline (mean ± SD): 26.7 ± 6.8 to 42.8 ± 16.9 ng/mL; P < 0.05] and remained elevated at 1 y (group-by-time interaction: P < 0.001). PTH decreased from baseline only in the vitamin D group (baseline: 89.1 ± 49.3 to 70.1 ± 24.8 pg/mL; P = 0.01) at 12 wk, but values were not significantly different from baseline at 1 y (75.4 ± 29.5 pg/mL; P = 0.16; group-by-time interaction: P = 0.09). Group differences were more pronounced in participants with secondary hyperparathyroidism (group-by-time interaction: P = 0.004). Blood pressure and FGF23 did not change in either group.. After 1 y, this oral cholecalciferol regimen was safe and sufficient to maintain serum 25(OH)D concentrations and prevent vitamin D insufficiency in early CKD. Furthermore, serum PTH improved after cholecalciferol treatment, particularly in patients who had secondary hyperparathyroidism.

Topics: Aged; Calcifediol; Cholecalciferol; Diet; Dietary Supplements; Double-Blind Method; Female; Fibroblast Growth Factor-23; Georgia; Hospitals, Veterans; Humans; Hyperparathyroidism; Hyperparathyroidism, Secondary; Intention to Treat Analysis; Male; Middle Aged; Parathyroid Hormone; Pilot Projects; Prevalence; Renal Insufficiency, Chronic; Severity of Illness Index; Vitamin D Deficiency

The optimal treatment of secondary hyperparathyroidism in chronic kidney disease (CKD) is unknown.. We conducted a randomized, blinded, 3-month trial in vitamin D-deficient CKD stage 3 and 4 patients with parathyroid hormone (PTH) values above the Kidney Disease Outcomes Quality Initiative target, comparing cholecalciferol (4000 IU/d x 1 month, then 2000 IU/d; n = 22) to doxercalciferol (1 microg/d; n = 25).. There was no difference in baseline demographics or lab tests, except a slightly higher estimated GFR (eGFR) in the doxercalciferol group. There was a significant increase in vitamin D level in the cholecalciferol group (14 +/- 6 to 37 +/- 10 ng/ml; P < 0.001) but no change in the doxercalciferol group. The PTH decreased by 27% +/- 34% in the doxercalciferol group (P = 0.002) and decreased by 10% +/- 31% in the cholecalciferol group (P = 0.16), but the difference between treatments was NS (P = 0.11). Similar results were found when absolute PTH change from baseline to end point was analyzed in a repeated-measures ANOVA model. The serum calcium and urine calcium excretions were not different. Additional non-mineral-related end points, albuminuria, and BP were evaluated, and although trends were present, this did not reach significance.. This prospective, randomized trial demonstrated a within-group reduction in PTH in the doxercalciferol-treated patients but no significant difference between the doxercalciferol and cholecalciferol patients. Larger, long-term studies are needed to demonstrate efficacy of mineral-related and non-mineral-related end points and safety.

Topics: Aged; Biomarkers; Calcium; Cholecalciferol; Chronic Disease; Ergocalciferols; Female; Humans; Hyperparathyroidism, Secondary; Kidney Diseases; Male; Middle Aged; Parathyroid Hormone; Prospective Studies; Single-Blind Method; Time Factors; Treatment Outcome; Vitamin D; Vitamin D Deficiency; Vitamins

To compare the effects on parathyroid hormone (PTH) and 25-hydroxy-vitamin D (25(OH)D) of two dosing regimens of cholecalciferol in women with secondary hyperparathyroidism (sHPTH) and hypovitaminosis D and to investigate variables affecting 25(OH)D response to cholecalciferol.. Randomized-controlled trial with 6-month follow-up.. Two osteoporosis centers in northern Italy.. Sixty community-dwelling women aged 65 and older with sHPTH and hypovitaminosis D, creatinine clearance greater than 65 mL/min and without diseases or drugs known to influence bone and vitamin D metabolism.. Cholecalciferol 300,000 IU every 3 months, once at baseline and once at 3 months (intermittent D(3) group) or cholecalciferol 1,000 IU/day (daily D(3) group).. Serum PTH, 25(OH)D, calcium, bone-specific alkaline phosphatase, β-C-terminal telopeptide of type I collagen, phosphate, 24-hour urinary calcium excretion.. The two groups had similar baseline characteristics. All participants had vitamin D deficiency [25(OH)D<20 ng/mL)], and 36 subjects (60%) had severe deficiency (<10 ng/mL), with no difference between the groups (severe deficiency: intermittent D(3) group, n=18; daily D(3) group, n=18). After 3 and 6 months, both groups had a significant increase in 25(OH)D and a reduction in PTH. Mean absolute increase ± standard deviation of 25(OH)D at 6 months was higher in the intermittent D(3) group (22.7±11.8 ng/mL) than in the daily D(3) group (13.7±6.7 ng/mL, P<.001), with a higher proportion of participants in the intermittent D(3) group reaching desirable serum concentration of 25(OH)D≥30 ng/mL (55% in the intermittent D(3) group vs 20% in the daily D(3) group, P<.001). Mean percentage decrease of PTH in the two groups was comparable, and at 6 months, a similar proportion of participants reached normal PTH values. 25(OH)D response to cholecalciferol showed a wide variability. In a logistic regression analysis, body mass index and type of treatment appeared to be significantly associated with normalization of 25(OH)D values.. Cholecalciferol 300,000 IU every 3 months was more effective than 1,000 IU daily in correcting vitamin D deficiency, although the two groups achieved similar effects on PTH at 6 months. Only 55% of the higher-dose intermittent group reached desirable concentrations of 25(OH)D, suggesting that yet-higher doses will be required for adequate vitamin D repletion.

Topics: Aged; Alkaline Phosphatase; Biomarkers; Calcium; Cholecalciferol; Collagen Type I; Dose-Response Relationship, Drug; Female; Humans; Hyperparathyroidism, Secondary; Parathyroid Hormone; Peptides; Phosphates; Vitamin D; Vitamin D Deficiency; Vitamins

Studies addressing the effects of vitamin D(3) supplementation on secondary hyperparathyroidism in patients with moderate chronic kidney disease are scarce.. Post hoc analysis of the randomized clinical trial Vitamin D, Calcium, Lyon Study II (DECALYOS II) to assess effects according to baseline estimated glomerular filtration rate (eGFR).. Multicenter, randomized, double-blinded, placebo-controlled study of 639 elderly women randomly assigned to calcium-vitamin D(3) fixed combination; calcium plus vitamin D(3) separate combination, or placebo.. Placebo or calcium (1,200 mg) and vitamin D(3) (800 IU) in fixed or separate combination.. Proportion of participants with a mean decrease in intact parathyroid hormone (iPTH) level of 30% or greater. eGFR was calculated using the 4-variable Modification of Diet in Renal Disease (MDRD) Study equation and categorized as 60 or greater, 45 to 59, and less than 45 mL/min/1.73 m(2).. 610 participants had an eGFR at baseline: 288 (47.2%), 222 (36.4%), and 100 (16.4%) were in each decreasing eGFR category. Across decreasing eGFR groups, 88%, 86%, and 89% had 25-hydroxyvitamin D (25[OH]D) levels less than 15 ng/mL at baseline. On treatment, similar improvements in the proportion of participants achieving 25(OH)D levels greater than 30 ng/mL at 6 months were seen in all kidney function groups (43%, 49%, and 41%, respectively). Active regimens versus placebo increased mean 25(OH)D levels from baseline in all eGFR groups at all times (P < 0.001 for all). The proportion with a 30% or greater decrease in iPTH level at 6 months was 50% in all eGFR groups on treatment versus 6% to 9% for placebo (P < 0.001 for all). The effects of the intervention on iPTH levels did not differ according to baseline eGFR (interaction P > 0.1 for all times).. This study included only elderly white women.. Vitamin D(3) was effective in increasing 25(OH)D and decreasing iPTH levels in patients with moderate chronic kidney disease.

Topics: Aged, 80 and over; Calcium, Dietary; Cholecalciferol; Chronic Disease; Dietary Supplements; Double-Blind Method; Female; Humans; Hyperparathyroidism, Secondary; Kidney Diseases; Parathyroid Hormone; Severity of Illness Index; Vitamins

By the time patients require dialysis replacement therapy, nearly all chronic kidney diseases (CKD) patients are affected with uremic bone diseases. High-turnover osteodystrophy can be prevented; patients with CKD should be monitored for imbalances in calcidiol (25 OH vitamin D), calcium, and phosphate homeostasis. We aimed to determine the effect of a monthly oral 300,000 IU vitamin D(3) (cholecalciferol) supplementation on the uremic bone diseases (UBD) markers such as iPTH and alkaline phosphatase in CKD patients. Among a total of 70 patients under treatment in the nephrology unit, 40 predialysis CKD patients (mean age of 49 +/- 14, male/female 20/20) were included the study. The patients were randomly divided into two groups. Treatment group included 20 patients (mean age of 51 +/- 14, male/female 9/11), and the control group comprised 20 patients (mean age of 47 +/- 14, male/female 9/11). Treatment group patients were given a single dose of Devit3 ampoule (300,000 U cholecalciferol) per month orally way. Patients in the control group did not take any vitamin D for a month. The level of calcidiol was lower than normal range in two groups. After a month, treatment group patient's calcidiol increased statistically significant (6.8 +/- 3.5 to 17.8 +/- 21.4 ng/mL, p < 0.001). After a month, iPTH level decreased in the treatment group statistically significantly (368 +/- 274 to 279 +/- 179 pg/ml, p < 0.001). At the 30(th) day of the treatment, in 9/20 of the treatment group patients (45%), the iPTH value decreased at least 30% (p < 0.001). We suggest that oral depot cholecalciferol treatment causes a statistically significant decrease of serum iPTH level but does not cause a statistically significant change in Ca, P, ratio of Ca x P, or urinary calcium creatinine rate in UBD predialysis CKD. This treatment can be used safely for the predialysis CKD patients, along with the cautious control of serum calcium and phosphor.

Topics: Absorptiometry, Photon; Administration, Oral; Adult; Bone Density; Bone Density Conservation Agents; Calcifediol; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Delayed-Action Preparations; Dose-Response Relationship, Drug; Drug Administration Schedule; Female; Follow-Up Studies; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Kidney Function Tests; Male; Middle Aged; Parathyroid Hormone; Probability; Prospective Studies; Reference Values; Renal Dialysis; Risk Assessment; Severity of Illness Index; Treatment Outcome

We designed a randomized, double-blind, controlled clinical trial to compare the effect of two regimens for administering cholecalciferol on the serum 25-hydroxycholecalciferol [25(OH)D] levels and in the reversion of secondary hyperparathyroidism in the elderly living in a low-income housing unit in the city of Porto Alegre, southern Brazil. We studied 28 individuals ranging in age from 65 to 102 years with serum parathyroid hormone (PTH) levels greater than 48 pg/ml and normal or reduced serum calcium levels. Subjects were randomized to receive oral cholecalciferol, as a single dose of 300 000 IU (group 1) or 800 IU (group 2) daily for 9 months. Both groups received 1250 mg calcium carbonate per day. Serum 25(OH)D and PTH levels were measured at baseline and after 1, 2, 3, 6, and 9 months. Serum 25(OH)D levels in group 1 were significantly higher than in group 2 during the study (P < 0.001). After 1 (P < 0.001) and 2 (P < 0.04) months of treatment, mean serum 25(OH)D levels were higher in group 1. The number of subjects who reached serum 25(OH)D levels >/=20 ng/dl was higher in group 1, after the first (P < 0.001) and third (P = 0.008) months. In the short term, a single 300 000 IU oral dose of vitamin D(3) was more effective than 800 IU per day to increase serum 25(OH)D levels in elderly persons, living in a low-income housing unit, who were taking 500 mg elementary calcium supplement per day.

Topics: Aged; Aged, 80 and over; Bone Density Conservation Agents; Brazil; Calcifediol; Calcium, Dietary; Cholecalciferol; Dietary Supplements; Double-Blind Method; Humans; Hyperparathyroidism, Secondary; Parathyroid Hormone; Poverty; Public Housing; Vitamin D; Vitamin D Deficiency

To evaluate the efficacy and safety of an annual intramuscular injection of cholecalciferol for vitamin D deficiency.. Prospective open-label study.. Five men and 45 women (mean age 66.3 years) with vitamin D deficiency who were given a single therapeutic intramuscular injection of 600 000 IU (15 mg) cholecalciferol (vitamin D(3)).. Serum levels of calcium, creatinine, 25-hydroxyvitamin D(3) (25OHD(3)) and parathyroid hormone, as well as early morning 2-hour urine calcium/creatinine excretion index. Specimens were collected at baseline and after 4 and 12 months of therapy. Data are reported as mean +/- 1 SD.. Vitamin D deficiency was severe (< 12.5 nmol/L) in one participant, moderate (12.5-24 nmol/L) in 14, and mild (25-49 nmol/L) in 35. Twenty-four participants (48%) had secondary hyperparathyroidism. Following intramuscular cholecalciferol injection, serum 25OHD(3) levels normalised in all participants and remained above 50 nmol/L throughout the study. Serum 25OHD(3) levels were significantly higher at 4 months (114 +/- 35 nmol/L), and 12 months (73 +/- 13 nmol/L) compared with baseline (32 +/- 8 nmol/L) (P < 0.001), increasing by an average of 128% over the 12 months. There was a corresponding decrease in serum parathyroid hormone levels at 4 months (6 +/- 3 pmol/L) and at 12 months (5.2 +/- 3 pmol/L), with a 30% decrease at 12 months from baseline (7.4 +/- 4 pmol/L) (P < 0.01). Primary hyperparathyroidism was unmasked in one participant at 4 months and mild hypercalcaemia (serum calcium, < 2.70 mmol/L) was noted in two participants (4%) at 12 months. Serum creatinine levels remained normal in all participants throughout the study, while increases in 2-hour urine calcium/creatinine excretion index were seen in 10 participants (20%) at 12 months, three of whom had had elevated values at baseline.. Once-yearly intramuscular cholecalciferol injection (600 000 IU) is effective therapy for vitamin D deficiency. While this therapy appears to be safe, the potential for developing hypercalciuria needs to be examined in a large randomised controlled trial.

Topics: Adult; Aged; Aged, 80 and over; Calcium; Cholecalciferol; Creatinine; Dose-Response Relationship, Drug; Drug Administration Schedule; Female; Humans; Hyperparathyroidism, Secondary; Injections, Intramuscular; Male; Middle Aged; Parathyroid Hormone; Prospective Studies; Treatment Outcome; Vitamin D; Vitamin D Deficiency

Topics: Alkaline Phosphatase; Calcium; Calcium Carbonate; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dialysis; Drug Therapy, Combination; Female; Humans; Hyperparathyroidism, Secondary; Male; Parathyroid Hormone; Phosphorus; Polyamines; Practice Guidelines as Topic; Sevelamer

Renal osteodystrophy is the major complication in patients with end-stage renal failure. Oral or intravenous vitamin D3 (D3) is given to these patients, but severe hypercalcaemia sometimes interrupts this therapy. This study was undertaken to determine whether the effectiveness and safety of D3 also depend on its dosing time during a repeated treatment.. A higher dose (3 micro g) was given orally to 13 haemodialysis patients at 08.00 h or 20.00 h for 12 months by a randomized, cross-over design.. Three patients were withdrawn due to severe hypercalcaemia after switching from 08.00 h to 20.00 h dosings. The elevation in serum calcium concentration was significantly (P < 0.001) greater during the 08.00 h dosing in the remaining ten patients. Mean serum Ca concentration after the trial was 10.92 (95% confidence interval (CI) 10.79, 11.06) and 9.55 mg dl-1 (95% CI 9.30, 9.71) by 08.00 h and 20.00 h dosing, respectively. On the other hand, the suppression of the elevated serum parathyroid hormone (PTH) and subsequent increment in bone density were significantly greater during the 08.00 h dosing. Mean PTH concentration after the trial was 414 (95% CI 360, 475) and 220 pg ml-1 (95% CI 202, 249) by 08.00 h and 20.00 h dosing, respectively (P = 0.02). Mean increment of bone density after the trial was 22 (95% CI 8, 32) and 57 g cm-3 (95% CI 43, 83) by 08.00 h and 20.00 h dosing, respectively (P = 0.04).. These results indicate that a higher dose of oral D3 is more effective and safe after dosing at evening in patients with renal osteodystrophy.

Topics: Administration, Oral; Adult; Aged; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Chronotherapy; Cross-Over Studies; Double-Blind Method; Female; Humans; Hypercalcemia; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis

Vitamin D insufficiency and low calcium intake contribute to increase parathyroid function and bone fragility in elderly people. Calcium and vitamin D supplements can reverse secondary hyperparathyroidism thus preventing hip fractures, as proved by Decalyos I. Decalyos II is a 2-year, multicenter, randomized, double-masked, placebo-controlled confirmatory study. The intention-to-treat population consisted of 583 ambulatory institutionalized women (mean age 85.2 years, SD = 7.1) randomized to the calcium-vitamin D3 fixed combination group (n = 199); the calcium plus vitamin D3 separate combination group (n = 190) and the placebo group (n = 194). Fixed and separate combination groups received the same daily amount of calcium (1200 mg) and vitamin D3 (800 IU), which had similar pharmacodynamic effects. Both types of calcium-vitamin D3 regimens increased serum 25-hydroxyvitamin D and decreased serum intact parathyroid hormone to a similar extent, with levels returning within the normal range after 6 months. In a subgroup of 114 patients, femoral neck bone mineral density (BMD) decreased in the placebo group (mean = -2.36% per year, SD = 4.92), while remaining unchanged in women treated with calcium-vitamin D3 (mean = 0.29% per year, SD = 8.63). The difference between the two groups was 2.65% (95% CI = -0.44, 5.75%) with a trend in favor of the active treatment group. No significant difference between groups was found for changes in distal radius BMD and quantitative ultrasonic parameters at the os calcis. The relative risk (RR) of HF in the placebo group compared with the active treatment group was 1.69 (95% CI = 0.96, 3.0), which is similar to that found in Decalyos I (RR = 1.7; 95% CI = 1.0, 2.8). Thus, these data are in agreement with those of Decalyos I and indicate that calcium and vitamin D3 in combination reverse senile secondary hyperparathyroidism and reduce both hip bone loss and the risk of hip fracture in elderly institutionalized women.

Topics: Aged; Aged, 80 and over; Analysis of Variance; Bone Density; Calcium; Cholecalciferol; Drug Therapy, Combination; Female; Femur Neck; Hip Fractures; Homes for the Aged; Humans; Hyperparathyroidism, Secondary; Institutionalization; Middle Aged; Radius; Risk; Ultrasonography

Supplementation of elderly institutionalized women with vitamin D and calcium decreased hip fractures and increased hip bone mineral density. Quantitative ultrasound (QUS) measurements can be performed in nursing homes, and easily repeated for follow-up. However, the effect of the correction of vitamin D deficiency on QUS parameters is not known. Therefore, 248 institutionalized women aged 62-98 years were included in a 2-year open controlled study. They were randomized into a treated group (n = 124), receiving 440 IU of vitamin D3 combined with 500 mg calcium (1250 mg calcium carbonate, Novartis) twice daily, and a control group (n = 124). One hundred and three women (42%), aged 84.5 +/- 7.5 years, completed the study: 50 in the treated group, 53 in the controls. QUS of the calcaneus, which measures BUA (broadband ultrasound attenuation) and SOS (speed of sound), and biochemical analysis were performed before and after 1 and 2 years of treatment. Only the results of the women with a complete follow-up were taken into account. Both groups had low initial mean serum 25-hydroxyvitamin D levels (11.9 +/- 1.2 and 11.7 +/- 1.2 micrograms/l; normal range 6.4-40.2 micrograms/l) and normal mean serum parathyroid hormone (PTH) levels (43.1 +/- 3.2 and 44.6 +/- 3.5 ng/l; normal range 10-70 ng/l, normal mean 31.8 +/- 2.3 ng/l). The treatment led to a correction of the metabolic disturbances, with an increase in 25-hydroxyvitamin D by 123% (p < 0.01) and a decrease in PTH by 18% (p < 0.05) and of alkaline phosphatase by 15% (p < 0.01). In the controls there was a worsening of the hypovitaminosis D, with a decrease of 25-hydroxyvitamin D by 51% (p < 0.01) and an increase in PTH by 51% (p < 0.01), while the serum calcium level decreased by only 2% (p < 0.01). After 2 years of treatment BUA increased significantly by 1.6% in the treated group (p < 0.05), and decreased by 2.3% in the controls (p < 0.01). Therefore, the difference in BUA between the treated subjects and the controls (3.9%) was significant after 2 years (p < 0.01). However, SOS decreased by the same amount in both groups (approximately 0.5%). In conclusion, BUA, but not SOS, reflected the positive effect on bone of supplementation with calcium and vitamin D3 in a population of elderly institutionalized women.

Topics: Aged; Aged, 80 and over; Bone and Bones; Bone Density; Calcium; Cholecalciferol; Female; Homes for the Aged; Humans; Hyperparathyroidism, Secondary; Institutionalization; Longitudinal Studies; Middle Aged; Ultrasonography; Vitamin D Deficiency

The objective of this study was to compare the effect of ultraviolet radiation (UV) and oral vitamin D3 on the vitamin D status and parathyroid hormone (PTH) concentration in elderly nursing home patients. The design of the study was a randomized clinical trial. The setting was a psychogeriatric nursing home. Subjects included 45 female psychogeriatric patients with a mean age of 85 years. Exclusion criteria were going outdoors more than once a week and the presence of actinic or cancer skin lesions. Intervention was random allocation of UV-B irradiation at half the minimal erythemal dose of the lower back, three times per week during 12 weeks (UV-B), or oral vitamin D3 400 IU/day during 12 weeks (VIT-D), or no treatment (CONTR). Main outcome measures were change in fasting serum levels of vitamin D metabolites at 0, 2, 4, 8, and 12 weeks in the treatment groups, compared with the control group. PTH(1-84) was measured at 0 and 12 weeks. Baseline serum 25-hydroxyvitamin D (25(OH)D) was lower than 30 nmol/l in 95% of the participants. It increased to a median value of around 60 nmol/l after 12 weeks both in the UV-B and VIT-D groups, whereas there was no change in the CONTR group. Serum 1,25-dihydroxyvitamin D increased significantly in the UV-B group. Serum calcium increased significantly in both treatment groups. Serum PTH decreased more than 30% in both treatment groups (p < 0.001), whereas there was no significant change in the control group. Irradiation with UV-B in the very elderly for a few minutes per day leads to adequate improvement of the vitamin D status. It is as effective as oral vitamin D3 in increasing serum 25(OH)D and suppressing secondary hyperparathyroidism.

Topics: Administration, Oral; Aged; Aged, 80 and over; Calcium; Cholecalciferol; Female; Humans; Hyperparathyroidism, Secondary; Netherlands; Nursing Homes; Parathyroid Hormone; Ultraviolet Rays; Vitamin D; Vitamin D Deficiency

Secondary hyperparathyroidism is one of the severe complications of chronic renal failure. In this study, we investigated the cellular components of parathyroid tissue, with measurements of various serum parathyroid hormone (PTH) types in the circulation, and evaluated their clinical significance in hemodialysis patients. Thirty-eight patients who underwent both subtotal parathyroidectomy and autotransplantation in Tokai University Hospital from 1979 to 1994 were divided into two groups. Group 1 (G-1) was not administered active-type vitamin D3 (VD; 19 patients; 15 males and 4 females), and group 2 (G-2) was administered VD (19 patients; 10 males and 9 females). The parathyroid tissues which were obtained from G-1 and G-2 patients were classified into three classes based on the size of the oxyphilic cell area (class I < 25%, class II 25-50% and class III > 50%). Our results showed that the proliferation index of parathyroid tissues in the oxyphilic cell area was higher in G-2 than that in G-1. Immunohistochemically, MIB-1 staining was more intense than that in the chief cell area in G-2 patients. Moreover, the proliferative index in the same specimen was also higher in the oxyphilic cell area than in the chief cell area. It was suggested that the oxyphilic cells proliferated independently. Furthermore, synthesis of PTH in the oxyphilic cell area was revealed immunohistochemically by the presence of PTH and was confirmed by positive staining of PTH mRNA in the oxyphilic cell area with in situ hybridization. HS(M-terminal)- and C-PTH levels in the serum were significantly higher in class III than in class I (p < 0.01). No significant difference of HS- and C-PTH levels between class II and class III was noted. Moreover, no significant difference of intact-PTH levels was found in all three classes. From the above findings, it was suggested that proliferation of the parathyroid tissues or secretory state of PTH in hemodialysis-maintained patients with secondary hyperparathyroidism, which was closely related to the proliferation of oxyphilic cells, can be more accurately reflected by HS- and C-PTH levels than by the intact-PTH level. Therefore, it was suggested that HS- and C-PTH levels in the serum are important indices for accurate evaluation of the pathology and suitable therapy of secondary hyperparathyroidism, as well as observation of the clinical course.

Topics: Adult; Antibodies, Monoclonal; Cell Division; Cell Nucleus; Cholecalciferol; Female; Humans; Hyperparathyroidism, Secondary; Immunohistochemistry; In Situ Hybridization; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Parathyroidectomy; RNA, Messenger

Supplementation with 800 IU of vitamin D and 1 g of calcium each day is recommended in institutionalized elderly subjects to prevent secondary hyperparathyroidism and its adverse skeletal effects. An original formulation (IDEOS) combining vitamin D and calcium has been developed for use in this end. The aim of this study was to determine whether administration of this association, of which each tablet contains 500 mg calcium and 400 IU vitamin D3, produces the same beneficial effects on laboratory parameters as separate administration of both active agents. A multicenter randomized study was conducted in 91 elderly institutionalized subjects (mean age 83.1 years) who had vitamin D deficiency [25-(OH)D < 6 ng/ml] without severe renal failure. Subjects were randomly assigned to one of the two treatment groups. Treatment duration was six months. One group (G1, n = 46) received one tablet of the new formulation twice daily. The other (G2, n = 45) received 8 drops of vitamin D3 (800 IU/day) and one calcium carbonate 500 mg tablet twice daily. Blood tests were carried out at inclusion and after three and six months of treatment. In group G1, plasma 25-(OH)D levels increased from 2.6 ng/ml at inclusion to 14.6 ng/ml at month 6 (p < 0.001), and iPTH fell from 63.2 pg/ml at inclusion to 33.8 pg/ml at month 6 (p < 0.001). In group G2, 25-(OH)D rose from 2.8 ng/ml at inclusion to 13.5 ng/ml at month 6 (p < 0.001), and iPTH fell from 55.4 pg/ml at inclusion to 32.5 pg/ml at month 6 (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aged; Aged, 80 and over; Alkaline Phosphatase; Calcium; Calcium Carbonate; Cholecalciferol; Creatinine; Drug Administration Schedule; Drug Combinations; Drug Therapy, Combination; Female; Humans; Hydroxycholecalciferols; Hyperparathyroidism, Secondary; Male; Parathyroid Hormone; Vitamin D Deficiency

The two main determinants of hip fractures are falls and bone loss leading to an intrinsic femoral fragility. Substantial femoral bone loss continues throughout old age, with a continuous and exponential increase in the risk of hip fracture; thus any reduction or arrest of this loss will induce an important reduction in the incidence of hip fracture. Preventive measures may be achieved during childhood by increasing peak bone mass with calcium and exercise, by using long-term estrogen replacement therapy after menopause, but also by using vitamin D and calcium supplements for late prevention in the elderly. Vitamin D insufficiency and a deficit in calcium intake are very common in the elderly living either in institutions or at home and the cumulative response to these deficits is a negative calcium balance which stimulates parathyroid hormone secretion. This senile secondary hyperparathyroidism is one of the determinants of femoral bone loss and can be reversed by calcium and vitamin D supplements. We have shown in a 3-year controlled prospective study that the daily use of supplements (1.2 g calcium and 800 IU vitamin D3) given in a large population of 3270 elderly ambulatory women living in nursing homes reduced the number of hip fractures by 23% (intention-to-treat analysis). In parallel, serum parathyroid hormone concentrations were reduced by 28% and low baseline serum 25-hydroxyvitamin D concentration returned to normal values. After 18 months of treatment the bone density of the total proximal femoral region had increased by 2.7% in the vitamin D3-calcium group and decreased by 4.6% in the placebo group (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Accidental Falls; Aged; Bone Density; Bone Resorption; Calcium Compounds; Cholecalciferol; Female; Hip Fractures; Humans; Hyperparathyroidism, Secondary; Osteoporosis; Prospective Studies; Risk Factors

Secondary hyperparathyroidism (SHPT) after bariatric surgery has significant adverse implications for bone metabolism, increasing the risk for osteoporosis and fracture. Our aim was to characterize prevalence and identify risk factors for SHPT in bariatric surgery patients.. We performed a single-institution, retrospective chart review of patients who underwent bariatric surgery from June 2017 through December 2021. Demographic and clinical data were collected, including serum parathyroid hormone, calcium, and vitamin D3 at enrollment and 3, 6, and 12-months postoperatively. Chi-square or Fisher's exact tests were used to analyze categorical data and Mann-Whitney U test for continuous data. Multivariable analysis using binomial logistic regression assessed risk factors for SHPT. P-values ≤ 0.05 were considered significant.. 350 patients were analyzed. SHPT prevalence at any time point was 72.9%. 65.8% had SHPT at enrollment; 45.9% resolved with intensive vitamin supplementation; and 19.7% had recurrent SHPT. New-onset SHPT occurred in 8.6%. Persistent SHPT was present in 42.4% at 1-year. Baseline SHPT correlated with black race and T2DM. SHPT at any time point correlated with T2DM and higher baseline BMI. 1-year SHPT correlated with RYGB, depression, and longer time in program. SHPT was not correlated with %TBWL at any time point. In patients with SHPT, vitamin D3 deficiency prevalence was significantly higher at baseline (77.0%) compared to all post-bariatric time points (16.7%, 17.3%, and 23.1%; P < 0.0001).. SHPT is highly prevalent in patients with obesity seeking weight loss surgery. 42% had persistent SHPT at 1-year despite appropriate vitamin supplementation. Current vitamin D3 and calcium supplementation protocols may not effectively prevent SHPT in many post-bariatric patients. Low prevalence of concomitant vitamin D3 deficiency with SHPT after bariatric surgery suggests that there may be alternative mechanisms in this population. Further studies are needed to develop effective treatment strategies to mitigate the adverse effects of bariatric surgery on bone metabolism.

Topics: Bariatric Surgery; Calcium; Cholecalciferol; Diabetes Mellitus, Type 2; Humans; Hyperparathyroidism, Secondary; Parathyroid Hormone; Prevalence; Retrospective Studies; Risk Factors; Vitamin D; Vitamin D Deficiency; Vitamins

Hyperuricemia is common among patients with chronic kidney disease (CKD). In the general population, hyperuricemia is associated with secondary hyperparathyroidism (SHPT), in a mechanism that involves vitamin D metabolism. Data for patients with CKD, however, are scarce. We aimed to evaluate the relationship between hyperuricemia and mineral and bone metabolism, particularly hyperparathyroidism.. This is a retrospective study that included 922 adult patients with stages 3, 4, or 5 CKD, not on dialysis. Clinical, demographic, and biochemical data were collected from charts and included uric acid, parathyroid hormone (PTH), 25(OH)-vitamin D, calcium, phosphate, renal function (estimated glomerular filtration rate-eGFR), and medications such as allopurinol, furosemide, and cholecalciferol. SHPT was defined as PTH > 65 pg/ml.. Our patients were mostly Caucasian women, with a mean age of 64 ± 16 years. SHPT and hyperuricemia were observed in 70% and 62.4% of patients, respectively. Patients with SHPT presented higher levels of uric acid (7.2 ± 1.8 vs. 6.6 ± 1.7 mg/dL, p = 0.0001) and a higher frequency of hyperuricemia (66% vs. 33%, p = 0.0001). Patients with hyperuricemia were mostly female, with lower eGFR, higher phosphate, and higher PTH. The risk of hypovitaminosis D was higher among patients with SHPT (69.7% vs. 53.1%, p = 0.0001). Hyperuricemia remained independently associated with hyperparathyroidism, (p = 0.033) even after adjustments for eGFR, calcium, phosphate, hypovitaminosis D, and use of allopurinol, calcitriol, furosemide, and cholecalciferol.. Hyperuricemia seems to be a contributing factor for SHPT in patients with CKD. The mechanisms behind this finding have yet to be elucidated.

Topics: Adult; Aged; Aged, 80 and over; Allopurinol; Calcium; Cholecalciferol; Female; Furosemide; Humans; Hyperparathyroidism, Secondary; Hyperuricemia; Male; Middle Aged; Parathyroid Hormone; Phosphates; Renal Insufficiency, Chronic; Retrospective Studies; Uric Acid; Vitamin D; Vitamin D Deficiency

Abnormalities related to mineral and bone metabolism are a common finding in chronic kidney disease (CKD). Vitamin D compounds are often prescribed to CKD patients with the purpose to control secondary hyperparathyroidism and reduce the risk of high-turnover bone disease. However, data on the effect of vitamin D sterols on bone histology in non-dialysis CKD is limited.. A prospective controlled study was conducted on a cohort of 56 patients with CKD stages 3 and 4. 19 patients on calcitriol and 12 patients on cholecalciferol were compared to a group of 25 age- and sex-matched controls. Participants underwent a tetracycline double-labelled transiliac bone biopsy before starting therapy and again 12 months later. Changes from baseline in circulating biomarkers and bone histomorphometric parameters were analyzed.. Low-turnover bone disease was the most common pattern of renal osteodystrophy on the initial biopsy. There was no difference in biochemical or histomorphometric values between the three study groups at baseline. Serum intact parathormone (iPTH) and bone formation rate decreased significantly in calcitriol-treated patients, with prevalence of low-turnover bone disease doubling from baseline. In contrast, no significant changes were noted in cholecalciferol-treated and control subjects.. Calcitriol was effective in preventing secondary hyperparathyroidism and high-turnover bone disease. However, it was associated with an increased risk of developing or aggravating low-turnover bone disease. In the absence of a bone biopsy, calcitriol use in pre-dialysis CKD should be reserved for patients with a progressive rise in iPTH levels, in whom high-turnover bone disease is suspected.

Topics: Calcitriol; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dialysis; Humans; Hyperparathyroidism, Secondary; Parathyroid Hormone; Prospective Studies; Renal Dialysis; Renal Insufficiency, Chronic; Sterols; Vitamin D; Vitamins

Obesity increases the risk of vitamin D insufficiency, which exacerbates secondary hyperparathyroidism in chronic kidney disease. Recent studies suggest that serum total 25-hydroxyvitamin D (25OHD) levels of ≥50 ng/mL are necessary to produce significant reductions in elevated parathyroid hormone levels in nondialysis patients. Data from real-world and randomized controlled trials (RCTs) involving these patients were examined for (1) relationships between vitamin D treatments and the achieved levels of serum 25OHD and between serum 25OHD and body weight (BW)/body mass index (BMI); and (2) the impact of BW/BMI on achieving serum 25OHD levels ≥50 ng/mL with extended-release calcifediol (ERC) treatment or vitamin D supplementation (cholecalciferol or ergocalciferol).. Data obtained from nondialysis patients participating in two real-world studies, one conducted in Europe (Study 1) and the other (Study 2) in the USA, and in two US RCTs (Studies 3 and 4) were analyzed for serum 25OHD outcomes after treatment with ERC, vitamin D supplements, or placebo.. More than 50% of subjects treated with vitamin D supplements in both real-world studies (Studies 1 and 2) failed to achieve serum 25OHD levels ≥30 ng/mL, a level widely viewed by nephrologists as the threshold of adequacy; only 7.3-7.5% of subjects achieved levels ≥50 ng/mL. Data from the European study (Study 1) showed that serum 25OHD levels had significant and nearly identical inverse relationships with BW and BMI, indicating that high BW or BMI thwarts the ability of vitamin D supplements to raise serum 25OHD. One RCT (Study 3) showed that 8 weeks of ERC treatment (60 μg/day) raised serum 25OHD levels to ≥30 and 50 ng/mL in all subjects, regardless of BW, while cholecalciferol (300,000 IU/month) raised serum 25OHD to these thresholds in 56% and 0% of subjects, respectively. The other RCT (Study 4) showed that ERC treatment (30 or 60 μg/day) successfully raised mean serum 25OHD levels to at least 50 ng/mL for subjects in all BW categories, whereas no increases were observed with placebo treatment.. Real-world studies conducted in Europe and USA in nondialysis patients (Studies 1 and 2) showed that vitamin D supplements (cholecalciferol or ergocalciferol) were unreliable in raising serum total 25OHD to targets of 30 or 50 ng/mL. In contrast, ERC was demonstrated to be effective in one real-world study (Study 2) and two RCTs (Studies 3 and 4) conducted in US nondialysis patients in raising serum 25OHD to these targeted levels irrespective of BW.

Topics: Calcifediol; Cholecalciferol; Ergocalciferols; Humans; Hyperparathyroidism, Secondary; Overweight; Parathyroid Hormone; Randomized Controlled Trials as Topic; Renal Insufficiency, Chronic; Vitamin D; Vitamin D Deficiency; Vitamins

Several studies have shown that cholecalciferol supplementation (25OHD-S) in chronic kidney disease (CKD) improves kidney injury by reducing fibrosis-related vascular calcification and declining apoptosis-linked nephron damage.. Vitamin D deficiency alters in the same manner CMet, CRenal, and others biomarkers in both groups SS; however, these disorders are more acute in blacks compared to whites SS. Oral 25OHD-S a highlighted improvement of eGFR drop, SHPT decrease, decline proteinuria, and cardiac failure risk (NT-proBNP and cTnT) attenuation. Concomitantly, 25OHD-S normalizes

Topics: Biomarkers; Cardio-Renal Syndrome; Cholecalciferol; Dietary Supplements; Humans; Hyperparathyroidism, Secondary; Renal Insufficiency, Chronic; Troponin T; Vitamin D Deficiency

Topics: Calcimimetic Agents; Calcitriol; Chelating Agents; Cholecalciferol; Ergocalciferols; Humans; Hyperparathyroidism, Secondary; Male; Middle Aged; Parathyroid Hormone; Parathyroidectomy; Phosphates; Phosphorus, Dietary; Polycystic Kidney, Autosomal Dominant; Renal Insufficiency, Chronic; Vitamin D; Vitamin D Deficiency

Topics: Body Mass Index; Calcium; Calcium Citrate; Cholecalciferol; Follow-Up Studies; Gastric Bypass; Humans; Hyperparathyroidism, Secondary; Postoperative Care; Postoperative Complications; Risk Factors

Vitamin D (VD) deficiency in chronic lymphocytic leukemia (CLL) is associated with inferior prognosis, shorter time to treatment and worse overall survival. VD deficiency is the first potentially modifiable prognostic factor in CLL. Currently, however, there is a lack of studies concerning VD supplementation in CLL patients.. To evaluate the efficacy and safety of VD supplementation in patients with CLL.. A 6-month interventional study was conducted in CLL patients with lower serum 25-OH-D3 concentrations (< 30 ng/ml) than currently recommended. Patients with VD insufficiency (20-30 ng/ml) received 2000 IU of cholecalciferol/day, patients with moderate deficiency (10-19.9 ng/ml) received 4000 IU/day, and patients with severe VD deficiency (<10 ng/ml) received 6000 IU/day.. In the analyzed group of 13 CLL subjects, only 1 patient had a VD level within the optimal range (30-80 ng/ml), 7 had an insufficient concentration, 4 had moderate deficiency, and 1 had severe deficiency. Secondary hyperparathyroidism was diagnosed in 4 subjects. Cholecalciferol supplementation (mean dose of 3384 ± 1211 IU) was followed by a significant increase in 25-OH-D3 concentration (from 17.3 ± 5.8 to 41.4 ± 17.5 ng/ml; p<0.05) and decrease in PTH (p<0.05). Five patients did not achieve the recommended 25-OH-D3 concentration. Calcium level remained unchanged and no patients developed hypercalcemia.. VD replenishment is safe and can be effectively achieved by means of the employed cholecalciferol dosage in the majority of patients. However, some subjects may require higher doses to obtain the optimal level and immune function.

Topics: Aged; Cholecalciferol; Chronic Disease; Dietary Supplements; Female; Humans; Hyperparathyroidism, Secondary; Leukemia, Lymphoid; Male; Middle Aged; Patient Safety; Treatment Outcome; Vitamin D; Vitamin D Deficiency

Traditionally, secondary hyperparathyroidism (SHPT) due to low calcitriol synthesis in failing kidneys has been treated with synthetic vitamin D receptor (VDR) activators. Recently, also the importance of low native vitamin D status beyond the issue of SHPT has been recognized in these patients. The aim of this work was to evaluate the effect of cholecalciferol supplementation in haemodialysis patients with low vitamin D serum levels. Another aim was to evaluate dual vitamin D therapy (cholecalciferol supplementation plus paricalcitol) in haemodialysis patients with vitamin D deficiency and concomitant SHPT.. Ninety clinically stable maintenance haemodialysis patients were included. Supervised cholecalciferol supplementation was administered due to low vitamin D status. Patients with SHPT were also treated with synthetic VDR activator. Two pre hoc subgroups for statistical analysis were formed: patients treated solely with cholecalciferol (N=34; 5,000 IU once weekly) and patients treated with a combination of cholecalciferol (identical dose, i.e. 5,000 IU/week) plus paricalcitol (N=34, median dose 10 μg/week). Follow-up visit was scheduled 15 weeks later. Serum concentrations of calcidiol (25-D), parathyroid hormone (PTH) and beta-cross laps (CTX) were assessed at baseline and at follow-up. Serum calcium, phosphate and alkaline phosphatase (ALP) were monitored monthly. Only non-calcium gastrointestinal phosphate binders were administered. Dialysate calcium was 1.5 mmol/L in all patients, and no oral calcium-containing preparations were prescribed. Depending on data distribution, parametric or nonparametric statistical methods were used for comparison within each group (i.e. baseline vs. follow-up data) as well as between groups.. In the whole group of 90 patients, mean baseline 25-D serum level was 20.3 (standard deviation 8.7) nmol/L, and it increased to 66.8 (19) nmol/L (p<0.0001) after supplementation. In both preformed subgroups, the effect of vitamin D supplementation was almost identical. In cholecalciferol monotherapy, 25-D levels increased from 18.4 (8.2) to 68.6 (21.2) and in dual vitamin D therapy from 18.4 (5.0) to 67.6 (17.7) nmol/L (both p<0.0001). In addition, both treatment modalities decreased serum PTH levels importantly: from 21.7 (interquartile range 17.3; 35.4) to 18.1 pmol/L (15.3; 24.7) in monotherapy (p=0.05) and from 38.6 (31.8; 53.3) to 33.9 pmol/L (26.1; 47.5) in dual vitamin D therapy (p=0.01). Serum calcium, phosphate, ALP and CTX did not change. We have not observed any episode of hypercalcemia in any subject during the whole period of follow-up. At baseline, slightly lower 25-D levels were observed in diabetic than in non-diabetic patients. This difference disappeared after substitution. Vitamin D status and its changes were not related to the patient's age.. Low 25-D levels were very common in haemodialysis patients. They were safely and effectively corrected with supervised low-dose cholecalciferol supplementation. In patients with higher baseline PTH levels, dual vitamin D therapy (cholecalciferol plus paricalcitol) was safely and effectively used.

Topics: Aged; Alkaline Phosphatase; Bone Density Conservation Agents; Calcifediol; Calcium; Cholecalciferol; Dietary Supplements; Drug Therapy, Combination; Ergocalciferols; Female; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Phosphates; Receptors, Calcitriol; Renal Dialysis; Vitamin D Deficiency; Vitamins

Secondary osteoporosis occurs in many diseases. Celiac disease-induced osteoporosis is the consequence of secondary hyperparathyroidism. Biochemical bone markers show predominance of bone resorption, thus making the bisphosphonates the first line therapy option. Intestinal mucosal changes are reversible on gluten-free diet. Osteoporosis reversibility is also possible, provided postmenopausal osteoporosis risk factors independent from celiac disease are not present.. We presented a postmenopausal woman with at least a 10-year history of celiac disease prior to diagnosis, which had overt secondary hyperparathyroidism with insufficient status of vitamin D and a significant bone mass reduction. At the time of diagnosis of celiac disease the patient was receiving 250 μg of levothyroxine daily without achieving optimal substitution. Three years after the initiation of gluten-free diet the patient was without any signs and symptoms of the disease. All laboratory findings were within normal range. It was decided to treat the underlying disease and to supplement calcium and vitamin D without the initiation of bisphosponate therapy.. Osteoporosis regression justified this therapeutic approach. The presence of primary autoimmune hypothyroidism makes this case specific, since the inability for optimal substitution therapy with a high daily dose of levothyroxine provoked the suspicion of celiac disease.

Topics: Calcium; Celiac Disease; Cholecalciferol; Diet, Gluten-Free; Female; Humans; Hyperparathyroidism, Secondary; Middle Aged; Osteoporosis, Postmenopausal; Thyroxine; Vitamin D; Vitamin D Deficiency

Brown tumours caused by vitamin D deficiency are rare. Most cases are caused by primary hyperparathyroidism, and are rarely caused by secondary hyperparathyroidism in cases of renal failure. We present a case of Brown tumours of the tibia and second metacarpal bone in a 50-year-old woman who had a low dietary intake of vitamin D and had worn a veil for most of her adult life. The Brown tumours were caused by vitamin D deficiency and secondary hyperparathyroidism. The patient improved on treatment with vitamin D3 and calcium supplements. This is a rare case and the first, to our knowledge, with a Brown tumour of the tibia caused by vitamin D deficiency due to decreased dietary intake and decreased exposure to sunlight. The course of treatment and investigations of the patient are described.

Topics: Bone Neoplasms; Calcium, Dietary; Cholecalciferol; Clothing; Diet; Female; Hand; Humans; Hyperparathyroidism, Secondary; Leg; Metacarpal Bones; Middle Aged; Osteitis Fibrosa Cystica; Sunlight; Tibia; Vitamin D Deficiency

A 93 year-old woman with Paget's disease of bone had been treated with etidronate without interruption during 20 years. The daily dose was usual (5mg/kg/day) but this prescription had never been stopped by her physicians. Two fractures had already occurred in pagetic (right tibia) and non pagetic bones (right fibula) within the last 2 years, and she presented rib fractures, another right tibia fracture and right femur fracture during hospitalization time. X-rays films showed major osteolysis of left ulna and right tibia. Blood samples and technetium bone scan brought no evidence for sarcoma or lytic evolution of the disease. A transiliac bone biopsy on non pagetic bone site confirmed the diagnosis of osteomalacia (increased osteoid parameters), with secondary hyperparathyroidism (hook resorption). In Paget's disease of bone, continuous treatment by etidronate may induce generalized osteomalacia, and increase the risk of fracture in both pagetic and non-pagetic bones. Whereas physicians and pharmaceutical industry try to improve the observance of those drugs, this striking observation also points out that a prescription always needs to be updated.

Topics: Aged, 80 and over; Alkaline Phosphatase; Biopsy; Bone Density Conservation Agents; Calcification, Physiologic; Calcium Carbonate; Cholecalciferol; Etidronic Acid; Female; Femoral Fractures; Fibula; Fractures, Spontaneous; Humans; Hyperparathyroidism, Secondary; Iatrogenic Disease; Osteitis Deformans; Osteolysis; Osteomalacia; Parathyroid Hormone; Radionuclide Imaging; Rib Fractures; Tibial Fractures; Ulna; Vitamin D

A dyshomeostasis of macro- and micronutrients, including vitamin D and oxidative stress, are common pathophysiologic features in patients with congestive heart failure (CHF). In African Americans (AA) with CHF, reductions in plasma 25(OH)D are of moderate-to-marked severity (<20 ng/mL) and may be accompanied by ionized hypocalcemia with compensatory increases in serum parathyroid hormone (PTH). The management of hypovitaminosis D in AA with CHF has not been established.. Herein, a 14-week regimen: an initial 8 weeks of oral ergocalciferol (50,000 IU once weekly); followed by a 6-week maintenance phase of cholecalciferol (1400 IU daily); and a CaCO₃ (1000 mg daily) supplement given throughout was designed and tested. Fourteen AA patients having a dilated (idiopathic) cardiomyopathy with reduced ejection fraction (EF, <35%) were enrolled: all completed the initial 8-week course; and 12 complied with the full 14 weeks. At baseline, 8 and/or 14 weeks, serum 25(OH)D and PTH; serum 8-isoprostane, a biomarker of lipid peroxidation, and echocardiographic EF were monitored.. Reduced 25(OH)D at entry (14.4 ± 1.3 ng/mL) was improved (P < 0.05) in all patients at 8 weeks (30.7 ± 3.2 ng/mL) and sustained (P < 0.05) at 14 weeks (30.9 ± 2.8 ng/mL). Serum PTH, abnormally increased in 5 patients at baseline (104.8 ± 8.2 pg/mL), was reduced at 8 and 14 weeks (74.4 ± 18.3 and 73.8 ± 13.0 pg/mL, respectively). Plasma 8-isoprostane at entry (136.1 ± 8.8 pg/mL) was reduced at 14 weeks (117.8 ± 7.8 pg/mL; P < 0.05), whereas baseline EF (24.3 ± 1.7%) was improved (31.3 ± 4.3%; P < 0.05).. Thus, the 14-week course of supplemental vitamin D and CaCO₃ led to healthy 25(OH)D levels in AA with heart failure having vitamin D deficiency of moderate-to-marked severity. Albeit a small patient population, the findings suggest that this regimen may attenuate the accompanying secondary hyperparathyroidism and oxidative stress and improve ventricular function.

Topics: Black or African American; Calcium Carbonate; Calcium, Dietary; Cardiomyopathy, Dilated; Cholecalciferol; Dietary Supplements; Dinoprost; Ergocalciferols; Female; Heart Failure; Humans; Hyperparathyroidism, Secondary; Male; Middle Aged; Parathyroid Hormone; Stroke Volume; Vitamin D; Vitamin D Deficiency

Two new clinical trials highlight refinements in the use of vitamin D and its analogs in the treatment of secondary hyperparathyroidism in end-stage renal disease (ESRD), and the treatment of proteinuria in diabetics. In patients with ESRD, alfacalcidol is as effective as paricalcitol in suppressing parathyroid hormone; the occurrence of hypercalcemia and hyperphosphatemia is infrequent and similar with the two analogs. Oral cholecalciferol reduces albuminuria and urinary transforming growth factor-β1 in patients with type 2 diabetes mellitus and proteinuria.

Topics: Albuminuria; Cholecalciferol; Diabetes Mellitus, Type 2; Diabetic Nephropathies; Ergocalciferols; Female; Humans; Hydroxycholecalciferols; Hyperparathyroidism, Secondary; Male; Renal Dialysis; Renin-Angiotensin System; Transforming Growth Factor beta1

Vitamin D insufficiency is common in patients with chronic kidney disease (CKD) and may contribute to mineral bone disease. In a prospective interventional study, we estimated the prevalence of vitamin D insufficiency (serum 25-hydroxyvitamin D3 [25OHD] < 30 ng/ml), and examined the effect of high-dose (600,000 IU) cholecalciferol supplementation after 6 weeks on serum 25OHD and parathyroid hormone (PTH) levels in children with CKD stages 2-4. Forty-two children (86% boys) with a mean age of 7.7 ± 3.8 (range 2--5) years were studied. Thirty-seven children (82.1%) had vitamin D insufficiency; 18 (42.8%) had 25OHD < 16 ng/ml. The median 25OHD increased significantly from 16.7 (95% CI 11.3, 19.8) to 46.2 (34.5, 44.6) ng/ml in patients with vitamin D insufficiency (P <0.001). The median PTH decreased significantly from 51.3 (95% CI 46.7, 71.5) to 37.1 (29.0, 54.6) pg/ml (P = 0.003). Nineteen patients (47.5%) had >30% reduction in the PTH after supplementation. Serum calcium, phosphorus, and estimated GFR did not change significantly. We conclude that vitamin D insufficiency is highly prevalent in children with CKD stages 2-4. High-dose cholecalciferol is safe and effective in correcting vitamin D insufficiency and results in a significant reduction in PTH levels in vitamin D-insufficient children.

Topics: Adolescent; Biomarkers; Calcifediol; Child; Child, Preschool; Cholecalciferol; Chronic Disease; Female; Humans; Hyperparathyroidism, Secondary; India; Kidney Diseases; Male; Parathyroid Hormone; Prevalence; Prospective Studies; Time Factors; Treatment Outcome; Vitamin D Deficiency; Vitamins

Various complications consequent on disordered calcium and phosphate homeostasis occur frequently in chronic kidney disease (CKD) patients. Particularly, vascular calcification has high morbidity and mortality rates. There is a clear need for a better CKD model to examine various aspects of this disordered homeostasis.. Oral dosing with adenine induced CKD in rats in only 10 days. Serum calcium, phosphate and parathyroid hormone were measured and calcification in aorta was assessed histologically. The effects of varying phosphorus content of diet or treatment with phosphate binders or active vitamin D(3) on these parameters were examined.. After adenine dosing, significant hyperphosphatemia, hypocalcemia and secondary hyperparathyroidism (2HPT) were observed during the experimental period of 15 weeks. Aortic calcification was detected in only some of the animals even at 15 weeks (approximately 40%). Treatment with vitamin D(3) for 18 days, even at a low dose (100 ng x kg(-1), 3-4 times week(-1), p.o), caused aortic calcification in all animals and increases in serum calcium levels up to the normal range. The vitamin D(3)-induced calcification was significantly inhibited by phosphate binders which lowered serum phosphate levels and the calcium x phosphate product, although serum calcium levels were elevated.. These data suggest that rats dosed orally with adenine provide a more useful model for analysing calcium/phosphate homeostasis in severe CKD. Controlling serum calcium/phosphate levels with phosphate binders may be better than vitamin D(3) treatment in hyperphosphatemia and 2HPT, to avoid vascular calcification.

Topics: Adenine; Animals; Aortic Diseases; Biomarkers; Blood Urea Nitrogen; Calcinosis; Calcium; Calcium Carbonate; Chelating Agents; Cholecalciferol; Chronic Disease; Creatinine; Disease Models, Animal; Disease Progression; Hyperparathyroidism, Secondary; Hyperphosphatemia; Hypocalcemia; Kidney Diseases; Male; Parathyroid Hormone; Phosphates; Polyamines; Rats; Rats, Wistar; Sevelamer; Severity of Illness Index; Time Factors

Cinacalcet is a calcimimetic drug for the treatment of secondary hyperparathyroidism (HPT). In a sequential open-label study, ten patients with persistent HPT after renal transplantation received first 30 and then 60 mg oral cinacalcet once daily over 2 weeks each. Cinacalcet steady state oral clearance was 131.1 +/- 20.9 l/h and 92.8 +/- 9.5 l/h (mean +/- SE) after 30 and 60 mg, respectively. Cinacalcet and parathyroid hormone (PTH) concentrations showed an inverse correlation and were fitted to a simple E(max) model (E(max) = 80% reduction vs. baseline, EC(50) = 13 ng/mL). A once daily administration of cinacalcet lowered serum calcium over 24 h without fluctuations. The 8-h fractional urinary excretion of calcium was increased after 60 mg cinacalcet (baseline 0.85 +/- 0.17%, 30 mg 1.53 +/- 0.35%, 60 mg 1.92 +/- 0.37%). Renal function remained stable. Cinacalcet pharmacokinetics and pharmacodynamics showed a pronounced interindividual variability. We conclude that the once daily administration of cinacalcet in patients with secondary HPT after renal transplantation effectively reduced iPTH and serum calcium. The transient calciuria could potentially favor nephrocalcinosis and reduce bone mineral density, suggesting that higher doses of cinacalcet need to be used with caution in renal transplant recipients with severe persistent hyperparathyroidism.

Topics: Area Under Curve; Calcitonin; Calcium Phosphates; Cholecalciferol; Cinacalcet; Dose-Response Relationship, Drug; Glomerular Filtration Rate; Humans; Hyperparathyroidism, Secondary; Kidney Transplantation; Naphthalenes; Parathyroid Hormone

Hypovitaminosis D (HD) and secondary hyperparathyroidism (SHP) are common in elders, and many factors could contribute to them. The objectives of this study were to estimate the prevalence of HD, SHP, and its associated factors, in individuals living in nonprofit homes for elders in south Brazil. Design Cross-sectional study.. Serum 25-hydroxyvitamin D 25(OH)D, intact parathyroid hormone (PTH), total calcium, phosphorus, alkaline phosphatase, magnesium, creatinine, and albumin levels were measured in late spring, November, 2005. The presence of factors potentially related with HD and SHP-age, sex, weight, height, skin phototype, sun exposure, exercise, smoking, use of < or = 5 medications or diuretics or alcohol, and daily calcium ingestion.. 102 subjects age 77.8 +/- 9.0 were included in the study. HD was found in 85.7% and SHP in 53% of the subjects. The estimated daily calcium ingestion was 720 mg. There was no association between serum 25(OH)D levels and any of the risk factors evaluated. Serum 25(OH)D levels were correlated with serum PTH (r = -0.358, P = 0.000), calcium (r = 0.306, P = 0.002), and albumin (r = 0.253, P = 0.011) levels. In univariate analysis, SHP was positively associated with age (P = 0.006), and female sex (0.007); and negatively associated with sunlight exposure (P = 0.020), GFR (P = 0.000), Ln25(OH)D (P = 0.002), and total serum calcium (P = 0.024). After multivariate model adjustment, age [OR 1.09 (CI 1.01-1.18); P = 0.024], Ln25(OH)D [OR 0.92 (CI 0.08-0.74); P = 0.013], GFR [OR 0.96 (CI 0.92-0.99); P = 0.013], and hydrochlorothiazide treatment [OR 7.63 (CI 1.67-34.9); P = 0.008] were independently associated with SHP.. HD and SHP are highly prevalent in elders living in old-age homes. No associations were established between common risk factors and low serum levels of 25(OH)D levels; however, SHP was independently related with age, 25(OH)D, GFR, and hydrochlorothiazide use.

Topics: Aged; Aged, 80 and over; Brazil; Cholecalciferol; Female; Humans; Hyperparathyroidism, Secondary; Male; Organizations, Nonprofit; Parathyroid Hormone; Prevalence; Residence Characteristics; Vitamin D Deficiency

To compare biochemical variables, renal function and calcium and vitamin D intakes in euparathyroid and hyperparathyroid patients with primary osteoporosis and osteopenia and describe the measures necessary to normalize serum PTH in the patients with secondary hyperparathyroidism.. We reviewed the charts of normocalcemic patients with primary osteoporosis and osteopenia first seen during the years 1991-2003 and identified 75 with elevated serum PTH levels at baseline. These patients were compared to all the 143 euparathyroid patients first seen in 1998 and 1999. Patients were restudied after 1 year and we attempted to follow patients with secondary hyperparathyroidism until PTH levels became normal.. At baseline serum PTH, ionized calcium, inorganic phosphate, alkaline phosphatase, creatinine, a complete blood count and serum 25 hydroxy vitamin D were measured in the early morning fasting state. These tests were repeated at follow up.. In one-third of the hyperparathyroid patients, the standard baseline treatment failed to correct the secondary hyperparathyroidism necessitating extraordinary measures including unusually large doses of vitamin D (i.e. 50 000 IU vitamin D(2) twice weekly) or the substitution of calcium citrate for calcium carbonate as a calcium supplement.. Large doses of vitamin D are frequently necessary to suppress secondary hyperparathyroidism in patients with primary osteoporosis and osteopenia. This suggests that vitamin D metabolism may be altered in some of these patients.

Topics: 25-Hydroxyvitamin D 2; Alkaline Phosphatase; Bone Diseases, Metabolic; Calcium; Calcium Citrate; Calcium, Dietary; Cholecalciferol; Creatinine; Female; Humans; Hyperparathyroidism, Secondary; Osteoporosis; Parathyroid Hormone; Phosphates; Retrospective Studies; Vitamin D

Topics: Adult; Celiac Disease; Cholecalciferol; Female; Humans; Hyperparathyroidism, Secondary; Osteomalacia; Pregnancy; Pregnancy Complications

Vitamin D is essential for intestinal calcium absorption, bone mineralisation and plays an important role in neuromuscular functions. Vitamin D insufficiency is highly prevalent among postmenopausal women with osteoporosis and in the elderly. In turn, supplements of vitamin D3 (cholecalciferol), and to a lesser extent vitamin D2 (ergocalciferol), may decrease falls and fracture risk by 25%. Despite some recent negative studies, the actual question is not to know whether vitamin D is necessary, but rather how much vitamin D is sufficient to prevent secondary hyperparathyroidism, falls and fractures. Moreover, the risk of osteoporosis and of fragility fractures may be influenced by genetic variation in the vitamin D receptor (VDR).

Topics: Accidental Falls; Aged; Bone Density Conservation Agents; Calcification, Physiologic; Calcium; Cholecalciferol; Ergocalciferols; Female; Fractures, Bone; Humans; Hyperparathyroidism, Secondary; Intestinal Absorption; Neuromuscular Junction; Osteoporosis; Osteoporosis, Postmenopausal; Receptors, Calcitriol; Vitamin D; Vitamins

Parathyroidectomy is the only effective therapy for osteitis fibrosa cystica in hyperparathyroidism.. The objective of this study was to describe the changes of skeletal and nonskeletal manifestations in a patient with hyperparathyroidism and renal failure after oral vitamin D therapy.. This was a descriptive case report.. The patient was followed up in a referral center.. A 55-yr-old male patient with moderate renal failure was referred for expansile lytic lesions affecting several ribs and the spinous process of T12. His creatinine was 1.8 mg/dl; calcium, 8.9 mg/dl; PTH, 666 pg/ml; and 1,25 dihydroxy-vitamin D, 27 pg/ml. Bone mineral density (BMD) Z-scores by dual-energy x-ray absorptiometry were -4.1 at the spine, -1.7 at the hip, and -4.3 at the forearm.. The main outcome measures were the skeletal manifestations of hyperparathyroidism.. At 10 months of therapy, calcium level was 10 mg/d, PTH level declined to 71 pg/ml, and BMD increased by 12% at the spine and 18% at the hip. Computerized tomography (CT) cuts revealed marked regression in the lytic lesions. At 2 yr, BMD increased by an additional 6% at the spine, and there were no further changes in the lytic lesions by CT. The vitamin D receptor genotype using the restriction enzymes Bsm1, Taq1, and Apa1 was Bb, tt, and AA.. We showed regression of severe skeletal abnormalities of hyperparathyroidism documented by serial CT images in response to oral vitamin D therapy. It is possible that the vitamin D receptor genotype of the patient modulated this response.

Topics: Bone Density; Bone Diseases; Calcium; Cholecalciferol; Genotype; Humans; Hydroxycholecalciferols; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Male; Middle Aged; Osteitis Fibrosa Cystica; Osteoporosis; Receptors, Calcitriol; Thalassemia; Tomography, X-Ray Computed; Vitamin D

Topics: Adult; Arthralgia; Bone Density Conservation Agents; Calcium; Celiac Disease; Cholecalciferol; Diagnosis, Differential; Drug Therapy, Combination; Female; Fractures, Bone; Humans; Hyperparathyroidism, Secondary; Neoplasms; Obesity; Treatment Outcome; Weight Loss

Topics: Administration, Oral; Calcium; Cholecalciferol; Female; Follow-Up Studies; Humans; Hyperparathyroidism, Secondary; Infant; Rickets; Time Factors; Vitamin D Deficiency

Secondary hyperparathyroidism (2HPT), which is related to renal osteodystrophy (ROD), may occur in patients in the comparatively early stage of chronic renal failure (CRF). Secondary hyperparathyroidism patients with parathyroid hyperplasia showed resistance to vitamin D(3) treatment during long-term dialysis. At present, evaluation by ultrasonography is considered to be useful for confirming parathyroid hyperplasia. There are no clinical data associated with imaging evaluation of 2HPT in CRF patients. In the present study, the relationship among clinical and biochemical data, and parathyroid hyperplasia by ultrasonography, was evaluated in 12 patients (six males and six females) with end-stage renal failure (ESRF) before and at initiation of dialysis. Five patients showed an enlargement of parathyroid glands in ultrasonography. Levels of serum-intact parathyroid hormone (PTH) in patients with parathyroid hyperplasia (positive group) were significantly higher than in those without hyperplasia (negative group; 97.6 +/- 36.65 vs 17.4 +/- 4.45 pmol/L; P < 0.05). The levels of intact PTH were above 35.0 pmol/L in all five patients with hyperplasia. All patients in the positive group had never taken vitamin D(3) supplements. Calcium-containing phosphate binders were not prescribed before the present study, except in one patient. Parathyroid hyperplasia caused by 2HPT was recognized in patients before and at initiation of dialysis in this study. It appears that untreated 2HPT in CRF patients may progress to advanced 2HPT in ESRF before and/or after the early stage of dialysis. The levels of serum intact PTH are useful in predicting parathyroid hyperplasia.

Topics: Adult; Aged; Alkaline Phosphatase; Biomarkers; Calcium; Calcium Carbonate; Cholecalciferol; Dialysis; Female; Humans; Hyperparathyroidism, Secondary; Hyperplasia; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Glands; Parathyroid Hormone; Ultrasonography, Doppler, Color; Vitamins

To investigate via the vitamin D status whether patients with peripheral arterial disease (PAD) tend to develop vitamin D deficiency that in turn influences their clinical symptoms.. Cross-sectional.. University hospital.. Three hundred twenty-seven patients were evaluated; subjects with secondary causes of bone disease or bone active medication were excluded. One hundred sixty-one patients with either PAD stage II (n = 84) or stage IV (n = 77) were enrolled and compared to 45 age- and sex-matched healthy controls.. All patients underwent determinations of serum chemistry, 25-hydroxyvitamin D (vitamin D3) intact parathyroid hormone (iPTH), alkaline phosphatase (ALP), and osteocalcin and were further stratified according to an individual restriction score into 3 groups: mildly, moderately, or severely restricted in daily life due to the underlying disease. Patients with PAD IV showed significantly lower vitamin D3 (P =.0001), and calcium (P =.0001) values and significantly higher iPTH (P =.0001), osteocalcin (P =.0001) and ALP (P =.02) levels as compared to patients with PAD II. Patients considering themselves as severely restricted due to the underlying disease showed lower vitamin D3 and higher iPTH levels than those who described only a moderate (vitamin D3: P <.001; iPTH: P <.01) or mild (vitamin D3: P <.001; iPTH: P <.001) restriction in daily life.. Patients with PAD IV, especially those who feel severely restricted due to the disease, are at high risk of developing vitamin D deficiency, secondary hyperparathyroidism, and ultimately osteomalacia due to immobilization and subsequent lack of exposure to sunlight, all of which in turn lead to further deterioration. Monitoring of vitamin D metabolism and vitamin D replacement therapy could be a simple, inexpensive approach to mitigating clinical symptoms and improving quality of life in patients with advanced PAD.

Topics: Activities of Daily Living; Aged; Cholecalciferol; Cross-Sectional Studies; Female; Humans; Hyperparathyroidism, Secondary; Immobilization; Male; Pain Measurement; Parathyroid Hormone; Peripheral Vascular Diseases; Prevalence; Quality of Life; Sunlight; Surveys and Questionnaires; Time Factors; Vitamin D Deficiency

The treatment of the secondary hyperparathyroidism of chronic renal failure patients has greatly improved during the last 2 decades. Significant progress has been made, in particular in the indication of 1alpha-hydroxylated vitamin D derivatives and patient management using these compounds. Treatment and prevention should start early during the development of chronic renal insufficiency. One of the major remaining problems in more advanced stages of renal failure is that control of plasma phosphate often remains extremely difficult. New inert oral phosphate binders are needed. The nephrology community is still waiting for the advent of nonhypercalcemic and nonhyperphosphatemic vitamin D analogs with PTH suppressive activity equal to the parent compound calcitriol or its immediate precursor, alfacalcidol.

Topics: Administration, Oral; Calcitriol; Cholecalciferol; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Vitamin D

We report autopsy findings of a 69-year-old man on long-term CAPD therapy for 13 years who showed linear peritoneal calcification. Continuous ambulatory peritoneal dialysis (CAPD) was started in 1982. He has been administered excessive amounts of vitamin D(3) derivatives (VitD) (2.0 to 2.5 microg daily) and calcium carbonate (4 g daily) for secondary hyperparathyroidism since initiation of CAPD. In May 1995, his intact parathyroid hormone (PTH) level increased over 1,000 pg/mL. Immediately after VitD was changed from pill to liquid, the dose was increased to 5 microg daily. Although the serum calcium level remained between 4.5 and 4.9 mEq/L, and serum phosphate level was 5.0 to 7.2 mg/dL, plain abdominal radiography and computed tomography showed continuous calcification along the intestinal wall in October 1995. In spite of the continuation of CAPD therapy, he remained asymptomatic until he died of congestive heart failure in January 1997. He experienced eight episodes of peritonitis during his clinical course. Autopsy showed that numerous calcified plaques were present on the submucosal portion between the thickened serosa and the longitudinal layer of the muscularis externa. The remainder of the subserosa was fibrotic, and the small arteries had markedly thickened intima and severely narrowed lumina.

Topics: Abdominal Muscles; Calcinosis; Calcium; Calcium Carbonate; Cholecalciferol; Humans; Hyperparathyroidism, Secondary; Male; Middle Aged; Peritoneal Dialysis, Continuous Ambulatory; Phosphates; Time Factors; Tomography, X-Ray Computed

Long-term vitamin D and calcium supplementation is effective in reducing nonvertebral fractures in elderly people. Increased bone fragility caused by secondary hyperparathyroidism (sHPT) and impaired balance are known risk factors for hip fractures. The hypothesis is that short-term therapy with calcium and vitamin D may improve body sway as well as sHPT more effectively than calcium monotherapy. The effects of 8 weeks of supplementation with vitamin D (cholecalciferol) and calcium on body sway and biochemical measures of bone metabolism were measured. The sample consisted of 148 women (mean [+/-SD] age, 74 +/- 1 years) with a 25-hydroxycholecalciferol level below 50 nmol/liter. They received either 1200 mg of calcium plus 800 IU of vitamin D or 1200 mg of calcium per day. We measured intact parathyroid hormone (PTH), markers of bone turnover, and body sway before and after treatment. Falls and fractures among the participants were followed over a 1-year period. Compared with calcium mono, supplementation with vitamin D and calcium resulted in an increase in serum 25-hydroxyvitamin D of 72% (p < 0.0001), a decrease in the serum PTH of 18% ( p = 0.0432), and a decrease in body sway of 9% (p = 0.0435). The mean number of falls per subject during a 1-year follow-up period was 0.45 for the calcium mono group and 0.24 for the calcium and vitamin D group (p = 0.0346). Short-term supplementation with vitamin D and calcium improves sHPT and body sway and therefore may prevent falls and subsequent nonvertebral fractures in elderly women.

Topics: Aged; Calcium; Cholecalciferol; Dietary Supplements; Female; Gait; Humans; Hyperparathyroidism, Secondary; Parathyroid Hormone; Time Factors; Vitamin D

Topics: Cholecalciferol; Humans; Hyperparathyroidism, Secondary; Kidney Diseases; Uremia

Vitamin D compounds are usually indicated for the treatment of secondary hyperparathyroidism in dialysis patients. The possibility to induce a reversal of hyperparathyroidism with calcium supplementation alone is controversial. The present study was conducted to assess if oral calcium carbonate may constitute a therapeutic option for the control of hyperparathyroidism in patients with high PTH concentrations at the beginning of the treatment with chronic hemodialysis.. Thirty-one patients with end-stage renal failure with an intact PTH concentration above 250 pg/ml at the beginning of chronic hemodialysis therapy were treated with high doses of calcium carbonate; no patient received either aluminium-containing binders or vitamin D compounds. To minimize hypercalcemia, a calcium dialysate concentration of 2.5 mEq/l was used in all patients. The goal of the study was to reduce the intact PTH concentration to 250 pg/ml with oral calcium carbonate supplements alone.. Throughout the first year on hemodialysis treatment, the intact PTH concentration decreased from 538 +/- 256 to 251 +/- 218 pg/ml (p < 0.001). By the end of the study, the therapeutic objective was achieved in 22 patients (71%) ('responder' group). The remaining 9 patients were classified as the 'treatment failure' group. The basal intact PTH concentration was not different between both groups (508 +/- 235 vs. 612 +/- 303 pg/ml, respectively, p = n.s.), but 5 'treatment failure' patients admitted to take a dose of calcium carbonate lower than that prescribed. There were 40 episodes of hyperphosphatemia (11% of all measurements) in 7 of 31 patients, 5 of them belonged to the noncompliance 'treatment failure' patients. Only 15 episodes (4% of all measurements) of transient hypercalcemia (range 11.1 - 11.9 mg/dl) were detected in 8 patients.. Secondary hyperparathyroidism in hemodialysis patients can often be reverted by oral calcium carbonate alone. But a good adherence to treatment is absolutely necessary.

Topics: Administration, Oral; Calcium Carbonate; Cholecalciferol; Female; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Renal Dialysis

The measurement of urinary deoxypyridinoline (DPD) constitutes a specific and sensitive marker of bone resorption. Total and free forms of DPD are determined by chromatographic method (HPLC) after or without hydrolysis of urine, respectively. Pyrilinks-D, a new immunoassay, allows to assess directly the free forms and needs an appropriate hydrolysis step for measuring the total form. We have compared the values of free (F), total (T) and conjugated (NF) forms of DPD determined by HPLC and Pyrilinks-D, in elderly women (n = 21, mean age: 83.5 +/- 1.5 years) with vitamin D insufficiency (25 OH D < 6 ng/mL) and Ca insufficiency responsible for a secondary hyperparathyroidism (iPTH = 45.3 +/- 22.7 pg/mL) and in healthy elderly women (n = 25, mean age: 76.6 +/- 3.1 years) with a normal vit D status (25 OH D > 10 ng/mL) as control group. We have also measured DPD during the course of vit D and Ca supplementation. At baseline, the HPLC and Pyrilinks-D values of DPD/Cr are highly correlated (DPD-T: r = 0.92, p < 0.001 and DPD-F: r = 0.76, p < 0.001), DPD-F and -NF values are correlated with those of DPD-T, while DPD-F and -NF are not correlated between themselves. In elderly with vit D insufficiency, the values obtained with Pyrilinks-D as compared to control subjects, show a significant increase of urinary excretion of DPD-F (8.5 +/- 3.1 vs 5.7 +/- 1.9 nmol/mmol, Cr, p < 0.0001), DPD-T (16.8 +/- 10.2 vs 9.9 +/- 3.5 nmol/mmol, Cr; p < 0.001) and DPD-NF (8.3 +/- 9.0 vs 4.5 +/- 3.3 nmol/mmol, Cr, p < 0.05). The administration of 800 IU of vit D and 1 g of elemental Ca during a course of 6 months normalize the iPTH values (24.4 +/- 11.8 and 30.9 +/- 14.6 pg/mL at 3 and 6 months). Simultaneously, the urinary excretion at 3 and 6 months of DPD-T (12.9 +/- 6.0 and 13.6 +/- 6.5 nmol/mmol, Cr) and of DPD-NF (4.5 +/- 3.3 and 5.5 +/- 4.8 nmol/mmol Cr) assessed by Pyrilinks-D as well as by HPLC decreased significantly, while no change was seen with DPD-F assessed by both methods. The decreases expressed as percent of baseline values were about 20% for DPD-T and more than 30% for DPD-NF, while DPD-F levels remain unchanged. We conclude that the Pyrilinks-D immunoassay presents reliable characteristics and allows to assess either free or total forms of DPD, like the HPLC technique. It constitutes an excellent reflection of bone resorption in elderly with vit D insufficiency. However its application to monitor therapy like vit D and Ca supplementation, needs a hydrolysis step

Topics: Aged; Aged, 80 and over; Amino Acids; Analysis of Variance; Calcifediol; Cholecalciferol; Chromatography, High Pressure Liquid; Creatinine; Enzyme-Linked Immunosorbent Assay; Female; Humans; Hyperparathyroidism, Secondary; Parathyroid Hormone; Vitamin D Deficiency

Twelve dialysis patients received oral pulse therapy with 1-alpha-hydroxyvitamin D3 in a dose of 0.1 microgram/kg body weight twice weekly and daily calcium carbonate (1.5-3.5 g) for a period of 8-12 months. This treatment was very effective in suppressing secondary hyperparathyroidism without causing hypercalcaemia and/or hyperphosphataemia.

Topics: Administration, Oral; Adolescent; Adult; Alkaline Phosphatase; Calcium; Child; Child, Preschool; Cholecalciferol; Female; Humans; Hyperparathyroidism, Secondary; Immunoradiometric Assay; Kidney Failure, Chronic; Male; Parathyroid Hormone; Peritoneal Dialysis, Continuous Ambulatory; Phosphorus; Renal Dialysis

Pulse vitamin D3 (3-5 micrograms po, twice a week) has been proposed for individuals with hyperparathyroidism resistant to daily po vitamin D3 therapy. While pulse vitamin D3 is effective, concerns regarding oversuppression of parathyroid hormone (PTH) values leading to adynamic bone disease have arisen. In view of these concerns, minibolus vitamin D3 po therapy was utilized in dosages varying from 0.25-1.0 micrograms twice a week in an effort to control elevated PTH values in patients who failed standard daily vitamin D3 therapy. Eleven patients were changed to minibolus vitamin D3 therapy from standard daily treatment (6 women, 5 men; mean age 55.8 +/- 14 years), on continuous ambulatory peritoneal dialysis (CAPD) for an average of 28.4 +/- 23 months. The mean intact PTH (iPTH) values on 0.25 microgram/day decreased by 54.5 +/- 167.8 pg/mL compared to pretreatment values. The mean iPTH on minibolus vitamin D3 therapy decreased by 165.1 +/- 104 pg/mL. The response to minibolus vitamin D3 was not truly predicted by the baseline PTH values. While the average decrease in PTH was greatest on 1.0 microgram two times a week, 2 patients experienced a decrease greater than 200 pg/mL in PTH on a lower dose. The greatest effect on PTH with minipulse vitamin D3 occurred when iPTH was < or = 500 pg/mL. While total calcium increased on daily vitamin D3, there was no significant change with minipulse therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Administration, Oral; Cholecalciferol; Drug Administration Schedule; Female; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Peritoneal Dialysis, Continuous Ambulatory

During the course of chronic renal failure (CRF) in man, renal osteodystrophy (osteitis fibrosa and/or osteomalacia) gradually develops. The present study aimed to establish a similar type of CRF leading to renal osteodystrophy in rats. During progressive CRF development over 225 days after 5/6 nephrectomy, the following serum variables were measured: creatinine, immunoreactive parathyroid hormone (iPTH), 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), a25-hydroxyvitamin D3, (25(OH)D3), alkaline phosphatase, albumin, phosphate, urea nitrogen, total calcium, and other blood electrolytes. Subsequent to sacrifice, mechanical properties of the rat femur, bone histomorphometry (osteoid and eroded surfaces) and bone contents of calcium, phosphate and hydroxyproline were also examined. Serum creatinine in rats with CRF gradually escalated by some 70%, while circulating 1,25(OH)2D3 was reduced beneath detection level. Total plasma calcium and phosphate concentrations were, however, almost unchanged indicating that PTH-induced bone remodeling due to moderate hyperparathyroidism sustained calcium homeostasis. Alkaline phosphatase levels were reduced by some 50%, which reflects chronically impeded bone formation. Bone histomorphometry assessment revealed substantial elevation of resorption with moderate accompanying fibrosis in about 70% of afflicted animals. Bone calcium, phosphate and hydroxypyrroline contents remained unaltered. However, hydroxyproline/calcium ratio was marginally reduced. These results, together with altered mechanical bending stress characteristics and diminished diaphysis cross section area, confirm development of mixed bone lesions in the uremic animals. Our results are compatible with the early development of CRF in man. The established rat model is therefore useful in elucidating the precipitation and early treatment of renal osteodystrophy in humans.

Topics: Alkaline Phosphatase; Animals; Biomarkers; Bone and Bones; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Disease Models, Animal; Female; Hydroxyproline; Hyperparathyroidism, Secondary; Nephrectomy; Parathyroid Hormone; Rats; Rats, Wistar; Second Messenger Systems; Stress, Mechanical; Uremia

We evaluated the degree of secondary hyperparathyroidism (SHPT) in the patients undergoing long-term hemodialysis treatment. Most patients showed improvement of SHPT by administration of the active vitamin D3 analogue. However, some patients developed overt SHPT even under intensive treatment. Pulse therapy with large dose of vitamin D3 for those who suffered from overt SHPT was an effective treatment modality at the initial stage, however, hypercalcemia which developed in the majority of the patients at the later stage of this treatment became an obstacle for the continuation of this treatment. Therefore, early detection of the hypersecretion state of parathyroid hormone (PTH) as well as earlier initiation of intensive therapy are important factors in preventing overt SHPT. Establishment of a suitable assay system for early detection of SHPT is an important task and the high sensitivity-PTH assay system may be the most desirable. Though diabetic patients were not likely to develop overt SHPT, this system could detect even the mild chronological increase of serum PTH level in diabetic patients. On the other hand, relatively earlier initiation of vitamin D3 therapy to the predialysis patients from the conservative treatment stage caused aggravation of deterioration of renal function. Therefore, we should be prudent to initiate vitamin D3 therapy on predialysis patients suffering from renal failure. Strict management of the patients by vitamin D3 as well as calcium supplement therapy along with evaluation of the serum PTH level is still an important measure to avoid overt SHPT.

Topics: Cholecalciferol; Diabetes Complications; Humans; Hyperparathyroidism, Secondary; Parathyroid Hormone; Renal Dialysis

Topics: Adult; Amyloidosis; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Kidney Transplantation; Male; Renal Dialysis

It has previously been shown in this laboratory that vitamin D3 is essential for normal insulin secretion from the perfused rat pancreas. In this present study, the influence of vitamin D status on insulin secretion in vivo was investigated. Intravenous glucose tolerance tests were performed on conscious vitamin D-deficient rats (-D), vitamin D-replete rats fed ad libitum (+D AL), and vitamin D-replete rats pair fed to the D-deficient animals (+D PF). Vitamin D deficiency, easily recognizable by low daily dietary intake and depressed plasma calcium levels, was found to impair plasma glucose clearance as characterized by an elevated KG value (representing a function of the area beneath the tolerance curve). KG values for the +D AL, +D PF, and -D groups were 504 +/- 15, 480 +/- 46, and 641 +/- 28, respectively. The increase in KG corresponded to a significant reduction in glucose-mediated insulin secretion as compared to the +D animals. This difference appeared not to be related to the increase caloric intake associated with vitamin D repletion, since +D rats which had been pair fed to the -D animals also exhibited restored plasma insulin levels in response to glucose. Plasma phosphorus concentrations were comparable in all three groups, and thus this parameter is also unlikely to be a contributory factor in the observed phenomenon. Additional experiments were conducted to evaluate the involvement of hypocalcemia in the observed impaired glucose tolerance. Normalization of plasma calcium levels (from 4.8 mg/100 ml to 9.6/100 ml) of the -D rats, by dietary calcium and phosphorus manipulation, failed to improve glucose clearance (KG for -D normocalcemic rats = 639 +/- 61) or insulin secretion. These results support the concept that vitamin D plays a physiological role in insulin secretion, acting, at least in part, independently of nutritional factors and the prevailing plasma calcium and phosphorus concentrations.

Topics: Animals; Blood Glucose; Calcium; Cholecalciferol; Energy Intake; Glucose Tolerance Test; Hyperglycemia; Hyperparathyroidism, Secondary; Insulin; Insulin Secretion; Islets of Langerhans; Male; Phosphates; Rats; Vitamin D; Vitamin D Deficiency

Topics: Adolescent; Adult; Aged; Alkaline Phosphatase; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Female; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Long-Term Care; Male; Middle Aged; Osteomalacia; Parathyroid Glands; Parathyroid Hormone; Phosphorus; Radiography; Receptors, Calcitriol; Receptors, Steroid; Renal Dialysis

Calcium and phosphate metabolism as well as those substances which are essential in regulating this metabolism (parathyroid hormone, thyrocalcitonin and cholecalciferol) are briefly discussed. Of three known forms of bone disease (nutritional secondary hyperparathyroidism, rickets and hypervitaminosis A), the clinical symptoms, radiological changes, (histo)pathological findings, therapeutic procedures as well as the aetiological, pathogenic and pathophysiological features will be reviewed.

Topics: Animal Nutritional Physiological Phenomena; Animals; Birds; Bone and Bones; Bone Diseases; Calcitonin; Cat Diseases; Cats; Cholecalciferol; Dog Diseases; Dogs; Hyperparathyroidism, Secondary; Minerals; Osteoporosis; Parathyroid Hormone; Rickets; Vitamin A

Topics: Animals; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dogs; Humans; Hyperparathyroidism, Secondary; Intestine, Small; Kidney; Kidney Failure, Chronic; Myocardium; Parathyroid Hormone; Vitamin D

Topics: Cholecalciferol; Humans; Hyperparathyroidism, Secondary; Ileum; Jejunum; Obesity; Postoperative Complications

Vitamin D-deficient osteomalacia with pronounced secondary hyperparathyroidism was observed in an acromegalic patient suffering from adult celiac disease. Two oral tests with tritiated vitamin D3 showed a nearly normal absorption coefficient, contrasting with a marked steatorrhea mainly due to functional and reversible pancreatic insufficiency. The urinary excretion of the radioactive label was strikingly increased and accounted for the completely flat curve of plasma radioactivity. This urinary loss of mainly water-soluble metabolite(s) of vitamin D3 represents a unique and presently unexplained feature.

Topics: Acromegaly; Celiac Disease; Cholecalciferol; Female; Humans; Hyperparathyroidism, Secondary; Middle Aged; Osteomalacia

Many clinical similarities between renal osteodystrophy and nutritional rickets have suggested that a defect in either the metabolism or action of vitamin D exists in chronic renal failure. The discovery of the kidney as the organ that manufactures the active metabolite of vitamin D has provided direct evidence for a relationship between renal failure and altered vitamin D metabolism. Other observations suggest that an abnormality of vitamin D action could underlie both osteomalacia and osteitis fibrosa (secondary hyperparathyroidism) observed in patients with chronic renal failure. The administration of the active vitamin D analogs, 25(OH)D3, 1,25(OH)2D3, and lalpha(OH)D3, to uremic patients with symptomatic bone disease is capable of reversing many of the abnormalities of divalent ion metabolism. The widespread availability of these agents in the future may provide the clinician the means to correct or even prevent the serious bone disease that frequently complicates the course of chronic renal failure.

Topics: Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols; Hyperparathyroidism, Secondary; Kidney; Kidney Failure, Chronic; Phosphorus; Vitamin D

Highly sensitive assays have been developed that enable 25-hydroxycholecalciferol (25-hydroxyvitamin D3) and 25-hydroxyergocalciferol (25-hydroxyvitamin D2) to be measured in the same serum sample. With these assays it has been shown that endogenously produced cholecalciferol (vitamin D3) is important in man; the findings further emphasize the role of vitamin D metabolites as hormones rather than vitamins in the traditional sense. Dietary sources of vitamin D appear to be inadequate and vitamin D deficiency has been shown to the cause of rickets and osteomalacia in Asian immigrants to Britain. This condition may be readily treated with small doses of vitamin D. In addition, sub-clinical deficiency was found in the Asian community. In the elderly, also, vitamin D deficiency was established as an important cause of osteomalacia and again evidence for the existence of a sub-clinical deficiency state was found. It is therefore suggested that the present prophylactic practices should be reviewed. Secondary hyperparathyroidism (reflected by elevated concentrations of circulating immunoassayable parathyroid hormone) was shown to be the rule rather than the exception in vitamin D deficiency. Some patients, however, had failed to respond to a hypocalcaemic stimulus. In others, there were high concentrations of parathyroid hormone despite normal serum calcium concentrations. Thus the relationship between parathyroid hormone and metabolites of vitamin D may not be mediated through changes in serum calcium alone, and it is postulated that metabolites of vitamin D may directly affect the secretion of parathyroid hormone.

Topics: Adolescent; Adult; Aged; Alkaline Phosphatase; Animals; Asia; Asian People; Child; Cholecalciferol; Ergocalciferols; Ethnicity; Humans; Hydroxycholecalciferols; Hyperparathyroidism, Secondary; London; Middle Aged; Osteomalacia; Parathyroid Hormone; Radioimmunoassay; Rats; Rickets; Submarine Medicine; United Kingdom; Vitamin D; Vitamin D Deficiency

The authors report osteomalacia in 3 cases of epilepsy and one case of coronary heart disease treated with phenobarbitone, either alone or associated with other anticonvulsants. There were clinical signs in all cases and typical radiological signs in 3 cases, a characteristic laboratory syndrome in 4 cases. In the 3 cases where it was estimated, serum levels of parathormone were high. Finally, in 3 cases where it was measured, daily urinary excretion of glucaric D acid was increased. The bony histological signs studied in 3 cases, were similar to those in deficiency osteomalacia. A study of Ca45 metabolism in one case, showed the characteristic changes found in osteomalacia. Finally, a study of the metabolism of tritiated vitamin D, or tritiated 25 OH CC, carried out in 3 cases, gave 3 different patterns; only one of them was characteristic of enzyme induction under the dependency of anticonvulsant. Started in 2 cases, treatment with 125 OH2CC, brought about a rapid fall in blood PTH levels which then rose again before falling progressively in one case, under treatment with 25 OH CC. The bony histological signs of hyperparathyroidism then regressed whilst serum PTH levels remained high. Phosphorous and calcium balance improved in only one case. Treatment with 25 OH CC in high dosage brought about clinical, radiological and laboratory cure of osteomalacia in both cases, reducing the frequency of fits in the epileptic patient.

Topics: Adult; Aged; Anticonvulsants; Calcium; Cholecalciferol; Female; Humans; Hydroxycholecalciferols; Hyperparathyroidism, Secondary; Hypnotics and Sedatives; Male; Middle Aged; Osteomalacia; Parathyroid Hormone; Phenobarbital; Phenytoin

Topics: Aluminum; Animals; Calcium; Carbonates; Cholecalciferol; Diet Therapy; Dogs; Glomerular Filtration Rate; Humans; Hydroxides; Hyperparathyroidism, Secondary; Kidney; Kidney Failure, Chronic; Kidney Tubules; Nephrons; Parathyroid Hormone; Phosphorus