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)

Anorexia, constipation, vomiting and somnolence in a 39-year-old woman were at first misinterpreted as being of psychological and autonomic nervous system origin. Further clinical and biochemical tests revealed hyperthyroidism associated with hypercalcaemia and hypercalciuria. Thyrostatic treatment for 12 days caused regression of the hypercalcaemia and, after subtotal resection, serum calcium levels and urinary calcium excretion returned to normal for good. The hypercalcaemia syndrome must therefore be assumed to have been the direct result of the hyperthyroidism.
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PMID:[Hyperthyroidism with hypercalcaemia (author's transl)]. 5 61

A 56-year-old man with a three-month history of fever, malaise, anorexia, mental confusion, and weight loss had hypercalcemia and azotemia. The chest roentgenogram was normal. Biopsy material removed 2 1/2 years previously showed noncaseating granulomas. Sarcoidosis was diagnosed, and prednisone was administered. Fever persisted, and the patient died 49 days after admission. Postmortem examination showed evidence of extensive disseminated histoplasmosis, interstitial nephritis, and papillary necrosis. This communication emphasizes the difficulty in diagnosing the etiology of disseminated, noncaseating granulomatous disease.
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PMID:Histoplasmosis with hypercalcemia, renal failure, and papillary necrosis. Confusion with sarcoidosis.. 57 82

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.
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PMID:[Immobilisation hypercalcaemia (author's transl)]. 59 68

Pseudohyperparathyroidism was diagnosed in a mature stallion presented for anorexia, weight loss, pollakiuria and constipation. Laboratory findings included hypercalcemia, hypophosphatemia, anemia and isosthenuria. Thoracocentesis indicated an exfoliating squamous cell carcinoma. At necropsy, a squamous cell carcinoma of the stomach with metastases to the abdominal and thoracic cavities was diagnosed. No osseous metastases were found. No gross or microscopic renal lesions were noted. Bone tissue showed arrested resorption, and the parathyroid gland was atrophic.
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PMID:Gastrict carcinoma with pseudohyperparathyroidism in a horse. 63 16

Two groups of weanling pigs, injected with 45Ca, were fed diets containing optimal calcium and phosphorus, and vitamin D3 at 1320 IU/kg feed in the control group, and 825,000 IU/kg feed in the test group. The groups were further subdivided with 2 pigs in each subgroup, with survival times of 1, 2, 3, 4, 7, and 14 days. Pigs fed the high level of vitamin D3 lost weight and anorexia, weakness, rough hair coat and labored breathing were observed. Hypercalcemia began at 12 hours and progressed rapidly after 2 days. Radioisotope sutdies interpreted in the light of histopathologic findings indicated that bone was the primary source of increased plasma calcium. Calcium was released at a rapid rate into blood from prelabeled bone which was undergoing necrosis; it was also removed from blood and deposited into bone at a slower rate due to decreased apposition. Histopathologic examination of bones from test pigs showed regressive changes in the osteocytes, chondrocytes and osteoblasts which bean within 1 day of treatment and resulted in evidence osteopenia within 7 days. Arrested osteocytic osteolysis led to the appearance of cementing lines and to chondroid core retention. Further regressive changes in the osteocytes resulted in osteocytic death and osteonecrosis with subsequent osteoclasia and osteopenia. Retardation and arrest of cartilage maturation as well as osteoblastic deficiency contributed to the osteopenia. The osteopenia was further evidenced by decreased specific gravity and ash content per unit volume of humerus. The initial negative effect on the osteocytes, chondrocytes and osteoblasts is attributed to a direct toxic effect of excessive dietary vitamin D3 since hypoparathyroidism and hypercalcitoninism, which occur secondarily to hypercalcemia, could not account for the rapid appearance of this effect, nor are they known to induce osteocytic death. The release of bone calcium and the resulting hypercalcemia in vitamin D3 toxicosis is therefore due to a direct toxic effect of the vitamin, or its metabolites, on the osteocyte resulting in osteonecrosis. It is not due to increased resorption as has been reported previously from both in vivo and in vitro investigations. Degeneration, with subsequent inflammation, but without calcification, was observed in the kidneys and in the lungs. Epithelial cells, basement membranes, and smooth muscle were affected. This conclusively demonstrates that degeneration is the primary soft tissue lesion in vitamin D3 toxicosis, and that the subsequent calcification is therefore dystrophic. Degenerative changes occurred in the parathyroid glands within 1 day of treatment resulting in necrosis, inflammation and atrophy within 4 days. Relative fibrosis was seen as the parenchyma receded. The parathyroid gland changes were considered a direct effect of vitamin D3 toxicity since they occurred with only mild hypercalcemia and since necrosis of parathyroid cells has not been demonstrated with hypercalcemia either in vivo or in vitro.
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PMID:Vitamin D toxicity. Initial site and mode of action. 66 94

Profound hypercalcemia associated with immobilization is rare. Hypercalcemic crisis occurring as a result of immobilization in which there was not a coexisting, contributing medical condition has not, to our knowledge, been reported previously. Failure to consider hypercalcemia as the source of progressive anorexia, nausea, vomiting, and irritability resulted in a respiratory arrest and nearly fatal outcome in the case of a 13-year-old boy one month after a simple femoral fracture. Therapy consisting of the intravenous administration of fluids and corticosteroids was successful in lowering the serum calcium level until mobilization could be accomplished. Review of previously reported cases emphasizes the difficulty in recognition and diagnosis of this unusual condition. Surgeons treating patients with fractures should be aware of this complication and familiar with its appropriate therapy.
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PMID:Immobilization hypercalcemia crisis. 105 62

The chronic ingestion of the leaves of the plant Solanum malacoxylon (SM) causes an endemic disease in the cattle of some areas of Buenos Aires province. The animals affected manifest loss of appetite and weight, hypercalcemia, hyperphosphatemia, and ectopic calcifications. In order to study the mechanism of the hypercalcemia provoked by the administration of SM, a calcium kinetic study was performed in control and treated adult intact rats. The animals receiving SM showed higher levels of serum calcium throughout the study. The body excretion of 47Ca and the size of the most rapidly exchangeable calcium pool were also elevated. On the other hand, the bone accretion rate and the urinary excretion of total hydroxyproline were significantly diminished. The results indicate that during the early phase of SM administration in intact rats, bone turnover rate is depressed.
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PMID:Calcium kinetics in the Solanum malacoxylon-treated rat. 119 17

Anorexia, severe skeletal demineralization, and muscular weaknesss developed in a 9 year-old Collie. Hypercalcemia, hypophosphatemia, and nephrocalcinosis were found on clinical evaluation. The surgical removal of a parathyroid adenoma was followed by profound hypocalcemia that was unresponsive to calcium therapy, and the dog died. The persistent hypocalcemia was attributed to increased deposition of calcium in mineral-deficient bone.
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PMID:Primary hyperparathyroidism in a dog. 126 47

A sixty nine-year-old woman was admitted to the hospital because of further examination of hypercalcemia. On July 1990, she complained of general fatigue and loss of appetite. She was pointed out to have hypercalcemia (15.1mg/dl), urolithiasis, and renal insufficiency. CT films of the chest showed swelling of the mediastinal lymphnodes and CT of the abdomen nephrocalcinosis. Ga-scintigraphy demonstrated an abnormal accumulation of gallium in the mediastinum. Levels of the parathyroid hormone was normal. Levels of the serum calcium (13.7mg/dl), angiotensin converting enzyme (30.4IU/L) and 1.25 (OH)2D (87PG/ml) were elevated. Giant cells were found in the biopsy specimen of the lung. A significant relationship between the serum calcium and creatinine were observed (r = 0.76, p < 0.02). Proximal fractional reabsorption of sodium showed to be suppressed (47.7%), and distal fractional reabsorption of sodium showed to be normal (88.4%). From these findings hypercalcemia and urolithiasis was suggested to result from sarcoidosis. The hypercalcemia and renal insufficiency improved with corticosteroid therapy.
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PMID:[A case of sarcoidosis with hypercalcemia, urolithiasis, nephrocalcinosis and renal insufficiency]. 148 16

A 34-year-old male was admitted to our hospital because of anorexia and nausea in September, 1987. On admission, anemia, thrombocytopenia and hypercalcemia were observed, and the peripheral blood showed leukocytosis with atypical plasma cells (50%). Bone marrow aspiration showed hypercellularity, with a presence of atypical plasma cells (82%). The M-type protein in the serum and urine was identified as lambda Bence Jones protein by immunoelectrophoresis. On systemic skeletal X-rays, osteolytic lesions were not detected. Thus, a diagnosis of plasma cell leukemia associated with hypercalcemia was made. Hypercalcemia was treated successfully with overhydration. However the disease was refractory to combination chemotherapy, and at 10 months after diagnosis, he died of septic candidiasis. Hypercalcemia associated with plasma cell leukemia in its initial stage is rare.
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PMID:[Primary plasma cell leukemia associated with hypercalcemia]. 194 29


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