Cases reported "Hypercalcemia"

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1/28. Regulatory hyperparathyroidism: the role of C-cell hyperplasia.

    Four cases with clinical and biochemical evidence of hyperparathyroidism are reported. The syndrome was due to DHT-intoxication of iatrogenic origin in the first case to histologically confirmed C-cell hyperplasia of the thyroid in the three others. The collective term "regulatory hyperparathyroidism" is porposed for the syndromes which, in distinction to secondary parathyroidisms, have a pathogenesis other than a negative calcium balance. Management of the syndrome is discussed with particular emphasis on the removal of the TCT-producing hyperplasia or adenoma, and the restoration of the electrolyte balance.
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2/28. hypercalcemia of the newborn: etiology, evaluation, and management.

    hypercalcemia in infants is uncommon but has potentially serious sequelae. This review examines four cases of neonatal hypercalcemia, emphasizing appropriate investigations and treatment of acute and chronic hypercalcemia. The paper provides additional information as to the mechanisms of calcium dysregulation in idiopathic infantile hypercalcemia, williams syndrome, vitamin d intoxication, and parathyroid and parathyroid-related protein disturbances.
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3/28. hypercalcemia-induced renal insufficiency during therapy with dihydrotachysterol.

    During vitamin-D therapy drug accumulation and intoxication should be considered. In the present study we report on five patients with renal insufficiency during therapy with dihydrotachysterol or calcitriol. Four patients received dihydrotachysterol for 29 (7-44) years and one patient received calcitriol for 4 years to treat hypoparathyroidism after thyroid surgery. As confirmed by renal biopsy impairment of renal function was due to calcifications as a consequence of prolonged hypercalcemia. The effective duration of dihydrotachysterol is ten days as compared with five days for calcitriol. Severe hypercalcemic episodes with dihydrotachysterol are longer-lasting than those with the shorter acting vitamin-D derivatives. Further, they occur with higher incidence as was shown by our own observations and previously published data by other workers. Hence, impairment of renal function during therapy with dihydrotachysterol should be considered as being due to hypercalcemia and hypercalciuria.
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4/28. liver granulomatosis is not an exceptional cause of hypercalcemia with hypoparathyroidism in dialysis patients.

    In 4 of our patients on chronic dialysis, we were intrigued by the association of hypercalcemia /- hyperphosphatemia and normal intact PTH, with anicteric cholestasis without cytolysis. This picture occurred in 2 patients after they resumed dialysis because of a transplant rejection and in a third one after discontinuation of corticosteroids, prescribed for an idiopathic thrombocytopenia. No patient was under calcitriol, CaCO3 therapy, and their hypercalcemia persisted on a low calcium dialyzate (1.25 mmol/l). Obvious etiologies of hypercalcemia were not found: vitamin d or A intoxication, hyperparathyroidism, aluminum intoxication, hemopathy, hiv infection. The hypothesis of a granulomatous disease was made and a liver biopsy was performed showing granulomas with giant epitheloid cells. In one case foreign material (silicon ?) was present in the macrophages. Extensive investigations for sarcoidosis, tuberculosis and mycosis were negative. In 2 cases the so-called "dialysis" granulomatosis actually occurred in transplanted patients, suggesting the role of a transplantation related factor (toxic or virus). In the last case HCV seroconversion was present. In the 4 cases, corticotherapy led to the disappearance of hypercalcemia and to an increase of PTH. Our patients had the biological pattern of low bone turnover disease (hypercalcemia and normal intact PTH) and bone biopsy performed in 2 showed osteomalacia or ABD without aluminum. The association of this pattern with cholestasis should evoke liver granulomatosis, which should be confirmed by a liver biopsy and lead to a treatment by corticosteroids. The masking effect of previous corticoid therapy for transplantation should be pointed out. In 2 cases serial monitoring of plasma calcitriol showed a relation between decreasing high normal calcitriol with prednisone and normalization of calcemia, suggesting the role of inappropriate synthesis of calcitriol by the granuloma. In conclusion, liver granulomatosis should be looked for in dialysis patients on the association of unexplained hypercalcemia and normal PTH with anicteric cholestasis, and confirmed by a liver biopsy. Although still of unknown etiology, its evolution is favourable under corticotherapy.
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keywords = intoxication
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5/28. hypercalcemia and human nature.

    patients on hemodialysis may develop severe and symptomatic hypercalcemia if skeletal buffering is ineffective. We report a case of persistent hypercalcemia with apparent extrarenal vitamin d synthesis. Associated aluminium intoxication was suggested on desferrioxamine challenge and adynamic uremic osteodystrophy confirmed on bone biopsy. plasma calcitriol did not suppress with corticosteroids but did with ketoconazole. No other evidence for underlying granulomatous disease was found. We discuss our approach to less usual causes of hypercalcemia, and emphasise the pitfalls associated with factitious disorders.
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6/28. hypercalcemia due to vitamin d intoxication with clinical features mimicking acute myocardial infarction.

    We report a case of hypercalcemia in an elderly patient due to vitamin d intoxication with clinical features and electrocardiogram (ECG) findings mimicking acute myocardial infarction. A 78-year-old man was referred to our department with symptoms of general fatigue, anorexia and chest pain. The ECG demonstrated ST elevation in leads V1 to V3 and diffuse T wave flattening, resulting in myocardial infarction being suspected. However, his symptoms, including chest pain, gradually improved and the ECG returned to normal in accordance with a fall in his serum calcium level. We introduce the use of QaTc interval shortening in differentiating ST-T changes of hypercalcemia from those of true myocardial ischemia.
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keywords = intoxication
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7/28. Lithium intoxication, hypercalcemia and "accidentally" induced food and water aversion: a case report.

    Lithium is widely used in the management of patients with affective and other behavioral disorders. In addition to its therapeutic role, it is important to recognize that it occasionally causes severe side effects. Associated with its long-term use, parathyroid hypersecretion and hypercalcemia is a rare but reported side effect. A 54-year-old patient is reported who previously had a good response to lithium carbonate treatment of his bipolar disorder. Suddenly, and after 15 years of lithium carbonate use, he presented food and water aversion, hypercalcemia, lithium intoxication (SLi of 4.30 mmol/l) and acute renal insufficiency. Haemodialysis was carried out and the patient improved dramatically.
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8/28. vitamin d intoxication and hypercalcaemia in an infant treated with pamidronate infusions.

    Bisphosphonates are used for the treatment of childhood hypercalcaemia, especially that due to malignancies. Here we report the use of intravenous pamidronate for the treatment of hypercalcaemia due to vitamin d intoxication in a 3-month-old infant. serum calcium levels were normalised without complications. CONCLUSION: pamidronate may be used in hypercalcaemia due to vitamin d intoxication in paediatric cases resistant to hydration, diuretics or corticosteroids.
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ranking = 6
keywords = intoxication
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9/28. role of dialysis in the treatment of severe hypercalcemia: report of two cases successfully treated with hemodialysis and review of the literature.

    The role of dialysis in the treatment of patients with severe hypercalcemia is uncertain. The fourteen previously reported cases of hypercalcemia treated with either peritoneal or hemodialysis have been reviewed. Two additional patients treated with hemodialysis are described in this report. Because the use of large volumes of intravenous fluids was contraindicated, each of the patients received a low calcium bath (0-1 mEq calcium per liter) hemodialysis for three and a half hours. After dialysis, the serum calcium fell to normal in both and remained normal thereafter with treatment of the underlying disease (multiple myeloma in one and vitamin d intoxication in the other). Hemodialysis can clear up to 682 mg of calcium per hour as compared to 124 mg per hour for peritoneal dialysis and 82 mg per hour with forced saline diuresis. Low calcium bath hemodialysis is indicated when the presence of renal and/or cardiac failure prevents the administration of large volumes of intravenous fluids to hypercalcemic patients.
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10/28. Oral alendronate therapy for severe vitamin d intoxication of the infant with nephrocalcinosis.

    vitamin d intoxication is a well-known cause of hypercalcemia in children. We report here the use of oral alendronate for the treatment of hypercalcemia due to vitamin d intoxication in a 7 month-old infant with nephrocalcinosis. The serum calcium levels were normalized without complications. Oral alendronate therapy may be safely used in hypercalcemia due to vitamin. D intoxication in pediatric patients with nephrocalcinosis resistant to hydration, diuretics or corticosteroids.
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ranking = 7
keywords = intoxication
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