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

In three patients with thyrotoxicosis and with symptomatic hypercalcaemia antithyroid therapy restored the plasma calcium concentration to normal, though initially in one case intravenous and oral neutral phosphate solution were required to curtail intractable vomiting.Nine cases have been recorded in which the plasma calcium concentration returned to normal after antithyroid treatment was started; all but one became normocalcaemic within eight weeks. It is suggested that in hypercalcaemic thyrotoxicosis a second pathological condition should be considered only if the plasma calcium concentration fails to return to normal within eight weeks.
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PMID:Symptomatic hypercalcaemia in thyrotoxicosis. 542 53

After 13 days therapy with 30 mg dihydrotachysterol (dihydrotachysterin, AT 10 (DHT3 daily in a 33-year-old female patient a severe intoxication developed. In addition to this the patient was twice administered calcium gluconate and vitamin D. Typical clinical symptoms of the developing hypercalcaemia syndrome consisted in adynamia, vomiting and obstipation. The occurring clinical symptom and findings are discussed on the basis of recent knowledge concerning efficacy and metabolism of DHT3 as well as vitamin D3.
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PMID:[Dihydrotachysterol poisoning]. 651 95

The most common cause of hypoadrenocorticism in dogs is idiopathic immune-mediated destruction of the adrenal cortex. Other causes include anterior pituitary insufficiency, pituitary or adrenal neoplasia, acute withdrawal of exogenous corticosteroids, and mitotane toxicity. Females are affected more often than males; only 1 feline case has been documented. Animals 2-5 years old are most commonly affected. Clinical signs include lethargy, weakness, weight loss, anorexia, vomiting, diarrhea and bradycardia. Hematologic and biochemical changes can include eosinophilia, lymphocytosis, anemia, hyperkalemia, hyponatremia and hypercalcemia. Diagnosis is by finding negligible resting levels of plasma cortisol and no response to ACTH administration, and a serum Na:K ratio of 20:1 or less. Treatment involves restoring fluid volume, correcting acidosis, and supplementing salt and glucocorticoids. Daily oral use of prednisone at 0.05 mg/kg can safely maintain most affected dogs. Some dogs only require glucocorticoids in stressful situations. Iatrogenic secondary adrenocortical insufficiency (iatrogenic Cushing's disease) may result from a single injection of long-acting glucocorticoids or from long-term use. Clinical signs are the same as for natural hyperadrenocorticism, but endogenous cortisol release is suppressed. Treatment is gradual withdrawal of the offending glucocorticoid and elimination of the cause that initially prompted glucocorticoid therapy.
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PMID:Diseases of the adrenal cortex of dogs and cats. 674 17

In outlining the pathology of various electrolyte metabolism abnormalities in cancer patients we considered the main clinical points between pathologies and emergency treatment. In regard to sodium (Na+) metabolism, one pathologic state that requires our attention is hypernatremia. Hypernatremia is accompanied with dehydration and is due to water loss, vomiting, diarrhea and renal insufficiency. One of the major causes of this condition is lack of the antidiuretic hormone due to intracranial metastasis of the tumor. When hypernatremia becomes severe, it is accompanied with circulatory failure, muscular asthenia, disorientation, convulsions, coma and other cerebral symptoms. Treatment consists of replenishing the water content by infusion of electrolyte solutions which should be carefully conducted after complete diagnose of the severity of the patient's pathological condition. Hyponatremia, like sick cell syndrome, is observed relatively frequently in cancer patients. When the serum Na level falls markedly, it induces cerebral edema and causes disorders of consciousness. The major treatment consists of providing both water and sodium supplements. Hyperkalemia is observed at the time of renal insufficiency, tissue lesions, vomiting, and diarrhea. When serum potassium level rises, it causes bradycardia, ventricular fibrillation, or cardiac arrest. It is important to diagnostically apprehend the severity of this condition using EKG and determining the serum K1+ level. For emergency treatment injection of calcium gluconate is very effective. Hypokalemia is often manifested by the loss of intestinal fluids due to diarrhea or during administration of diuretic agents. Clinical symptoms include neural paralysis but emergencies occur relatively infrequently. K C1 injections are used in treating this condition. Hypercalcemia is manifested in cancer patients during hyperparathyroidism. Its clinical symptoms include lassitude, tachycardia, nausea, vomiting, and renal dys-function, leading to neural symptoms in severe cases. The main treatment consists of injection of physiological saline solution and administration of calcitonin, mithramycin. Hypocalemia is manifested during renal insufficiency, lack of vitamin D, and hypothyroidism. In classic cases it causes tetanic spasms. Injection of calcium is an effective treatment but since during tetanic spasms alcalosis may easily occur, treatment should only be provided after obtaining a complete understanding of the patient's condition. The pathological conditions described above can not be said to specific to cancer but it should be kept in mind that one of their main causative factors is the involvement of mechanism which produces ectopic hormones from cancerous tissues.
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PMID:[Electrolyte metabolism and emergency]. 688 72

Studies have suggested that both natural and synthetic retinoids have extensive chemopreventive activity against a variety of carcinogens in vivo and in vitro. We have previously shown that growth of human breast cancer cells can be inhibited by retinoids, and retinoic acid-binding proteins have been demonstrated in these cell lines and tumor biopsies. We studied the activity of 13-cis-retinoic acid in the treatment of 18 patients with advanced breast cancer refractory to standard cytotoxic and/or endocrine therapy. Patients began on 0.5 mg/kg and escalated to 8 mg/kg over a one-month period unless toxicity (dry skin, dry mucosa, cheilitis, conjunctivitis) forced dose reduction. All these toxicities responded promptly to dose reduction. Four patients exhibited drug related hypercalcemia, 2 complained of severe earache and several had nausea, vomiting and abdominal cramping. There were no objective responses as defined by standard criteria. One patient with thrombocytopenia secondary to documented marrow involvement demonstrated a recovery of platelet count from 9000 to 110,000. 13-cis-Retinoic acid is not of apparent value in women with heavily pretreated breast cancer.
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PMID:Phase II trial of 13-cis-retinoic acid in metastatic breast cancer. 696 67

Thirty-seven cases of canine hypoadrenocorticism were compared with 39 previously reported cases. The 2 series were compared because it was believed that a study of 37 consecutive cases diagnosed at 1 institution (Michigan State University) and compiled by 1 group of veterinarians would yield data that were more representative of the disease than multiple cases from various institutions. Age, sex, and breed data were similar in both series. The frequency of anorexia, vomiting, depression, and the mean values for the clinicopathologic data were similar for both series except for blood glucose concentration (P less than 0.025). The Michigan State University series was different in that it had a lower frequency of eunatremia, increased plasma total solids, and hypoglycemia but a higher frequency of lymphocytosis, lymphopenia, hyponatremia, hyperglycemia, and hypercalcemia. Further, 3 dogs in the Michigan State University series had azotemia plus near isosthenuric urine, suggesting renal disease, but they seemingly responded to therapy for hypoadrenocorticism. Only 1 such case was identified in the literature. Finally, we detected fewer instances of P waves not being evident in lead II of an electrocardiogram.
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PMID:Canine hypoadrenocorticism: report of 37 cases and review of 39 previously reported cases. 703 23

Hyperparathyroid crisis is a rare disease but should be suspected in acutely ill patients complaining of weakness, lethargy, nausea, vomiting, confusion and abdominal pain. Despite the variety of clinical manifestations, the syndrome forms a distinctive pattern which, in the presence of a serum calcium level greater than 16 mg/100 ml, should be recognized. The most difficult problem in diagnosis is the differentiation of hyperparathyroid crisis from ectopic parathyroid hormone-producing tumors. The disease is an endocrine emergency which requires prompt surgery after rapid correction of dehydration and hypercalcemia. The best results are achieved by removing offending parathyroid tissue within 72 hours after the onset of symptoms.
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PMID:Primary hyperparathyroidism: hyperparathyroid crisis. 730 6

A female infant who was anoxic at birth had lesions of subcutaneous fat necrosis at the age of 16 days. She also had problems with poor feeding, frequent vomiting, and failure to thrive. Hypercalcemia was discovered at the age of 28 days and she died at 11 1/2 weeks despite return of the serum calcium level to normal with oral prednisone therapy and a diet low in calcium and devoid of vitamin D. Fourteen other cases of idiopathic hypercalcemia in patients with subcutaneous fat necrosis of the newborn have been reported. Most of these infants were full-term with prenatal complications. The hypercalcemia was usually diagnosed much later than the subcutaneous fat necrosis. Both conditions generally resolved without sequelae, but two of the 14 infants died. The causal relation between these two entities, if one exists, remains unknown. Infants with subcutaneous fat necrosis should have serial serum calcium determinations and should be observed closely for signs and symptoms of hypercalcemia, which include irritability, anorexia, constipation, and failure to thrive.
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PMID:Subcutaneous fat necrosis of the newborn and idiopathic hypercalcemia. Report of a case. 742 62

To determine the frequency of gastrointestinal symptoms in primary hyperparathyroidism, we retrospectively analyzed 100 consecutive patients seen at Emory University Hospital from Jan 1, 1977 through March 1, 1979. At the time of diagnosis, 28 patients complained of nausea, 19 of vomiting, 29 of abdominal pain, and 33 of constipation. One patient presented with acute pancreatitis and 14 had ulcer disease (two gastric and 12 duodenal ulcers). Hypercalcemia increases gastric acid secretion and may account for associated ulcer disease and the ulcer-like pain in primary hyperparathyroidism. The mechanisms causing the other gastrointestinal symptoms in hypercalcemia remain to be elucidated. These symptoms abate on correction of hyperparathyroidism.
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PMID:Primary hyperparathyroidism and the gastrointestinal tract. 746 39

Cimadronate (YM175) is a novel bisphosphonate with potent inhibitory activity on bone resorption under development for the treatment of tumor-induced hypercalcemia, metastatic bone disease and osteoporosis. We conducted intravenous single and repeated dose toxicity studies of cimadronate in beagle dogs. In the single dose study, animals received a single dose of 0.3, 1, 3 or 10 mg/kg of cimadronate and the animals were observed for at least 14 days. At 10 mg/kg, both the male and female dog showed toxic signs such as vomiting, decreased locomotor activities and hypothermia and were killed in extremis within a week after dosing. In the 30-day study, animals received cimadronate at a dosage of 0 (vehicle), 0.03, 0.1, 0.3 or 1 mg/kg/day. At 0.03 mg/kg/day or more, histological findings indicated an increased amount of primary spongiosa in the rib and ilium. At 1 mg/kg/day, degenerative nephropathy, aggregation of spermatozoa and glandular hypoplasia of the prostate gland were observed. On day 16 of dosing one male animal died of acute renal failure. In the 26-week study, animals received cimadronate once weekly at a dosage of 0 (vehicle), 0.31, 0.62, or 1.25 mg/kg. Histopathological examination showed an increased amount of primary spongiosa in the rib at all dosage levels. In addition, similar findings were observed in the lumbar vertebrae at 1.25 mg/kg/week. Histopathological changes in the kidney and male reproductive organs were not observed.
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PMID:Intravenous single and repeated dose toxicity studies of cimadronate (YM175), a novel bisphosphonate, in beagle dogs. 749 Jul 87


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