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)

White Leghorn chick embryos were injected on the 15th day of incubation with 70 to 300 pmoles 1,25-(OH)2D3. All doses produced hypercalcemia; with the highest dose, the concentration of calcium in serum started to rise 4 h after the injection, reached a peak 20 h after, and was still high 48 h after. Twenty hours after the injection of the same dose, the concentration of inorganic phosphorus in the serum was significantly lower than in the corresponding controls. The tibias from 17-day-old chick embryos injected with 300 pmoles on day 15 were shorter, lighter, and had a lower ash content than those from controls. Histological signs of resorption appeared to be reduced with respect to controls, but no precise quantitation was conducted. The fact that hypercalcemia was not accompanied by hyperphosphatemia may suggest that the vitamin stimulates resorption of calcium from the shell, which is mainly formed by calcium carbonate rather than from the bone from which calcium and phosphate are usually resorbed together.
Calcif Tissue Res 1978 Dec 08
PMID:Effects produced by the administration of high doses of 1,25-dihydroxycholecalciferol to the chick embryo. 57 6

Hypercalcaemia would seem to be rare during immobilisation, whilst osteoporosis and hypercalciuria are constant. In fact, it often goes unnoticed. The case presented here confirms its predominance in the adolescent male. The reason for immobilisation seems to be irrelevant. The clinical symptoms are very variable: polydipsia, nausea, headache, apathy, anorexia. Blood calcium levels are raised, up to 14 mg%. This hypercalcaemia is due to very marked bone loss in adolescents, secondary to hyper-resorption and a temporary stoppage in osseous formation. The differential diagnosis from primary hyperparathyroidism is sometimes difficult but is aided by laboratory and histological findings. The essential is to consider the possibility of immobilisation hypercalcaemia in the presence of any suggestive symptoms in an immobilised adolescent. Treatment includes a return to weight bearing, adequate water intake and the administration of phosphorus, calcitonin, furosemide, and corticosteroids.
Nouv Presse Med 1977 Dec 03
PMID:[Immobilisation hypercalcaemia (author's transl)]. 59 68

Our reported experience with ninety-seven hypercalcemic patients having resected adenomas with no recurrent hypercalcemia or hypocalcemia had led us to continue a conservative approach. Twelve patients with multiple parathyroid gland involvement proven by biopsy were treated with three and one-half gland resection and autotransplantation.
Am J Surg 1977 Dec
PMID:Surgical treatment of primary hyperparathyroidism. 59 43

All patients with hyperparathyroidism seen in a large referral military hospital within a twenty month period underwent neck exploration by one of us (HN). Three patients were found to have an unsuspected solid thyroid nodule measuring 0.5 to 1.5 cm. All were widely excised by thyroid lobectomy and isthmectomy and found to be follicular or papillary carcinoma of the thyroid. These three patients join thirty-one previously reported clinical cases documenting an association between parathyroid adenoma and nonmedullary carcinoma of the thyroid. Because of the high potential for malignancy in this clinical setting, we urge careful examination and palpation of the thyroid gland during neck exploration for hypercalcemia in order to detect and cure "early" malignancies of the thyroid.
Am J Surg 1977 Dec
PMID:Unsuspected nonmedullary carcinoma of the thyroid in patients with hyperparathyroidism. 59 48

The present study is an investigation of the mechanism of hypercalcemia and hyperphosphatemia induced by the intravenous injection of lead acetate (Pb-Ac). A total of 118 male rats were injected with 30 mg/kg of Pb-Ac, or with 16.5 mg/kg of sodium acetate as the control. The levels of serum calcium, phosphorus and lead were then determined at various time periods after the injections. Serum calcium and phosphorus levels increased with time after Pb-Ac injection and the maximum values of calcium (17 mg%) were found after 1 h and of phosphorus (13.5 mg%) after 30 min. Both calcium and phosphorus levels reverted to the normal range after 12 h. The maximum net rates of increase of calcium and phosphorus were found immediately after Pb-Ac injection. At that time, deposition of lead at the calcifying sites of bone and incisor dentin was demonstrated by a histochemical examination. In other experiments the changes in the calcium and phosphorus contents in the medium after shaking bone powder in serum with Pb-Ac in an in vitro system were studied. It was confirmed that the calcium and phosphorus were displaced from the bone mineral, the extent of the displacement being correlated with the concentration of the Pb-Ac added to the medium, and that these displacements were very rapid reactions. These results suggest that hypercalcemia and hyperphosphatemia following Pb-Ac injection results from a direct action of lead on the bone mineral.
Calcif Tissue Res 1977 Dec 14
PMID:Mechanism of induction of hypercalcemia and hyperphosphatemia by lead acetate in the rat. 59 44

Between 1972 and 1976 15 patients with chronic renal failure of different aetiology and varying severity were observed who developed 23 hypercalcaemic phases during treatment with calcium-containing drugs. 12 instances of hypercalcaemia occurred during conservative treated during conservative treatment (serum creatinine 177-1061 mumol/l, equivalent to 20-120 mg/l) and 11 during chronic haemodialysis (serum creatinine 707-1061 mumol/l, equivalent to 80-120 mg/l). In 15 cases hypercalcaemia was caused by a hexacalciumhexasodium-heptacitratehydrate complex (Acetolyt), in 6 cases by the combined use of this drug with calcium ion-exchange resins on a calciumpolystyrolsulfonate base, and in two cases by the use of calcium tablets and calciumpolystyrolsulfonate, respectively. The daily doses of these drugs were in the usual therapeutic range in most cases. Deterioration of renal function was observed in two cases and coma in a further two cases. In 5 cases gastric ulcers were demonstrated. Three patients died. In no patient was there evidence of florid hyperparathyroidism. Treatment with calcium-containing drugs in patients with renal failure should only be carried out under regular control of calcium concentrations.
Dtsch Med Wochenschr 1977 Dec 30
PMID:[Hypercalcaemic crises in patients with chronic renal failure caused by ion-exchange resins, antacidotics and other calcium-containing drugs (author's transl)]. 59 99

The effect of induced hypercalcemia on serum gastrin concentrations, measured by radioimmunoassay, and gastric acid secretion was studied in 20 healthy subjects, 8 patients after antrectomy and gastroduodenostomy (Billroth I), 12 patients after antrectomy and gastrojejunostomy (Billroth II) and in 9 patients after total gastrectomy and esophagojejunostomy. In normal man calcium stimulates gastric secretion and gastrin release. After antrectomy gastric secretion is still stimulated by calcium without changing serum gastrin levels. After total gastrectomy basal serum gastrin concentration is further reduced; calcium does not liberate gastrin. These results show that calcium-induced gastric secretion is caused by direct action at the parietal cell level besides the gastrin release from the antrum. In man, extra antral gastrin cannot be released by induced hypercalcemia.
Klin Wochenschr 1977 Dec 01
PMID:[The effect of antrectomy or total gastrectomy on calcium-induced gastrin secretion and gastrin release in man (author's transl)]. 59 73

Balance studies were performed in thirty-three post-menopausal women (all but five having vertebral crush fractures or femoral neck fractures) in the basal state and on treatment with 1alpha-hydroxyvitamin D3 and/or oestrogenic hormones. The results suggest that the effectiveness of oestrogen therapy is limited by calcium malabsorption and the effectiveness of 1alpha-hydroxyvitamin D3 is limited by oestrogen deficiency. The best results were obtained with combined therapy to remedy what appears to be two distinct deficiencies. To minimize the risks of hypercalcaemia and the possible risks of hormone therapy, we suggest that the treatment of choice in post-menopausal osteoporosis may be 1alpha-hydroxyvitamin D3 1microgram daily and ethinyloestrodiol 25 microgram daily for 3 weeks in every 4. Patients on a low dietary intake of calcium should probably be given calcium supplements. With this regimen, it should not be necessary to screen patients initially for calcium malabsorption or oestrogen deficiency because the majority of patients present with a combination of the two factors.
Clin Endocrinol (Oxf) 1977 Dec
PMID:The effect of 1alpha-hydroxyvitamin D3 with and without oestrogens on calcium balance in post-menopausal women. 60 14

The surgical management of primary hyperparathyroidism with severe bone disease (and tertiary hyperparathyroidism) has frequently been complicated by severe and prolonged post-operative hypocalcaemia. In seven such cases a short-pre-operative course of 1alpha-hydroxyvitamin D3 has been found to abolish these adverse features virtually completely and even to diminish pre-operative symptoms where present. Exacerbation of hypercalcaemia has not occurred and this regimen is thus recommended as a routine measure.
Clin Endocrinol (Oxf) 1977 Dec
PMID:1alpha-hydroxyvitamin D3 in primary hyperparathyroidism. 60 19

The high circulating concentrations of immunoassayable parathyroid hormone observed in chronic renal failure are due to a number of factors. These include altered metabolism of the hormone and also end-organ unresponsiveness which may, indirectly, cause increased secretion of parathyroid hormone. The response of the overactive parathyroid glands to changes in plasma calcium and magnesium is variable and caution is needed in evaluating the suppressibility of parathyroid hormone secretion in acute studies. 1alpha-Hydroxylated derivatives of vitamin D can effectively suppress parathyroid gland overactivity. This effect may not necessarily be medicated through hypercalcaemia and vitamin D metabolites may act directly on the parathyroid glands.
Clin Endocrinol (Oxf) 1977 Dec
PMID:Hyperparathyroidism in chronic renal failure. 60 26


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