cholecalciferol and Hypoparathyroidism

Hypoparathyroidism (HypoPT) is a rare endocrine disorder characterized by the absence or insufficient parathyroid hormone production resulting in chronic hypocalcemia. Complications of HypoPT include perturbation of several target organs. The conventional treatment consists of the administration of active vitamin D, namely calcitriol. Regarding vitamin D status, few data are available, mostly in HypoPT subjects supplemented with parent vitamin D. In addition, perturbation of vitamin D metabolism has been poorly investigated, as well as the contribution of altered vitamin D status on the clinical expression of the disease. The most recent consensus on the management of chronic HypoPT suggests the baseline evaluation of serum 25-hydroxy-vitamin D [25(OH)D] and supplementation with parent vitamin D with the aim to achieve and maintain serum 25(OH)D levels in the range of 30-50 ng/mL. The rationale for using supplementation with parent vitamin D (either ergocalciferol or cholecalciferol) in HypoPT would be to provide sufficient 25(OH)D substrate to the residual 1-α-hydroxylase activity, thus ensuring its conversion to active vitamin D in renal and extra-renal tissues. More data from experimental and clinical studies are needed for better assessing how these mechanisms may significantly influence metabolic control in HypoPT and eventually skeletal and extra-skeletal manifestation of the disease. Finally, future data will clarify how the currently available parent vitamin D compounds (ergocalciferol, cholecalciferol, calcifediol) would perform in addressing these specific issues.

Topics: Calcifediol; Calcitriol; Cholecalciferol; Ergocalciferols; Humans; Hypoparathyroidism; Parathyroid Hormone; Vitamin D; Vitamin D Deficiency; Vitamins

Isolated and acquired hypoparathyroidism occurs as an autoimmune disorder either alone or in association with other autoimmune diseases. Reduced PTH (parathyroid hormone) secretion due to disorder of Ca-sensing regulation in parathyroid gland is most commonly caused by activating mutations of the CaSR (Ca-sensing receptor) gene. There has been accumulating evidence that it also occurs as a result of activating autoantibodies directed to CaSR. Hypoparathyroidism is one of the most common endocrine manifestation in APECED (Autoimmune Polyendocrinopathy-Candidiasis-Ectodermal Dystrophy) , which is also known as APS (Autoimmune Polyendocrinopathy Syndrome) type I . In APECED, the spectrum of epitope responsible for the hypoparathyroidism is presumably CaSR. It remains unclear how autoimmunity against CaSR occurs and how much patients caused by this disorder exist.

Topics: Autoantibodies; Autoimmune Diseases; Cholecalciferol; Humans; Hypoparathyroidism; Polyendocrinopathies, Autoimmune; Receptors, Calcium-Sensing

Topics: AIRE Protein; Autoimmunity; Calcium; Cholecalciferol; Diagnosis, Differential; GATA3 Transcription Factor; Humans; Hypoparathyroidism; Mutation; Nuclear Proteins; Parathyroid Hormone; Prognosis; Receptors, Calcium-Sensing; Transcription Factors

Topics: Cholecalciferol; Diagnosis, Differential; DNA-Binding Proteins; High Mobility Group Proteins; Humans; Hypoparathyroidism; Magnesium Deficiency; Mutation; Nuclear Proteins; Parathyroid Hormone; Prognosis; SOXB1 Transcription Factors; Transcription Factors

Topics: Cholecalciferol; Humans; Hypocalcemia; Hypoparathyroidism; Mental Disorders; Neuromuscular Diseases; Parathyroid Hormone

Topics: Autoantibodies; Calcium-Binding Proteins; Cholecalciferol; Diagnosis, Differential; Humans; Hypoparathyroidism; Parathyroid Hormone

The term vitamin D is generally used to describe a number of chemically related compounds with common antirachitic properties, but which have differences in the rapidity of their action, the way they are produced in the body, and the conditions under which their results are optimal. Ergocalciferol, cholecalciferol, 25-hydroxycholecalciferol (calcifediol), dihydrotachysterol, 1 alpha-hydroxycholecalciferol (alfacalcidol), and 1,25-dihydroxycholecalciferol (calcitriol) are currently the most commonly used vitamin D metabolites. In man, cholecalciferol produced on the skin and the fraction obtained from the diet in the gastrointestinal tract are converted in the liver to 25-hydroxycholecalciferol and then in the kidney to 1,25-dihydroxycholecalciferol. The demonstration of these metabolic pathways has helped to elucidate the aetiology of such conditions a hepatobiliary osteodystrophy, drug-induced anticonvulsant osteomalacia, the hypocalcaemia of hypoparathyroidism and above all azotaemic osteodystrophy. In the therapy of azotaemic osteodystrophy, the period of 'vitamin D resistance' when large doses of vitamin D2 and D3 had to be used is now over, and these patients can be efficiently and successfully treated with almost physiological doses of 1 alpha-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol. Attention to diet, calcium supplements and oral phosphate binders are also important. During repetitive haemodialysis, the above principles still hold true, but in some of these patients an osteomalacic syndrome resistant to 1,25-dihydroxycholecalciferol has been recognised. These patients readily become hypercalcaemic when given 1,25-dihydroxycholecalciferol and their fractures and osteomalacia do not improve. Aluminium intoxication, possibly related to the use of impure dialysis fluid, is currently thought to be the most likely explanation of this dialysis osteomalacic syndrome.

Topics: Bone Diseases; Cholecalciferol; Ergocalciferols; Humans; Hypoparathyroidism; Vitamin D

A rapidly growing understanding of the biochemical and physiological processes that underlie the metabolism of vitamin D has provided new insights into the pathogenesis of oestomalacia. Many of the vitamin D--resistant osteomalacia syndromes can now be explained on the basis of defects in the metabolic conversion of vitamin D to the biologically active dihydroxylated metabolite 1,25(OH)2D and perhaps, in some instances, to impairement of the actions of 1,25(OH)2D on target tissues. The availability of this new information has made possible the synthesis of 1-hydroxylated forms of the vitamin for therapeutic use in states of vitamin D resistance. Although many questions regarding the pathogenesis and most effective approaches in the management of osteomalacia remain unanswered, considerable progress has been made in this direction as a result of continued research on the subject.

Topics: Bone Neoplasms; Chemical Phenomena; Chemistry; Cholecalciferol; Dihydroxycholecalciferols; Ergocalciferols; Giant Cell Tumors; Humans; Hydroxycholecalciferols; Hypoparathyroidism; Hypophosphatemia, Familial; Kidney Failure, Chronic; Metabolism, Inborn Errors; Nephrectomy; Osteomalacia; Phosphates; Pseudohypoparathyroidism; Vitamin D; Vitamin D Deficiency

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

Topics: Bone and Bones; Bone Diseases; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Hydroxycholecalciferols; Hypoparathyroidism; Hypophosphatemia, Familial; Kidney; Liver Cirrhosis; Parathyroid Hormone; Phosphates; Protein Precursors; Pseudohypoparathyroidism; Vitamin D

Topics: Adrenal Cortex Hormones; Animals; Anticonvulsants; Bone and Bones; Calcium; Carrier Proteins; Cholecalciferol; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols; Hypocalcemia; Hypoparathyroidism; Hypophosphatemia, Familial; Intestinal Absorption; Kidney; Kidney Failure, Chronic; Kidney Tubules; Liver; Mixed Function Oxygenases; Parathyroid Hormone; Phosphorus; Vitamin D; Vitamin D Deficiency

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

Topics: Acute Kidney Injury; Animals; Bone Diseases; Calcium; Cholecalciferol; Deficiency Diseases; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols; Hypoparathyroidism; Kidney; Kidney Transplantation; Nephrectomy; Phosphorus; Rickets; Structure-Activity Relationship; Vitamin D

Topics: Anticonvulsants; Bone and Bones; Bone Diseases; Calcium; Cell Membrane Permeability; Cholecalciferol; Cholesterol; Ergocalciferols; Gastrointestinal Diseases; Humans; Hypoparathyroidism; Hypophosphatemia, Familial; Intestinal Mucosa; Kidney; Kidney Failure, Chronic; Parathyroid Hormone; Sarcoidosis; Skin; Vitamin D

Topics: Animals; Biological Transport; Bone Development; Bone Diseases; Calcification, Physiologic; Calcium; Cholecalciferol; Fanconi Syndrome; Humans; Hypoparathyroidism; Intestinal Absorption; Kidney; Liver; Rats; Rickets; Uremia; Vitamin D; Vitamin D Deficiency

Topics: Acetates; Calcium; Calcium Chloride; Calcium Phosphates; Cholecalciferol; Citrates; Dihydrotachysterol; Ergocalciferols; Gluconates; Humans; Hypoparathyroidism; Lactates; Magnesium; Parathyroid Hormone; Potassium; Salicylates; Thiosulfates; Vitamin D

Vitamin D deficiency has potential roles in breast cancer etiology and progression. Vitamin D deficiency has also been associated with increased toxicity from bisphosphonate therapy. The optimal dose of vitamin D supplementation is unknown, but daily sunlight exposure can generate the equivalent of a 10,000-IU oral dose of vitamin D(3). This study therefore aimed to assess the effect of this dose of vitamin D(3) in patients with bone metastases from breast cancer.. Patients with bone metastases treated with bisphosphonates were enrolled into this single-arm phase 2 study. Patients received 10,000 IU of vitamin D(3) and 1000 mg of calcium supplementation each day for 4 months. The effect of this treatment on palliation, bone resorption markers, calcium metabolism, and toxicity were evaluated at baseline and monthly thereafter.. Forty patients were enrolled. No significant changes in bone resorption markers were seen. Despite no change in global pain scales, there was a significant reduction in the number of sites of pain. A small but statistically significant increase in serum calcium was seen, as was a significant decrease in serum parathyroid hormone. Treatment unmasked 2 cases of primary hyperparathyroidism, but was not associated with direct toxicity.. Daily doses of 10,000 IU vitamin D(3) for 4 months appear safe in patients without comorbid conditions causing hypersensitivity to vitamin D. Treatment reduced inappropriately elevated parathyroid hormone levels, presumably caused by long-term bisphosphonate use. There did not appear to be a significant palliative benefit nor any significant change in bone resorption.

Topics: Adult; Aged; Aged, 80 and over; Biomarkers; Bone Neoplasms; Bone Resorption; Breast Neoplasms; Cholecalciferol; Dietary Supplements; Diphosphonates; Female; Humans; Hypoparathyroidism; Middle Aged; Pain

Although there have been some case reports suggesting that bone in patients with pseudohypoparathyroidism (PHP) might respond to parathyroid hormone (PTH), no information is available as to whether serum PTH concentration is related to bone metabolic markers or to bone mineral density (BMD) in PHP.. To address these relationships, by comparing intact serum PTH, bone metabolic markers and BMD in patients with PHP with those in patients with idiopathic hypoparathyroidism (IHP) and postoperative hypoparathyroidism (OHP).. Intact serum PTH, bone metabolic markers (osteocalcin, tartrate-resistant acid phosphatase, pyridinoline, deoxypyridinoline) and BMD by dual-energy X-ray absorptiometry or single-photon absorptiometry were measured in patients with PHP Ia (n=2) and PHP Ib (n=8). The results were compared with those in patients with IHP (n=5) and OHP (n=14).. All bone metabolic markers measured were present in significantly greater amounts in patients with PHP Ib than in those with IHP+OHP. The Z score (standard deviation of average BMD at each age) of the BMD of femoral neck was significantly lower in patients with PHP Ib than in those with IHP+OHP. The Z scores of BMD of lumbar spine and radius were also lower in patients with PHP Ib than in those with IHP+OHP, but the difference was not significant. Moreover, the intact serum PTH concentrations were significantly and positively related to bone metabolic marker levels in all patients, and the intact serum PTH concentrations were significantly and negatively related to BMD of lumbar spine in PHP patients.. These results suggest that PTH stimulates bone turnover in PHP Ib patients, resulting in a relatively lower BMD in PHP Ib patients than in IHP+OHP patients. The present study indicates that bones of most cases of PHP could respond to PTH.

Topics: Acid Phosphatase; Adult; Aged; Amino Acids; Biomarkers; Bone Density; Cholecalciferol; Creatinine; Cyclic AMP; Erythrocyte Membrane; Female; GTP-Binding Protein alpha Subunits, Gs; Humans; Hypoparathyroidism; Isoenzymes; Kidney; Male; Middle Aged; Osteocalcin; Parathyroid Hormone; Phosphates; Postoperative Complications; Pseudohypoparathyroidism; Tartrate-Resistant Acid Phosphatase

Activating mutations of the calcium-sensing receptor (CaR) can cause isolated hypoparathyroidism. Treatment of hypocalcemia in these patients remains to be optimized, because the use of 1-hydroxylated vitamin D3 derivatives can cause hypercalciuria and nephrocalcinosis. We identified activating CaR mutations in 8 (42%) of 19 unrelated probands with isolated hypoparathyroidism. The severity of hypocalcemic symptoms at diagnosis was independent of age, mutation type, or mode of inheritance but was related to the degree of hypocalcemia; serum Ca was 1.97 +/- 0.08, 1.82 +/- 0.14, and 1.54 +/- 0.22 mmol/liter, respectively, in asymptomatic (n = 7), mildly symptomatic (n = 8), and severely symptomatic patients (n = 6). Hypocalcemia segregated with the CaR mutation, but no phenotype-genotype relationships were identified. Fourteen patients received regular 1-hydroxylated vitamin D3 treatment (mean duration, 7.2 +/- 4.9 yr). Nine had hypercalciuric episodes, which were associated with nephrocalcinosis in eight cases. Serum Ca during treatment predicted hypercalciuria and nephrocalcinosis poorly, because either or both of the latter could develop in hypocalcemic patients. Thus, mutational analysis of the CaR gene should be considered early in the work-up of isolated hypoparathyroidism. Treatment options should be weighed carefully in patients with serum Ca below 1.95 mmol/liter. The risk of nephrocalcinosis during treatment can be minimized by carefully monitoring urinary Ca excretion.

Topics: Aging; Amino Acid Substitution; Calcium; Cholecalciferol; DNA Mutational Analysis; Female; Humans; Hypocalcemia; Hypoparathyroidism; Male; Middle Aged; Nephrocalcinosis; Parathyroid Hormone; Pedigree; Receptors, Calcium-Sensing; Receptors, Cell Surface; Reverse Transcriptase Polymerase Chain Reaction; Treatment Outcome

Topics: Adolescent; Cholecalciferol; Clinical Trials as Topic; Dihydrotachysterol; Drug Evaluation; Female; Humans; Hypoparathyroidism; Male

In order to clarify the mechanisms of thiazide diuretic-induced hypocalciuria, the effect of a thiazide was studied for 7 days in seven patients with hypoparathyroidism on Vitamin D and one on calcium infusion, and seven euparathyroid patients with hypercalciuria. In the control group, calcium excretion (mg/24 hr) fell by 44% from 415 to 232 within 4 days and remained at this level. Plasma total calcium corrected for total protein did not change. In the hypoparathyroid group, calcium excretion fell by 11% from 351 to 311 and then returned to the base line level. Plasma total calcium (mg/100 ml) increased from 10.09 to 10.88, 11.29 and 10.77 at the end of the 2nd, 4th, and 7th day of thiazide administration. In the patient having i.v. calcium and no Vitamin D, neither plasma nor urinary calcium changed significantly. In both groups sodium excretion increased on the first 2 days and fell to or below base line level thereafter. Urinary phosphate, magnesium, and potassium increased, plasma phosphate rose, and magnesium and potassium fell. It is concluded that: (a) The hypocalciuric effect of thiazides requires the presence of parathyroid hormone and is not solely a result of sodium depletion. (b) The hypercalcemic effect of thiazides in hypoparathyroidism is due to increased release of calcium from bone and requires the presence of a pharmacologic dose of Vitamin D. (c) Thiazides enhane the action of parathyroid hormone on bone and kidney; Vitamin D can replace parathyroid hormone in this interaction in bone but not in kidney.

Topics: Adult; Aged; Bone and Bones; Calcium; Chlorothiazide; Cholecalciferol; Clinical Trials as Topic; Dihydrotachysterol; Drug Interactions; Ergocalciferols; Female; Humans; Hypoparathyroidism; Kidney Tubules; Magnesium; Male; Methyclothiazide; Middle Aged; Natriuresis; Parathyroid Hormone; Phosphates; Potassium; Urinary Calculi; Vitamin D

Hypoparathyroidism occurs due to insufficient parathyroid gland activity leading to abnormal calcium and phosphate levels. The presentation of hypoparathyroidism is rare in adults and mostly encountered in the paediatric population. We present a case of a 3.5-month-old male infant with the presenting complaint of an episode of afebrile generalized tonic-clonic seizure. Haematological, urinary, cerebro-spinal fluid and radiological investigations were unremarkable but a biochemical profile revealed hypocalcaemia, hyperphosphataemia and lowered vitamin D3 levels. Parathyroid hormone profile showed a decreased level, confirming diagnosis of hypoparathyroidism. Intravenous administration of calcium and magnesium in combination with oral activated vitamin D3 and phosphate binders managed to resolve symptoms and maintain normal levels. The rationale of this case is to confirm the necessity of early diagnosis to prevent irreversible sequelae of hypocalcaemia and regular monitoring of treatment to avoid side-effects of medication.

Topics: Calcium; Cholecalciferol; Humans; Hypocalcemia; Hypoparathyroidism; Infant; Male; Parathyroid Hormone; Phosphates

To describe the clinical presentation and outcome of a dog with primary hypoparathyroidism secondary to cervical bite wounds.. A 3-year-old male intact Chihuahua presented after being attacked by a large breed dog. The dog sustained severe cervical lacerations, exposing the trachea and jugular veins. A portion of the right thyroid gland was missing. The dog was stabilized before wound debridement and closure. Ionized calcium concentrations were within reference range at the time of presentation. Forty-eight hours after the initial trauma, the dog was presented in lateral recumbency with signs of hypovolemic shock, muscle tremors, and hyperthermia. Bloodwork showed severe ionized hypocalcemia with low normal parathyroid hormone concentration consistent with acute primary hypoparathyroidism. The dog was managed initially with IV calcium gluconate and calcitriol, then long-term oral calcium carbonate and vitamin D3. After 6 months, the dog was successfully weaned off calcium supplementation.. This is the first described case of traumatic primary hypoparathyroidism after a bite injury to the neck in a dog.

Topics: Animals; Bites and Stings; Calcium; Calcium Gluconate; Cholecalciferol; Dog Diseases; Dogs; Female; Humans; Hypocalcemia; Hypoparathyroidism; Male; Parathyroid Hormone; Wounds and Injuries

Calcium and vitamin D treatment does not improve reduced quality of life (QOL) in hypoparathyroidism. Recombinant human (rh) PTH(1-84) therapy improves QOL metrics for up to 5 years. Data on QOL beyond this time point are not available.. To evaluate the effects of 8 years of rhPTH(1-84) therapy on QOL and factors associated with long-term benefit.. Prospective, open-label trial.. Referral center.. Twenty patients with hypoparathyoidism.. RAND 36-Item Short Form Health Survey (SF-36).. rhPTH therapy led to substantial improvement in five of the eight SF-36 domains [vitality, social functioning (SF), mental health (MH), bodily pain (BP) and general health] and three of these domains (SF, MH, BP) were no longer lower than the reference population. The improvement in the mental component summary (MCS) score was sustained through 8 years, while the physical component summary (PCS) score improved through 6 years. A lower baseline QOL score was associated with greater improvement. A threshold value <238 (MCS) and <245 (PCS) predicted long-term improvement in 90% and 100% of the cohort, respectively. In patients whose calcium supplementation was reduced, MCS and PCS scores improved more than those whose supplementation did not decline to the same extent. Improvement in PCS was greater in patients whose calcitriol dosage was reduced and duration of disease was shorter.. rhPTH(1-84) improves long-term well-being in hypoparathyroidism. The improvements are most prominent in those with impaired SF-36 at baseline and those whose requirements for conventional therapy decreased substantially.

Topics: Adult; Aged; Calcitriol; Calcium; Calcium-Regulating Hormones and Agents; Cholecalciferol; Ergocalciferols; Female; Humans; Hypoparathyroidism; Longitudinal Studies; Male; Middle Aged; Parathyroid Hormone; Prospective Studies; Quality of Life; Recombinant Proteins; Treatment Outcome; Vitamin D

We here report the case of a 38-year old woman with dilated cardiomyopathy induced by hypocalcaemia secondary to hypoparathyroidism. The patient had low calcium level (30 mg/L) and echocardiography showed dilated-hypokinetic cardiomyopathy with reduced left ventricular ejection fraction (31.4%). She received calcitherapy associated with vitamin D3 and her evolution was marked by the normalization of the size of the cardiac cavities and of the left ventricular ejection fraction after normocalcemia.

Topics: Adult; Calcium; Cardiomyopathy, Dilated; Cholecalciferol; Female; Humans; Hypocalcemia; Hypoparathyroidism; Stroke Volume; Thyroidectomy; Treatment Outcome

Topics: Biomarkers; Calcium; Cholecalciferol; Dietary Supplements; Female; Humans; Hyperparathyroidism, Primary; Hypocalcemia; Hypoparathyroidism; Infant, Newborn; Infant, Newborn, Diseases; Male; Pregnancy; Recurrence; Risk Factors; Seizures; Tetany; Time Factors; Treatment Outcome

Topics: Agammaglobulinemia; Autoimmune Diseases; Autoimmunity; B-Lymphocytes; Bacterial Infections; Calcium; Cholecalciferol; Electrolytes; Female; Humans; Hypocalcemia; Hypokalemia; Hypoparathyroidism; Hypophosphatemia; Immunoglobulins, Intravenous; Immunologic Deficiency Syndromes; Magnesium; Middle Aged; Thymoma; Weight Loss

Hypercalcemia associated with lymphomas can be secondary to increased calcitriol [1,25(OH)2 vitamin D3], PTHrP, or osteolytic metastases.. A case of calcitriol-mediated hypercalcemia secondary to non-Hodgkin lymphoma in a patient with postsurgical hypoparathyroidism is presented.. Single patient managed at a tertiary health care facility in the United States.. A 55-year-old white woman had a total thyroidectomy and radioiodine ablation for a 3.5-cm follicular carcinoma. Surgery was complicated by permanent hypoparathyroidism treated with calcium, calcitriol, and cholecalciferol. For over 16 years she had no evidence of either residual thyroid tissue in the neck or metastasis. Her corrected serum calcium levels were appropriately maintained in the low-normal range. During a routine clinic visit, she had mild hypercalcemia; calcium and cholecalciferol were reduced by 50%, while calcitriol was continued. Two weeks later, she presented with nausea, abdominal pain, and multiple rapidly enlarging cervical and axillary lymph nodes with elevated calcium and calcitriol. A fluorine-18 fluorodeoxyglucose positron emission tomography/computed tomography scan and lymph node biopsy were diagnostic for non-Hodgkin lymphoma.. Calcium and calcitriol were stopped; hypercalcemia was corrected with iv fluids. Chemotherapy resulted in an excellent response within 7 weeks; calcitriol normalized, and the patient developed recurrent hypocalcemia. Positron emission tomography/computed tomography scans at 7 weeks and 3 months after treatment documented near-complete resolution of the lesions. Outcome and Result: Sixteen months after the treatment of lymphoma, the patient remains free of disease and is on calcium, calcitriol, and cholecalciferol.. Clinicians should have a high index of suspicion for malignancy when patients presents with rapid and high elevations of serum calcium.

Topics: Adenocarcinoma, Follicular; Calcitriol; Calcium; Cholecalciferol; Female; Humans; Hypercalcemia; Hypocalcemia; Hypoparathyroidism; Lymphoma, Non-Hodgkin; Middle Aged; Thyroid Neoplasms; Thyroidectomy; Treatment Outcome

Long-term management of patients with differentiated thyroid cancer (DTC) commonly includes TSH-suppressive therapy with L-T4 and, in case of postsurgical hypoparathyroidism, Calcium-D3 supplementation, both of which may affect skeletal health. Experience with female patients treated for DTC at a young age and who were then receiving long-term therapy with L-T4 and Calcium-D3 medication is very limited to date. This cross-sectional study set out to investigate effects of Calcium-D3 supplementation and TSH-suppressive therapy on bone mineral density (BMD) in 124 young female patients treated for DTC at a mean age of 14 years and followed-up for an average of 10 years. BMD was found to be significantly higher in patients receiving Calcium-D3 medication than in patients not taking supplements. The level of ionized calcium was the strongest factor determining lumbar spine BMD in patients not receiving Calcium-D3 supplementation. Pregnancy ending in childbirth and HDL-cholesterol were associated with a weak adverse effect on spine and femoral BMD. No evidence of adverse effects of L-T4 and of radioiodine therapies on BMD was found. We conclude that Calcium-D3 medication has a beneficial effect on BMD, and that TSH-suppressive therapy does not affect BMD in women treated for DTC at young age, at least after 10 years of follow-up.

Topics: Adolescent; Bone Density; Bone Density Conservation Agents; Bone Resorption; Calcium, Dietary; Chernobyl Nuclear Accident; Cholecalciferol; Combined Modality Therapy; Cross-Sectional Studies; Dietary Supplements; Female; Follow-Up Studies; Hormone Replacement Therapy; Humans; Hypoparathyroidism; Incidence; Iodine Radioisotopes; Neoplasms, Radiation-Induced; Postoperative Complications; Radiopharmaceuticals; Republic of Belarus; Risk Factors; Thyroid Neoplasms; Thyroidectomy; Thyroxine

To assess the efficacy and safety of a single administration of vitamin D3 for postoperative hypoparathyroidism.. Twelve patients with postoperative hypoparathyroidism were enrolled for this study. They had taken calcium and vitamin D3 orally after the surgery and had shown no symptoms of hypoparathyroidism. Then, all patients had changed their regimen to a single administration of vitamin D3 (1α(OH)D3) with monitoring of serum calcium, urine calcium (u-Ca) and creatinine (u-Cre). The dose of vitamin D3 was started at 2.0μg/day and appropriately adjusted to maintain the ratio of u-Ca and u-Cre (u-Ca/u-Cre) at less than 0.3. The physical findings were carefully checked and the serum intact-parathyroid was also estimated. Those data and physical findings were monitored for at least two years.. The maintenance dose of vitamin D3 varied from 0.5 to 3.5μg/day, and the mean dose was 2.04μg/day. All patients tolerated changes of regimen without any symptoms of hyper-/hypocalcemia.. A single administration of vitamin D3 is not only safe but also an easy and cost-effective regimen. This also makes drug control easy and worthwhile both for patients and clinicians.. 2c.

Topics: Adult; Aged; Cholecalciferol; Cohort Studies; Female; Humans; Hypoparathyroidism; Hypopharyngeal Neoplasms; Laryngeal Neoplasms; Male; Middle Aged; Parathyroidectomy; Prospective Studies; Thyroid Neoplasms; Thyroidectomy; Treatment Outcome; Vitamins

Fahr's syndrome is a rare disorder characterized by abnormal deposits of calcium in areas of the brain that control movement, including the basal ganglia and the cerebral cortex associated with many neurological and psychiatric abnormalities such as a rigid hypokinetic syndrome, mood disorders and cognitive impairment. Fahr's syndrome is secondary to some disorders, such as hypoparathyroidism.. We report the case of a 56 year-old man, with a history of cataract, who was admitted to our psychiatric hospital for the first time in his life because of psychotic symptoms associated with irritability and aggressiveness. Since the age of 38 the patient had become nervous, 10 years later he developed tonic-clonic seizures. Two months ago, he began expressing delusions of persecution against his wife and sons and making fugues. According to his family during this period, he was agitated, aggressive, and suffered from insomnia and anorexia. The general and psychiatric examination showed an upright and bronzed patient with neglected hygiene. He was indifferent to his environment and expressed poor mimics and gestures. He was anxious, suspicious and not very talkative. He was conscious but his attention was slightly decreased. Moreover, he was not aware of his problems. The neurological examination showed extrapyramidal syndrome with postural tremor and cerebellar ataxia. A cranial computed tomography brain scan found bilateral, symmetric basal ganglia calcifications, in favour of Fahr's syndrome. Phosphocalcic investigations revealed low concentration of serum calcium at 1.01mmol/L (normal 2.15 to 2.57mmol/L) and hyperphosphoremia at 2.69mmol/L (normal 0.81 to 1.55mmol/L). He also had low concentrations of 25-OH vitamin as well as decreased urinary levels of phosphate and calcium. The blood level of parathyroid hormone was 0ng/L. The diagnosis of Fahr's syndrome, revealing a hypoparathyroidism was posed. He was supplemented with calcium and alpha cholecalciferol and treated with clozapine (100mg per day). After four weeks, psychotic symptoms responded well to this treatment without expressing any side effects, notably seizures.. Psychotic symptoms seen in Fahr's disease include auditory and visual hallucinations, complex perceptual distortions, delusions, and fugue state. Some of them were manifest in this patient. It is likely that the psychosis in both Fahr's disease and schizophrenia share a similar pathology. Positive psychotic symptoms, hallucinations, and paranoia are not necessarily generated by the classical hypothesis of dopamine-mediated attachment of salience to internally generated stimuli. Still, there is some evidence that disruption of the cortex involved in the pathophysiology of schizophrenia is also seen in Fahr's disease, particularly in areas of the limbic system.. Psychiatrists should consider Fahr's syndrome as a differential diagnosis in the evaluation of psychosis associated with seizures. This case, along with others in the literature, further emphasizes the importance of the role of neuro-imaging and the search for disrupted phosphocalcic metabolism in patients with atypical psychotic symptoms. Moreover, further research should focus on pharmacologic interventions. The efficacy and risks of neuropharmacologic and psychopharmacologic interventions in Fahr's syndrome, and correlates of good and poor outcome with these interventions remain to be defined.

Topics: Basal Ganglia; Basal Ganglia Diseases; Brain Diseases; Calcinosis; Calcium; Cholecalciferol; Clozapine; Humans; Hypoparathyroidism; Male; Middle Aged; Neurocognitive Disorders; Neurodegenerative Diseases; Tomography, X-Ray Computed

A 55 years old man was extubated on first postoperative day following coronary artery bypass grafting at 7:30 am. The same day at 5 pm, he became drowsy but arousable only on painful stimuli with severe generalized hypertonia and bilateral upgoing plantars. He was reventilated and a provisional diagnosis of cerebrovascular accident was made. CT scan of brain was normal except for bilateral basal ganglia calcification. On further investigations, he was found to be severely hypocalcaemic due to hypoparathyroidism. All symptoms resolved on the treatment of his hypocalcaemia. There was no history of neck surgery in this patient and the case additionally highlights important interaction between parathyroid hormone (PTH) in calcium metabolism.

Topics: Cholecalciferol; Coronary Angiography; Coronary Artery Bypass; Humans; Hypocalcemia; Hypoparathyroidism; Male; Middle Aged; Parathyroid Hormone; Postoperative Complications; Severity of Illness Index; Treatment Outcome

Wilson's disease (WD) is not as rare as once believed, and has a wide range of presentations with equally wide range of age of onset. Sometimes the primary presentation might be unusual and may require a thorough investigation to avoid a misdiagnosis. Our case presented with uncontrolled seizures, severe hypokalemia, renal failure, and hypoparathyroidism. After being diagnosed as WD and treated for the same patient made a remarkable recovery.

Topics: Adolescent; Cholecalciferol; Hepatolenticular Degeneration; Humans; Hypocalcemia; Hypokalemia; Hypoparathyroidism; Renal Insufficiency; Seizures; Treatment Outcome; Vitamins; Zinc Acetate

A 56-year-old patient with postsurgical hypothyroidism and hypoparathyroidism associated with gastrointestinal malabsorption syndrome was prescribed with L: -thyroxine and 1alpha(OH)D(3) at a massive daily dosage of 600 and 39 mug, respectively. Although the patient became nearly euthyroid, she had been hypocalcemic, requiring frequent intravenous injection of calcium gluconate to prevent tetany. Because the serum level of 1,25(OH)(2)D hardly increased after an oral intake of 21 microg 1alpha(OH)D(3), vitamin D(3) was administered intramuscularly. After stoss therapy (600,000 IU), the patient has been receiving 300,000 IU vitamin D(3) at intervals of 2-4 months so that she remained slightly hypocalcemic (7-8 mg/dl). At 1.5 years later, serum levels of 25(OH)D and 1,25(OH)(2)D were maintained at about 60 ng/ml and 30-50 pg/ml, respectively, and renal function was maintained well. These data suggest that intramuscular injection of 300,000 IU vitamin D(3) at an interval of a few months to maintain a slightly increased serum level of 25(OH)D and a slightly decreased serum level of calcium is a safe and cost-effective treatment in such a parathyroid hormone-deficient hypoparathyroid patient with malabsorption syndrome.

Topics: Abdomen; Cholecalciferol; Female; Graves Disease; Humans; Hypocalcemia; Hypoparathyroidism; Hypothyroidism; Injections, Intramuscular; Malabsorption Syndromes; Middle Aged; Reoperation; Thyroidectomy; Treatment Outcome

Concurrent vitamin D(3) deficiency is common in primary hyperparathyroidism (pHPT). We aimed to examine the clinicopathologic features and short-term outcomes of vitamin D(3)-deficient patients after minimally invasive parathyroidectomy (MIP).. Over 2-year period, 80 consecutive MIP patients had preoperative-fasting 25-hydroxyvitamin D(3) (25OHD(3)) checked. Forty-five patients had a 25OHD(3) level <20 ng/ml and were defined as deficient. Intraoperative parathyroid hormone (IOPTH) assay was used for all MIP. Postoperative adjusted calcium (Ca) was checked at 6, 16 (with intact PTH), and 24 h. Oral calcium and vitamin D supplements were given if hypocalcemic symptoms developed or Ca < 2.00 mmol/l. Late-onset hypocalcemia (LOH) was defined as symptoms developed after 24 h.. Both deficient and nondeficient groups had similar demographic data and bone density scores. The deficient group had significantly higher PTH (190 vs. 121 pg/ml, p = 0.015). Although IOPTH in the deficient group were higher at induction and 0 min after excision, the percentage drop from induction to 10 min after excision was similar. Ca was similar at 6 and 16 h in the two groups but was significantly lower in the deficient group at 24 h (2.10 vs. 2.45 mmol/l, p = 0.033). At 1 week, the proportion of LOH was significantly higher in the deficient group (12/42 vs. 3/34, p = 0.043) and in those with preoperative PTH > 100 pg/ml (15/57 vs. 0/19, p = 0.013).. Vitamin D(3) deficiency was associated with a higher preoperative PTH level and a greater risk of LOH after MIP. However, the likely cause of LOH remains unclear as both low preoperative vitamin D(3) and high PTH levels could be responsible.

Topics: Adult; Aged; Aged, 80 and over; Chi-Square Distribution; China; Cholecalciferol; Female; Humans; Hypocalcemia; Hypoparathyroidism; Male; Middle Aged; Minimally Invasive Surgical Procedures; Parathyroidectomy; Radionuclide Imaging; Statistics, Nonparametric; Vitamin D Deficiency

A family with hereditary (familial) hypoparathyroidism is reported where three of the total four siblings were affected and each presented with different manifestation-one brother with refractory epilepsy since early childhood, another brother with unilateral extrapyramidal features in adult life, and their only sister having recurrent attacks of tingling and numbness due to hypocalcemia since 12 years of age.

Topics: Calcium; Cholecalciferol; Diagnosis, Differential; Female; Humans; Hypoparathyroidism; Pedigree; Tomography, X-Ray Computed; Vitamins; Young Adult

Hypocalcemia caused by transient or definitive hypoparathyroidism is the most frequent complication after thyroidectomy. We aimed to compare the impact of incidental parathyroidectomy and serum vitamin D(3) level on postoperative hypocalcemia after total thyroidectomy (TT) or near total thyroidectomy (NTT).. Two hundred consecutive patients with nontoxic multinodular goiter treated by TT and NTT were included prospectively in the present study. Group 1 (n = 49) consisted of patients with a postoperative serum calcium level < or =8 mg/dL, and group 2 (n = 151) had a postoperative serum calcium level greater than 8 mg/dL. Patients were evaluated according to age, preoperative serum 25-hydroxy vitamin D (25-OHD) levels, postoperative serum calcium levels, incidental parathyroidectomy, and the type of thyroidectomy.. Patients in group 1 (n = 49) were hypocalcemic, whereas patients in group 2 (n = 151) were normocalcemic. Preoperative serum 25-OHD levels in group 1 were significantly lower than in group 2 (P < .001). The incidence of hypoparathyroidism was significantly higher following TT (13.5%) than following NTT (2.5%) (P < .05). The risk for postoperative hypocalcemia was increased 25-fold for patients older than 50 years, 28-fold for patients with a preoperative serum 25-OHD level less than 15 ng/mL, and 71-fold for patients who underwent TT. Incidental parathyroidectomy did not have an impact on postoperative hypocalcemia. The highest risk of postoperative hypocalcemia was found in the patients with all of the above variables.. Age, preoperative low serum 25-OHD, and TT are significantly associated with postoperative hypocalcemia. Patients with advanced age and low preoperative serum 25-OHD levels should be placed on calcium or vitamin D supplementation after TT to avoid postoperative hypocalcemia and decrease hospital stay.

Topics: Adolescent; Adult; Aged; Cholecalciferol; Female; Goiter; Humans; Hypocalcemia; Hypoparathyroidism; Male; Medical Errors; Middle Aged; Parathyroidectomy; Thyroidectomy; Young Adult

Topics: Calcinosis; Calcium Gluconate; Cholecalciferol; Female; Fingers; Goiter; Hand Deformities, Acquired; Humans; Hypoparathyroidism; Hypothyroidism; Middle Aged; Thyroid Hormones; Thyroidectomy; Thyroxine

A now 65-year-old man had undergone a subtotal thyroidectomy over 40 years ago, which postoperatively resulted in hypoparathyroidism. His doctor began daily intravenous injections of a calcium preparation (1880 mg to 3760 mg calcium per day, over 40000 injections during this period), a regimen continued subsequently by a total of more than 15 other doctors for over 40 years. On admission the patient complained of oral paresthesias and paresthesias of the limbs.. Low calcium and parathormone levels confirmed the diagnosis of hypoparathyroidism.. Normal levels of calcium were achieved after a short course of 1.25-dihydroxycalciferol. This was followed by the administration of cholecalciferol and calcium. The patient soon became symptom-free and calcium levels returned to normal. Late sequelae have been calcification of the basal ganglia, first signs of nephrocalcinosis and bilateral cataract.. This case demonstrates that appropriate treatment of hypoparathyroidism [corrected] might not be given in every case.

Topics: Aged; Basal Ganglia; Calcinosis; Calcitriol; Calcium; Cholecalciferol; Humans; Hypocalcemia; Hypoparathyroidism; Injections, Intravenous; Male; Parathyroid Hormone; Paresthesia; Thyroidectomy

Paroxysmal kinesigenic dyskinesia (PKD) is an uncommon neurological disorder characterised by abnormal episodic brief movements induced by sudden movements of the body. The recognition and understanding of this disorder has increased over the past few decades. While most cases are idiopathic, the association of PKD with various disorders, including metabolic abnormalities has also been reported. We report an interesting case of a 52 year old male who presented with PKD manifesting as subtle facio-brachial movements and apraxia of eyelid opening (ALO) secondary toidiopathic hypoparathyroidism.

Topics: Arm; Brain Diseases; Calcinosis; Calcium Carbonate; Cholecalciferol; Chorea; Epilepsy, Tonic-Clonic; Eyelids; Facial Muscles; Humans; Hypoparathyroidism; Male; Middle Aged; Movement; Shoulder

Topics: Cholecalciferol; Humans; Hypoparathyroidism; Male; Middle Aged; Nervous System Diseases

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

The clinical manifestations of hypoparathyroidism are mainly characterised by increased neuromuscular irritability as a consequence of hypocalcaemia. Occasionally, elevation of the muscle enzymes may mimic polymyositis. Reduced parathyroid hormone production, but also vitamin D treatment and calcium supplementation, may contribute to the increased bone mass found in patients with postsurgical hypoparathyroidism. We report the case of a 36-year-old woman with untreated idiopathic hypoparathyroidism and a high bone mass despite severe muscle impairment due to hypocalcaemic myopathy.

Topics: Absorptiometry, Photon; Adult; Bone and Bones; Bone Density; Calcium; Cholecalciferol; Diagnosis, Differential; Electromyography; Female; Humans; Hypocalcemia; Hypoparathyroidism; Muscular Diseases

The sigmoidal curves plotting serum parathyroid hormone (PTH) against serum Ca in primary hyperparathyroidism and secondary hyperparathyroidism due to renal failure deviate to the right. We previously found the leftward curve shift in PTH-deficient hypoparathyroidism. In the present study, we investigated the curve shift in pseudohypoparathyroidism (PHP) with secondary hyperparathyroidism due to target organ resistance to PTH. In renal failure the sigmoidal curves move to the left after vitamin D3 treatment. We also examined the effect of vitamin D3 on the curve shift in pseudohypoparathyroidism (PHP) and idiopathic hypoparathyroidism (IHP). Before vitamin D3 treatment, the sigmoidal curve deviated to the left in both types of hypoparathyroidism. After vitamin D3 treatment it moved to the right. These results indicate that vitamin D3 and/or extracellular Ca modify the relationship between PTH and Ca dynamics even in hypoparathyroid disorders with decreased or increased maximum serum PTH. Following vitamin D3 treatment, the point plotting baseline serum PTH against baseline serum Ca moved to the right at first in accordance with the rightward shift of the sigmoidal curve and then the point moved downward in PHP or downward in IHP. These changes suggest that vitamin D3 resets PTH secretion at a higher extracellular Ca level at first and then suppresses it in a time-dependent manner. 1, 25(OH)2D3 and/or extracellular Ca may be the determinant factors of the sigmoidal curve shift in hypoparathyroid disorders. Mechanisms other than the Ca sensing system error may contribute to the curve shift.

Topics: Adult; Calcitriol; Calcium; Cholecalciferol; Dose-Response Relationship, Drug; Female; Humans; Hypoparathyroidism; Middle Aged; Parathyroid Hormone; Pseudohypoparathyroidism; Time Factors; Vitamin D

Hypoparathyroidism is a rare disease with hypocalcemia as the leading symptom. In adults, hypocalcemia is mainly due to postoperative hypoparathyroidism. Hypoparathyroidism requires lifelong therapy with vitamin D or metabolites. Genuine vitamin D3 (Vigantol) is the most economic treatment of hypoparathyroidism; however, vitamin D3 has a very long biologic half life with the subsequent danger of chronic vitamin D intoxication. Dihydrotachysterol (A.T.10), an analogue of vitamin D, acts similarly and can be used alternatively. 1,25-dihydroxyvitamin D3 (Rocaltrol), the biologically active metabolite of vitamin D3, is very potent, but bears the danger of causing acute intoxication; it has a short half life and is more expensive than vitamin D3. A further metabolite, 1-hydroxy-vitamin D3 (alfacalcidol, Doss, EinsAlpha) is available for therapeutic use. Clinical intervention trials concerning the best therapy and management of hypoparathyroidism are lacking. We therefore surveyed German physicians treating hypoparathyroidism. Furthermore, we carried out a retrospective study of 45 patients treated in our endocrinology department during the last 8 years and examined whether measurement of 25(OH)-vitamin D3 is helpful in managing hypoparathyroidism. The data from 59 children and 270 adults could be completed in the survey. 1,25-dihydroxyvitamin D3 was the only vitamin D agent that was administered in the treatment of children, whereas in adults 52% were treated with dihydrotachysterol, 28% with genuine vitamin D3, and 20% with 1,25-dihydroxyvitamin D3. There was a positive correlation between serum 25(OH)-vitamin D3 levels and administered vitamin D3 doses. In patients treated with vitamin D3, serum calcium levels correlated significantly with serum 25(OH)-vitamin D3 levels whereas they did not correlate with administered calcium doses. Thus: (1) in Germany dihydrotachysterol is preferred for therapy of hypoparathyroidism in adults and (2) measurement of serum 25(OH)-vitamin D3 may be helpful in assessing efficacy of therapy and compliance in patients treated with vitamin D3.

Topics: Adult; Aging; Calcifediol; Calcitriol; Calcium; Child; Cholecalciferol; Dihydrotachysterol; Endocrinology; Germany; Half-Life; Humans; Hypoparathyroidism; Physicians; Retrospective Studies; Surveys and Questionnaires

The relationship between parathyroid hormone (PTH) secretion and extracellular calcium (Ca) level is reciprocal causality. The equilibrium operating point determines basal PTH secretion rate and basal extracellular Ca level. We studied how this equilibrium was achieved in the subjects with decreased PTH secretion or decreased parathyroid glands number. Basal/maximum ratio of serum PTH, which reflects the basal secretory state of parathyroid glands, was increased in 9 hypoparathyroid patients treated with vitamin D3 (VD3) [7 patients with idiopathic hypoparathyroidism] and in seven of nine parathyroid adenectomized patients. There was a negative correlation between the ratio and basal serum Ca level in the patients with IHP after VD3 treatment (r = 0.7167, P < 0.05) and in the patients after parathyroid adenectomy (r = 0.7760, P < 0.05). The regression curves in these two groups coincided regardless of the difference in maximum PTH secretion rate, which suggested that the basal secretory state of parathyroid glands was determined by extracellular Ca level in a similar manner in these subjects. There was a sigmoidal relationship between basal/maximum ratio of serum PTH and basal serum Ca level, when the data were collected from 15 hypoparathyroid patients before or after VD3 treatment, 9 parathyroid adenectomized patients, and 10 normal subjects (r = 0.9057, P < 0.001). This sigmoidal curve is thought to represent the fundamental relationship between the basal secretory state of parathyroid glands and extracellular Ca level.

Topics: Adenoma; Adolescent; Adult; Aged; Calcium; Child; Cholecalciferol; Humans; Hyperthyroidism; Hypoparathyroidism; Middle Aged; Parathyroid Hormone; Parathyroid Neoplasms; Parathyroidectomy

Topics: Basal Ganglia Diseases; Calcinosis; Calcium; Cholecalciferol; Drug Therapy, Combination; Humans; Hypoparathyroidism; Male; Middle Aged; Syndrome

Topics: Calcium; Cholecalciferol; Forearm; Glucose; Humans; Hypoparathyroidism; Insulin; Ischemia; Muscles; Muscular Diseases; Phosphates; Physical Exertion; Uric Acid

Extracellular fluid calcium is a tightly controlled variable. Hypoparathyroid state may result in profound calcium imbalance and moderate to severe hypocalcaemia. During 1974-89, 108 cases of hypoparathyroidism (97 post-surgical and 11 idiopathic) were seen. In the post-thyroidectomy group, 83 cases (85%) presented with acute transient hypocalcaemia with spontaneous recovery within 7-10 days. Chronic hypoparathyroidism was seen in 25 cases (14 post-surgical and 11 idiopathic). Convulsions resembling epileptic fits were seen in 9 cases (36%). Pseudopapilloedema was seen in three cases presenting with fits. The administration of phenobarbitone and dilantin aggravated convulsions in 9 patients. The other manifestations were psychiatric illness, cataract and calcification of basal ganglion. Biochemical findings included persistent hypocalcaemia with normal or raised serum phosphorus and lowered daily urinary excretion of calcium. Twenty three of 25 chronic hypoparathyroid cases were treated with vitamin D3 (1-3 mg/day) and calcium supplements (600-1000 mg/day)while 1 alfa-calcidol or calcitriol was used in two patients. Four patients receiving treatment with vitamin D3 developed transient hypercalcaemia with raised plasma levels of 25 hydroxy-vitamin D3. They responded to a reduction in dosage of vitamin D3. One patient was later changed over to 1-alfa-calcidol and another to calcitriol.

Topics: Acute Disease; Adolescent; Adult; Aged; Calcium, Dietary; Child; Cholecalciferol; Chronic Disease; Humans; Hydroxycholecalciferols; Hypocalcemia; Hypoparathyroidism; Middle Aged

Topics: Calcium; Cholecalciferol; Combined Modality Therapy; Humans; Hypoparathyroidism; Iatrogenic Disease; Seasons; Ultraviolet Therapy

In two patients suffering from hypoparathyroidism (HP) whose serum calcium and -phosphate could not be normalized with Vitamin D3-resp. Calcitriol and who continued to have tetanic convulsions, synthetic 1-38 human parathyroid hormone (1-38 hPTH) was used for treatment. In both patients the intravenous administration of 1-38 hPTH provoked a rapid increase of phosphaturia and cAMP-excretion and an increase of the serum calcium level into the normal range. The same effects, only slightly delayed, could be achieved with subcutaneous injections which the patients had learned to do themselves. In case 1, a boy aged 14 years with autoimmune-HP, the daily administration of 8.5 U/kg BW caused hypercalcemia on the 6th day of treatment; therefore the dosis was reduced to alternate day administration. In case 2, a girl aged 17 1/2 years with idiopathic HP, treatment was started with alternate day administration (7.7 U/kg BW/day of injection); serum calcium increased to levels of about 2.2 mmol/1. Side effects could not be seen. Case 1, however, developed resistance to 1-38 hPTH after 10 weeks of therapy. 1-38 hPTH can be classified as an effective substance in the treatment of HP. Optimal dose and frequency of administration cannot yet be pointed out.

Topics: Adolescent; Calcium; Cholecalciferol; Creatinine; Female; Follow-Up Studies; Humans; Hypoparathyroidism; Male; Parathyroid Hormone; Peptide Fragments; Phosphates

A 48-year-old woman developed a hypocalcaemic cardiomyopathy, the hypocalcaemia being due to hypoparathyroidism after three previous thyroid operations for goitre with tracheal compression. She had signs of severe cardiac failure, but no tetany. She was put on calcium and vitamin D3 medication which raised calcium concentration. The cardiac status improved, as did the radiological and echocardiographic findings, without the patient having received any diuretics, digitalis or afterload lowering drugs.

Topics: Calcium; Cardiomyopathy, Dilated; Cholecalciferol; Female; Humans; Hypocalcemia; Hypoparathyroidism; Middle Aged; Thyroidectomy

Forty-four patients suffering of hypoparathyroidism were receiving in the complex treatment vitamin D3. Blood calcium and phosphorus, parathyroid hormone, urinary excretion of calcium were determined. The primary clinical effect was manifest on the 3-7 day of treatment; the effect achieved its maximum in most patients by the 2-3 week and in some cases by the 3-6 months of treatment.

Topics: Adolescent; Adult; Child; Cholecalciferol; Combined Modality Therapy; Drug Evaluation; Female; Humans; Hypoparathyroidism; Male; Middle Aged; Time Factors

Serum osteocalcin was measured in patients with idiopathic hypoparathyroidism or pseudohypoparathyroidism, before or during the treatment with active vitamin D3 (1,25(OH)2D3 or 1 alpha OHD3). Serum osteocalcin and plasma 1,25(OH)2D were decreased in 11 patients with idiopathic hypoparathyroidism before treatment (2.8 +/- 1.27 ng/ml, P less than 0.001 and 14.3 +/- 4.27 pg/ml, P less than 0.001, respectively). In 24 patients with idiopathic hypoparathyroidism during the treatment, serum osteocalcin and plasma 1,25(OH)2D were within the normal range (4.5 +/- 0.74 ng/ml and 25.7 +/- 5.69 pg/ml, respectively). In five patients with pseudohypoparathyroidism before treatment, plasma 1,25(OH)2D was decreased (15.6 +/- 10.6 pg/ml, P less than 0.001) but serum osteocalcin was normal (7.8 +/- 1.66 ng/ml). In nine patients with pseudohypoparathyroidism during the treatment with active vitamin D3, serum osteocalcin and plasma 1,25(OH)2D were normal (6.8 +/- 1.47 ng/ml and 27.2 +/- 6.0 pg/ml, respectively). Serum PTH in pseudohypoparathyroidism was increased before treatment (0.70 +/- 0.34 ng/ml, P less than 0.05) and was normal during the treatment (0.50 +/- 0.13 ng/ml). In idiopathic hypoparathyroidism, the active vitamin D3 increased serum osteocalcin without PTH. In pseudohypoparathyroidism, PTH may increase serum osteocalcin or modulate the effect of active vitamin D3 on serum osteocalcin.

Topics: Adult; Calcitriol; Calcium; Calcium-Binding Proteins; Cholecalciferol; Female; Humans; Hypoparathyroidism; Male; Middle Aged; Osteocalcin; Parathyroid Hormone; Phosphorus; Pseudohypoparathyroidism

Topics: Adult; Aged; Calcifediol; Calcium; Cholecalciferol; Female; Humans; Hypoparathyroidism; Male; Middle Aged; Phosphates; Postoperative Complications

Topics: Aged; Calcium; Cholecalciferol; Creatine Kinase; Female; Humans; Hypocalcemia; Hypoparathyroidism; Isoenzymes; L-Lactate Dehydrogenase; Phosphates

This interlaboratory study on determination of 25-hydroxyvitamin D (25-OH-D) in serum involved 15 laboratories in eight European countries. All could distinguish between normal (50 +/- 31 nmol/L, mean +/- SD) and grossly increased concentrations, but for eight laboratories the results for serum samples with low and normal 25-OH-D content overlapped. In general, values were well reproducible, but interlaboratory variation in 25-OH-D measurement was large, 24,25(OH)2D3 interfering in most of the assays. We present evidence in favor of chromatography before assay, as opposed to nonchromatographic methods. Liquid chromatography with ultraviolet detection for quantifying 25-OH-D2 and 25-OH-D3 appears to be an appropriate reference method, whereas competitive protein binding assay is the method of choice for routine determinations. Control sera with subnormal, normal, and above-normal concentrations of 25-OH-D3 are needed for use in standardization of 25-OH-D assays.

Topics: 25-Hydroxyvitamin D 2; Calcifediol; Carrier Proteins; Charcoal; Chemistry, Clinical; Cholecalciferol; Chromatography, High Pressure Liquid; Ergocalciferols; Europe; False Positive Reactions; Humans; Hypoparathyroidism; Spectrophotometry, Ultraviolet; Vitamin D; Vitamin D-Binding Protein

Topics: Calcifediol; Calcitriol; Cholecalciferol; Dihydrotachysterol; Drug Resistance; Female; Humans; Hypoparathyroidism; Middle Aged

The effects of chronic hypocalcaemia on serum basal and chlorpromazine-stimulated prolactin (Prl) levels were studied in 16 patients with idiopathic or secondary hypoparathyroidism. These results were compared with the results of other chlorpromazine stimulation tests which were made in the normocalcaemic state after treatment with vitamin D, and in normal subjects. In hypocalcaemic and normocalcaemic states (mean serum Ca 5.8 +/- 0.24 mg/dl and 9.5 +/- 0.11 mg/dl, respectively) basal Prl levels were within the normal range and during stimulation the maximal stimulated levels in each state were not significantly different from each other. Also, the mean serum Prl levels obtained from a control group were not different from values in the normocalcaemic state. It is concluded that chronic hypocalcaemia does not inhibit Prl secretion and low serum parathyroid hormone levels do not affect basal and chlorpromazine-stimulated Prl secretion.

Topics: Adult; Calcium; Chlorpromazine; Cholecalciferol; Female; Humans; Hypocalcemia; Hypoparathyroidism; Male; Middle Aged; Parathyroid Hormone; Prolactin

Topics: Adult; Brain Diseases, Metabolic; Calcinosis; Cholecalciferol; Female; Humans; Hypoparathyroidism; Syndrome; Vitamin D Deficiency

Recognition over the last ten years of the fact that vitamin D does not act as such, but must be converted into a hormonal form, has filled in the picture physiological endocrine regulation of calcium and phosphate homeostasis. While vitamin D has thus lost the dietetic significance associated with it for over 50 years. Nevertheless, new interpretations of the aetiopathogenesis of many demineralizing bone diseases are of much greater utility. Nor is it futuristic to suppose that all the biochemical parameters establishing one of the metabolisms that are under strict homeostatic control in the body, such as that of calcium and that of phosphate, are understood.

Topics: Bone Diseases; Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Glucocorticoids; Humans; Hypoparathyroidism; Iatrogenic Disease; Intestinal Absorption; Osteomalacia; Osteoporosis; Phosphates; Rickets; Vitamin D

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

Topics: Aged; Cholecalciferol; Fecal Incontinence; Humans; Hypoparathyroidism; Male; Urinary Incontinence

Elucidation of the vitamin D endocrine system and the availability of potent metabolites have led to new approaches to vitamin D therapy. The traditional management of exogenous (sunlight) or endogenous (malabsorption) vitamin D deficiency without evidence of disordered vitamin D metabolism has not changed, since it consists of treatment with vitamin D itself--a therapy which preserves the normal intrinsic mechanisms for regulating the rate of production of 1,25-dihydroxycholecalciferol. 1,25-DHCC and the analogue compound 1 alpha-CC should be reserved for treatment of hypocalcemia consequent on chronic renal failure or hypoparathyroidism, where 1-hydroxylation is lacking or impaired. Hypophosphatemic rickets has been treated with 1-hydroxylated compounds, with promising results; this use of the latter metabolites warrants further investigation. The use of vitamin D metabolites and of pharmacological doses of vitamin D itself must be regarded as substitution of a hormone or hormone precursors. Therefore, careful monitoring of serum and urine calcium is required in every patient receiving these compounds, in order to avoid excessive dosage. Special attention must be paid to patients with sarcoidosis since they often develop hypercalcemia after vitamin D or UV-light exposure, as a result of an intrinsic regulation defect in 1,25-DHCC synthesis.

Topics: Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols; Hypoparathyroidism; Osteomalacia; Phosphates; Vitamin D; Vitamin D Deficiency

Topics: Calcium Metabolism Disorders; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Ergocalciferols; Humans; Hypoparathyroidism; Osteomalacia; Osteoporosis; Phosphorus Metabolism Disorders; Renal Dialysis; Vitamin D

A half century ago, vitamin D was recognized as a vitamin. Now it has become clear that it is also a hormone--indeed the biochemical cornerstone of a major hormonal system involved in regulating the body's calcium economy. The active metabolite, calcitriol, produced in the kidney, acts on bone and intestine and has been found effective in therapy of osteodystrophy and perhaps other metabolic bone diseases.

Topics: Calcium; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Hypoparathyroidism; Hypophosphatemia, Familial; Osteoporosis; Phosphates; Phosphorus; Vitamin D

Calcium balance studies and measurement of 25-hydroxyvitamin D3 (25[OH]D3) levels were performed on a vitamin D intoxicated, hypoparathyroid patient before, during, and after successful management of hypercalcemia with oral prednisone therapy. Prednisone effected a dramatic reduction in both mean serum calcium levels and mean 24-hour urinary calcium excretion within four days on two separate occasions. No changes were apparent in fecal calcium excretion. Calcium balance became less negative with prednisone treatment. Levels of 25(OH) D3 during the same period did not change. Decreased calcium mobilization from bone best accounted for the glucocorticoid-mediated amelioration of hypercalcemia.

Topics: Calcium; Calcium, Dietary; Cholecalciferol; Female; Humans; Hypercalcemia; Hypoparathyroidism; Middle Aged; Prednisone; Vitamin D

Topics: Carrier Proteins; Cholecalciferol; Glycoproteins; Humans; Hypoparathyroidism; Hypophosphatemia, Familial; Immunoassay; Polymorphism, Genetic; Rickets

Endotoxin-stimulated NBT-tests were carried out in 15 patients with hypocalcemia of varying etiology and in 14 normocalcemic children free of infection. In the control group the formazan cell percentage (FCP) was 73.8 +/- 1.6% (range 63% to 83%). In 5 patients with hypoparathyroidism or pseudohypoparathyroidism the FCP before treatment was lower than normal. Vitamin D3 therapy produced a rapid increase of serum calcium but normalisation of NBT-test was only achieved after a latent period of one or more months. Patients with hypocalcemic rickets and children with an acute relapse of the nephrotic syndrome also showed abnormal results. The clinical significance of the NBT-test in hypocalcemic conditions is discussed.

Topics: Adolescent; Adult; Child; Child, Preschool; Cholecalciferol; Endotoxins; Female; Humans; Hypocalcemia; Hypoparathyroidism; Infant; Lymphocyte Activation; Male; Nephrotic Syndrome; Nitroblue Tetrazolium; Pseudohypoparathyroidism; Rickets; Tetrazolium Salts

Topics: Adult; Cholecalciferol; Drug Evaluation; Female; Humans; Hypoparathyroidism; Male; Middle Aged

Topics: Adolescent; Adult; Animals; Bone and Bones; Bone Resorption; Calcium; Child; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Humans; Hypoparathyroidism; Intestinal Mucosa; Kidney; Liver Cirrhosis, Biliary; Malabsorption Syndromes; Osteomalacia; Parathyroid Glands; Phosphorus; Rats; Renal Tubular Transport, Inborn Errors; Vitamin D

25-Hydroxyvitamin D (25-OHD) levels were measured in 39 patients with metabolic bone disease or hypoparathyroidism who had been treated with a constant high dose of vitamin D2 or D3 for at least 12 weeks. Plasma 25-OHD levels rose with increasing dosage, the relationship between dose and plasma level being approximately linear whether or not the dose was expressed on a weight-corrected basis. A therapeutic range of 25-OHD to be expected when patients with these conditions are treated with vitamin D has been established. There may be certain exceptions in which plasma 25-OHD levels within the range are associated with either an inadequate response to treatment or, conversely, the hypercalcaemia of vitamin D toxicity. There was no correlation between plasma calcium level and 25-OHD concentration in the group of patients studied. There was also no difference between the dose/25-OHD relationship of patients treated with vitamin D2 and that of patients receiving vitamin D3. Ten patients were started on treatment with large doses of vitamin D during the period of the study. The rate of rise of plasma 25-OHD was followed during treatment. The incremental rise in 25-OHD was calculated at the end of the first week of treatment in terms of dose per unit body weight. The rate of rise of plasma 25-OHD level was highly correlated with the dose used. Plasma 25-OHD levels after one weeks' treatment were only 15-20% of the expected steady-state level on the same dosage. The importance of a high priming dose when a rapid response is needed is thus emphasised.

Topics: Adolescent; Adult; Aged; Body Weight; Bone Diseases; Child; Child, Preschool; Cholecalciferol; Dose-Response Relationship, Drug; Ergocalciferols; Female; Humans; Hydroxycholecalciferols; Hypercalcemia; Hypoparathyroidism; Infant; Male; Middle Aged; Vitamin D

Two patients with profound hypocalcaemia due to uraemia and hypoparathyroidism respectively presented with alterations of mental state as their dominant symptom. 1-Alpha-hydroxycholecalciferol (1-alpha-OHD3) was chosen as the principal therapy because of its potency and rapid action. In both patients the plasma calcium was restored towards normal and the symptoms relieved within a very short period. The cases illustrate the role of 1-alpha-OHD3 in severe hypocalcaemia due to two different causes and provide experience on which to base treatment regimes for future patients similarly afflicted.

Topics: Calcium; Cholecalciferol; Female; Humans; Hydroxycholecalciferols; Hypocalcemia; Hypoparathyroidism; Middle Aged; Psychotic Disorders; Uremia

Topics: Child; Cholecalciferol; Humans; Hypoparathyroidism; Intellectual Disability; Male; Phenobarbital

Topics: Age Factors; Cholecalciferol; Gastrectomy; Humans; Hypoparathyroidism; Vitamin D; Vitamin D Deficiency

In hypoparathyroidism and pseudohypoparathyroidism, pharmacologic doses of vitamin D correct hypocalcemia, but the mechanism is unknown. In two children with hypoparathyroidism and one with pseudohypoparathyroidism we tested the hypothesis that in these conditions there is a defect in synthesis of 1 alpha,25-dihydroxyvitamin D3, the principal active metabolite of vitamin D. In both conditions, minute doses of the metabolite (0.04 to 0.08 mug per kilogram of body weight per day) quickly corrected hypocalcemia and increased intestinal calcium absorption. On the other hand, the effective dose of 25-hydroxyvitamin D3 to maintain normocalcemia was 3 to 4 mug per kilogram per day in the two conditions. Thus, the dosage ratio of 25-hydroxyvitamin D3 to 1 alpha,25-dihydroxyvitamin D3 approximated 100:1. By contrast this ratio was approximately 3:1 in two infants with vitamin D deficiency, a condition in which optimal metabolism of vitamin D would be expected. These findings suggest an impaired conversion of 25-hydroxyvitamin D to 1 alpha,25-dihydroxyvitamin D in both hypoparathyroidism and pseudohypoparathyroidism.

Topics: Administration, Oral; Adolescent; Calcium; Child; Cholecalciferol; Dihydroxycholecalciferols; Female; Humans; Hydroxycholecalciferols; Hypoparathyroidism; Injections, Intravenous; Intestinal Absorption; Male; Phosphates; Pseudohypoparathyroidism

Topics: Cholecalciferol; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols; Hydroxylation; Hypoparathyroidism; Pseudohypoparathyroidism; Vitamin D

Topics: Aged; Calcium; Cholecalciferol; Ergocalciferols; Esophagus; Female; Humans; Hypercalcemia; Hypoparathyroidism; Laryngectomy; Male; Middle Aged; Parathyroid Hormone; Pharyngectomy; Postoperative Complications; Vitamin D

Topics: Animals; Antigens; Calcium; Cholecalciferol; Humans; Hypoparathyroidism; Parathyroid Hormone; Phosphorus; Rickets; Seasons; Sterols; Tritium; Vitamin D

Topics: Cholecalciferol; Creatine Kinase; Female; Humans; Hypoparathyroidism

Topics: Cholecalciferol; Ergocalciferols; Humans; Hypercalcemia; Hypoparathyroidism; Vitamin D

Topics: Adolescent; Adult; Calcium; Cholecalciferol; Dihydrotachysterol; Female; Follow-Up Studies; Humans; Hydroxyproline; Hypoparathyroidism; Kidney Failure, Chronic; Male; Middle Aged; Spectrum Analysis; Thyroidectomy; Vitamin D

Topics: Calcium; Cholecalciferol; Humans; Hypoparathyroidism; Vitamin D

Topics: Calcium; Cholecalciferol; Ergocalciferols; Humans; Hypoparathyroidism; Osteomalacia; Rickets; Vitamin D

Topics: Adolescent; Body Height; Bone Diseases; Calcium; Child; Cholecalciferol; Diagnosis, Differential; Female; Humans; Hyperparathyroidism; Hypocalcemia; Hypoparathyroidism; Phosphorus Metabolism Disorders; Tetany

Topics: Adult; Bone and Bones; Calcium; Calcium Isotopes; Cholecalciferol; Creatine; Dihydrotachysterol; Humans; Hydroxyproline; Hypocalcemia; Hypoparathyroidism; Male; Parathyroid Hormone; Phosphates; Radiometry; Tritium; Vitamin D