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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The state of vitamin D nutrition depends on synthesis in the skin under the influence of sunlight as well as on dietary intake. In European countries that do not fortify milk with vitamin D, reduced sun exposure is the major factor leading to a fall in body stores of vitamin D with age and to a high frequency of hypovitaminosis D in the elderly sick. In the US, because vitamin D is added to milk and the use of vitamin D supplements is more common, the dietary intake of vitamin D is relatively more important than in Europe, and the total vitamin D intake and body stores of vitamin D are generally higher. Nevertheless, body stores of vitamin D probably fall with age in the US as they do in Europe, and it is likely that some sick elderly persons in the US, especially among those confined to institutions, become vitamin D deficient. For several reasons, the vitamin D requirement increases with age, and a total supply of 15 to 20 micrograms/day (600 to 800 IU) from all sources is recommended. Special attention should be paid to persons most likely to need supplementation, such as the housebound, persons with malabsorption, and persons with interruption of the enterohepatic circulation. Osteomalacia, the bone disease produced by severe vitamin D deficiency, is less common in the US than in Europe, but subclinical vitamin D deficiency may contribute to the pathogenesis of hip fractures, both through increased liability to fall and through PTH-mediated bone loss. The extent to which vitamin D deficiency contributes to hip fractures in the US is unknown, and is an important area for future research. Excess intake of vitamin D or of its metabolites may result in hypercalcemia and extra-osseous calcification, particularly in arterial walls and in the kidney, leading to chronic renal failure. The dose of vitamin D that causes significant hypercalcemia is highly variable between individuals but is rarely less than 1000 micrograms/day. Smaller doses can cause hypercalciuria and nephrolithiasis and possibly impaired renal function. Vitamin D administration may raise plasma cholesterol but there is no convincing evidence that the risk of myocardial infarction is increased. The recommended total supply for the elderly of 20 micrograms/day is most unlikely to be harmful, except in patients with sarcoidosis or renal calculi.
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PMID:Vitamin D and bone health in the elderly. 676 68

Four families with familial hypocalciuric hypercalcaemia were studied. The probands presented with abdominal pain, which in three was due to acute pancreatitis; in two the condition was life threatening. Serum concentrations of calcium, magnesium, phosphate, and immunoassayable parathyroid hormone, urinary calcium excretion, and the rate of renal tubular reabsorption of phosphate were measured; the findings were compared with results in 10 patients with primary hyperparathyroidism matched for serum calcium concentration to establish differences between the diseases. Familial hypocalciuric hypercalcaemia should be suspected in patients with hypercalcaemia in whom daily urinary calcium excretion is below 5 mmol (200 mg) provided renal insufficiency, vitamin D deficiency, and ingestion of drugs that reduce calcium excretion have been excluded. Most cases appear to run a benign course, but some may suffer considerable morbidity. Surgical treatment should be reserved for patients with severe complications, when all parathyroid tissue should be removed.
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PMID:Familial hypocalciuric hypercalcaemia and acute pancreatitis. 678 29

The physiological mechanisms involved in the alterations in calcium homeostasis during pregnancy are complex. The fetal acquisition of calcium, for skeletal growth, is obtained by an increase in intestinal calcium absorption in the mother with transplacental calcium transfer to the fetus. The regulation of calcium homeostasis during the transition from the intrauterine to the extrauterine environment is complex and poorly understood. Within the first few hours of life the serum calcium concentrations begins to fall progressively reaching a "trough" value by the second or third day of life and then increases to normal values by the tenth day of life. In some neonates the fall in calcium concentration is sufficient to be associated with either tetany or convulsions. Hypocalcemia is probably the commonest disturbance of calcium homeostasis that occurs in the neonate and can be subdivided into three main groups on the basis of the etiological mechanism involved. Other disorders of calcium homeostasis that may affect the neonate include hypoparathyroidism, either congenital or acquired, pseudohypoparathyroidism, and vitamin D deficiency. Hypercalcemia may occur, but is a relatively rare occurrence in the neonate.
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PMID:Disorders of calcium homeostasis in the fetus and neonate. 704 84

It has been widely believed that phosphate deficiency causes osteomalacia. Based on this belief, the rickets of familial hypophosphatemia has been attributed to phosphate deficiency associated with the hypophosphatemia. The present studies on rats have, however, demonstrated significant differences between the effects of phosphate deficiency on bone metabolism and the characteristic features of rickets. Weanling rats, maintained on a mildly phosphate deficient diet, had hypercalcemia and hypophosphatemia, and impairment of body growth, bone growth, and bone mineralization. The maximum effect was observed at 5 wk; between 5 and 20 wk the rats improved despite persistent hypophosphatemia. Histologically, at 5 wk the bone showed thick unmineralized osteoid seams covering most bone surfaces, but the epiphyseal cartilage was normal. In addition, the excess osteoid readily incorporated tetracycline indicating normal mineralization and, based on a new sequential pulse labeling technique, the linear bone apposition rate (LBA) was significantly (p < 0.001) increased above control values. This increase was observed within the initial 4 days of phosphate (P) deficiency and persisted up to 15 wk. This effect of P deficiency on LBA was dependent on vitamin D activity. At 4 wk, the mean LBA was 0.106 +/- 0.003 (1 SE) in control rats, 0.149 +/- 0.008 microns/hr in P deficient rats, 0.083 +/- 0.004 microns/hr in vitamin D deficient rats and 0.086 +/- 0.006 microns/hr in rats deficient in both P and vitamin D. We have reported a similar increase in LBA with parathyroid hormone activity. With vitamin D deficiency, phosphate deficient rats showed all the characteristic features of rickets; disorganization of epiphyseal cartilage, excessive unmineralized osteoid, and reduced mineralization based on the incorporation of tetracycline. We conclude that the effects of phosphate deficiency on bone metabolism more closely resembles the effects of PTH activity than the characteristic effects of osteomalacia and rickets.
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PMID:Differences between the effects of phosphate deficiency and vitamin D deficiency on bone metabolism. 745 66

Vitamin D deficiency is common in the elderly, especially in countries where effective sunlight or exposure to sunlight is limited. Two regimes for vitamin D supplementation--low-dose daily oral administration and intermittent high-dose administration--were examined with regard to safety and effectiveness. Eleven papers reporting studies in 449 elderly subjects were reviewed. On low-dose continuous supplementation mean concentration of 25 hydroxyvitamin D (25(OH)D) ranged from 57 to 105 nmol/L compared to 55 to 87 nmol/L following high-dose supplementation. These mean values fall within the physiological range for young adults. Hypercalcemia occurred in only 3 subjects and was associated with a predisposing cause in 2 of 3 subjects. We suggest that low dose continuous supplementation (10 to 20 micrograms daily) is the regime of choice but high-dose intermittent supplementation (2.5 mg six monthly) may be suitable where compliance is poor.
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PMID:Vitamin D supplementation in the elderly: review of safety and effectiveness of different regimes. 764 77

This article begins with a discussion on changes in the maternal calcium-parathyroid axis in response to pregnancy, followed by calcium disorders that can take place during pregnancy. Hypercalcemia and its subsequent disorders, including hyperparathyroidism, hypocalciuric hypercalcemia, and thyroid disease, are reviewed. Also, hypocalcemia and its subsequent disorders, including hypoparathyroidism, vitamin D deficiency, and hypomagnesemia, are addressed. Concluding the article are discussions on bone status and osteoporosis, calcium metabolism in pregnancy-induced hypertension and preeclampsia, and nephrolithiasis in pregnancy.
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PMID:Calcium disorders of pregnancy. 778 23

Antituberculous chemotherapy agents, particularly rifampicin and isoniazid, affect vitamin D metabolism and can create biochemical evidence of vitamin D deficiency. Vitamin D deficiency induces a state of resistance to parathyroid hormone. This study sought to explain the temporary resolution of hypercalcaemia and hypercalciuria, during antituberculous chemotherapy with rifampicin and isoniazid, in a subject with a surgically proven parathyroid adenoma and coincidental spinal tuberculosis. Serum ionized calcium, 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, plasma parathyroid hormone, and 24-hour urine excretions of calcium, inorganic phosphorus and hydroxyproline were sequentially measured over a 3-year interval that included 18 months of antituberculous chemotherapy. Initial serum ionized calcium was 1.52 mmol/l (normal 1.20-1.35 mmol/l), 24-hour urine calcium excretion was 9.40 mmol/day (normal 1.25 to 7.50 mmol/day) and plasma intact PTH was 9.2 pmol/l (normal 0.0-4.5 pmol/l). During antituberculous chemotherapy the serum ionized calcium and 24-hour urine calcium excretion were normal but the plasma PTH rose to higher levels. Following completion of the chemotherapy, hypercalcaemia and hypercalciuria returned with levels similar to those observed pretreatment. Serum 25-hydroxyvitamin D was low at 6.25 nmol/l (normal 20 to 90 nmol/l) during antituberculous chemotherapy, but was normal before and after. Serum 1,25-dihydroxyvitamin D was normal throughout the 3-year interval. We conclude that the antituberculous chemotherapy induced relative vitamin D deficiency and resistance to parathyroid hormone action, thereby masking the hyperparathyroidism and hypercalcaemia until the chemotherapy was completed.
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PMID:Primary hyperparathyroidism masked by antituberculous therapy-induced vitamin D deficiency. 764 6

Neonatal primary hyperparathyroidism is a life threatening disorder that is associated with severe hypercalcaemia, hypotonia, bone demineralization, fractures and respiratory distress. Treatment consists of total parathyroidectomy and without this affected infants will usually die by the age of three months. We report a patient with neonatal primary hyperparathyroidism who survived without fractures or parathyroidectomy to an age of nine months, and in whom the hypercalcaemia became masked by vitamin D deficiency. At surgery, four-gland hyperplasia was demonstrated and total parathyroidectomy followed by oral calcitriol treatment has restored well-being and normocalcaemia. An absence of skeletal complications, a survival beyond three months of age without parathyroidectomy and the masking of the hypercalcaemia by vitamin D deficiency represents a unique combination of metabolic abnormalities in a patient with neonatal primary hyperparathyroidism.
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PMID:Neonatal primary hyperparathyroidism masked by vitamin D deficiency. 795 63

Forty-five subjects (41 women and 4 men) in long-stay and medium-stay facilities, aged 74 to 95 years (mean 86.4 years), with 25-hydroxy-vitamin D levels less than 12 ng/ml, were treated for six consecutive months with two tablets per day of a preparation containing vitamin D3 (800 IU/day) and calcium carbonate (1 g elemental calcium/day). Serum levels of 25-hydroxy-vitamin D were very low at baseline (5.6 +/- 0.4 ng/ml) and rose significantly under treatment, to normal values, 33.2 +/- 1.2 and 40.9 +/- 2.1 ng/ml after three and six months, respectively (p < 0.001 for both comparisons). Serum calcium increased significantly, by 4.5% (p < 0.001) during the first three months, and remained at a plateau thereafter. Corrected serum calcium rose by 8.9% (p < 0.001) during the trial. No patient developed hypercalcemia. Serum parathyroid hormone levels, which were elevated at baseline (71.6 +/- 5.8 pg/ml; normal, 12 to 54 pg/ml), decreased gradually and significantly throughout the treatment period, by 43.0% and 67.1% after three and six months, respectively (p < 0.001 for both comparisons). Serum alkaline phosphatase activity fell concomitantly, by 9.9% after three months (p < 0.01) and 36.5% after six months (p < 0.001). In conclusion, the preparation used in our study is effective in correcting both the vitamin D deficiency that is prevalent in elderly institutionalized patients and the resultant increase in bone turnover.
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PMID:Biochemical effects of calcium and vitamin D supplementation in elderly, institutionalized, vitamin D-deficient patients. 868 85

Primary hyperparathyroidism causes excessive bone resorption with a decrease in bone mineral density. Fractures of the vertebras and appendicular bones, however, seem uncommon, even in the long term. We report three patients who presented with bone insufficiency fractures as the inaugural symptom of primary hyperparathyroidism. The three patients were women, aged 62, 65 and 86 years, respectively, who presented with fractures of the medial tibial plateau, femoral neck of femoral neck and tarsus. Laboratory tests showed hypercalcemia, hypophosphatemia and elevated parathyroid hormone levels. Apart from confusion in the 86-year-old patient, there were no clinical manifestations. A bone biopsy obtained in one patient showed increased resorption parameters with no loss of bone trabecular volume; the two other patients underwent absorptiometry, which disclosed a marked decrease in bone mineral density at the spine and femoral neck. There were no risk factors for osteopenia apart from advanced age and female gender. A parathyroid adenoma was removed surgically in all three cases. Vitamin D deficiency was a concomitant abnormality that probably exacerbated the adverse effects of hyperparathyroidism on the skeleton.
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PMID:Bone insufficiency fractures as an inaugural manifestation of primary hyperparathyroidism. 889 60


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