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

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

A 21-year-old man suffered severe (up to 15.5 mg%) and prolonged (7 months) hypercalcaemia as a result of immobilisation following severe trauma. During the period of hypercalcaemia, plasma parathormone and calcitonin levels were undetectable. A study using radioactive calcium revealed a very marked increase in bone resorption, a moderate increase in accretion and virtually no intestinal absorption. Iliac biopsy revealed dense calcification front and there was no osteoid substance. This hypercalcaemia appeared to be due to increased bone resorption, while the synthesis of osteoid substance seemed to be insufficient to permit an equivalent increase in calcium accretion.
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PMID:[Immobilisation hypercalcaemia. 1 case (author's transl)]. 63 83

To determine the effect of thyroid-stimulating hormone (TSH) on secretion of calcitonin by the thyroid, 50 male Sprague-Dawley rats were randomly separated into seven groups. The groups received different diets, medications, or operations [propylthiouracil (PTU), iodine-deficient diet, (LID), acute or chronic thyroxine treatment, sham operation (SO), hemithyroidectomy (Htx), and total thyroidectomy (Ttx)]. two weeks to six months later, serum TSH concentrations were increased in the Htx, Ttx, and LID groups when compared with SO animals. Serum calcitonin concentrations were increased in the LID- and PTU-treated groups and were decreased in animals that chronically received thyroxine. Serum calcium concentrations were increased in the LID animals, decreased in the Ttx animals, and were similar in the other groups. These findings suggest that TSH stimulates both follicular and parafollicular cells in the rat thyroid and that iodine deficiency causes hypercalcemia and hypercalcitonemia.
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PMID:Iodine deficiency produces hypercalcemia and hypercalcitonemia in rats. 64 56

Immobilization hypercalcemia following a single limb fracture of one weight bearing bone has been reported rarely in the pediatric age group. Nevertheless, in six of 12 patients immobilization hypercalcemia developed, associated with elevations in the urinary calcium/creatinine ratio and serum levels of ionized calcium after a single limb fracture of a weight-bearing bone during this two-year study period. We suggest that immobilization hypercalcemia occurs frequently in both children and adolescents after a single limb fracture of one weight-bearing bone, exercises in bed fail to prevent immobilization hypercalcemia, serial measurements of the serum ionized calcium and the urinary calcium/creatinine ratio are critical measures in treating such patients, and though complete mobilization is curative, transient calcitonin therapy is highly effective in reversing the disorders in calcium metabolism.
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PMID:Immobilization hypercalcemia after single limb fractures in children and adolescents. 65 37

Autopsy examination of a patient with well-documented supravalvular aortic stenosis and other characteristic features of the idiopathic infantile hypercalcemia syndrome revealed previously unreported hyperplasia of parafollicular cells (C cells). Immunohistochemical analysis demonstrated up to 30 calcitonin-containing cells per high power field, whereas normal glands contain only 4 to 10 cells per low power field in areas of highest concentration. The parathyroid glands were found to be normal both grossly and microscopically, whereas the bones showed thickened trabeculas, normal Haversian canals and no apparent increase in osteoblast or osteoclast activity, suggesting normal parathyroid hormone, but increased thyrocalcitonin activity. We suggest that C-cell hyperplasia has occurred in response to a persistent, rather than transient, elevation in serum calcium levels and that thyrocalcitonin function is augmented, rather than impaired in this disorder. The primary biochemical defect promoting hypercalcemia remains to be clarified, as well as the role, if any, such a defect plays in producing significant pathology in the central nervous system and in the cardiovascular, renal and skeletal systems.
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PMID:Supravalvular aortic stenosis with parafollicular cell (C-cell) hyperplasia. 65 98

The thyroidal content of calcitonin was investigated in patients with euthyroid goitre, patients undergoing laryngectomies or neck operations and finally patients with primary hyperparathyroidism using method of biological titration. Patients with primary hyperparathyroidism had markedly decreased content of calcitonin in the thyroid gland when compared with the content of calcitonin of both groups of patients without calcium metabolism disturbance. Decreased content of calcitonin in patients with primary hyperparathyroidism can be explained by long lasting hypercalcaemia during which the rate of biosynthesis of calcitonin in the C cells does not keep up with the rate of release of calcitonin into the circulation.
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PMID:Calcitonin activity of the thyroid gland in primary hyperparathyroidism. 69 67

The paper presents the case history of a 15-year-old boy with traumatic tetraplegia who developed hypercalcaemia within 6 weeks of injury. The condition was initially controlled by the infusion of intravenous fluids in large amounts and by the administration of calcitonin. After 3 weeks, calcitonin became ineffective. Eventually the hypercalcaemia responded to cortisone administered in low dosage. The endocrinologic implications of this observation are discussed.
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PMID:Hypercalcaemia in adolescent tetraplegic patients: case report and review. 73 87

The importance of calcitonin (CT) in calcaemic homeostasis has been studied in control subjects and in thyroidectomized patients. After administration per os of a calcium load together with a radioactive tracer, calcaemia increases more markedly in thyroidectomized cases while the radioactivity curve shows no difference between the two groups. Unlike the controls, in patients the absorption-induced calcaemic increment curve coincided with the cumulative intestinal calcium absorption curve evaluated by the biradioisotopic method. Thus absorption-induced hypercalcaemia in athyroid subjects would not seem to be controlled by homeostatic factors. Through CT, the thyroid exerts an evident, though limited, braking action on calcaemic increase due to absorption. Considering that absorption of calcium is prolonged for a number of hours, CT secretion will last at least as long as will its action on the skeleton. The saving of skeletal mineral that follows may be considered to be physiologically more important than the effect of the hormone on calcaemic homeostasis.
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PMID:[Importance of the thyroid gland in calcemic homeostasis during intestinal calcium absorption in man]. 85 28

Two cases of neonatal hypophosphatasia are described. In case 1, hypercalcemia developed at 2 1/2 months of age and continued until death at 10 1/2 months of age. Serum calcium levels decreased transiently in response to phosphate supplementation, prednisolone, and calcitonin. Significantly elevated levels of PTH were detected at 2 1/2 months of age. At autopsy, no parathyroid glands were found. In case 2, hypercalcemia was not detected in his course. Elevated level of serum PTH was recorded on the 17th day of life. A post-mortem examination revealed the presence of one normal parathyroid gland.
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PMID:Neonatal hypophosphatasia with elevated serum parathyroid hormone. 85 8

Hypercalcemia of multiple myeloma has been discussed widely in the medical literature. The role of calcitonin and phosphate in the treatment of hypercalcemia of multiple myeloma has not yet been studied to our knowledge, although experimental animal models have been pointing to the role of phosphate supplement to calcitonin treatment in multiple myeloma. A patient had multiple myeloma and hypercalcemia. The usual medical treatment for hypercalcemia failed; however, the treatment with combined orally administered phosphate and calcitonin was successful. The role of phosphate depletion in this setting is brought up as an important factor in the failure of calcitonin therapy.
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PMID:Combined calcitonin and oral phosphate treatment for hypercalcemia in multiple myeloma. 87 32


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