Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Skeletal muscle calcium metabolism and contractile force in vitamin D-deficient chicks. 22 25

Ten years of experience with daily prophylaxis of rickets brought about isolated knowledge which corrected old mistakes and demands a revision of older attitudes towards the usual prophylaxis. Prophylaxis of vitamin D according to the most modern and reliable knowledge in the best way promotes the growth and mineralisation of the skeleton with dosages of 400 to 800 I.U. smaller or higher dosages are disadvantageous. By observing the above given dosage, rickets and hypercalcaemia are rare and only conceivable under special pathological conditions. The diagnosis of beginning rickets must be well known, otherwise unspecific symptoms of rickets may induce the administration of unnecessarily high amounts of vitamin D. The symptoms of rickets show a gradual increase: the increase of serum alkaline phosphatase precedes the clinical and radiological symptoms. The reliable radiographic deformities of the hand can first be seen at the Ulna, then at the Radius and later at the secondary centers of Metacarpals. Among the relatively reliable clinical symptoms there its first the rosary later the Marfan-sign and eventually the deformation of the long bones. For infants protected by vitamin D, craniotabes as a sign of rickets is completely unreliable as well as the Harrison grooves and rachitic kyphosis. If one observes all these rules and rachitic kyphosis. If one observes all these rules and criterions vitamin D is as reliable in the prophylaxis as in the therapy of vitamin D deficiency rickets.
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PMID:[Ten years' daily prophylaxis against rickets--review and outlook (author's transl)]. 119 21

High calcium leads to the secretion of calcitonin, and the administration of 1,25-dihydroxyvitamin D3 leads to a decreased transcription of the calcitonin gene. We now report the effect of chronic hypercalcemia, hypocalcemia, and vitamin D deficiency on calcitonin gene expression in vivo in the rat. Hypercalcemia was created by calcium infusions for 6 h, a high-calcium diet given to weanling rats for 3 weeks, and the transplantation of the Walker carcinosarcoma 256 cell line. Despite serum calcium as high as 22 mg/dl, there was no difference in calcitonin mRNA levels among these rats. The control genes studied, actin and somatostatin, which is specific for C cells in the thyroparathyroid tissue, also did not differ among the different groups of rats. Injected 1,25-(OH)2D3 decreased calcitonin mRNA levels at 6 h, as previously reported. Hypocalcemia, created by feeding diets deficient in calcium and vitamin D to weanling rats for 3 weeks, had no effect on calcitonin mRNA levels, in contrast to the large increases in PTH mRNA levels. These results demonstrate that calcitonin gene expression in vivo in the rat is regulated by administered 1,25-(OH)2D3 but not by changes in serum calcium.
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PMID:Regulation of calcitonin gene expression by hypocalcemia, hypercalcemia, and vitamin D in the rat. 136 Jul 44

In primary hyperparathyroidism, hypercalcaemia is due to inappropriate hypersecretion of parathormone (PTH). Yet, the intestinal or osseous origin of the excess in plasma calcium and the symptoms of the disease are largely conditioned by vitamin D reserve and metabolism. In cases with sufficient vitamin D reserve and normal metabolism, the primary disorder is hyperabsorption of calcium by the intestine, and there is a risk of renal stone formation. In patients with vitamin D deficiency, there is a significant increase of bone resorption accompanied by osteoarticular symptoms. In addition, other factors, as yet unidentified, seem to intervene in the reabsorption of calcium by the renal tubule, which commands the degree of hypercalcaemia. Hypersecretion of parathormone may be due either to a reduced sensitivity of parathyroid cells to calcium (as in adenomas) or to an increase of the PTH-secreting thyroid mass (as in hyperplasia and some adenomas).
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PMID:[Primary hyperparathyroidism. Mechanisms of hypercalcemia]. 167 65

A clinical trial carried out during the autumn/winter season in 46 institutionalized elderly subjects (35 women, 11 men) (group mean age = 83 +/- 2 years) revealed a severe deficiency in vitamin D in these subjects (25-hydroxyvitamin D level less than or equal to 3 ng/ml). After oral administration of 100,000 IU of vitamin D3, an increase in 25-hydroxyvitamin D levels above the 10 ng/ml threshold was observed and maintained for three months. A second dose, administered after 3 months, made it possible to sustain this level. No sign of toxicity was detected, notably no trace of hypercalcemia. In contrast, no change in the deficit (25-hydroxyvitamin D level less than or equal to 3 ng/ml) was seen in the placebo population. Three-monthly administration of the moderate dosage of 100,000 IU of vitamin D3 all year round would offer a simple, effective and risk-free system to counteract vitamin D deficiency in the elderly and of preventing the risk of osteomalacia, thus reducing the incidence of fractures.
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PMID:[Vitamin D supplementation in institutionalized elderly. Effects of vitamin D3 (100,000 IU) orally administered every 3 months on serum levels of 25-hydroxyvitamin D]. 196 39

Neurofibromatosis is sometimes complicated by impaired renal tubular reabsorption of phosphate, hypophosphatemia, and osteomalacia. Hyperparathyroidism has also been reported in patients with neurofibromatosis. When hypercalcemia and elevated levels of parathyroid hormone are found in osteomalacia, however, it may be difficult to determine if the hyperparathyroidism was primary or tertiary. We describe a patient with neurofibromatosis, hypercalcemic hyperparathyroidism, hypophosphatemic osteomalacia, vitamin D deficiency, and clear-cell hyperplasia of all four parathyroid glands. Serial biomechanical, bone biopsy, and densitometric studies confirmed that treatment with ergocalciferol, calcium, and phosphate supplements significantly improved the osteomalacia but caused increased parathyroid overactivity. After subtotal parathyroidectomy, the parathyroid hormone concentration became normal and the bone mineral content increased at the spine and hip, but inappropriate phosphaturia persisted. The findings indicate that hyperparathyroidism, osteomalacia, and vitamin D deficiency adversely affect each other.
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PMID:Hypercalcemic hyperparathyroidism and hypophosphatemic osteomalacia complicating neurofibromatosis. 211 9

The influence of vitamin D and ultraviolet irradiation (UVI), used for prevention of vitamin D deficiency, on the state of phosphoric-calcium metabolism was studied in experiments on rats. It has been shown that daily injections of 1-5 IU of vitamin D, and UVI in biodoses from 1/8 to 1/4 promote the maintainance of the normal level of phosphoric-calcium metabolism. When UVI was applied according to the widely used "basic scheme" (in biodoses from 1/4 to 2 1/2) the following anomalies were recorded: a three-fold increase of 25-ON-D3 concentration in the blood plasma, hyperphosphatemia, a tendency to hypercalcemia. The use of higher doses of UVI led to a further increase of 25-OH-D3 level, hypophosphatemia, hypercalcemia, kidney and heart calcification. The data obtained have evidenced a possibility of vitamin D intoxication during UVI.
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PMID:[Experimental research on the effect of ultraviolet irradiation on the phosphorus-calcium metabolic status]. 216 9

1. The serum concentrations of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were measured in 44 patients with primary hyperparathyroidism. 2. In 14 patients the serum concentration of 1,25-dihydroxyvitamin D was greater than normal (142-337 pmol/l). One patient had a subnormal concentration of 1,25-dihydroxyvitamin D (36 pmol/l) but no other evidence of vitamin D deficiency. 3. The possible biological determinants of the serum concentration of 1,25-dihydroxyvitamin D were sought by multivariate analysis of relevant variables. The serum concentration of 1,25-dihydroxyvitamin D was found to be significantly and positively correlated with the serum concentrations of 25-hydroxyvitamin D (P less than 0.001) and parathyroid hormone (P less than 0.003), and with the glomerular filtration rate (P less than 0.03), and negatively correlated with the serum concentrations of calcium (P less than 0.02) and phosphate (P = 0.055) (multiple R = 0.638, P less than 0.002). 4. In primary hyperparathyroidism the major determinant of serum 1,25-dihydroxyvitamin D is the availability of precursor 25-hydroxyvitamin D. 5. The finding that serum 1,25-dihydroxyvitamin D is commonly normal in patients with primary hyperparathyroidism despite an adequate state of vitamin D nutrition, can be explained in terms of the constraining influences of hypercalcaemia and variable degrees of renal dysfunction on the biosynthesis of 1,25-dihydroxyvitamin D.
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PMID:Determinants of the serum concentration of 1,25-dihydroxyvitamin D in primary hyperparathyroidism. 253 4

This study deals with the relationship between the occurrence of hypercalcemia and the administration of prophylactic doses of vitamin D in children with hypothyroidism, before and during L-thyroxine (LT4) treatment. The goal of the study was to determine the dosage of vitamin D necessary to prevent rickets without inducing hypercalcemia. There was a 23% prevalence of hypercalcemia at the time of the diagnosis of hypothyroidism by screening whereas it was 21% in the children who were not given vitamin D during the first 3 months of LT4 treatment. This figure was significantly higher in those who were given vitamin D during the first 3 months of treatment and reached 70%. However, one of the 19 children not given vitamin D presented with biological signs evoking vitamin D deficiency. In conclusion, in hypothyroid infants, vitamin D should be administered carefully during the first 6 months of treatment and restricted to children at risk for developing vitamin D deficiency.
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PMID:[Prophylaxis of vitamin D deficiency in hypothyroidism in the newborn infant]. 260 8

Characteristics of secondary hyperparathyroidism were evaluated in dogs with mild vitamin D deficiency. The animals were normocalcemic with reduced concentrations of 1,25-dihydroxy vitamin D3 [1,25(OH)2D3] and elevations in parathyroid hormone (PTH) concentrations, parathyroid mass, and prepro PTH mRNA levels. Dynamic testing revealed a sigmoidal relationship between plasma calcium and PTH, although PTH concentrations were increased relative to values in vitamin D-sufficient dogs. Infusions of chelator elicited lower plasma calcium levels and greater augmentations in biologically active PTH in vitamin D-deficient than in D-sufficient animals. Induced hypercalcemia lowered both immunoreactive and bioactive hormone to stable but detectable levels. The results demonstrate the decreased capacity of vitamin D-deficient animals to defend against acute hypocalcemia, despite the presence of abundant PTH, and indicate that increased circulating PTH levels in early vitamin D deficiency is due predominantly to an augmentation in the quantity of releasable hormone. The latter appears secondary to an increase in parathyroid mass and synthetic activity regulated by 1,25(OH)2D3 per se.
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PMID:Characteristics of secondary hyperparathyroidism in vitamin D-deficient dogs. 273 2


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