cholecalciferol has been researched along with Hyperparathyroidism* in 50 studies
14 review(s) available for cholecalciferol and Hyperparathyroidism
Article | Year |
---|---|
[Absolute risk for fracture and WHO guideline. Treatment of patients with secondary osteoporosis].
There has been accumulating evidence that various diseases and drugs cause increased risk of fracture. Although the treatment of primary diseases and discontinuation of drugs are the first and ideal option for the cure of secondary osteoporosis, medical intervention for osteoporosis is often necessary. The mechanisms, which induce bone fragility, are supposed to be different, depending on diseases and drugs. Guidelines for the evaluation and treatment of secondary osteoporosis have not been established except glucocorticoid-induced osteoporosis. In patients with osteoporosis caused by primary hyperparathyroidism, hyperthyroidism, diabetes mellitus as well as hormone deprivation therapy, bisphosphonate is effective in increasing bone mineral density but no data have been available about the fracture risk. Guidelines on the management and treatment of each secondary osteoporosis are desirable. Topics: Aromatase Inhibitors; Bone Density Conservation Agents; Cholecalciferol; Diabetes Complications; Diphosphonates; Glucocorticoids; Humans; Hyperparathyroidism; Hyperthyroidism; Osteoporosis; Parathyroidectomy; Risk; Vitamin K 2 | 2007 |
[Dementia in parathyroid disease].
Topics: Biomarkers; Calcium; Cholecalciferol; Dementia; Humans; Hypercalcemia; Hyperparathyroidism; Hyperparathyroidism, Secondary; Hypocalcemia; Hypothyroidism; Parathyroid Hormone; Parathyroidectomy; Phosphorus | 2004 |
Primary hyperparathyroidism: a case study.
Primary hyperparathyroidism is a hypercalcemic condition generated as a result of overproduction of parathyroid hormone (PTH) by one or more of the parathyroid glands. The cause is usually an abnormal group of cells forming a benign adenoma and rarely carcinoma. The condition is usually discovered by routine serum chemistry analysis showing hypercalcemia, hypophosphatemia, and elevated PTH levels. Elevated 24-hour urine calcium provides further confirmation. During the last decade, three procedures have been developed to help diagnose the affected parathyroid gland(s) in preparation for surgical intervention: computerized nuclear scanning with technetium-99-m sestamibi performed preoperatively; radio-guided probes; and rapid PTH assay (RPHA), both used intraoperatively. These three techniques have been reported to reduce the need for immediate frozen section diagnosis; shorten the length of the incision, surgical time, and length of hospital stay; produce less pain and discomfort; reduce surgical cost; and produce a quicker return to normal life. This article follows the surgical experience of a patient with a diagnosis of hyperparathyroidism and a history of postoperative nausea and vomiting who was scheduled as 23-hour stay. Topics: Biopsy; Calcitonin; Calcium; Cholecalciferol; Female; Humans; Hyperparathyroidism; Length of Stay; Middle Aged; Nurse's Role; Parathyroid Hormone; Parathyroidectomy; Perioperative Care; Postanesthesia Nursing; Radiosurgery; Technetium Tc 99m Sestamibi | 2004 |
[Nephrocalcinosis].
Nephrocalcinosis is used to describe renal parenchymal calcification. Causes of nephrocalcinosis include persistent hypercalcemia, hypercalciuria, acid-base disorders, hyperoxaluria and urinary stasis. Patients with nephrocalcinosis initially present no symptom. However, advanced nephrocalcinosis is irreversible and causes impaired renal function. Therefore, careful observation for the presence and progression of nephrocalcinosis is necessary for patients who have risk factors for this disorder. Topics: Acid-Base Imbalance; Calcium; Cholecalciferol; Humans; Hypercalcemia; Hyperoxaluria; Hyperparathyroidism; Nephrocalcinosis; Risk Factors; Urinary Retention | 2004 |
Effects of drugs and systemic factors on orthodontic treatment.
Orthodontic tooth movement and bone remodeling activity are dependent on systemic factors such as nutritional factors, metabolic bone diseases, age, and use of drugs. Therefore, a comprehensive review of the effects of these factors on orthodontic tooth movement is attempted in this article. Systemic hormones such as estrogen, androgen, and calcitonin are associated with an increase in bone mineral content, bone mass, and a decrease in the rate of bone resorption. Consequently, they could delay orthodontic tooth movement. On the contrary, thyroid hormones and corticosteroids might be involved in a more rapid orthodontic tooth movement during orthodontic therapy and have a less stable orthodontic result. Drugs such as bisphosphonates, vitamin D metabolites, and fluorides can probably cause a reduction of tooth movement after the orthodontic force is applied. Nonsteroidal anti-inflammatory drugs have also been shown to reduce bone resorption. Long-term administration of these drugs may therefore delay the necessary bone response to respective tooth-borne pressure and should not be administered for long periods of time to patients undergoing orthodontic tooth movement. Attention has also been focused on the effects of prostaglandins and leukotrienes in orthodontic tooth movement. It seems that they might have future clinical applications that could result in enhanced tooth movement. The use of the above drugs should be considered by every dentist in evaluating the treatment time and in planning treatment when tooth movement is attempted. Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Bone Remodeling; Cholecalciferol; Diphosphonates; Eicosanoids; Fluorides; Hormones; Humans; Hyperparathyroidism; Osteoporosis; Tooth Movement Techniques | 2001 |
Oral vitamin D or calcium carbonate in the prevention of renal bone disease?
It is well known that hyperparathyroidism begins early in renal failure and progresses, probably not linearly, throughout the natural course of renal diseases and dialysis therapy. Recent progress in basic medical science has improved our understanding of the mechanisms by which the classically known stimuli for parathyroid hormone synthesis and secretion may act, including hypocalcaemia, hyperphosphataemia and vitamin D3 metabolism disturbances. In the treatment of hyperparathyroidism, although some authors stress the benefit of treating one of these stimuli, it is probably more effective to combine the treatment of them all. There is conclusive recent work showing the efficacy of using both CaCO3 and vitamin D3, either in chronic renal failure or in dialysis patients at every stage of hyperparathyroidism. Therefore, the treatment of hyperparathyroidism should start early, long before dialysis, and it should aim to correct any of the causal factors. Both CaCO3 and vitamin D3 derivatives may be used in the prevention and treatment of renal bone disease. The limits of this association are the increasingly often reported adynamic bone disease, which in our experience has not yet given major clinical problems, and hyperphosphataemia. Uncontrolled serum phosphate levels would counterbalance the beneficial effect of vitamin D3 derivatives on hyperparathyroidism. Topics: Administration, Oral; Animals; Bone Diseases; Calcium; Calcium Carbonate; Cholecalciferol; Humans; Hyperparathyroidism; Kidney Failure, Chronic; Phosphates; Renal Dialysis | 1996 |
[Vitamin D deficiency and hip fracture].
Vitamin D deficiency is common in the elderly, especially in patients with hip fracture. Elderly people infrequently stay outside in the sunshine, and nutrition is deficient in vitamin D. In addition, the hydroxylation of vitamin D into active metabolites decreases with age. Vitamin D deficiency ultimately leads to osteomalacia, but in an earlier stage it causes secondary hyperparathyroidism, which is accompanied by increased bone turnover and cortical bone loss. Along these pathways vitamin D deficiency may contribute to the pathogenesis of hip fractures. In a survey in Amsterdam vitamin D deficiency was observed in more than 60% of the patients with hip fracture. Transilial bone biopsy showed signs of high turnover and cortical bone loss in more than 20% of patients. The elderly which are institutionalized carry an increased risk. Prevention or vitamin D deficiency is possible by adequate exposure to ultraviolet light. Primarily, the elderly should be encouraged to go out into the sunshine regularly. Advice on nutrition may be given additionally. When sunshine exposure is negligible, as in many disabled and institutionalized elderly, a daily supplement of vitamin D3 400 IU should be given. Preventive measures have to be evaluated prospectively. Vitamin D deficiency is not the most important risk factors for hip fractures, but the easiest to correct. Topics: Adult; Aged; Aging; Cholecalciferol; Hip Fractures; Humans; Hydroxylation; Hyperparathyroidism; Middle Aged; Nutritional Requirements; Osteomalacia; Sunlight; Vitamin D; Vitamin D Deficiency | 1985 |
A review of the aetiology and pathogenesis of hypercalcaemia.
Topics: Alkalosis; Benzothiadiazines; Calcinosis; Cholecalciferol; Diuretics; Humans; Hypercalcemia; Hyperparathyroidism; Isotretinoin; Lithium; Osteitis Deformans; Sarcoidosis; Sodium Chloride Symporter Inhibitors; Tamoxifen; Tretinoin; Vitamin A | 1984 |
Recent advances in the understanding of the metabolism and functions of vitamin D.
Many advances have been made in the past several years in our understanding of the metabolism and mechanism of action of vitamin D. Recognition of the clinical implications of this knowledge continues to grow. Despite these gains, however, many questions remain unanswered. These include the role of 24,25(OH)2D3 in physiologic processes, the nature of the contribution of vitamin D metabolism to bone growth and development, the responses of other possible target tissues such as the pancreas and parathyroid gland, and the further elucidation of interactions between vitamin D metabolites and parathyroid hormone in the maintenance of calcium and phosphorus homeostasis. The next decade of research is bound to bring insight into these and other questions. Topics: Bone and Bones; Calcium; Chemical Phenomena; Chemistry; Cholecalciferol; Humans; Hydroxycholecalciferols; Hyperparathyroidism; Intestinal Mucosa; Kidney; Mixed Function Oxygenases; Osteomalacia; Parathyroid Glands; Phosphates; Pseudohypoparathyroidism; Rickets; Vitamin D | 1980 |
Calcium metabolism and disorders of parathyroid glands.
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 | 1977 |
Hormonal control of skeletal and mineral homeostasis.
Topics: Bone and Bones; Calcification, Physiologic; Calcitonin; Calcium; Calcium Carbonate; Cholecalciferol; Cyclic AMP; Dihydroxycholecalciferols; Feedback; Homeostasis; Humans; Hydroxycholecalciferols; Hyperparathyroidism; Osteoclasts; Osteocytes; Parathyroid Hormone; Vitamin D; Vitamin D Deficiency | 1974 |
[Hypercalciuria--nephrocalcinosis-- and calcium calculi of the kidney. Differential diagnosis and clinical aspects of pathological renal calcium transport].
Topics: Calcium; Calcium Metabolism Disorders; Cholecalciferol; Cushing Syndrome; Diagnosis, Differential; Fanconi Syndrome; Fractures, Bone; Glomerular Filtration Rate; Humans; Hypercalcemia; Hyperparathyroidism; Hyperthyroidism; Kidney Calculi; Nephrocalcinosis; Osteitis Deformans; Osteoporosis; Parathyroid Hormone; Sarcoidosis | 1974 |
Metabolism and action of the hormone vitamin D. Its relation to diseases of calcium homeostasis.
Extensive experimental evidence has established a significant role of calciferol in the maintenance of normal calcium homeostasis. Present knowledge indicates that vitamin D(3) must first be converted to 25-OH-D(3) and then to 1,25(OH)(2)D(3), the most active known form of the steroid. Many of the factors regulating the rate of production of this last steroid from its precurser have been evaluated, and the concept that vitamin D functions as a steroid hormone seems to be well established. Deranged action of calciferol, caused by impaired metabolism of the steroid or through altered sensitivity of target tissues, may be involved in the pathophysiology of several disease states with abnormal calcium metabolism. It is noted that liver disease, osteomalacia due to anticonvulsant therapy, chronic renal failure, hypophosphatemic rickets, hypoparathyroidism, hyperparathyroidism, sarcoidosis and idiopathic hypercalciuria have possible relation to alterations in metabolism or action of vitamin D. The future clinical availability of 1,25(OH)(2)D(3) and other analogs of this steroid may offer potential therapeutic benefit in the treatment of certain of the disease entities discussed. Topics: Animals; Biological Transport, Active; Bone Resorption; Calcium; Calcium Metabolism Disorders; Cholecalciferol; Collagen; Homeostasis; Humans; Hydroxycholecalciferols; Hyperparathyroidism; Hypoparathyroidism; Hypophosphatemia, Familial; Intestinal Absorption; Kidney; Kidney Diseases; Liver; Liver Diseases; Sarcoidosis; Skin; Ultraviolet Rays; Vitamin D; Vitamin D Deficiency | 1974 |
[Treatment of parathyroid diseases].
Topics: Calcitonin; Calcium; Cholecalciferol; Humans; Hyperparathyroidism; Hypocalcemia; Kidney Failure, Chronic; Osteitis Fibrosa Cystica; Osteomalacia; Parathyroid Glands; Phosphorus | 1971 |
9 trial(s) available for cholecalciferol and Hyperparathyroidism
Article | Year |
---|---|
The effect of vitamin D3 supplementation on markers of cardiovascular health in hyperparathyroid, vitamin D insufficient women: a randomized placebo-controlled trial.
Emerging data supports an association between parathyroid hormone (PTH) and aldosterone. It has been speculated, that potential adverse cardiovascular effects of vitamin D insufficiency may partly be caused by the development of secondary hyperparathyroidism with increased activity of the renin-angiotensin-aldosterone system (RAAS). We aimed to investigate the effect of normalizing vitamin D status and/or reducing PTH levels on RAAS activity and other markers of cardiovascular health.. In a double-blinded study during wintertime, we randomized 81 healthy postmenopausal women with secondary hyperparathyroidism (PTH > 6.9 pmol/l) and 25-hydroxy-vitamin D (25(OH)D) levels < 50 nmol/l to 12 weeks of treatment with vitamin D3 70 µg/day (2800 IU/day) or identical placebo. Markers of cardiovascular health were defined as changes in the plasma RAAS, glycated hemoglobin, lipids, and lipoproteins, blood pressure, vascular stiffness, heart rate, and cardiac conductivity.. Compared to placebo, vitamin D3 treatment significantly increased plasma levels of 25(OH)D and 1,25(OH). Vitamin D3 supplementation normalized vitamin D levels and reduced PTH. The supplement increased levels of HDL, but had no effects on RAAS activity or other indices of cardiovascular health. Topics: Aged; Aged, 80 and over; Blood Pressure; Cardiovascular System; Cholecalciferol; Double-Blind Method; Female; Heart Rate; Hormone Replacement Therapy; Humans; Hyperparathyroidism; Middle Aged; Treatment Outcome; Vascular Stiffness; Vitamin D Deficiency | 2018 |
The effect of cholecalciferol for lowering albuminuria in chronic kidney disease: a prospective controlled study.
Growing evidence indicates that vitamin D receptor activation may have antiproteinuric effects. We aimed to evaluate whether vitamin D supplementation with daily cholecalciferol could reduce albuminuria in proteinuric chronic kidney disease (CKD) patients.. This 6-month prospective, controlled, intervention study enrolled 101 non-dialysis CKD patients with albuminuria. Patients with low 25(OH) vitamin D [25(OH)D] and high parathyroid hormone (PTH) levels (n = 50; 49%) received oral cholecalciferol (666 IU/day), whereas those without hyperparathyroidism (n = 51; 51%), independent of their vitamin D status, did not receive any cholecalciferol, and were considered as the control group.. Cholecalciferol administration led to a rise in mean 25(OH)D levels by 53.0 ± 41.6% (P < 0.001). Urinary albumin-to-creatinine ratio (uACR) decreased from (geometric mean with 95% confidence interval) 284 (189-425) to 167 mg/g (105-266) at 6 months (P < 0.001) in the cholecalciferol group, and there was no change in the control group. Reduction in a uACR was observed in the absence of significant changes in other factors, which could affect proteinuria, like weight, blood pressure (BP) levels or antihypertensive treatment. Six-month changes in 25(OH)D levels were significantly and inversely associated with that in the uACR (Pearson's R = -0.519; P = 0.036), after adjustment by age, sex, body mass index, BP, glomerular filtration rate and antiproteinuric treatment. The mean PTH decreased by -13.8 ± 20.3% (P = 0.039) only in treated patients, with a mild rise in phosphate and calcium-phosphate product [7.0 ± 14.7% (P = 0.002) and 7.2 ± 15.2% (P = 0.003), respectively].. In addition to improving hyperparathyroidism, vitamin D supplementation with daily cholecalciferol had a beneficial effect in decreasing albuminuria with potential effects on delaying the progression of CKD. Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Albuminuria; Cholecalciferol; Dietary Supplements; Disease Progression; Female; Humans; Hyperparathyroidism; Male; Middle Aged; Parathyroid Hormone; Phosphates; Prospective Studies; Renal Insufficiency, Chronic; Vitamin D; Vitamin D Deficiency; Vitamins; Young Adult | 2014 |
Vitamin D treatment in primary hyperparathyroidism: a randomized placebo controlled trial.
Low 25-hydroxyvitamin D levels are common in patients with primary hyperparathyroidism (PHPT) and associated with higher PTH levels and hungry bone syndrome after parathyroidectomy (PTX). However, concerns have been raised about the safety of vitamin D supplementation in PHPT.. We aimed to assess safety and effects on calcium homeostasis and bone metabolism of supplementation with high doses of vitamin D in PHPT patients.. This was an investigator-initiated double-blind, randomized, placebo-controlled, parallel-group trial from a single center.. Forty-six PHPT patients were recruited, with a mean age of 58 (range 29-77) years, and 35 (76%) were women.. Intervention included daily supplementation with 70 μg (2800 IU) cholecalciferol or identical placebo for 52 weeks. Treatment was administered 26 weeks before PTX and continued for 26 weeks after PTX.. PTH, calcium homeostasis, and bone metabolism were evaluated.. Preoperatively, 25-hydroxyvitamin D increased from 50 to 94 nmol/L in the treatment group and decreased from 57 to 52 nmol/L in the placebo group (P < .001). Compared with placebo, vitamin D decreased PTH significantly by 17% before PTX (P = .01), increased lumbar spine bone mineral density by 2.5% (P = .01), and decreased C-terminal β-CrossLaps by 22% (P < .005). The trabecular bone score did not change in response to treatment, but improved after PTX. Postoperatively, PTH remained lower in the cholecalciferol group compared with the placebo group (P = .04). Plasma creatinine and plasma and urinary calcium did not differ between groups.. Daily supplementation with a high vitamin D dose safely improves vitamin D status and decreases PTH in PHPT patients. The vitamin D treatment is accompanied by reduced bone resorption and improved bone mineral density before operation. Topics: Adult; Aged; Bone Density; Calcium; Cholecalciferol; Female; Humans; Hyperparathyroidism; Male; Middle Aged; Parathyroid Hormone; Phosphates; Placebos; Vitamin D | 2014 |
High-dose cholecalciferol reduces parathyroid hormone in patients with early chronic kidney disease: a pilot, randomized, double-blind, placebo-controlled trial.
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 | 2012 |
Effect of cholecalciferol on parathyroid hormone and vitamin D levels in chronic kidney disease.
We aimed to determine the effect of a monthly oral vitamin D on the serum 25-hydroxyvitamin D levels and iPTH levels in patients with CKD.. This was a prospective controlled trial of 48 patients with CKD stage 3-4. Patients were divided into two groups Group1 the cholecalciferol treatment group, Group 2, the control group. One patient in Group 1, and 3 patients in Group2 were excluded after the baseline 25(OH)D levels were determined to be greater than 30ng/ml. Two patients in Group1, and one patient in Group 2 were excluded after the baseline iPTH was determined to be less than 70 pg/ml and greater than 300 pg/ml. Five patients in both groups were lost to follow-up. Thus, a total of 16 patients in Group 1 and 15 patients in Group2 completed the three month study. Group1 patients received 300,000 IU month oral cholecalciferol.. The mean serum 25(OH)D concentration of the group1 was significantly higher at baseline (P=0.039). At the end of the three months; serum 25 (OH) D level increased significantly in Group1 (P=0.001). iPTH level of Group1 was significantly lower at baseline (P=0.034). The values of the group1 before and end of third month was compared, serum Ca (P=0.011), P (P=0.013) level showed significant increase, but no significant increase in the Group 2 (P>0.05). The groups had not a clinically significant change in serum Ca and P level (P>0.05).. Oral cholecalciferol supplementation can be used safely and effective in reducing iPTH levels and correcting vitamin D insufficiency/deficiency in patients with CKD. Topics: Administration, Oral; Adult; Aged; Bone Density Conservation Agents; Cholecalciferol; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Diabetic Nephropathies; Female; Follow-Up Studies; Glomerulonephritis; Humans; Hyperparathyroidism; Hypertension; Male; Middle Aged; Parathyroid Hormone; Prospective Studies; Renal Insufficiency, Chronic; Risk Factors; Treatment Outcome; Vitamin D | 2011 |
Sensitivity analysis for the estimation of rates of change with non-ignorable drop-out: an application to a randomized clinical trial of the vitamin D3.
The vitamin D(3) trial was a repeated measures randomized clinical trial for secondary hyperparathyroidism in haemodialysis patients where the efficacy of the vitamin D(3) infusions for suppressing the secretion of parathyroid hormone (PTH) was compared among four dose groups over 12 weeks. In this trial, patients terminated the study before the scheduled end of the study due to their elevated serum calcium (Ca) level, that is, the administration of the vitamin D(3) was expected to cause hypercalcaemia as an adverse event. In this setting of monotone missingness, there is a potential for bias in estimation of mean rates of decline in PTH for each treatment group using the standard methods such as the generalized estimating equations (GEE) which ignore the observed past Ca histories. We estimated the treatment-group-specific mean rates of decline in PTH by the inverse probability of censoring weighted (IPCW) methods which account for the observed past histories of time-dependent factors that are both a predictor of drop-out and are correlated with the outcomes. The IPCW estimator can be viewed as an extension of the GEE estimator that allows for the data to be MAR but not MCAR. With missing data, it is rarely appropriate to analyse the data solely under the assumption that the missing data process is ignorable, because the assumption of ignorable missingness cannot be guaranteed to hold and is untestable from the observed data. We proposed a sensitivity analysis that examines how inference about the IPCW estimates of the treatment-group-specific mean rates of decline in PTH changes as we vary the non-ignorable selection bias parameter over a range of plausible values. Topics: Bias; Calcium; Cholecalciferol; Computer Simulation; Data Interpretation, Statistical; Dialysis; Humans; Hyperparathyroidism; Models, Statistical; Parathyroid Hormone; Randomized Controlled Trials as Topic; Sensitivity and Specificity | 2003 |
[Treatment of severe uremic hyperparathyroidism using a method for percutaneous injection of the parathyroid glands with ethanol].
The results of recent studies suggest that uremic patients with large parathyroid hyperplasia are often resistant to active vitamin D3 therapy. Percutaneous ethanol injection has become an interesting option in such cases, although there are only a few publications on that subject. In this work we would like to present our experience with this method. 20 patients with serum iPTH > 400 pg/ml and 1-4 hyperplastic parathyroids (mean volume 1.07) underwent 56 percutaneous ethanol injection sessions under ultrasonographic guidance. In 9 patients a marked (> 75%), long-term (12-24 months) decrease in serum iPTH was achieved; lesser (> 50%) reduction in parathyroid activity persisted for 36-42 months in 5 out of 9 patients observed in this period. In almost every patient a significant reduction of alphacalcidol dose was possible. Our data confirm that percutaneous ethanol injection therapy is a useful and safe adjunct in severe uremic hyperparathyroidism treatment strategy which allows to restore the responsiveness to active vitamin D3 metabolites. Topics: Adult; Aged; Cholecalciferol; Drug Resistance; Ethanol; Female; Humans; Hyperparathyroidism; Hyperplasia; Injections, Subcutaneous; Male; Middle Aged; Parathyroid Glands; Parathyroid Hormone; Ultrasonography; Uremia | 1999 |
Comparison of the efficacy of two injectable forms of vitamin D3 and oral one-alpha in treatment of secondary hyperparathyroidism in patients on maintenance hemodialysis.
In the present study, we compared the efficacy of two intravenous forms of vitamin D3[Calcijex: 1,25(OH)2D3 and One-Alpha: 1(OH)D3] and that of oral One-Alpha in the treatment of secondary hyperparathyroidism in patients receiving maintenance hemodialysis. Twenty patients were assigned to 1 of 2 treatment groups (A and B) which were matched for age, sex, and duration of maintenance hemodialysis. None of the patients included had chronic liver disease or had received drugs known to interfere with hepatic enzymes. All patients had received a stable dose of oral calcium and One-Alpha for a minimum period of 1 year, which maintained corrected serum calcium at the upper limit of the normal range. At the start of the study, oral One-Alpha was replaced by Calcijex in group A and injectable One-Alpha in group B. Treatment was maintained for 3 months (phase I). Subsequently, injectable vitamin D3 was discontinued and all patients received their previous dose of oral One-Alpha for a period of 1 month. Finally, oral One-Alpha was discontinued again and the injectable forms of vitamin D3 were crossed over in the 2 treatment groups for another 3 months (phase II). The results showed that the serum concentrations of 1,25(OH)2D3, measured 48 h after intravenous injection of One-Alpha, were not different from that produced by an equivalent dose of Calcijex in the same group of patients. Furthermore, overall analysis of intact parathyroid levels during the cross-over, using ANOVA with repeated responses, indicated that the two analogues were equipotent as regards suppression of PTH secretion. In our study, treatment with intravenous vitamin D3 led to significant suppression of PTH secretion. These results were achieved by a lower drug dosage of vitamin D3 and at lower trough blood levels of 1,25(OH)2D3 as compared to those of oral One-Alpha. Our findings are in favor of the early use of either forms of injectable vitamin D3 in the treatment of secondary hyperparathyroidism. Topics: Adenoma; Administration, Oral; Adult; Analysis of Variance; Calcitriol; Cholecalciferol; Female; Humans; Hyperparathyroidism; Injections, Intravenous; Male; Middle Aged; Parathyroid Glands; Parathyroid Hormone; Parathyroid Neoplasms; Random Allocation; Renal Dialysis; Treatment Outcome; Ultrasonography | 1997 |
Different responses of free and peptide-bound cross-links to vitamin D and calcium supplementation in elderly women with vitamin D insufficiency.
Recent findings have shown that bisphosphonates had different effects on the urinary excretion of free and peptide-bound cross-links. Because of this discrepancy, we investigated the effects of another antiresorptive therapy, i.e. vitamin D (vitD) and calcium (Ca) supplementation (800 IU vit D3 and 1 g elemental calcium daily for 6 months) in elderly women (n = 21, age: 83.5 +/- 1.5 yr) with vitD insufficiency and secondary hyperparathyroidism (mean level 25 hydroxy vitamin D = 3.17 +/- 1.2 ng/mL, mean level of intact parathormone = 45.3 +/- 22.7 pg/mL) on the urinary excretion of free and peptide-bound cross-links. A group of free-living, healthy elderly women (n = 25, age: 76.6 +/- 3.1 yr) with a normal vitD status (mean level of 25 OH D = 23.4 +/- 8.9 ng/mL, intact parathormone = 30.2 +/- 11.2 pg/mL) was simultaneously studied. Bone resorption was assessed by total (T), free (F), peptidyl (P) hydroxylysylpyridinoline (HP) and lysylpyridinoline (LP) measured with high performance liquid chromatography, by F-LP determined with enzyme linked immunosorbent assay (iF-LP) and by the N- and C-terminal telopeptides of type I collagen (NTX and Cross-laps) before and after (3 and 6 months) therapy. Comparison of the two groups of elderly women at baseline showed that the urinary excretion of pyridinoline cross-links (T, F, and peptide-bound forms) and of telopeptide fragment of type I collagen were all increased in patients with a low vitD status. Highly significant differences were seen principally for T-HP, F-HP, and F-LP (P < 0.001). Correlation studies between each marker showed that the values of pyridinoline cross-links (T and peptide-bound forms) and of the telopeptide fragments of type I collagen correlated well, but the correlation was slightly less pronounced between free pyridinolines and the other markers. After treatment, the response to therapy was greatest for peptide-bound cross-links assessed by high performance liquid chromatography and for telopeptide fragments of type I collagen (percent change at 6 months: -21% for P-HP P < 0.05, -26% for P-LP P < 0.05, -31% for NTX P < 0.01, and -51% for CLaps P < 0.001). In contrast, free pyridinolines excretion (F-HP and F-LP) assessed by high performance liquid chromatography as well as by immunoassay remained unchanged at 3 and 6 months. Because marked and significant changes were seen with peptide-bound cross-links only and not with free forms, we conclude that vitD and Ca therapy has the same effects Topics: Aged; Aged, 80 and over; Amino Acids; Biomarkers; Bone Resorption; Calcifediol; Calcium; Cholecalciferol; Chromatography, High Pressure Liquid; Collagen; Collagen Type I; Enzyme-Linked Immunosorbent Assay; Female; Humans; Hyperparathyroidism; Parathyroid Hormone; Peptides; Vitamin D Deficiency | 1996 |
27 other study(ies) available for cholecalciferol and Hyperparathyroidism
Article | Year |
---|---|
Lessons learned from the management of Hungry Bone Syndrome following the removal of an Atypical Parathyroid Adenoma.
Hungry Bone Syndrome (HBS) refers to rapid, profound, and prolonged hypocalcemia associated with hypophosphatemia and hypomagnesemia occurring in patients with increased bone turnover after successful management of the underlying disorder. We describe a male patient with primary hyperparathyroidism (PHPT), in whom HBS was diagnosed 6 months after parathyroidectomy. Histopathologic examination revealed an atypical parathyroid adenoma (APA), while immunohistochemistry showed cell proliferation index Ki-67 10% and overexpression of cyclin D1 (>90%). Preoperative treatment with vitamin D3 had normalized 25OHD and alkaline phosphatase levels, reflected in an improvement in bone turnover prior to surgery. Postoperative treatment for HBS with alfacalcidol, calcium, vitamin D3 and magnesium was administered for a long period. This treatment prevented severe postoperative hypocalcemia and he was discharged two days later. Preoperative cinacalcet treatment did not reduce hypercalcemia implying that the tumor had lack of calciumsensing receptors (CaSR). In conclusion, preoperative restoration of low 25OHD levels is essential for prevention of HBS. Postoperative treatment with active metabolites of vitamin D must be initiated as early as possible, in order to prevent or minimize the development of HBS, and to reduce the duration of hospitalization. Topics: Adenoma; Adult; Bone Density Conservation Agents; Calcium; Calcium-Regulating Hormones and Agents; Cholecalciferol; Cinacalcet; Humans; Hydroxycholecalciferols; Hyperparathyroidism; Hypocalcemia; Hypophosphatemia; Magnesium; Male; Parathyroid Neoplasms; Parathyroidectomy; Postoperative Complications; Syndrome | 2019 |
Normocalcemia in the Face of Marked Hypervitaminosis D: The Utility of Vitamin D Metabolite Profiling.
Topics: Aged, 80 and over; Calcium; Cholecalciferol; Cinacalcet; Dietary Supplements; Dose-Response Relationship, Drug; Ergocalciferols; Female; Humans; Hyperparathyroidism; Nutrition Disorders; Parathyroid Hormone; Vitamin D; Vitamin D Deficiency | 2019 |
Denosumab-induced Normocalcemic Hyperparathyroidism in a Woman with Postmenopausal Osteoporosis and Normal Renal Function.
Elevations in serum Parathyroid Hormone (PTH) levels after denosumab administration have been described in medical literature among patients with renal impairment or intestinal malabsortion syndromes.. To present a case of denosumab-induced normocalcemic hyperparathyroidism in a woman with postmenopausal osteoporosis without renal impairment or malabsorption syndrome.. A 62-year-old woman was diagnosed with postmenopausal osteoporosis (serum iPTH: 61pg/mL) and received anti-osteoporotic medication (70mg alendronate sodium once weekly and 1g/800IU calcium carbonate/cholecalciferol daily). Because of severe gastrointestinal symptoms, the alendronate sodium was discontinued and replaced it with denosumab 60mg/mL subcutaneously. Three months after first receiving denosumab, the serum iPTH, 25[OH]D and calcium levels were 1350pg/mL, 24.8ng/ml and 8.4mg/dL, respectively. This dramatic elevation of serum iPTH was attributed to receiving denosumab, as other causes of normocalcemic hyperparathyroidism were excluded. So, an interruption of denosumab for the second semester and reception only 2g/1600IU calcium carbonate/cholecalciferol daily was decided. Twelve months later the serum iPTH, 25[OH]D and calcium levels were 71pg/mL, 33.2ng/ml and 9.4mg/dL, respectively.. A close monitoring of all patients prior to and during treatment with denosumab is suggested. Topics: Bone Density Conservation Agents; Calcium; Calcium Carbonate; Cholecalciferol; Denosumab; Female; Humans; Hyperparathyroidism; Kidney Function Tests; Middle Aged; Osteoporosis, Postmenopausal; Parathyroid Hormone | 2018 |
A model of calcium homeostasis in the rat.
We developed a model of calcium homeostasis in the rat to better understand the impact of dysfunctions such as primary hyperparathyroidism and vitamin D deficiency on calcium balance. The model accounts for the regulation of calcium intestinal uptake, bone resorption, and renal reabsorption by parathyroid hormone (PTH), vitamin D Topics: Animals; Bone Resorption; Calcium; Cholecalciferol; Homeostasis; Hyperparathyroidism; Intestinal Mucosa; Models, Biological; Parathyroid Hormone; Rats; Receptors, Calcium-Sensing; Vitamin D Deficiency | 2016 |
Recommendations of the Brazilian Society of Endocrinology and Metabology (SBEM) for the diagnosis and treatment of hypovitaminosis D.
The objective is to present an update on the diagnosis and treatment of hypovitaminosis D, based on the most recent scientific evidence.. The Department of Bone and Mineral Metabolism of the Brazilian Society of Endocrinology and Metabology (SBEM) was invited to generate a document following the rules of the Brazilian Medical Association (AMB) Guidelines Program. Data search was performed using PubMed, Lilacs and SciELO and the evidence was classified in recommendation levels, according to the scientific strength and study type.. A scientific update regarding hypovitaminosis D was presented to serve as the basis for the diagnosis and treatment of this condition in Brazil. Topics: Bariatric Surgery; Brazil; Calcifediol; Calcium, Dietary; Cholecalciferol; Databases, Bibliographic; Ergocalciferols; Evidence-Based Medicine; Humans; Hyperparathyroidism; Malabsorption Syndromes; Osteoporosis; Osteoporotic Fractures; Parathyroid Hormone; Risk Factors; Vitamin D Deficiency | 2014 |
Impact of cholecalciferol treatment on biomarkers of inflammation and myocardial structure in hemodialysis patients without hyperparathyroidism.
Vitamin D (25-hydroxyvitamin D, 25(OH)D) deficiency, hypovitaminosis D, is highly prevalent in chronic kidney disease patients and is potentially involved with complications in the hemodialysis (HD) population. The aim of this study was to evaluate the impact of cholecalciferol supplementation on biomarkers of mineral metabolism, inflammation, and cardiac function in a group of HD patients presenting with hypovitaminosis D and low intact parathyroid hormone (iPTH) levels.. HD patients with iPTH levels of <300 pg/mL, not receiving vitamin D therapy, and presenting with 25(OH)D levels of <30 ng/mL were enrolled in this prospective study. Oral cholecalciferol was prescribed once a week in the first 12 weeks (50,000 IU) and in the last 12 weeks (20,000 IU) of the study. High-sensitivity C-reactive protein, interleukin-6, and serum albumin were used as inflammatory markers. Echocardiograms were performed on a midweek interdialytic day at baseline and after 6 months of cholecalciferol supplementation.. In all, 30 patients were included in the final analysis. We observed a significant increase in serum 25(OH)D levels after 3 months (46.2 ± 14.4 ng/mL vs. 18.1 ± 6.6 ng/mL; P < .001) and after 6 months (40.4 ± 10.4 ng/mL vs. 18.1 ± 6.6 ng/mL; P < .001) of cholecalciferol supplementation. There were no significant changes in alkaline phosphatase, iPTH, phosphorus, and serum albumin levels, but there was a slight but significant increase in calcium levels after 6 months of cholecalciferol supplementation (9.4 ± 0.6 mg/dL vs. 9.0 ± 0.6 mg/dL; P = .02). Additionally, we observed a significant reduction in high-sensitivity C-reactive protein levels after 3 months (median: 0.62 [0.05 to 29.6] mg/L vs. 0.32 [0.02 to 3.13] mg/L; P = .02) and after 6 months (median: 0.62 [0.05 to 29.6] mg/L vs. 0.50 [0.02 to 5.66] mg/L; P = .04) of cholecalciferol supplementation, as well as a significant reduction in interleukin-6 levels (median: 6.44 pg/mL vs. 3.83 pg/mL; P = .018) after 6 months of supplementation. Left ventricular mass index was significantly reduced at the end of supplementation (159 ± 55 g/m(2) vs. 175 ± 63 g/m(2); P = .03).. Cholecalciferol supplementation in HD patients was found to be safe and efficient to correct hypovitaminosis D and established little impact on mineral metabolism markers. Additionally, we observed a reduction in important surrogate markers of cardiovascular risk, namely systemic inflammation and left ventricular hypertrophy, suggesting an anti-inflammatory action and possibly an improvement of cardiac dysfunction. Topics: Aged; Alkaline Phosphatase; Biomarkers; C-Reactive Protein; Calcium; Cholecalciferol; Dietary Supplements; Female; Humans; Hyperparathyroidism; Inflammation; Interleukin-6; Male; Middle Aged; Myocardium; Parathyroid Hormone; Phosphorus; Prospective Studies; Renal Dialysis; Serum Albumin; Vitamin D; Vitamin D Deficiency; Vitamins | 2012 |
Vitamin D repletion in patients with primary hyperparathyroidism and coexistent vitamin D insufficiency.
Vitamin D insufficiency is common in patients with primary hyperparathyroidism (PHPT) and may be associated with more severe and progressive disease. Uncertainty exists, however, as to whether repletion of vitamin D should be undertaken in patients with PHPT. Here we report the effects of vitamin D repletion on biochemical outcomes over 1 yr in a group of 21 patients with mild PHPT [serum calcium <12 mg/dl (3 mmol/liter)] and coexistent vitamin D insufficiency [serum 25 hydroxyvitamin D [25(OH)D] <20 microg/liter (50 nmol/liter)]. In response to vitamin D repletion to a serum 25(OH)D level greater than 20 microg/liter (50 nmol/liter), mean levels of serum calcium and phosphate did not change, and serum calcium did not exceed 12 mg/dl (3 mmol/liter) in any patient. Levels of intact PTH fell by 24% at 6 months (P < 0.01) and 26% at 12 months (P < 0.01). There was an inverse relationship between the change in serum 25(OH)D and that in intact PTH (r = -0.43, P = 0.056). At 12 months, total serum alkaline phosphatase was significantly lower, and urine N-telopeptides tended to be lower than baseline values (P = 0.02 and 0.13, respectively). In two patients, 24-h urinary calcium excretion rose to exceed 400 mg/d, but the group mean 24-h urinary calcium excretion did not change. These preliminary data suggest that vitamin D repletion in patients with PHPT does not exacerbate hypercalcemia and may decrease levels of PTH and bone turnover. Some patients with PHPT may experience an increase in urinary calcium excretion after vitamin D repletion. Topics: Adult; Aged; Bone Remodeling; Cholecalciferol; Female; Humans; Hyperparathyroidism; Male; Middle Aged; Parathyroid Hormone; Vitamin D; Vitamin D Deficiency | 2005 |
Risk factors associated to kidney stones in primary hyperparathyroidism.
Nephrolithiasis is the most important clinical manifestation of primary hyperparathyroidism (PHPT), although nowadays this disorder is often asymptomatic. Clinical or biochemical differences between PHPT patients with and without nephrolithiasis have not been clearly identified in most of the previous studies. The aim of the study was to investigate clinical and biochemical parameters in kidney stone former (SF) and non-stone former (NSF) patients with PHPT in order to identify potential risk factors. Serum and plasma samples from 55 consecutive patients (43 females, 12 males) with PHPT were collected after overnight fasting; 24-h urine collection and a fresh sample of urine for sediment analysis were obtained from all patients. Clinical data were recorded in all. Out of 55 patients, 22 had kidney stones, which were symptomatic in 73%. SFs showed circulating PTH, total and ionized calcium, 1,25 dihydroxyvitamin D3, urinary calcium excretion and 24-h urine oxalate levels significantly higher than NSFs. Hypercalciuria was often concomitant with massive quantities of calcium oxalate crystals in urine sediment. Hypercalciuria and relatively high oxaluria were associated with stone formation with an odds ratio (OR) of 4.0 and 7.0, respectively, which rose to 33.5 when they coexisted. Hypomagnesuria and hypocitraturia were common in at least one third of all PHPT patients, but they were not associated to an increased OR. As expected, they were positively correlated with urine calcium excretion, suggesting that calcium, magnesium and citrate are commonly regulated at renal level. In conclusion, hypercalciuria, higher oxalate excretion and severe PHPT are associated with kidney stones in PHPT. Topics: Aged; Calcium; Calcium Oxalate; Cholecalciferol; Female; Humans; Hyperparathyroidism; Kidney; Kidney Calculi; Male; Middle Aged; Oxalates; Risk Factors; Severity of Illness Index | 2005 |
[Calcium needs in hemodialyzed-parathyroidectomized patients].
Parathyroidectomy changes the homeostasis of calcium balance in patients under dialysis for kidney failure. The aim of this work is to value calcium needs in 20 hemodialysed patients who underwent parathyroidectomy, in the department of nephrology of UHC Ibn Rochd of Casablanca from January 1994 to June 1999. These patients, 12 women (60%) and 8 men (40%), aged between 14 and 70 years (mean=46.10+/-13.62 years). Hungry bone syndrome was noted in 8 patients and postoperative hypocalcemia in 15 (75%). Mean minimal serum calcium was 196+/-0.21 mmol/l, with clinical signs in 6 patients. Mean calcium supplement the first postoperative week was 18.1+/-0,54 g/day in the 8 patients with hungry bone syndrome and 14.28+/-0,86 g/day in the 12 remaining patients. Between 6 and 18 months postoperatively, required calcium supplementation was 4.5 to 12 g/day in patients with hungry bone syndrome compared with 3 to 6g/day at the remaining patients. Mean serum calcium remained stable between 2.16 mmol/l to the 3(rd) month and 2.48 mmol/l to the 36(th) month. Postoperative hypocalcemia remains a major concern after parathyroidectomy requiring massive substitution with calcium and active vitamin D metabolite under close supervision to spare these patients from hypercalcemia resulting from parathyroid dysfunction. Topics: Adolescent; Adult; Aged; Calcium Carbonate; Cholecalciferol; Drug Therapy, Combination; Female; Humans; Hyperparathyroidism; Hypocalcemia; Male; Middle Aged; Parathyroidectomy; Renal Dialysis; Renal Insufficiency; Retrospective Studies; Treatment Outcome | 2002 |
Estimation and comparison of rates of change in repeated-measures studies with planned dropout.
Many repeated-measures studies are designed to compare rates of change over time in responses among treatment groups. In such studies, some responses are often censored because some individuals drop out before completing the study. The Vitamin D(3) Trial was a repeated-measures, randomized clinical trial for secondary hyperparathyroidism in hemodialysis patients in which the efficacy of vitamin D(3) infusions for suppressing the secretion of parathyroid hormone (PTH) was compared among four dose groups during dialysis over 12 weeks. In this trial some patients dropped out because the protocol stated that any individual should have been off protocol if his or her serum calcium (Ca) level exceeded 11.5 mg/dL. While the dropout mechanism for the Ca level (secondary response) corresponded to the missing at random (MAR) assumption (because whether patients dropped out or not depended only on their previously recorded Ca level), the MAR assumption for the PTH level (primary response) was not justifiable without taking into account the effect of the Ca level. We consider estimation and comparison of several estimators of mean rate of change in the presence of dropout due to the selection process inherent in a study design like the Vitamin D(3) Trial. Simulation experiments are used to compare the bias and efficiency of several estimators of mean rate of change. The estimators based on a bivariate mixed-effects model outperform all other estimators in the primary response as well as in the secondary response. These estimators are applied to the Vitamin D(3) Trial data. Topics: Cholecalciferol; Humans; Hyperparathyroidism; Linear Models; Patient Dropouts; Randomized Controlled Trials as Topic | 2001 |
[Parathyroid function after total or subtotal thyroidectomy].
Postoperative parathyroid function was evaluated in 24 total thyroidectomy and 8 subtotal thyroidectomy patients seen by our department between January 1995 and July 1997. Parathyroid function was assessed by measuring the level of serum intact parathyroid hormon (intact-PTH). Hypoparathyroidism was avoided in 23 patients (95.8%) who received a total thyroidectomy and in 7 patients (87.5%) who received a subtotal thyroidectomy. Supplementary therapy for hypoparathyroidism was not required as long as the blood supply to more than two parathyroid glands was preserved. Half of the patients in this study did not require any postoperative supplementary therapy. Thus, the preservation of more than two parathyroid glands is essential for the prevention of hypoparathyroidism. In cases where the parathyroid glands had been resected, parathyroid gland transplantation were performed. In all cases, supplementary therapy was eventually no longer required. In two cases requiring supplementary therapy, a normal range of parathyroid activity was observed 30 months after surgery. The administration of vitamin D3 may suppress the recovery of parathyroid function in patients recieving parathyroid transplantations. Topics: Biomarkers; Cholecalciferol; Humans; Hyperparathyroidism; Hypoparathyroidism; Parathyroid Glands; Parathyroid Hormone; Postoperative Care; Postoperative Complications; Thyroid Neoplasms; Thyroidectomy | 2000 |
Ratio of baseline level/maximum level of serum PTH in pseudohypoparathyroidism and primary hyperparathyroidism.
The ratio of baseline level/maximum level of serum parathyroid hormone (PTH) is high in PTH-deficient hypoparathyroidism and it decreases after vitamin D3 treatment. There is a reversed sigmoidal relationship between the ratio and baseline serum Ca level. In this study, we further investigated the value of this ratio as a parameter of Ca-dependent changes of serum PTH in hyperparathyroid subjects. As in PTH-deficient hypoparathyroidism, the ratio in pseudohypoparathyroidism was high before vitamin D3 treatment and it decreased after 1,25(OH)2D3 treatment. The increased ratio may reflect the stimulated baseline PTH secretion from parathyroid cells perceiving the decrease in baseline extracellular Ca level. The points plotting the ratio against baseline serum Ca level were on the regression curve deduced from the data in PTH-deficient hypoparathyroidism. This result indicates that the relationship between the ratio and the baseline extracellular Ca level is unrelated to the variation in maximum secretion. The sigmoidal changes of serum PTH in patients with parathyroid adenoma were classified as follows. The first was with the upward and rightward curve shift, the second was only with the rightward curve shift, and the third was with the rightward curve shift, the increased minimum serum PTH, and the increased baseline/maximum ratio of serum PTH. These findings suggest that the decreased suppressibility of PTH secretion and the stimulated baseline secretion may develop without the increase in maximum secretion in some cases with parathyroid adenoma. In conclusion, the ratio of baseline level/maximum level of serum PTH may unfold a new aspect of secretion abnormality of parathyroid glands in several forms of parathyroid disorders. Topics: Adolescent; Adult; Analysis of Variance; Calcium; Cholecalciferol; Female; Humans; Hyperparathyroidism; Male; Middle Aged; Parathyroid Hormone; Pseudohypoparathyroidism | 1998 |
Vitamin D receptors and hyperparathyroidism.
Topics: Adult; Aged; Aged, 80 and over; Cholecalciferol; Gene Frequency; Humans; Hyperparathyroidism; Japan; Middle Aged; Polymorphism, Genetic; Prevalence; Receptors, Calcitriol | 1996 |
Biochemical variables associated with bone density in patients with primary hyperparathyroidism.
To clarify the association between primary hyperparathyroidism and cortical osteopenia.. Open study.. Department of Surgery, University of Lund, Sweden.. 38 patients with primary hyperparathyroidism.. Correlation between bone density (measured by single photon absorption) and age; sex; serum concentrations of parathyroid hormone and ionised calcium; serum alkaline phosphatase activity; and serum concentration of calcium, phosphate, creatinine, urea, osteocalcin, 25 hydroxycholecalciferol, and 1,25 dihydroxycholecalciferol.. There was no difference in bone density between men and women. There was no correlation between bone density and severity of hypercalcaemia or age. No biochemical abnormality was peculiar to the seven patients whose bone density was more than two SD below the population mean. Serum concentrations of 1,25 dihydroxycholecalciferol and osteocalcin both correlated significantly with bone density (p < 0.05) and there was a strong correlation between serum osteocalcin and serum intact parathyroid hormone (p < 0.001). Serum osteocalcin had the strongest correlation with bone density of any of the biochemical variables.. There is little association between bone density and serum concentration of parathyroid hormone. Topics: Absorptiometry, Photon; Bone Density; Calcium; Cholecalciferol; Female; Humans; Hyperparathyroidism; Male; Middle Aged; Osteocalcin; Parathyroid Hormone | 1992 |
Vitamin D3 3 beta sulfate has less biological activity than free vitamin D3 during pregnancy in rats.
The biological activities of free (D3) and sulfoconjugated (SD3) vitamin D3 were compared after 6 weeks of oral administration to D-deficient (-D) female rats which were mated in the meantime. Mothers and pups were sacrificed 1-2 days following parturition and mineral and hormonal plasma status was determined in mothers and bone mineral determinations and bone histomorphometric studies performed. In newborns, plasma levels of Ca, P and 25-hydroxyvitamin D (25(OH)D) were measured. After parturition, -D mothers had decreased body weight (BW) as well as decreased plasma levels of Ca, P and 1,25-dihydroxyvitamin D (1,25(OH)2D) associated with undetectable levels of 25(OH)D. Plasma levels of immunoreactive calcitonin and parathormone, by contrast, were higher than in vitamin D-replete (+D) control mothers. Bone histomorphometric analysis showed osteomalacia and secondary hyperparathyroidism in -D mothers. After parturition, -D +SD mothers had reduced BW compared to D-treated mothers and the plasma parameters measured were abnormal. Almost all bone histomorphometric parameters were found to be intermediate between +D and -D groups without reaching values of +D mothers. By contrast, -D +D mothers had most of the bone formation parameters identical to those of +D mothers. However, bone resorption was still higher while plasma levels of P and 25(OH)D remained slightly, but significantly lower than in +D mothers. In pups, plasma Ca in both D3- and SD3-treated groups was similar to values in +D-treated rats. However, pups from SD3-treated mothers still showed plasma levels of P and 25(OH)D lower than in +D pups. In conclusion, treatment with SD3 in -D mother rats significantly improves the biochemical plasma parameters of pups, but complete normalization can be achieved only in the D3-treated group. Our results show that when administered at equal amounts, SD3 has a much lower biological activity than D3 in -D female rats and cannot therefore replace vitamin D3 particularly during pregnancy. Topics: Animals; Animals, Newborn; Body Weight; Bone and Bones; Calcifediol; Calcitriol; Calcium; Cholecalciferol; Female; Hyperparathyroidism; Osteomalacia; Parathyroid Hormone; Phosphorus; Pregnancy; Pregnancy Complications; Rats; Vitamin D Deficiency | 1985 |
[Studies on the measurement of vitamin D derivatives in human plasma. III. Plasma concentrations of vitamin D derivatives in various diseases (author's transl)].
Plasma concentrations of vitamin D3, 25-OH-D3, 24, 25(OH)2D3 and 1, 25(OH)2D3 were measured in patients with various diseases using the multiple assay system previously reported. In patients with hyperparathyroidism, the plasma levels of 1, 25(OH)2D3 tended to increase, while the levels of 24, 25(OH)2D3 tended to decrease in many cases. On the other hand, plasma 1, 25(OH)2D3 levels were low, while 24, 25(OH)2D3 levels were high in patients with hypoparathyroidism. No significant differences in the levels of plasma D3 derivatives among idiopathic-, postoperative- and pseudo- hypoparathyroidism were observed. In a majority of hemodialyzed patients with advanced renal failure who showed no overt bone changes on X-ray films, both the plasma 1, 25(OH)2D3 and 24, 25(OPH)2D3 levels were distributed from normal to very low. In a majority of patients with osteoporosis and hypoparathyroidism, plasma 1, 25(OH)2D3 levels rose quickly after the administration of 1 alpha-OH-D3. In hypophosphatemic vitamin D resistant rickets, however, the response to the relatively large amounts of 1 alpha-OH-D2 was poor, although the concentrations of plasma 24, 25(OH)2D3 were elevated by the 1 alpha-OH-D3 administration in most of these cases. The plasma 1, 25(OH)2D3 and 24, 25(OH)2D3 concentrations in patients with senile osteoporosis were distributed from lower to higher range than those of normal adults. There was a relatively good correlation between plasma levels of 25-OH-D3 and D3 only in cases with plasma D3 levels higher than 5 ng/ml. In addition, a hyperbolic regression curve was obtained between the plasma D3 and 25-OH-D3 ratio. These results may indicate that a possible negative feedback homeostatic mechanism exists between plasma levels of D3 and 25-OH-D3, but only with low plasma levels of D3. Topics: Calcitriol; Cholecalciferol; Humans; Hydroxycholecalciferols; Hyperparathyroidism; Hypoparathyroidism; Kidney Diseases; Parathyroid Diseases; Pseudohypoparathyroidism | 1982 |
[Neonatal hypocalcemia with hyperparathyroidism in the mother (author's transl)].
A report on two siblings, on formula feeding, who had fits in the second week of life. Cause of the hypocalcemic cramps was a formerly undetected hyperparathyroidism in the mother. Topics: Adult; Calcium; Cholecalciferol; Female; Humans; Hyperparathyroidism; Hypocalcemia; Infant, Newborn; Male; Phosphates | 1981 |
The multiple causes of hypercalcemia in malignant disease.
Topics: Animals; Bone Neoplasms; Cholecalciferol; Cyclic AMP; Diagnosis, Differential; Humans; Hypercalcemia; Hyperparathyroidism; Mice; Neoplasms; Paraneoplastic Syndromes; Parathyroid Hormone; Peptides | 1980 |
[Disorders of calcium metabolism].
Topics: Acid-Base Equilibrium; Adolescent; Adult; Aged; Calcitonin; Calcium; Child; Child, Preschool; Cholecalciferol; Cholesterol; Humans; Hyperparathyroidism; Hypocalcemia; Infant; Infant, Newborn; Intestinal Absorption; Middle Aged; Osteoporosis; Parathyroid Hormone; Phosphates; Tetany; Vitamin D | 1980 |
1,25-Dihydroxycholecalciferol in human serum and its relationship with other metabolites of vitamin D-3.
A competitive protein binding assay for 1,25-dihydroxycholecalciferol has been developed using the hormone's nuclear receptor protein from chick intestinal mucosa. This nuclear receptor protein can be stored at -70 degrees C for several months and bound and free hormone can be separated easily with dextran coated charcoal. Results obtained using this assay agree well with those reported by other groups of workers. Serum levels of other vitamin D-3 metabolites, namely 25-hydroxycholecalciferol and 24,25-dihydroxycholecalciferol have also been measured and are shown in relation to 1,25-(OH)2D3 levels. Topics: Animals; Cell Nucleus; Cholecalciferol; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols; Hyperparathyroidism; Intestinal Mucosa; Kidney Failure, Chronic; Kinetics; Microchemistry; Osteomalacia; Radioligand Assay; Receptors, Drug | 1979 |
Progressive renal bone disease--an assessment of long-term therapy with vitamin D analogues.
Topics: Adult; Bone and Bones; Bone Diseases, Metabolic; Calcium; Cholecalciferol; Female; Humans; Hyperparathyroidism; Kidney Failure, Chronic; Male; Renal Dialysis; Vitamin D Deficiency | 1979 |
[Parathyroid and C-cell function in normocalcemic hypercalcuria].
Topics: Adolescent; Adult; Aged; Calcitonin; Calcium; Cholecalciferol; Female; Humans; Hyperparathyroidism; Hypocalcemia; Intestinal Absorption; Kidney Tubules; Male; Middle Aged; Parathyroid Glands; Parathyroid Hormone; Phosphorus; Urinary Calculi | 1977 |
Osteomalacia associated with increased renal tubular resorption of phosphate (hypohyperparathyroidism).
Topics: Child; Cholecalciferol; Female; Humans; Hyperparathyroidism; Hypocalcemia; Osteomalacia; Phosphates | 1976 |
[Osteomalacia and antiepileptic drugs: study on the pathogenesis].
Severe osteomalacia with secondary hyperparathyroidism was observed in a 19-year-old mentally retarded girl, who had been treated for several years with antiepileptic drugs. Vitamin D3 orally administered in low doses led to complete reversal of all symptoms and normalization of blood chemistry, X-ray pictures demonstrated healing of all lesions. It is suggested that the alterations of vitamin-D metabolism occuring during the administration of phenobarbital and hydantion are of importance only in patients with an already lowered intake of vitamin D3 or reduced exposure to ultraviolet rays. Topics: Adult; Anticonvulsants; Bicarbonates; Blood Proteins; Calcium; Cholecalciferol; Cholesterol; Creatinine; Female; Fractures, Bone; Hematocrit; Hemoglobins; Humans; Hyperparathyroidism; Osteomalacia; Vitamin B 12 | 1975 |
Vitamin D-dependent rickets: actions of parathyroid hormone and 25-hydroxycholecalciferol.
Topics: Adenosine Monophosphate; Adolescent; Alkaline Phosphatase; Amino Acids; Bone and Bones; Child; Child, Preschool; Cholecalciferol; Creatinine; Digestive System; Dihydrotachysterol; Humans; Hydroxycholecalciferols; Hyperparathyroidism; Hypocalcemia; Kidney; Male; Parathyroid Hormone; Rickets; Vitamin D | 1972 |
Calcium and the nervous system.
Topics: Adenylyl Cyclases; Anticonvulsants; Calcitonin; Calcium; Cholecalciferol; Cyclic AMP; Diagnosis, Differential; Humans; Hydroxycholecalciferols; Hypercalcemia; Hyperparathyroidism; Osteitis Deformans; Osteitis Fibrosa Cystica; Osteomalacia; Parathyroid Hormone; Pseudohypoparathyroidism; Radioimmunoassay; Thyroid Neoplasms | 1972 |
Hypo-hyperparathyroidism.
Topics: Adolescent; Body Height; Bone Diseases; Calcium; Child; Cholecalciferol; Diagnosis, Differential; Female; Humans; Hyperparathyroidism; Hypocalcemia; Hypoparathyroidism; Phosphorus Metabolism Disorders; Tetany | 1968 |