cholecalciferol and Hypocalcemia

Routine prophylaxis for at-risk patients may reduce the occurrence of postoperative hypocalcemia but is not widely adopted due to a lack of evidence on the efficacy of available prophylactic strategies. In this study, we compared the relative efficacy of prophylactic strategies for postthyroidectomy hypocalcemia with a systematic review and network meta-analysis.. PubMed, Embase, and Cochrane Library were searched, covering the period from 1980 to May 2022, for randomized controlled trials (RCTs) comparing calcium, vitamin D 3 , activated vitamin D 3 , teriparatide, steroids, and magnesium with placebo or each other in patients receiving total or completion thyroidectomy. Involved RCTs reporting symptomatic or biochemical hypocalcemia. The primary outcome was symptomatic hypocalcemia, defined as circumoral tingling, and Chvostek and Trousseau signs. The secondary outcome was biochemical hypocalcemia. Risk of bias was assessed using the Cochrane risk of bias assessment tool for randomized trials. Pooled estimates were calculated using a random-effects inverse-variance weighting model. The network meta-analysis was performed under the frequentist framework. This meta-analysis was registered on the PROSPERO (International prospective register of systematic reviews) (CRD42022299982).. Twenty-seven RCTs comprising 3382 patients are included. Prophylactic strategies of teriparatide, oral calcium plus vitamin D 3 , and oral calcium plus activated vitamin D 3 are superior to placebo in reducing symptomatic hypocalcemia. Teriparatide emerged as the most effective strategy for symptomatic hypocalcemia [relative risk (RR): 0.18; 95% CI: 0.03-0.98], followed by oral calcium plus activated vitamin D 3 (RR: 0.42; 95% CI: 0.25-0.73) and oral calcium plus vitamin D 3 (RR: 0.43; 95% CI: 0.26-0.71). Evidence on monotherapy with either oral calcium or vitamin D 3 in reducing symptomatic hypocalcemia is insufficient. Intravenous calcium and oral calcium are effective in reducing biochemical hypocalcemia.. This network meta-analysis provides information on the relative efficacy of current prophylactic strategies for postthyroidectomy hypocalcemia. Teriparatide performed better than other interventions and would seem appropriate for deployment among high-risk populations.

Topics: Calcium; Cholecalciferol; Humans; Hypocalcemia; Network Meta-Analysis; Teriparatide

This systematic review aimed to establish the evidence behind the use of pre-operative calcium, vitamin D or both calcium and vitamin D to prevent post-operative hypocalcaemia in patients undergoing thyroidectomy.. This review included prospective clinical trials on adult human patients that were published in English and which studied the effects of pre-operative supplementation with calcium, vitamin D or both calcium and vitamin D on the rate of post-operative hypocalcaemia following total thyroidectomy.. Seven out of the nine trials included reported statistically significantly reduced rates of post-operative laboratory hypocalcaemia (absolute risk reduction, 13-59 per cent) and symptomatic hypocalcaemia (absolute reduction, 11-40 per cent) following pre-operative supplementation.. Pre-operative treatment with calcium, vitamin D or both calcium and vitamin D reduces the risk of post-operative hypocalcaemia and should be considered in patients undergoing total thyroidectomy.

Topics: Calcitriol; Calcium; Calcium Carbonate; Calcium-Regulating Hormones and Agents; Cholecalciferol; Humans; Hydroxycholecalciferols; Hypocalcemia; Postoperative Complications; Preoperative Care; Thyroidectomy; Vitamin D; Vitamins

The aim was to assess the effectiveness of routine administration of calcium +/- vitamin D3 compared with a serum calcium level-based strategy to prevent symptomatic hypocalcaemia after thyroidectomy.. RCTs comparing routine supplementation of calcium +/- vitamin D3 with treatment based on serum calcium levels measured after total thyroidectomy, published between 1980 and 2017, were identified in MEDLINE, Embase, LILACS and Google Scholar databases. Risk of bias was evaluated using the Cochrane Collaboration tool. Risk differences were calculated by random-effects meta-analysis. Meta-regression and cumulative meta-analysis were used to explore the best therapeutic approach.. Fifteen studies with 3037 patients were included, and seven treatment comparisons were made. Routine supplementation with calcium + vitamin D3 offered a lower risk of symptomatic (risk difference (RD) -0·25, 95 per cent c.i. -0·32 to -0·18) and biochemical (RD -0·24, -0·31 to -0·17) hypocalcaemia than treatment based on measurement of calcium levels. The number needed to treat was 4 (95 per cent c.i. 3 to 6) for symptomatic hypocalcaemia. No publication bias was found; although heterogeneity was high for some comparisons, sensitivity analysis did not change the main results.. Routine postoperative administration of calcium + vitamin D3 is effective in decreasing the rate of symptomatic and biochemical hypocalcaemia.

Topics: Calcium; Cholecalciferol; Dietary Supplements; Humans; Hypocalcemia; Postoperative Complications; Thyroidectomy

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

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

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

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

Topics: Alcoholism; Calcium; Cholecalciferol; Humans; Hypocalcemia; Magnesium; Magnesium Deficiency; Phosphorus Acids

Topics: Aged; Aging; Calcium; Cholecalciferol; Color; Humans; Hypocalcemia; Light; Lighting; Osteoporosis; Sunlight; Ultraviolet Rays; Vision, Ocular; Vitamin D; Vitamin D Deficiency

Animal-experimental examinations show that the peroral or intramuscular application of a high dose of vitamin D2 or of D3 leads to a toxic effect of these compounds on the osteocytes and that the hypercalcaemia evoked by this is mainly to be traced back to an increased deliberation of calcium from the bones. After application of a larger dose of vitamin D the activation mechanism in the liver and in the kidneys is much inhibited for several weeks so that no formation of 1,25-hydroxy-vitamin-D takes place; consequently, no furthering effect on the mineralisation of the bones is performed. Therefore, it is recommended to use physiological doses in the prevention of rachitis (500-1,000 IU a day). During the pregnancy the activity of the enzymes which participate in the activation of the D-vitamins increases in the liver and the kidneys. The kidneys of the fetuses are able to form 1,25-hydroxy-vitamin-D. Vitamin D and 25-hydroxy-vitamin-D transgress through the placenta into the fetuses. Due to the adaptation mentioned and the increased formation of 1,25-hydroxy-vitamin-D the absorption of calcium and phosphate increases during pregnancy. Recent pathobiochemical knowledge concerning the metabolism of the D-vitamins in several diseases are described.

Topics: Bone and Bones; Calcium; Cholecalciferol; Ergocalciferols; Female; Glomerular Filtration Rate; Humans; Hypocalcemia; Infant, Newborn; Infant, Premature, Diseases; Intestinal Absorption; Liver; Osteogenesis; Osteoporosis; Parathyroid Hormone; Phosphates; Pregnancy; Rickets; Skin; Vitamin D

Topics: Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Ergocalciferols; Feedback; Humans; Hypocalcemia; Kidney Diseases; Liver; Osteomalacia; Parathyroid Hormone; Rickets; Seasons; Ultraviolet Rays; Vitamin D

Topics: Animals; Calcium; Cattle; Chickens; Cholecalciferol; Cyclic AMP; Dihydroxycholecalciferols; Feedback; Humans; Hydroxycholecalciferols; Hypocalcemia; Kidney; Mitochondria; Mixed Function Oxygenases; Parathyroid Hormone; Phosphates; Rats

Topics: Adolescent; Adult; Aged; Alkaline Phosphatase; Anticonvulsants; Bone Diseases; Child; Child, Preschool; Cholecalciferol; Diagnosis, Differential; Epilepsy; Female; Humans; Hypocalcemia; Infant; Male; Middle Aged; Osteomalacia; Phosphates; Rickets; Time Factors; Vitamin D; Vitamin D Deficiency

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

Topics: Animals; Biological Transport; Calcium; Cholecalciferol; Dactinomycin; Dihydroxycholecalciferols; Ethane; Homeostasis; Hydroxycholecalciferols; Hydroxylation; Hypercalcemia; Hypocalcemia; Intestinal Mucosa; Kidney; Mitochondria; Mitochondrial Swelling; Mixed Function Oxygenases; Organophosphonates; Parathyroid Hormone; Phosphorus; Vitamin D; Vitamin D Deficiency

Topics: Acute Disease; Adult; Animals; Calcitonin; Calcium; Calcium, Dietary; Cholecalciferol; Chronic Disease; Fatty Acids; Homeostasis; Humans; Hypocalcemia; Hypophysectomy; Malabsorption Syndromes; Pancreas; Pancreatic Diseases; Pancreatitis; Parathyroid Hormone; Pituitary Gland; Thyroxine

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

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

Topics: Binding Sites; Calcium Metabolism Disorders; Cholecalciferol; Female; Hypocalcemia; Rickets; Tritium; Vitamin D

Topics: Calcitonin; Calcium; Cholecalciferol; Humans; Hyperparathyroidism; Hypocalcemia; Kidney Failure, Chronic; Osteitis Fibrosa Cystica; Osteomalacia; Parathyroid Glands; Phosphorus

Transient hypocalcemia due to parathyroid gland or vessel manipulation is a common complication following thyroidectomy. Considering the role of 25-hydroxyvitamin D (25(OH)D) in calcium hemostasis, this study aimed to evaluate the effect of preoperative vitamin D supplementation on hypocalcemia incidence in thyroidectomy patients.. In this randomized clinical trial, 100 patients scheduled for total thyroidectomy and suffering from preoperative moderate or severe vitamin D deficiency were enrolled. Patients were randomly allocated to either study or control groups using the sealed envelope method. Patients in the study group received vitamin D3 50,000-unit pearl weekly for 4 weeks prior to the operation. The control group received placebo. Total and ionized serum calcium levels were checked before surgery, the day after surgery, and 2 weeks postoperatively.. No significant difference was observed in terms of demographic data. During serial total calcium checks (5 episodes), total calcium levels changed significantly in patients who had received vitamin D supplements compared to the control group (P = 0.043). Symptomatic hypocalcemia incidence was significantly lower in patients supplemented with 25-hydroxyvitamin D (25(OH)D) (P = 0.04). Also, the requirement for intravenous calcium administration in order to treat the hypocalcemia symptoms was significantly lower in the study in comparison to the control group (P = 0.03).. Vitamin D supplementation in patients with vitamin D deficiency might lead to a lower incidence of early-onset symptomatic hypocalcemia; hence, requiring less calcium supplementation for the management of hypocalcemia.

Topics: Adenocarcinoma, Follicular; Adult; Calcium; Cholecalciferol; Female; Goiter, Nodular; Humans; Hypocalcemia; Male; Postoperative Complications; Preoperative Care; Thyroid Cancer, Papillary; Thyroid Diseases; Thyroid Neoplasms; Thyroidectomy; Vitamin D; Vitamin D Deficiency; Vitamins

Post-thyroidectomy hypocalcaemia is a significant cause of morbidity and prolonged hospitalization, usually due to transient parathyroid gland damage, treated with calcium and vitamin D supplementation. We present a randomized, double-blinded placebo-controlled trial of preoperative loading with high-dose cholecalciferol (300 000 IU) to reduce post-thyroidectomy hypocalcaemia.. Patients (n = 160) presenting for thyroidectomy at tertiary hospitals were randomized 1:1 to cholecalciferol (300 000 IU) or placebo 7 days prior to thyroidectomy. Ten patients withdrew prior to surgery. The primary outcome was post-operative hypocalcaemia (corrected calcium <2.1 mmol/L in first 180 days).. The study included 150 patients undergoing thyroidectomy for Graves' disease (31%), malignancy (20%) and goitre (49%). Mean pre-enrolment vitamin D was 72 ± 26 nmol/L. Postoperative hypocalcaemia occurred in 21/72 (29%) assigned to cholecalciferol and 30/78 (38%) participants assigned to placebo (P = 0.23). There were no differences in secondary end-points between groups. In pre-specified stratification, baseline vitamin D status did not predict hypocalcaemia, although most individuals were vitamin D replete at baseline. Post-hoc stratification by day 1 parathyroid hormone (PTH) (<10 pg/mL, low vs ≥10 pg/mL, normal) was explored due to highly divergent rates of hypocalcaemia in these groups. Using a Cox regression model, the hazard ratio for hypocalcaemia in the cholecalciferol group was 0.56 (95%CI 0.32-0.98, P = 0.04) after stratification for Day 1 PTH. Further clinical benefits were observed in these subgroups.. Pre-thyroidectomy treatment with high-dose cholecalciferol did not reduce the overall rate of hypocalcaemia following thyroidectomy. In subgroups stratified by day 1 PTH status, improved clinical outcomes were noted.

Topics: Adult; Calcium-Regulating Hormones and Agents; Cholecalciferol; Female; Humans; Hypocalcemia; Male; Middle Aged; Premedication; Preoperative Care; Thyroidectomy; Treatment Outcome

There are several studies in which a correlation between maternal vitamin D deficiency and serum mineral disorders in the mother and the newborn has been reported. The present randomised clinical trial was designed to investigate the effect of vitamin D administration on maternal and fetal Ca and vitamin D status. The trial was carried out on 160 pregnant women. Vitamin D-deficient (25-hydroxyvitamin D (25(OH)D) < 30 ng/ml) pregnant women were recruited at 26-28 weeks of pregnancy. In the control group, a multivitamin supplement containing 400 IU vitamin D3/d was given. Patients in the treatment group were treated with 50 000 IU vitamin D3 weekly for a total duration of 8 weeks. At delivery, maternal and fetal Ca and 25(OH)D levels in both groups were compared. In total, 81 % of pregnant women were vitamin D deficient. At the time of delivery, Ca and vitamin D levels were higher in the treatment group compared with the control group (92 (SD 3) v. 85 (SD 4) mg/l, respectively, P= 0·001 for serum Ca; 47·8 (SD 11·1) v. 15·9 (SD 6·6) ng/ml, respectively, P< 0·001 for vitamin D). At the time of delivery, 32·7 % of women in the control group had hypocalcaemia, while no hypocalcaemic case was detected in the vitamin D-treated group. Mean neonatal serum 25(OH)D was higher in the treatment group compared with the control group (27·7 (SD 5·2) v.10·9 (SD 4·4) ng/ml, respectively, P< 0·01). The neonatal Ca level in the treatment group was significantly higher than that of the control group (99 (SD 3) v. 91 (SD 3) mg/l, respectively, P< 0·001). The administration of vitamin D to pregnant women with vitamin D deficiency improves both maternal and neonatal Ca levels.

Topics: Adult; Calcium; Cholecalciferol; Dietary Supplements; Female; Fetus; Humans; Hypocalcemia; Infant, Newborn; Pregnancy; Pregnancy Complications; Prevalence; Vitamin D; Vitamin D Deficiency; Young Adult

The purpose of this study was to determine the effectiveness of oral calcium plus vitamin D supplementation and to compare the effects of cholecalciferol versus calcitriol treatments on postoperative hypocalcemia.. After total thyroidectomy with central neck dissection, 306 patients were divided into 4 groups according to "routine use versus on-demand use" and "cholecalciferol versus calcitriol.". Hypocalcemic symptoms developed in 101 patients (33.0%). Hypocalcemia developed less frequently in patients receiving routine supplementation regardless of vitamin D type. However, routine supplementation did not prevent severe hypocalcemia. In patients receiving on-demand supplements, calcitriol was more effective and faster acting than was cholecalciferol.. Routine oral calcium and vitamin D supplements are beneficial after total thyroidectomy with central neck lymph node dissection with no difference between cholecalciferol and calcitriol. If taken after the onset of hypocalcemia, however, calcitriol along with calcium carbonate seems to be more effective than is cholecalciferol with calcium carbonate.

Topics: Administration, Oral; Adult; Aged; Bone Density Conservation Agents; Calcitriol; Calcium Carbonate; Cholecalciferol; Female; Humans; Hypocalcemia; Male; Middle Aged; Neck Dissection; Prospective Studies; Severity of Illness Index; Thyroidectomy; Young Adult

The aim of this study was to find an effective treatment for hypocalcemic symptoms during plateletpheresis and to evaluate if a combination of calcium, magnesium and vitamin D3 is more effective in comparison to routine calcium supplementation.. A study group consisting of 10 donors, having a history of previous hypocalcemic symptoms during plateletpheresis, donated platelets twice in a one-month period. During the first donation combination tablets (600mg Ca+300mg Mg+100IU vitamin D3) were used to treat hypocalcemic symptoms while routine treatment calcium carbonate tablets (1000mg Ca) were used during the second donation. If symptoms persisted after 10min the same dose was repeated. A control group, with no supplementation, consisting of five donors, with no history of hypocalcemic symptoms, were included. Donor subjective symptoms were graded and recorded on four occasions: at the start of plateletpheresis, when symptoms appeared, 10min after the first tablet and at the end of donation. Samples for analysis of ionized calcium (iCa), magnesium and potassium were also taken at the same occasions.. All donors from the study group experienced minor or medium hypocalcemic symptoms and needed a second dose of supplementation. Calcium carbonate tablets completely relieved the hypocalcemic symptoms in six donors, it had no effect on three donors and one donor experienced aggravated symptoms. The combination tablets completely relieved the symptoms in three donors, one donor experienced a partial relief and six donors had no relief of symptoms. There were no significant differences in iCa, potassium and magnesium levels were noted in the study group irrespective of which tablets were used for treatment of hypocalcemic symptoms. After plateletpheresis the median iCa levels declined by 30% and potassium levels declined by 3-11% in all donors while the magnesium levels were not significantly affected. There was no correlation between the presence of symptoms and the changed levels of iCa or magnesium.. Addition of magnesium and vitamin D3 to calcium seems to have no beneficial effect in the treatment of hypocalcemic symptoms in plateletpheresis donors.

Topics: Calcium; Case-Control Studies; Cholecalciferol; Drug Therapy, Combination; Humans; Hypocalcemia; Magnesium; Plateletpheresis; Potassium; Premedication; Treatment Outcome

Age, postoperative serum parathormone (PTH) level, and preoperative serum 25-hydroxyvitamin D(3) (25-OHD) level predict postoperative hypocalcemia after total thyroidectomy.. Prospective clinical trial.. Tertiary referral center.. One hundred thirty patients with nontoxic multinodular goiter. Patients were divided into 2 groups according to the postoperative serum calcium level. Group 1 (n = 32) consisted of patients with a postoperative serum calcium level of 8 mg/dL or less, and group 2 (n = 98) consisted of patients with a postoperative serum calcium level higher than 8 mg/dL.. The preoperative serum 25-OHD level and preoperative and postoperative serum calcium and PTH levels were determined.. The number of patients developing hypocalcemia and prediction of postoperative hypocalcemia by the serum 25-OHD and PTH levels.. Hypocalcemia developed in 32 patients (24.6%) (group 1). The preoperative serum 25-OHD level and postoperative serum calcium and PTH levels in group 1 were significantly lower than in group 2 (P = .001). With logistic regression analysis, factors that were predictive of postoperative hypocalcemia included a preoperative serum 25-OHD level less than 15 ng/mL (P < .001; odds ratio, 558.5), a postoperative serum PTH level less than 10 pg/mL (P = .01; odds ratio, 16.4), and being older than 50 years (P = .01; odds ratio, 4.6).. Age, a low preoperative serum 25-OHD level, and a low postoperative serum PTH level are significantly associated with postoperative hypocalcemia. The low preoperative serum 25-OHD level was more significant than the low postoperative serum PTH level in the prediction of postoperative hypocalcemia.

Topics: Adolescent; Adult; Aged; Cholecalciferol; Female; Goiter, Nodular; Humans; Hypocalcemia; Male; Middle Aged; Parathyroid Hormone; Predictive Value of Tests; Prospective Studies; Thyroidectomy

Hypocalcemia is one of the most frequent complications after total extracapsular thyroidectomy (TET). In most of cases it is a transient phenomenon. The aim of this study is to evaluate if and how the oral administration of calcium or calcium combined with D-vitamin could effectively prevent post-thyroidectomy hypocalcemia. A randomized prospective study was performed, recruiting 120 patients who underwent total thyroidectomy. The patients in our series were randomly assigned to one of two groups: group A--patients who received calcium lactogluconate/calcium carbonate (mg 300 per day); group B--patients who received calcium carbonate/cholecalciferol therapy (calcium carbonate: 1500 mg per day; cholecalciferol 400 UI per day). The groups were well matched for age, sex and pathologies. Patients of both A and B groups were divided in two subgroups: those operated on for benign thyroid diseases (A1 and B1) and those operated on for malignancy (A2, B2). Serum calcium assays, performed 24, 48 and 72 hours after surgery, showed mean values of calcemia higher in patients of the B1 and B2 group. Statistical analysis was performed using a Student's t test. Mean serum calcium concentrations on post-operative day one, two and three were higher in patients of the group B (p<<0.01). Early and combined oral administration of both calcium and vitamin D seemed to prove major efficacy in preventing and treating post-operative hypocalcemia, showing mean serum calcium levels higher than those of patients who received only oral calcium administration. Nevertheless, further studies are necessary to validate these data.

Topics: Adult; Antacids; Calcium Carbonate; Cholecalciferol; Drug Therapy, Combination; Female; Gluconates; Humans; Hypocalcemia; Male; Middle Aged; Prospective Studies; Thyroidectomy; Treatment Outcome; Vitamins

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

Fifty elderly patients with hypocalcaemia were randomly treated for 8 weeks with either oral dihydrotachysterol, parenteral cholecalciferol or oral alfacalcidol. All three treatments were successful in normalizing the serum calcium levels in most patients within 2 weeks. Hypercalcaemia was seen only with alfacalcidol but was rapidly reversed once treatment was discontinued. Hypercalcaemia was not observed with either dihydrotachysterol or cholecalciferol. These therefore, require less frequent biochemical monitoring. A single cholecalciferol injection eliminates the problems of compliance.

Topics: Aged; Aged, 80 and over; Cholecalciferol; Dihydrotachysterol; Humans; Hydroxycholecalciferols; Hypocalcemia

Denosumab is known to cause abnormalities in calcium homeostasis. Most of such cases have been described in patients with underlying chronic kidney disease or severe vitamin D deficiency. Previous bariatric surgery could also contribute to hypocalcemia and deterioration in bone health.. We present a case of a 61-year-old Malay female with worsening bilateral limb weakness, paresthesia, and severe carpopedal spasm a week after receiving subcutaneous denosumab for osteoporosis. She had a history of gastric bypass surgery 20 years ago. Post gastric bypass surgery, she was advised and initiated on lifelong calcium, vitamin D, and iron supplementations that she unfortunately stopped taking 5 years after surgery. Her last serum blood tests, prior to initiation on denosumab, were conducted in a different center, and she was told that she had a low calcium level; hence, she was advised to restart her vitamin and mineral supplements. Laboratory workup revealed severe hypocalcemia (adjusted serum calcium of 1.33 mmol/L) and mild hypophosphatemia (0.65 mmol/L), with normal magnesium and renal function. Electrocardiogram showed a prolonged QTc interval. She required four bolus courses of intravenous calcium gluconate, and three courses of continuous infusions due to retractable severe hypocalcemia (total of 29 vials of 10 mL of 10% calcium gluconate intravenously). In view of her low vitamin D level of 33 nmol/L, she was initiated on a loading dose of cholecalciferol of 50,000 IU per week for 8 weeks. However, despite a loading dose of cholecalciferol, multiple bolus courses, and infusions of calcium gluconate, her serum calcium hovered around only 1.8 mmol/L. After 8 days of continuous intravenous infusions of calcium gluconate, high doses of calcitriol 1.5 μg twice daily, and 1 g calcium carbonate three times daily, her serum calcium stabilized at approximately 2.0 mmol/L. She remained on these high doses for over 2 months, before they were gradually titrated down to ensure sustainability of a safe calcium level.. This case report highlights the importance of screening for risk factors for iatrogenic hypocalcemia and ensuring normal levels before initiating denosumab. The patient history of bariatric surgery could have worsened the hypocalcemia, resulting in a more severe presentation and protracted response to oral calcium and vitamin D supplementation.

Topics: Bariatric Surgery; Calcium; Calcium Gluconate; Cholecalciferol; Denosumab; Female; Humans; Hypocalcemia; Middle Aged; Vitamin D; Vitamins

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

Hypomagnesemia with secondary hypocalcemia (HSH) is a genetic disorder arising from the body's impaired capacity to absorb and retain magnesium (Mg2+) consumed through diet. Consequently, Mg2+ levels in blood are significantly reduced, a condition referred to as hypomagnesemia. Insufficient levels of Mg2+ and calci-um (Ca2+) can lead to neurological complications that manifest during infancy, such as painful muscle spasms (tet-any) and seizures.. We reported a case of HSH involving a 10-year-old male patient from a Han Chinese family. He was admitted due to recurrent convulsions experienced over the past two years. The patient's initial episode occurred two years prior, when he collapsed without apparent cause and exhibited limb numbness, convulsions, and a disordered state of consciousness, accompanied by hypocalcemia. Cranial CT scans revealed multiple symmetrical calcifications in the basal ganglia, corona radiata, and cerebellar dentate nucleus.. During the hospital stay, the patient was administered the following treatments: Calcium Carbonate and Vitamin D3 Tablets (1.5 g of calcium carbonate and 125 IU of Vitamin D3 per tablet, 1 tablet/time) once daily, Calcitriol Soft Capsules (0.25 μg of calcitriol per capsule, 1 capsule/time) twice daily, Potassium Chloride Sustained-release Tablets (0.5 g of potassium chloride per tablet, 1 tablet/time) thrice daily, Potassium Aspartate and Mag-nesium Aspartate Tablets (158 mg of potassium aspartate and 140 mg of magnesium aspartate per tablet, 1 tablet/ time) thrice daily, and intravenous infusions of Magnesium Sulfate Injection (2.5 g/time) twice daily. After three days in the hospital, the patient's initial symptoms subsided, resulting in discharge with a prescription of ongoing oral medications including Calcium Carbonate and Vitamin D3 Tablets, Calcitriol Soft Capsules, and Potassium Aspartate and Magnesium Aspartate Tablets, with the same usage and dosage as the above three drugs. A month subsequent, the serum levels of Mg2+, Ca2+, potassium (K+), and phosphorus were 0.96 mmol/L, 2.52 mmol/L, 4.06 mmol/L, and 1.63 mmol/L, respectively.. Primary HSH is an uncommon manifestation of parathyroid hypoplasia, clinically characterized by low levels of Mg2+, Ca2+, and K+ in the blood. Our findings serve to enrich and consolidate the knowledge for future case studies and follow-up investigations.

Topics: Aspartic Acid; Calcitriol; Calcium; Calcium Carbonate; Child; Cholecalciferol; Humans; Hypocalcemia; Magnesium; Male; Potassium Chloride; Seizures; Tablets

Denosumab can improve bone health in advanced kidney disease (CKD) but is associated with hypocalcemia. We created a clinical care pathway focused on the safe provision of denosumab in advanced CKD that reduced the risk of hypocalcemia by 37% at our hospital. Similar pathways could be adopted and tested in other centers.. There is an increased risk of hypocalcemia with denosumab in advanced chronic kidney disease (CKD). We aimed to reduce the proportion of patients with advanced CKD who experienced denosumab-induced hypocalcemia at our center.. There were 6 patients with advanced CKD treated with denosumab prior to the implementation of our care pathway (March 2015-October 2020; 83% receiving dialysis). At the time of their denosumab injection, 83% were using 500-1000 mg of calcium, and 83% used 1000-2000 IU of vitamin D. A clinical care pathway focused on the safe provision of denosumab in advanced CKD reduced the risk of hypocalcemia in patients treated in our hospital. Similar pathways could be adopted and tested in other centers.

Topics: Bone Density Conservation Agents; Calcium; Cholecalciferol; Denosumab; Humans; Hypercalcemia; Hyperphosphatemia; Hypocalcemia; Quality Improvement; Renal Insufficiency, Chronic

Denosumab-induced hypocalcemia is sometimes severe, and although a natural vitamin D/calcium combination is used to prevent hypocalcemia, some patients rapidly develop severe hypocalcemia even under supplementation. It is clinically important to predict this risk. This study aimed to develop a risk prediction model for grade ≥2 hypocalcemia within 28 days after the first denosumab dose under natural vitamin D/calcium supplementation. Using a large database containing multicenter practice data, 2399 patients with bone metastasis who were treated with denosumab between June 2013 and May 2020 were retrospectively analyzed. Background factors in patients who developed grade ≥2 hypocalcemia within 28 days after the first denosumab dose and those who did not were compared by univariate analysis. Multivariate analysis was conducted to develop a risk prediction model. The model was evaluated for discriminant performance (receiver operating characteristic-area under the curve, sensitivity, specificity) and predictive performance (calibration slope). A total of 124 patients in the hypocalcemia group and 1191 patients in the nonhypocalcemia group were extracted. A risk prediction model consisting of sex, calcium, albumin, alkaline phosphatase, osteoporosis, breast cancer, gastric cancer, proton pump inhibitor combination, and pretreatment with zoledronic acid was developed. The receiver operating characteristic-area under the curve was 0.87. Sensitivity and specificity were 83% and 81%, respectively, and the calibration slope indicated acceptable agreement between observed and predicted risk. This model appears to be useful to predict the risk of denosumab-induced hypocalcemia and thus should be helpful for risk management of denosumab treatment in patients with bone metastases.

Topics: Bone Density Conservation Agents; Bone Neoplasms; Calcium; Cholecalciferol; Denosumab; Humans; Hypocalcemia; Retrospective Studies; Vitamin D

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

Topics: Calcium Gluconate; Cholecalciferol; Humans; Hypocalcemia; Infant; Male; Rickets; Seizures

Due to the sudden increase of calcium demand at the onset of lactation many high yielding dairy cows experience a certain level of hypocalcaemia following parturition. The incidence of hypocalcaemia (parturient paresis) increases with age but also depends on many other factors such as the acid-base status and the availability of calcium as well as other minerals and trace elements. Hypocalcaemia can easily be treated by supplementation of calcium parenterally or orally, nonetheless, prophylaxis of the condition should be the main focus in modern dairy farming, in order to avoid its negative effects. Oral administration of calcium around parturition is the simplest way of prophylaxis, but results in a high work load and requires exact knowledge of the date of parturition. The latter also applies for the parenteral administration of vitamin D. Durch den laktationsbedingten sprunghaften Anstieg des Kalziumbedarfs nach der Geburt können hochleistende Milchkühe in eine hypokalzämische Stoffwechsellage geraten. Die Anfälligkeit für das Auftreten einer Gebärparese steigt dabei mit zunehmendem Alter der Tiere, hängt aber auch von zahlreichen anderen Faktoren wie dem Säure-Basen-Haushalt und der Versorgung mit Kalzium sowie anderen Mineralstoffen und Spurenelementen ab. Die Therapie erfolgt durch Kalziumapplikation, meist in Kombination mit Magnesium. Um die negativen Folgen des Kalziummangels zu vermeiden, sollte das Augenmerk jedoch auf dessen Prophylaxe liegen. Die peripartale orale Applikation von Kalziumverbindungen, eine der einfachsten Prophylaxemaßnahmen, ist mit einem hohen Arbeitsaufwand verbunden und setzt eine genaue Kenntnis des Geburtstermins voraus. Letzteres trifft auch für die parenterale Applikation von Vitamin D

Topics: Administration, Oral; Animals; Calcium; Cattle; Cattle Diseases; Cholecalciferol; Diet; Female; Hypocalcemia; Ions; Parturient Paresis; Potassium; Pregnancy; Time-to-Treatment

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

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

The objectives of the experiment were to evaluate the effects of feeding diets with distinct dietary cation-anion difference (DCAD) levels and supplemented with 2 sources of vitamin D during the prepartum transition period on postpartum health and reproduction in dairy cows. The hypotheses were that feeding acidogenic diets prepartum would reduce the risk of hypocalcemia and other diseases, and the benefits of a negative DCAD treatment on health would be potentiated by supplementing calcidiol compared with cholecalciferol. Cows at 252 d of gestation were blocked by parity (28 nulliparous and 52 parous cows) and milk yield within parous cows, and randomly assigned to 1 of 4 treatments arranged as a 2 × 2 factorial, with 2 levels of DCAD, positive (+130 mEq/kg) or negative (-130 mEq/kg), and 2 sources of vitamin D, cholecalciferol or calcidiol, fed at 3 mg for each 11 kg of diet dry matter. The resulting treatment combinations were positive DCAD with cholecalciferol (PCH), positive DCAD with calcidiol (PCA), negative DCAD with cholecalciferol (NCH), and negative DCAD with calcidiol (NCA), which were fed from 252 d of gestation to calving. After calving, cows were fed the same lactation diet supplemented with cholecalciferol at 0.70 mg for every 20 kg of dry matter. Blood was sampled 7 d before parturition, and at 2 and 7 d postpartum to evaluate cell counts and measures of neutrophil function. Postpartum clinical and subclinical diseases and reproductive responses were evaluated. Feeding a diet with negative DCAD eliminated clinical hypocalcemia (23.1 vs. 0%) and drastically reduced the incidence and daily risk of subclinical hypocalcemia, and these effects were observed in the first 48 to 72 h after calving. The diet with negative DCAD tended to improve the intensity of oxidative burst activity of neutrophils in all cows prepartum and increased the intensity of phagocytosis in parous cows prepartum and the proportion of neutrophils with killing activity in parous cows postpartum (58.5 vs. 67.6%). Feeding calcidiol improved the proportion of neutrophils with oxidative burst activity (60.0 vs. 68.7%), reduced the incidences of retained placenta (30.8 vs. 2.5%) and metritis (46.2 vs. 23.1%), and reduced the proportion of cows with multiple diseases in early lactation. Combining the negative DCAD diet with calcidiol reduced morbidity by at least 60% compared with any of the other treatments. Cows with morbidity had lower blood ionized Ca and serum total Ca con

Topics: Animal Feed; Animals; Anions; Asymptomatic Diseases; Calcifediol; Cations; Cattle; Cattle Diseases; Cholecalciferol; Diet; Dietary Supplements; Female; Hypocalcemia; Pregnancy; Pregnancy, Animal; Random Allocation; Vitamin D

Topics: Bone Density Conservation Agents; Calcium Citrate; Cholecalciferol; Female; Fractures, Bone; Humans; Hypocalcemia; Ibandronic Acid; Middle Aged; Osteoporosis; Pubic Bone; Sacrum; Vitamin D Deficiency

A 58-year-old male patient was admitted at the São Bernardos's Hospital (Setúbal, Portugal) with generalised muscle spasms, dyspnoea, laryngospasm and bronchospasm in the context of severe hypocalcaemia. Despite efforts to correct serum calcium, it remained below average, leading to question the true cause of hypocalcaemia. Low parathyroid hormone and 25-hydroxyvitamin D, along with facial anomalies, palate defect and cognitive impairment with concomitant psychiatric disorder led to a suspicion of a DiGeorge/velocardiofacial/22q11.2 deletion syndrome (DS), which was confirmed through genetic testing. The 22q11.2 DS has a wide phenotypic expression and there are growing reports of diagnosis being made in adulthood. This case report highlights the importance of understanding the cause of refractory hypocalcaemia and alerts medical community to carefully access these patients, for this metabolic disorder may only present in later stages of life.

Topics: Antacids; Bone Density Conservation Agents; Bronchial Spasm; Calcium Carbonate; Cholecalciferol; DiGeorge Syndrome; Dyspnea; Humans; Hypocalcemia; Laryngismus; Male; Middle Aged; Spasm; Treatment Outcome

There is clinical uncertainty as to the testing of serum 25--Hydroxy vitamin D (25[OH]D) concentrations and when to use high-dose supplementation. Data show that there has been a rapid increase in the number of tests performed within the Northumbria Healthcare NHS Foundation Trust over the past 8 years and an increase in high-dose supplementation over the past 5 years. We performed a retrospective analysis of the 25(OH)D test requests over the period from January to -October 2017. A total of 17,405 tests were performed in this time period. The overall average concentration was 57.5 nmol/L and this figure was similar across age groups, although a larger proportion of patients aged over 75 had a concentration <25 nmol/L. Test requests were classified into 'appropriate', 'inappropriate' and 'uncertain' categories based on current expert opinion. We found that between 70.4% and 77.5% of tests could be inappropriate, depending on whether the 'uncertain' categories of falls and osteoporosis are considered to be justified. Tiredness, fatigue or exhaustion was the reason for testing in 22.4% of requests. We suggest that a more rational approach to testing, and subsequent treating, could lead to reductions in costs to the healthcare system and patients.

Topics: Accidental Falls; Adult; Aged; Alkaline Phosphatase; Cholecalciferol; Clinical Laboratory Techniques; Dietary Supplements; Female; Humans; Hypocalcemia; Hypophosphatemia; Male; Medical Overuse; Middle Aged; Osteoporosis; Retrospective Studies; State Medicine; United Kingdom; Vitamin D; Vitamin D Deficiency; Vitamins

In dairy cows, hypocalcemia is caused by the sudden calcium demand by the mammary gland at the onset of lactation. Calcitriol (1,25-dihydroxy vitamin D; 1,25-VitD) increases the intestinal calcium absorption and the renal calcium reabsorption. Daylight contributes to the formation of 1,25-VitD, as it transforms 7-dehydrocholesterol into cholecalciferol, a 1,25-VitD precursor. Calving pens are usually set in quiet places where cows can stay calm and relaxed before parturition. However, those pens often have poor lighting conditions and therefore cows may become vitamin D deficient because of inadequate daylight exposure. Therefore, we have tested the hypothesis that direct daylight exposure supports the synthesis of 1,25-VitD and consequently attenuates the decline of calcium concentrations at parturition. Twenty Holstein dairy cows were randomly assigned to 2 experimental groups (daylight group, DL; and control group). Beginning on d -10 before expected parturition, both groups were placed in a standard indoor calving pen from 1700 h to 800 h. From 800 h to 1700 h cows from the DL group were moved into a contiguous open pen with direct access to daylight whereas controls remained at the standard indoor calving pen. After parturition both groups were permanently placed in an indoor calving pen until the end of the experimental period (d 30 postpartum). Blood samples were collected daily from d -10 prior to expected parturition through d 7 postpartum with an additional sample on d 30 postpartum. Milk yield was recorded at each milking during the whole experimental period. In the DL group, 25-hydroxyvitamin D (25-VitD), 1,25-VitD and total calcium concentrations around parturition were higher than in the controls. Higher parathyroid hormone concentrations were observed in the control group compared to the DL group at parturition. Pyridinoline concentrations did not differ between groups on d 1, and therefore it is assumed that the intensity of calcium transfer from the bones to the bloodstream was not affected by the increased daylight exposure. The measured plasma metabolites (β-hydroxybutyrate, fatty acids and glucose) as well as milk yield were not affected by the increased daylight exposure. In conclusion, the increased daylight exposure before parturition increased 25-VitD and 1,25-VitD concentrations, preventing a considerable decline of total calcium concentrations around parturition.

Topics: 3-Hydroxybutyric Acid; Animals; Calcifediol; Calcium; Cattle; Cholecalciferol; Dehydrocholesterols; Female; Hypocalcemia; Lactation; Light; Milk; Parathyroid Hormone; Parturition; Postpartum Period; Pregnancy; Random Allocation; Vitamin D

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

Denosumab-associated hypocalcaemia (DAH) has been reported in patients with osteoporosis or metastatic bone disease and is associated with stages 4 and 5 chronic kidney disease (CKD, estimated glomerular filtration rate <30 mL/min/1.73m. Retrospective cohort study between June 2013 and June 2014 of patients administered denosumab (60/120 mg) at a tertiary hospital in Melbourne, Australia, to identify the incidence of an albumin-adjusted serum calcium concentration <2.10 mmol/L or ionized calcium <1.13 mmol/L within 6 months of treatment. Univariable and multivariable logistic regression analyses were performed to identify clinical features associated with DAH.. One hundred and fifty-five patients were administered denosumab (100 osteoporosis, 55 bone metastases). Twenty-two patients (14% [95%CI 9.1-20.7]) developed hypocalcaemia: 55% were men, and 55% had osteoporosis. Eighty-six per cent had a 25-hydroxyvitamin D concentration >50 nmol/L, and 91% were on calcium/colecalciferol supplementation. Stages 4 and 5 CKD (adjusted odd ratio [aOR] 4.71, 95%CI 1.61-13.79, p = 0.005) and male sex (aOR 4.30, 95%CI 1.69-10.96, p = 0.002) were associated with DAH. No patients were documented as having hypocalcaemic symptoms. One patient received intravenous calcium gluconate treatment.. The incidence of denosumab-associated hypocalcaemia was 14% (95%CI 9.1-20.7) within 6 months of treatment despite widespread use of appropriate calcium/colecalciferol supplementation. Stages 4 and 5 CKD and male sex were associated with subsequent hypocalcaemia. Copyright © 2016 John Wiley & Sons, Ltd.

Topics: Aged; Aged, 80 and over; Australia; Bone Density Conservation Agents; Calcium; Cholecalciferol; Cohort Studies; Denosumab; Female; Glomerular Filtration Rate; Humans; Hypocalcemia; Incidence; Male; Renal Insufficiency, Chronic; Retrospective Studies; Risk Factors; Severity of Illness Index; Sex Factors; Tertiary Care Centers; Vitamin D

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

Topics: Aged, 80 and over; Bone Density Conservation Agents; Calcitriol; Calcium Carbonate; Cholecalciferol; Denosumab; Female; Fractures, Bone; Humans; Hypercalcemia; Hypocalcemia; Medication Errors; Renal Insufficiency, Chronic; Tetany

The main barriers to short stay thyroidectomy are haemorrhage, bilateral recurrent laryngeal nerve palsy causing respiratory compromise and hypocalcaemia. This study assessed the safety and effectiveness of thyroidectomy as a 23-hour stay procedure.. All patients undergoing total or completion thyroidectomy were prescribed calcium and vitamin D3 supplements following surgery. Retrospective analysis identified patients admitted for longer than 23 hours and any readmissions.. A total of 164 patients were admitted for 23-hour stay thyroid surgery over a 25-month period between 2008 and 2010. Four patients (2%) required admission for longer than 23 hours. No patients required emergency intervention for postoperative haemorrhage or airway compromise. Biochemical hypocalcaemia (despite calcium supplements) was detected in one patient when measured at the outpatient clinic two weeks following surgery. Twelve patients (7.3%) attended the accident and emergency department following discharge; four required admission for intravenous antibiotics for wound infection and one for biochemical hypocalcaemia.. This single centre UK experience demonstrates that thyroidectomy can be carried out both safely and effectively as a 23-hour stay procedure. Prophylactic prescription of calcium and vitamin D3 reduces hypocalcaemia, and thereby also prolonged admission and readmission due to hypocalcaemia. Supplements are an acceptable, cost effective method of reducing hypocalcaemia and shortening postoperative length of stay.

Topics: Ambulatory Surgical Procedures; Calcium; Cholecalciferol; Humans; Hypocalcemia; Length of Stay; Patient Readmission; Retrospective Studies; Thyroid Diseases; Thyroidectomy; Vitamins

Hypocalcemia is a rare condition that causes dilated cardiomyopathy and can result in heart failure. Patients with hypocalcemia have been reported to recover in 3 to 12 months after calcium and vitamin D replacement therapy as well as treatment of heart failure. A 6-month-old male patient who presented with dyspnea was admitted to the intensive care unit with severe heart failure and dilated cardiomyopathy. Blood biochemistry revealed hypocalcemia and vitamin D deficiency. After administration of anticongestive treatment, positive inotropic support, as well as vitamin D and calcium supplementation, cardiac function returned to normal in a week. Our case is the first report of such a rapid improvement in cardiac morphology and function in a patient with hypocalcemic dilated cardiomyopathy and heart failure.

Topics: Calcium Gluconate; Cardiomyopathies; Cholecalciferol; Heart Failure; Humans; Hypocalcemia; Infant; Male; Remission Induction; Time Factors; Vitamin D Deficiency; Vitamins

Rickets was first described in the 17th century and vitamin D deficiency was recognized as the underlying cause in the early 1900s. Despite this long history, vitamin D deficiency remains a significant health concern. Currently, vitamin D supplementation is recommended in Canada for breast fed infants. There are no recommendations for supplementation in formula-fed infants.. The objective of this report is to bring attention to the risk of severe vitamin D deficiency in high risk, formula fed infants.. A retrospective chart review was used to create this clinical case series.. Severe vitamin D deficiency was diagnosed in six formula-fed infants over a two-and-a-half year period. All six infants presented with seizures and they resided in First Nation communities located at latitude 54 in the province of Manitoba. While these infants had several risk factors for vitamin D deficiency, they were all receiving cow's milk based formula supplemented with 400 IU/L of vitamin D.. This report suggests that current practice with regards to vitamin D supplementation may be inadequate, especially for high-risk infants. Health care professionals providing service to infants in a similar situation should be aware of this preventable condition. Hopefully this would contribute to its prevention, diagnosis and management.

Topics: Arctic Regions; Calcitriol; Calcium; Canada; Cholecalciferol; Dietary Supplements; Humans; Hypocalcemia; Infant; Infant Formula; Infant, Newborn; Inuit; Retrospective Studies; Risk Factors; Severity of Illness Index; Vitamin D Deficiency

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 man presented with an exacerbation of heart failure following coronary artery bypass grafting. He was found to be severely hypocalcaemic secondary to a combination of decreased parathyroid reserve and severe vitamin D deficiency. On treatment of his hypocalcaemia, all symptoms resolved. This case highlights the importance of recognising that metabolic derangement can affect cardiac function.

Topics: Aged; Calcifediol; Calcium; Cholecalciferol; Coronary Artery Bypass; Diagnosis, Differential; Heart Failure; Humans; Hypocalcemia; Male; Vitamin D Deficiency

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 98-year-old woman was referred to our hospital because of myoclonia. The concentration of calcium and vitamin D in the serum was low. In this context, we concluded of neuromuscular irritability secondary to hypocalcaemia. The symptoms disappeared after a treatment of intravenous calcium. This case shows how important it is to investigate electrolytes in case of neuromuscular irritability symptoms in elderly people.

Topics: Acute Disease; Age Factors; Aged, 80 and over; Calcium; Cholecalciferol; Diagnosis, Differential; Female; Humans; Hypocalcemia; Injections, Intravenous; Magnesium; Myoclonus; Time Factors; Vitamin D

We report two patients with vitamin D deficiency due to unbalanced diet. The patients initially presented with severe hypocalcemia, normophosphatemia and markedly elevated serum PTH levels. Although nutritional vitamin D deficiency was suspected from their history of gastrointestinal problems and dietary restriction, we conducted Ellsworth- Howard test to exclude the possibility of pseudohypoparathyroidism (PHP). Both patients showed no incremental response of urinary phosphate excretion. However, the urinary cAMP response to exogenous PTH was different between the two. Case 1 showed a blunted response (5-fold and 1.54 micro mol/h increase) and case 2 showed a normal response (39-fold and 3.04 micro mol/h increase). According to the criteria of Ellsworth-Howard test, the data of case 1 was compatible with PHP type I, and of case 2 with PHP type II. The final diagnosis of vitamin D deficiency was established in both patients based on very low serum 25-hydroxyvitamin D levels (less than 5 ng/mL) and the effect of treatment. After calcium supplementation with or without vitamin D, their biochemical abnormalities disappeared. They maintained normocalcemia without medication after correction of their unbalanced diet. The present study indicated that patients with vitamin D deficiency occasionally showed biochemical findings suggestive of PHP and that such patients could exhibit not only PHP type II pattern of response to exogenous PTH but also of type I pattern. Thus our clinical observation suggests the complexity of PTH resistance in vitamin D deficiency and underscores the importance of diet to prevent the disorder.

Topics: Adult; Calcium, Dietary; Cholecalciferol; Cyclic AMP; Diagnosis, Differential; Diet; Female; Humans; Hypocalcemia; Parathyroid Hormone; Phosphates; Pseudohypoparathyroidism; Vitamin D; Vitamin D Deficiency

Hypovitaminosis D is a risk factor for transplant-related osteoporosis. Its contribution to severe hypocalcemia in transplant recipients is less well recognized. We present 2 cases to illustrate how risk factors specific to transplant recipients significantly increase the risk of development of severe hypocalcemia, on a background of unrecognized vitamin D deficiency. Regular surveillance of calcium homeostasis should be incorporated into routine clinical care of transplant recipients.

Topics: Calcitriol; Calcium; Cholecalciferol; Cystic Fibrosis; Humans; Hypocalcemia; Immunosuppressive Agents; Lung Transplantation; Magnesium; Male; Middle Aged; Pulmonary Fibrosis; Reference Values; Treatment Outcome; Vitamin D; Vitamin D Deficiency

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

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

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

Paget's disease is a relatively rare disorder of the bone with only a few reports and case series observations from India. Hypocalcaemia is rare in Paget's disease, usually occurring as a consequence of therapy with bisphosphonates. We report a 65-year-old woman with Paget's disease who had hypocalcaemia secondary to vitamin D deficiency. On further evaluation, she also had severe osteoporosis. How vitamin D deficiency affects the diagnosis and monitoring of Paget's disease and the relationship between the three diseases are discussed. This case illustrates an interesting situation with abnormal bone turnover, remodelling and mineralisation in the form of Paget's disease with osteomalacia and osteoporosis.

Topics: Absorptiometry, Photon; Aged; Bone and Bones; Bone Density; Calcium Carbonate; Cholecalciferol; Diphosphonates; Female; Humans; Hypocalcemia; Imidazoles; Lumbar Vertebrae; Osteitis Deformans; Osteomalacia; Vitamin D Deficiency; Zoledronic Acid

Topics: Adult; Ascorbic Acid; Calcium; Cholecalciferol; Female; Fractures, Bone; Humans; Hypocalcemia; Osteomalacia; Pregnancy; Pregnancy Complications; Vitamin D Deficiency

Vitamin D3 may have therapeutic potential in several diseases, including multiple sclerosis. High doses of vitamin D(3) may be required for therapeutic efficacy, and yet tolerability--in the present context, defined as the serum concentration of 25-hydroxyvitamin D [25(OH)D] that does not cause hypercalcemia--remains poorly characterized.. The objective of the study was to characterize the calcemic response to specific serum 25(OH)D concentrations.. In a 28-wk protocol, 12 patients in an active phase of multiple sclerosis were given 1200 mg elemental Ca/d along with progressively increasing doses of vitamin D3: from 700 to 7000 microg/wk (from 28 000 to 280 000 IU/wk).. Mean (+/- SD) serum concentrations of 25(OH)D initially were 78 +/- 35 nmol/L and rose to 386 +/- 157 nmol/L (P < 0.001). Serum calcium concentrations and the urinary ratio of calcium to creatinine neither increased in mean values nor exceeded reference values for any participant (2.1-2.6 mmol/L and <1.0, respectively). Liver enzymes, serum creatinine, electrolytes, serum protein, and parathyroid hormone did not change according to Bonferroni repeated-measures statistics, although parathyroid hormone did decline significantly according to the paired t test. Disease progression and activity were not affected, but the number of gadolinium-enhancing lesions per patient (assessed with a nuclear magnetic brain scan) decreased from the initial mean of 1.75 to the end-of-study mean of 0.83 (P = 0.03).. Patients' serum 25(OH)D concentrations reached twice the top of the physiologic range without eliciting hypercalcemia or hypercalciuria. The data support the feasibility of pharmacologic doses of vitamin D3 for clinical research, and they provide objective evidence that vitamin D intake beyond the current upper limit is safe by a large margin.

Topics: Adult; Bone Density Conservation Agents; Calcium; Cholecalciferol; Creatinine; Dietary Supplements; Disease Progression; Dose-Response Relationship, Drug; Female; Humans; Hypocalcemia; Liver; Magnetic Resonance Imaging; Male; Multiple Sclerosis; Multiple Sclerosis, Relapsing-Remitting; No-Observed-Adverse-Effect Level; Parathyroid Hormone; Reference Values; Risk Factors; Safety; Time Factors; Treatment Outcome; Vitamin D; Vitamin D Deficiency

Topics: Aged; Calcium; Cholecalciferol; Female; Humans; Hypocalcemia

Topics: Adolescent; Adult; Age Factors; Anticonvulsants; Calcium; Child; Child, Preschool; Cholecalciferol; Electroencephalography; Epilepsy; Female; Humans; Hypocalcemia; Magnesium; Male; Middle Aged; Minerals; Phosphorus; Sex Factors; Time Factors

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

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

Gain-of-function mutations of the calcium-sensing receptor (CaR) gene cause autosomal dominant and/or sporadic hypocalcemia with hypercalciuria. Because treatment of the hypocalcemia with vitamin D and/or calcium in patients with such mutations results in increased hypercalciuria, nephrocalcinosis, and renal impairment, its use should be limited to alleviating the symptoms of symptomatic patients. Because thiazide diuretics have been successfully used to treat patients with hypercalciuria and hypoparathyroidism, they are theoretically useful in reducing urine calcium excretion and maintaining serum calcium levels in patients with gain-of-function mutations of the CaR gene. In this study, we report on the clinical course, molecular analysis, and effects of hydrochlorothiazide therapy in two Japanese patients with gain-of-function mutations of the CaR gene. Within a few weeks after birth, they developed generalized tonic seizures due to hypocalcemia (serum calcium values: 1.1 mmol/liter and 1.3 mmol/liter, respectively). Despite treatment with the standard dose of 1,25-dihydroxyvitamin D(3) in one patient and 1alpha-hydroxyvitamin D(3) in the other, acceptable serum calcium levels near the lower limit of normal were not established, and their urinary calcium excretion inappropriately increased. Addition of hydrochlorothiazide (1 mg/kg) reduced their urinary calcium excretion and maintained their serum calcium concentrations near the lower limit of normal, allowing the 1,25-dihydroxyvitamin D(3) and 1alpha-hydroxyvitamin D(3) doses to be reduced, and it alleviated their symptoms. A heterozygous missense mutation was identified in both patients. In one patient, the mutation was A843E in the seventh transmembrane domain of the CaR, and in the other it was L125P in the N-terminal extracellular domain. In vitro transient transfection of their mutant CaR cDNAs into HEK293 cells shifted the concentration-response curve of Ca(2+) to the left. In conclusion, two sporadic cases of hypercalciuric hypocalcemia were due to de novo gain-of-function mutations of the CaR gene. Hydrochlorothiazide with vitamin D(3) successfully reduced the patients' urinary calcium excretion and controlled their serum calcium concentrations and symptoms. Thiazide diuretics are effective in patients with gain-of function mutations of the CaR gene.

Topics: Adolescent; Amino Acid Sequence; Base Sequence; Calcium; Cell Line; Cholecalciferol; Diuretics; Drug Therapy, Combination; Female; Humans; Hydrochlorothiazide; Hypocalcemia; Male; Molecular Sequence Data; Mutation, Missense; Receptors, Calcium-Sensing; Receptors, Cell Surface; Sodium Chloride Symporter Inhibitors

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

Gain-of-function mutations of the calcium-sensing receptor gene have recently been identified as a cause of familial hypercalciuric hypocalcemia. There have been no earlier reported cases of pregnancy among patients with this disorder.. A 26-year-old woman, gravida 1, para 0, was diagnosed at age 18 as being a heterozygous carrier of a mutation in the calcium-sensing receptor gene. Stable maternal hypocalcemia was achieved during pregnancy with high-dose calcium and 1,25-dihydroxyvitamin D3 therapy. Prenatal diagnosis was accomplished via amniocentesis at 16 weeks' gestation. The patient underwent cesarean delivery at 35 5/7 weeks' gestation after developing the HELLP syndrome.. Patients with mutations of the calcium-sensing receptor may have a successful pregnancy outcome. This abnormality may be transmitted to the fetus via an autosomal dominant pattern.

Topics: Adult; Calcium; Calcium Metabolism Disorders; Cholecalciferol; Female; Humans; Hypocalcemia; Mutation; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Receptors, Calcium-Sensing; Receptors, Cell Surface

Calcium plays an important role in various myopathies. We report on an animal model with increased plasma creatine kinase (CK) resulting from hypocalcemia that will provide clues for studying human hypocalcemic myopathy. Male Wistar rats were pair-fed either a control or a calcium- and vitamin D3-deficient diet for 1, 2, 3, 4, or 5-6 weeks after weaning (3 weeks old). In the deficient diet-fed rats, plasma creatine kinase was increased and was accompanied by marked hypocalcemia. The omission of calcium and vitamin D3 from the diet for 1 or 2 weeks was enough to cause increased plasma creatine kinase; the creatine kinase ratio of deficient diet-fed rats to controls was 4.84 (1,777 IU L(-1)/367 IU L(-1)), and the calcium ion ratio was 0.41 (1.8 mg dL(-1)/4.4 mg dL(-1)) after 2 weeks. These values returned to control levels on treatment of the rats with the control diet and 1alpha-OH-vitamin D3 for 1 week.

Topics: Animals; Calcium; Calcium, Dietary; Cholecalciferol; Creatine Kinase; Hydroxycholecalciferols; Hypocalcemia; Male; Muscle Proteins; Muscular Diseases; Rats; Rats, Inbred Lew; Rats, Wistar; Rickets; Specific Pathogen-Free Organisms; Vitamin D Deficiency

Several lines of evidence indicate that calcium deficiency is associated with cellular defects in many tissues and organs. Owing to the large in vivo gradient between ionized extra- and intracellular Ca2+ concentrations ([Ca2+]i), it is generally recognized that the prevailing circulating Ca2+ does not significantly affect resting cytosolic Ca2+. To probe the consequences of hypocalcemia on [Ca2+]i, a model of chronic hypocalcemia secondary to vitamin D (D) deficiency was used. Hepatocytes were isolated from livers of hypocalcemic D-deficient, of normocalcemic D3-repleted, or of normal control rats presenting serum Ca2+ of 0.78 +/- 0.02, 1.24 +/- 0.03, or 1.25 +/- 0.01 mM, respectively (P < 0.0001). [Ca2+]i was measured in cell couplets using the fluorescent probe Fura-2. Hepatocytes of normocalcemic D3-repleted and of normal controls exhibited similar [Ca2+]i of 227 +/- 10 and 242 +/- 9 nM, respectively (NS), whereas those of hypocalcemic rats had significantly lower resting [Ca2+]i (172 +/- 10 nM; P < 0.0003). Stimulation of hepatocytes with the alpha 1-adrenoreceptor agonist phenylephrine illicited increases in cytosolic Ca2+ leading to similar [Ca2+]i and phosphorylase a (a Ca(2+)-dependent enzyme) activity in all groups but in contrast to normocalcemia, low extracellular Ca2+ was often accompanied by a rapid decay in the sustained phase of the [Ca2+]i response. When stimulated with the powerful hepatic mitogen epidermal growth factor (EGF), hepatocytes isolated from hypocalcemic rat livers responded with a blunted maximal [Ca2+]i of 237.6 +/- 18.7 compared with 605.2 +/- 89.9 nM (P < 0.0001) for their normal counterparts, while the EGF-mediated DNA synthesis response was reduced by 50% by the hypocalcemic condition (P < 0.03). Further studies on the possible mechanisms involved in the perturbed [Ca2+]i homeostasis associated with chronic hypocalcemia revealed the presence of an unchanged plasma membrane Ca2+ ATPase but of a significant decrease in agonist-stimulated Ca2+ entry as indicated using Mn2+ as surrogate ion (P < 0.03). Our data, thus indicate that, in rat hepatocytes, the in vivo calcium status significantly affects resting [Ca2+]i, and from this we raise the hypothesis that this lower than normal [Ca2+]i may be linked, in calcium disorders, to inappropriate cell responses mediated through the calcium signaling pathway as illustrated by the response to phenylephrine and EGF.

Topics: Animals; Calcium; Cells, Cultured; Cholecalciferol; Epidermal Growth Factor; Homeostasis; Hypocalcemia; Liver; Male; Phenylephrine; Rats; Rats, Sprague-Dawley; Vitamin D Deficiency

We studied serum concentrations of calcium, phosphate, intact parathyroid hormone (PTH) and vitamin D3 metabolites in 41 patients with nephropathia epidemica. Thirty-four of the 41 patients had a mild to moderate, mostly nonoliguric acute renal failure (ARF). Hypocalcemia developed in relation to the severity of renal failure, and parathyroid gland response to hypocalcemia was normal. The serum concentration of 1,25-dihydroxyvitamin D3 was lower than normal in patients who developed ARF. Serum phosphate was the most important factor in regulating the serum 1,25(OH)2D3 level, though only mild phosphate retention was seen in the patients. We observed normal or slightly elevated serum phosphate, hypocalcemia accompanied by elevated PTH levels and a decreased serum concentration of 1,25(OH)2D3 in patients with ARF caused by nephropathia epidemica.

Topics: Acute Kidney Injury; Adolescent; Adult; Aged; Calcium; Cholecalciferol; Female; Hemorrhagic Fever with Renal Syndrome; Humans; Hypocalcemia; Male; Middle Aged; Nephritis, Interstitial; Orthohantavirus; Parathyroid Hormone; Phosphates

1,25-Dihydroxyvitamin D3 [1,25-(OH)2D3] is known to influence cell proliferation/maturation, whereas epidermal growth factor (EGF) is a potent stimulant of proliferation. Recently, hypocalcemia of vitamin D (D) deficiency was shown to significantly perturbe hepatic regeneration, which could be only partly restored by normalizing extracellular calcium, whereas normalization of 1,25-(OH)2D3 fully restored the process. To define the calcium- and/or D3-sensitive mechanisms associated with liver growth, a study of the initial events transduced by EGF was initiated by probing EGF receptor (EGFR) density and affinity, its subsequent autophosphorylation, and the level of its steady state transcript. Studies were carried out in D-depleted rats kept either untreated or supplemented with D3, 1,25-(OH)2D3, or calcium alone. The hepatic EGFR number (picomoles per mg microsomal protein) was significantly affected by hypocalcemic D-depleted (0.82 +/- 0.2), but responded with similar increases to calcium (1.7 +/- 0.09; P < 0.05), D3 (1.6 +/- 0.3; P < 0.05), and 1,25-(OH)2D3 (2.1 +/- 0.3; P < 0.01). The EGFR mRNA level revealed, however, no significant effect of the calcium or D3 status, indicating that posttranscriptional events were playing an important role. Phosphorylation studies showed that EGFR autophosphorylation and tyrosine protein kinase activity paralleled receptor density, with the lowest autophosphorylation values obtained in hypocalcemic D-depleted rats (D-depleted hypocalcemic vs. D3 repleted, P < 0.007). When normalized for receptor number, however, EGFR autophosphorylation increased in D-depleted hypocalcemic rats to a level comparable to that observed in all other groups. To dissociate the effect of the D3 hormone from that of calcium alone on EGFR, D-depleted rats were treated with the nonhypercalcemic 1,25-(OH)2D3 analog 22-OXA-1,25-(OH)2D3 (OCT), with or without calcium supplementation. Hypocalcemic OCT-treated rats did not exhibit any increase in EGFR number (0.6 +/- 0.1) compared to D-depleted hypocalcemic rats, but the addition of dietary calcium to OCT restored extracellular calcium concentrations and EGFR density (1.8 +/- 0.2; P < 0.002) to values comparable to those observed after D3 or 1,25-(OH)2D3 treatment. EGFR autophosphorylation was also decreased in hypocalcemic OCT-treated animals (P < 0.03), but after normalization for receptor density, full restoration of EGFR autophosphorylation was achieved. Our data demonstrate that in normal hepat

Topics: Animals; Calcitriol; Calcium; Cholecalciferol; Epidermal Growth Factor; ErbB Receptors; Female; Hypocalcemia; Liver; Male; Phosphorylation; Rats; Rats, Sprague-Dawley; RNA, Messenger; Transforming Growth Factor alpha; Vitamin D Deficiency

Investigations on the efficacy of high doses of cholecalciferol and flumethasone for prophylaxis of hypocalcemic milk fever were performed in dairy cows. Only one cow in the group of 25 treated animals diseased by milk fever, but 5 of 25 control animals showed signs of hypocalcemia. A placenta retention was observed in three treated animals and in four control animals. The results show that the additional application of flumethasone for birth induction after the injection of vitamin D3 was unchanged.

Topics: Animals; Cattle; Cattle Diseases; Cholecalciferol; Drug Therapy, Combination; Female; Flumethasone; Hypocalcemia; Parturient Paresis; Pregnancy

We report a case of thyrotoxicosis with prolonged post-treatment muscle cramp and hypocalcemia. A 36 year-old woman with hyperthyroidism was treated with Methimazole (MMI). As plasma levels of T4 and T3 were normalized, hypocalcemia was noted and severe cramp of skeletal muscle appeared so that the patient was unable to walk. The cramp was gradually relieved as the levels of thyroid hormones re-increased by discontinuance of MMI, and recurred as the hormone levels were normalized by readministration of MMI. The plasma levels of free calcium ion was positively correlated with those of thyroid hormones, and the muscle cramp was worsened with lowering of the calcium level. Serum examination also revealed vitamin D-deficiency, which was probably due to an unbalanced diet of the patient. A therapeutic trial with 1 alpha-vitamin D3 and calcium lactate in addition to MMI improved both thyrotoxicosis and muscle cramp. These findings suggested that hypocalcemia due to vitamin D-deficiency was involved in the exceptionally prolonged muscle cramp associated with the treatment of hypothyroidism in this patient.

Topics: Adult; Cholecalciferol; Female; Humans; Hypocalcemia; Lactates; Lactic Acid; Methimazole; Muscle Cramp; Thyrotoxicosis; Vitamin D Deficiency

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

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

Male Fischer-344 rats, 21 days old, were fed diets containing 0 (LOD), 2,200 (CONT), or 440,000 (HID) international units of vitamin D3 per kilogram for 12 weeks. [Ca] was measured in plasma, CSF, brain, and choroid plexus. In addition, 45Ca and 36Cl transfer coefficients (KCa and KCl) for uptake from blood into CSF and brain were determined. Although plasma ionized [Ca]s in LOD and HID rats were 50% and 136%, respectively, of values in CONT animals, CSF and brain [Ca]s ranged from only 85% to 110% of respective CONT values. Choroid plexus [Ca] was increased by 37% after HID diet, but was decreased only 10% after LOD. KCa values at CSF, parietal cortex, and pons-medulla were negatively correlated with plasma ionized [Ca], whereas KCl values at CSF and brain were not different between the diet groups. The findings demonstrate that central nervous system [Ca] is maintained during chronic hypo- or hypercalcemia by saturable transport of Ca at brain barrier membranes. This transport does not seem to involve modulation by 1,25-dihydroxyvitamin D3.

Topics: Animals; Brain; Calcium; Calcium Radioisotopes; Chlorides; Cholecalciferol; Choroid Plexus; Diet; Hypercalcemia; Hypocalcemia; Male; Potassium; Rats; Rats, Inbred F344; Sodium; Vitamin D

Serum levels of 25-hydroxyvitamin D [25-(OH)D], calcium, phosphate and alkaline phosphatase activity were measured between December and July in 110 pregnant women during the last trimester of pregnancy, and in their infants on the fifth day of life. This study showed a fall, during spring, below 6 ng/ml, of the maternal 25-(OH)D concentration at the time of delivery, and a fall of the 25-(OH)D and calcium concentrations in newborns. The existence of a positive correlation between calcium and 25-(OH)D levels in the newborns suggests that the low calcium concentrations found in the infants born in spring is related to a vitamin D deficiency of the infant and therefore of the mother. The administration of a single low dose of vitamin D3 (100,000 I.U.) on the sixth or seventh month of pregnancy allowed to prevent the seasonal fall in serum calcium and 25-(OH)D concentrations. This dosage appears therefore to be sufficient to reduce the risk of vitamin D deficiency of the newborn and the occurrence of neonatal hypocalcemia.

Topics: Adult; Alkaline Phosphatase; Cholecalciferol; Female; Humans; Hydroxycholecalciferols; Hypocalcemia; Infant, Newborn; Phosphates; Pregnancy; Seasons; Vitamin D Deficiency

We examined the calcium contents of desheathed peripheral nerve, perineurial sheath, and whole sciatic nerve in the frog as a function of the steady-state plasma concentration of ionized calcium. Chronic hypocalcemia was induced by parathyroidectomy and by bathing frogs in a phosphate medium. Chronic hypercalcemia was induced by administering vitamin D3 and by bathing frogs for up to 2 wk in medium containing 50 mM CaCl2. Calcium was measured with a calcium-sensitive electrode and by atomic absorption spectroscopy. The calcium contents (mmol/kg wet wt) in whole nerve, desheathed nerve, and the perineurial sheath varied linearly with slopes of 0.72, 0.71, and 1.72, respectively, with plasma concentration (mM) of ionized calcium, which ranged from 0.3 to 8.0 mM. In the same animals the calcium content in the cerebrum was independent of plasma calcium between 0.5 and 1.5 mM but rose at higher plasma concentrations. Our results indicate that net calcium concentration in the frog peripheral nerve is not regulated during chronic hypocalcemia and hypercalcemia, whereas brain calcium is regulated at plasma calcium concentrations less than 1.5 mM. The lack of calcium regulation in the nerve is attributed to the lack of calcium regulation in the endoneurial compartment.

Topics: Animals; Brain Chemistry; Calcium; Cholecalciferol; Homeostasis; Hypercalcemia; Hypocalcemia; Male; Rana pipiens; Sciatic Nerve; Spectrophotometry, Atomic

Topics: Calcium; Calcium Channel Blockers; Cholecalciferol; Diuretics; Homeostasis; Humans; Hypercalcemia; Hypocalcemia; Kidney; Nephrons

We have previously identified a receptor for 1,25-dihydroxyvitamin D3 in myocardial cells (Simpson, R.U. 1983. Circulation. 68:239.). To establish the relevance of this observation, we evaluated the role of the prohormone vitamin D3 in regulating cardiovascular function. In rats maintained on a vitamin D3-deficient diet for nine weeks, increases in systolic blood pressure (BP) and serum creatine phosphokinase (CPK) were observed. These increases coincided with a reduction of serum calcium from 10.3 to 5.6 mg/dl. However, while serum calcium remained depressed throughout the study, increases in BP and serum CPK were transient. After nine weeks of vitamin D3-depletion, but not after six weeks, ventricular and vascular muscle contractile function were also markedly enhanced. The increase in ventricular contractile function could not be prevented by maintaining serum calcium at 9.0 mg/dl during the period of D3-depletion. These observations suggest a primary role for the vitamin D3-endocrine system in regulating cardiovascular function.

Topics: Animals; Aorta; Blood Pressure; Calcium; Cholecalciferol; Creatine Kinase; Hypocalcemia; Male; Muscle Contraction; Muscle, Smooth, Vascular; Myocardial Contraction; Phosphates; Rats; Rats, Inbred Strains; Receptors, Calcitriol; Receptors, Steroid

Topics: Calcium; Calcium Gluconate; Cardiomyopathy, Dilated; Cholecalciferol; Heart Failure; Humans; Hypocalcemia; Male; Middle Aged

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

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

Serum 1,25-dihydroxyvitamin D3 concentration and renal 25-hydroxyvitamin D 1 alpha-hydroxylase activity were measured in rats fed various levels of calcium, phosphorus and vitamin D3. Both calcium deprivation and phosphorus deprivation greatly increased circulating levels of 1,25-dihydroxyvitamin D3. The circulating level of 1,25-dihydroxyvitamin D3 in rats on a low-calcium diet increased with increasing doses of vitamin D3, whereas it did not change in rats on a low-phosphorus diet given increasing doses of vitamin D3. In concert with these results, the 25-hydroxyvitamin D 1 alpha-hydroxylase activity was markedly increased by vitamin D3 administration to rats on a low-calcium diet, whereas the same treatment of rats on a low-phosphorus diet had no effect and actually suppressed the 1 alpha-hydroxylase in rats fed an adequate-calcium/adequate-phosphorus diet. The administration of 1,25-dihydroxyvitamin D3 to vitamin D-deficient rats on a low-calcium diet also increased the renal 25-hydroxy-vitamin D 1 alpha-hydroxylase activity. These results demonstrate that the regulatory action of 1,25-dihydroxyvitamin D3 on the renal 25-hydroxyvitamin D3 1 alpha-hydroxylase is complex and not simply a suppressant of this system.

Topics: 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; Animals; Calcitriol; Calcium; Calcium, Dietary; Cholecalciferol; Hypocalcemia; Kidney; Male; Phosphates; Phosphorus; Rats; Steroid Hydroxylases; Stimulation, Chemical; Vitamin D Deficiency

This study involved comparison of the distribution and integrity of perforating epiphyseal and marrow vessels with the stage of development and integrity of chondrocytes and the distribution of insoluble calcium in the proximal tibial growth plate of 3-week-old vitamin-D3-deficient hypocalcemic chicks and 3-week-old D3-deficient chicks 12, 36, 72, and 120 hours after an oral dose of 10,000 units vitamin D3. The aim was to clarify the mechanisms responsible for chondrocyte hypertrophy and cartilage calcification in the avian growth plate. Within 12 hours after administration of vitamin D3, serum calcium levels rose to normocalcemic levels. The following morphologic changes were first recognizable at the times indicated. Distal portions of previously elongated perforating epiphyseal vessels and adjacent proliferative and maturing chondrocytes underwent necrosis by 12 hours. Chondrocyte necrosis was not preceded by hypertrophy. By 36 hours, vascular and chondrocyte necrosis involved large portions of the thickened proliferating and maturing zone, and perforating epiphyseal vessels were shortened to a normal length. By 72 hours, chondrocyte hypertrophy and calcification resumed around the shortened epiphyseal vessels. By 120 hours, marrow had removed the necrotic cartilage, and morphologically normal growth plate was restored, with perforating epiphyseal and marrow vessels, both ending in a narrow hypertropic cartilage zone. The results indicate that proximity of chondrocytes to perforating epiphyseal vessels is necessary for their viability, but loss of these vessels does not cause hypertrophy. Since hypertrophy and calcification both occur in the proximity of perforating epiphyseal vessels in normocalcemic animals but not in hypocalcemic animals, it is likely that the vessels influence hypertrophy and calcification by delivering calcium to chondrocytes.

Topics: Animals; Bone Marrow; Cartilage, Articular; Chickens; Cholecalciferol; Epiphyses; Hypocalcemia; Necrosis; Rickets; Vitamin D Deficiency

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

Kidneys of adult rats were removed and perfused with semisynthetic media with the object of elucidating the separate actions of factors implicated as modulators of renal metabolism of 25-hydroxyvitamin D3 (25(OH)D3). During a 3-h perfusion with 3[H]25(OH)D3, the kidney produced high yields of 24,25-dihydroxyvitamin D3 (24,25(OH)2D3) or 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) depending on whether the rat had previously been, respectively, normocalcemic, normophosphatemic, vitamin D-replete or hypocalcemic, hypophosphatemic, vitamin D-deplete. With longer perfusion (up to 12 h), kidneys from normocalcemic, normophosphatemic, vitamin D-replete rats mainly produced 24,25(OH)2D3 but also amounts of 1,25(OH)2D3. This pattern was unaltered by reducing Ca or Pi concentrations of perfusate or by adding parathyroid hormone. Kidneys of hypocalcemic, hypophosphatemic, vitamin D-deplete rats perfused with low Ca, low Pi medium for 12 h at first produced 1,25(OH)2D3 exclusively. However, 24,25(OH)2D3 appeared after 4 h and accumulated thereafter, whereas 1,25(OH)2D3 synthesis ceased after 7 h, a metabolic pattern unaffected by the concentration of substrate or end products in the perfusate or by addition of cyclic AMP. The model shows promise for studying regulation of 25(OH)D3 metabolism by the kidney.

Topics: Animals; Cholecalciferol; Chromatography, High Pressure Liquid; Hypocalcemia; In Vitro Techniques; Kidney; Male; Methods; Perfusion; Phosphates; Rats; Vitamin D Deficiency

Topics: Animals; Calcium; Cattle; Cholecalciferol; Dihydroxycholecalciferols; Female; Hydroxyproline; Hypocalcemia; Magnesium; Phosphorus; Postpartum Period; Pregnancy

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

Topics: Acute Disease; Age Factors; Cholecalciferol; Humans; Hypocalcemia; Infant; Infant, Newborn; Tetany

The myopathy associated with vitamin D deficiency has not been well characterized, and it is not known if weakness is a result of a specific effect of vitamin D deficiency on skeletal muscle. Chicks were raised from hatching on a vitamin D-deficient diet, and by 3 wk of age were hypocalcemic and appeared weak. Tension generated by triceps surae during repetitive stimulation of posterior tibial nerve was significantly less than that developed by chicks given vitamin D(3) supplements (309 g tension/g wet weight of triceps surae, SD 60, for vitamin D-deficient chicks; 470, SD 77, for vitamin D(3)-treated chicks, P < 0.01). Histochemical and electron microscopic examination of skeletal muscles of these chicks showed no abnormalities, and there were no electrophysiologic evidences of motor nerve or neuromuscular junction dysfunction. The concentration of ATP in skeletal muscle of the vitamin D-deficient chicks (5.75 mumol/g wet weight, SD 0.17) was not significantly different from that in vitamin D-treated chicks (5.60, SD 0.50). There was no correlation between strength and serum calcium, serum inorganic phosphate, or skeletal muscle inorganic phosphate. Relaxation of tension after tetanic stimulation was slowed in the vitamin D-deficient chicks (20.6 ms, SD 1.7, vs. 15.4, SD 1.3, in vitamin D-treated chicks and 15.3, SD 1.0, in normal control chicks), and in vitro (45)Ca(++) transport by sarcoplasmic reticulum from the vitamin D-deficient chicks was reduced. Calcium content of mitochondria prepared from leg muscles of vitamin D-deficient chicks (24 nmol/mg mitochondrial protein, SD 6) was considerably lower than that of mitochondria from normal control chicks (45, SD 8) or from chicks treated with vitamin D for 2 wk or more (66-100, depending upon level and duration of therapy). Treatment of the vitamin D-deficient chicks from hatching with sufficient dietary calcium to produce hypercalcemia did not significantly raise skeletal muscle mitochondrial calcium content (31 nmol/mg mitochondrial protein, SD 7) and did not prevent weakness. These studies demonstrate objective weakness as a result of myopathy in vitamin D-deficient chicks, and provide evidence that vitamin D deficiency has effects on skeletal muscle calcium metabolism not secondary to altered plasma concentrations of calcium and phosphate.

Topics: Animals; Calcium; Calcium Chloride; Chickens; Cholecalciferol; Hypocalcemia; Mitochondria, Muscle; Muscle Contraction; Muscle Hypotonia; Vitamin D Deficiency

We evaluated oral 1,25-vitamin D3 for as long as 26 months in six prepubescent children with renal osteodystrophy previously treated with vitamin D2. Therapy was given at 14 to 41 ng per kilogram per day to correct hypocalcemia and reverse bone disease. Serum levels of 1,25-vitamin D3 were initially reduced at 15 +/- 5 pg per milliliter (mean +/- S.E.M.) and after treatment rose to 54 +/- 13. Serum calcium rose from 7.5 +/- 1.6 mg per deciliter (mean +/- S.D.) to 9.8 +/- 0.6 after one month (P less than 0.02). Alkaline phosphatase activity fell from 536 +/- 298 to 208 +/- 91 IU per liter after 12 months (P less than 0.05). Serum immunoreactive parathyroid levels fell from 900 +/- 562 microliter eq per milliliter 411 +/- 377. Healing of rickets and subperiosteal erosions was found. Remineralization of bone was demonstrated by the photon absorption technic. In four patients growth velocity, evaluated for 12 months before and after therapy, increased from 2.6 +/- 0.8 to 8.0 +/- 3.2 cm per year. Growth velocity per year increased from less than third percentile in each to the 10th to 97th percentile after therapy. Height increment ranged from 27 to 113 per cent of that expected for change in chronologic age and 40 to 114 per cent expected for change in bone age after therapy. This trial demonstrates that oral 1,25-vitamin D3 can reverse renal bone disease and increase growth in uremic children.

Topics: Administration, Oral; Adolescent; Alkaline Phosphatase; Body Height; Bone and Bones; Calcium; Child; Child, Preschool; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Female; Growth; Humans; Hypocalcemia; Infant; Magnesium; Male; Minerals; Parathyroid Hormone; Phosphorus; Radiography

1. Cholecalciferol, radioactively labelled with both (14)C and (3)H, was administered weekly for 7 weeks to rats that had been depleted of vitamin D for 4 weeks before repletion with the radioactive vitamin. This permitted measurement of the steady-state effect on vitamin D metabolism of low-calcium and low-phosphorus regimens, as compared with a normal mineral intake. These dietary manoeuvres were carried out during the last 3 weeks of repletion. Cholecalciferol, 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol were determined in plasma, intestine, kidney and bone. Ca(2+)-binding-protein content was measured in intestine and kidneys of comparable animals. 2. In rats on the low-calcium diets, 1,25-dihydroxycholecalciferol concentration was elevated in plasma, bone, kidney and intestine, and intestinal Ca(2+)-binding protein was increased to over twice the concentration found in the control animals. 3. The low-phosphorus regimens led to a decrease in plasma phosphate and 1,25-dihydroxycholecalciferol in all tissues studied, for the latter to the point where it was undetectable in plasma and bone. Intestinal and renal concentrations of Ca(2+)-binding protein were unchanged in the low-phosphate-intake group and decreased in the very-low-phosphate-intake group. 4. It is concluded that in the rat, unlike in the chick, hypophosphataemia is not associated with a stimulation of the production of 1,25-dihydroxycholecalciferol or its expression in the synthesis of Ca(2+)-binding protein. Therefore the plasma phosphate concentration does not appear to be directly involved in the regulation of the functional metabolism of vitamin D.

Topics: Animals; Bone and Bones; Calcium; Calcium, Dietary; Carrier Proteins; Cholecalciferol; Diet; Dihydroxycholecalciferols; Hypocalcemia; Intestinal Mucosa; Kidney; Phosphorus; Rats; Vitamin D

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: Adolescent; Adult; Aged; Calcitonin; Calcium; Cholecalciferol; Female; Humans; Hyperparathyroidism; Hypocalcemia; Intestinal Absorption; Kidney Tubules; Male; Middle Aged; Parathyroid Glands; Parathyroid Hormone; Phosphorus; Urinary Calculi

Topics: Child; Cholecalciferol; Female; Humans; Hyperparathyroidism; Hypocalcemia; Osteomalacia; Phosphates

Topics: Calcium; Child; Cholecalciferol; Chromosome Aberrations; Chromosome Disorders; Ergocalciferols; Female; Humans; Hypocalcemia; Hypophosphatemia, Familial; Infant; Intestinal Absorption; Male; Phosphates; Rickets; Vitamin D; Vitamin D Deficiency

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: Biopsy; Bone Neoplasms; Calcitonin; Calcium; Cholecalciferol; Humans; Hypocalcemia; Intestinal Absorption; Male; Middle Aged; Neoplasm Metastasis; Osteomalacia; Phosphorus; Prostatic Neoplasms

Report on a boy aged 6-1/2 years with pseudohypoparathyroidism. This is due to a genetic lack of PTH inducible adenocyclase. Even during vitamin D treatment renal camp formation by giving PTH extract cannot be stimulated, while in this situation. PTH shows a clearly phosphaturic effect. Whether this is due to a PTH potentiated vitamin D effect is discussed. The assay of camp in urine before and after stimulation with PTH extract has proved the most certain diagnostic criterion.

Topics: Alkaline Phosphatase; Child; Cholecalciferol; Cyclic AMP; Humans; Hypocalcemia; Kidney Function Tests; Male; Phosphates; Pseudohypoparathyroidism

Topics: Adolescent; Adult; Alkaline Phosphatase; Calcium; Child; Cholecalciferol; Diet; Diet, Vegetarian; Ergocalciferols; Female; Humans; Hypocalcemia; Male; Middle Aged; Osteomalacia; Phosphorus; Rickets; Seasons; United Kingdom; Vitamin D Deficiency; White People

Rickets, hypocalcemia, decreased duodenal calcium transport, and reduction of calcium binding protein have been produced in chicks treated with diphenylhydantoin. These effects are directly related to diphenylhydantoin dose and inversely related to the intake of vitamin D(3) (cholecalciferol).

Topics: Animals; Body Weight; Bone and Bones; Calcium; Calcium Radioisotopes; Chickens; Cholecalciferol; Dose-Response Relationship, Drug; Duodenum; Hypocalcemia; Intestinal Mucosa; Male; Phenytoin; Protein Binding; Rickets; Vitamin D Deficiency

Topics: Aged; Animals; Antineoplastic Agents; Child, Preschool; Cholecalciferol; Humans; Hypocalcemia; Leukemia, Lymphoid; Lymphoma; Male; Neoplasms; Phosphates; Uric Acid

Topics: Animal Nutritional Physiological Phenomena; Animals; Body Weight; Bone and Bones; Bone Development; Calcium; Chickens; Cholecalciferol; Dose-Response Relationship, Drug; Elements; Femur; Hypocalcemia; Magnesium; Male; Organ Size; Phosphates; Vitamin D Deficiency

Topics: Aluminum; Calcium Carbonate; Cholecalciferol; Humans; Hypocalcemia; Kidney Failure, Chronic; Male; Middle Aged; Phosphates

Topics: Animals; Anticonvulsants; Avitaminosis; Body Weight; Calcium; Calcium Radioisotopes; Cholecalciferol; Enzyme Induction; Epilepsy; Humans; Hypocalcemia; Intestinal Absorption; Liver; Long-Term Care; Mice; Osteomalacia; Phenobarbital; Phenytoin; Rats; Vitamin D

Topics: Administration, Oral; Animals; Cattle; Cattle Diseases; Cholecalciferol; Female; Hypocalcemia; Pregnancy; Puerperal Disorders

Topics: Animals; Calcium; Cholecalciferol; Diet; Hypocalcemia; Hypophosphatemia, Familial; Inositol; Male; Nutritional Requirements; Osteomalacia; Rats; Spectrophotometry, Atomic

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

Topics: Cholecalciferol; Deficiency Diseases; Female; Humans; Hypocalcemia; Hypophosphatemia, Familial; Infant; Male; Parathyroid Hormone; Vitamin D

Topics: Animals; Bone and Bones; Bone Resorption; Calcium; Calcium Isotopes; Cholecalciferol; Culture Techniques; Cyclic AMP; Drug Antagonism; Hypocalcemia; Imidazoles; Male; Parathyroid Glands; Parathyroid Hormone; Phosphorus; Rats; Theophylline; Thyroid Gland

Topics: Alkaline Phosphatase; Animal Nutritional Physiological Phenomena; Animals; Arthritis; Bone Development; Bone Diseases; Bone Resorption; Calcium; Cholecalciferol; Diet; Hypocalcemia; Male; Phosphorus; Rhinitis, Atrophic; Swine; Zinc

Topics: Animals; Calcitonin; Calcium; Calcium, Dietary; Cholecalciferol; Hypocalcemia; Injections, Subcutaneous; Male; Parathyroid Glands; Phosphorus; Rats; Thyroid Gland; Thyroidectomy; Tissue Extracts

Topics: Adenine Nucleotides; Animals; Bone and Bones; Bone Resorption; Calcium; Calcium Isotopes; Cholecalciferol; Culture Techniques; Cyclic AMP; Depression, Chemical; Glucagon; Hypercalcemia; Hypocalcemia; Male; Parathyroid Glands; Parathyroid Hormone; Rats; Thyroidectomy

Topics: Age Factors; Animals; Animals, Newborn; Biological Assay; Bone and Bones; Bone Development; Calcitonin; Calcium; Cholecalciferol; Hypercalcemia; Hypocalcemia; Rats; Secretory Rate; Thyroid Gland

Topics: Acidosis; Alkaline Phosphatase; Animals; Bone and Bones; Bone Development; Bone Resorption; Calcitonin; Calcium; Cholecalciferol; Chromium Isotopes; Citrates; Cortisone; Dogs; Hydrochloric Acid; Hydrogen-Ion Concentration; Hypercalcemia; Hypocalcemia; Metatarsus; Microradiography; Osteoclasts; Parathyroid Hormone; Perfusion; Phosphates; Phosphorus; Thyroxine

Topics: Animals; Calcium; Cholecalciferol; Female; Hypocalcemia; Lactation; Magnesium; Pregnancy; Pregnancy Complications; Sheep; Sheep Diseases

Topics: Animals; Calcium; Cholecalciferol; Hypercalcemia; Hypocalcemia; Neoplasm Metastasis; Parathyroid Glands; Rats; Sarcoma, Experimental; Thyroidectomy

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

Topics: Animals; Calcium; Chickens; Cholecalciferol; Chromatography, Gel; Guinea Pigs; Hypocalcemia; Male; Parathyroid Glands; Parathyroid Hormone; Peptides; Phosphates; Rats; Vitamin D; Vitamin D Deficiency

Topics: Animals; Bone Diseases; Cholecalciferol; Deficiency Diseases; Hypocalcemia; Osteoporosis; Rats; Rickets

Topics: Blood; Calcium; Calcium, Dietary; Cholecalciferol; Humans; Hypocalcemia; Liver Diseases; Vitamin D; Vitamins