1/242. Unaccountable severe hypercalcemia in a patient treated for hypoparathyroidism with dihydrotachysterol.This report describes a forty-seven-year-old female patient with a complex medical history. She was suffering from an unspecified interstitial lung disease, papillary thyroid carcinoma which had been treated, hypoparathyroidism after thyroidectomy for which she was receiving dihydrotachysterol and calcium, and atrial fibrillation and congestive heart failure as a result of mitral stenosis. Shortly after mitral valve replacement she developed a severe hypercalcemia (serum calcium 5.95 mmol/l) during a febrile illness. At that time anti-tuberculous agents were also being administered for presumed tuberculosis. The possible mechanisms for this severe elevation of the calcium level are discussed. immobilization, while Paget's bone disease was present, and perhaps enhanced activation of dihydrotachysterol by rifampicin, could have led to increased calcium-release into the circulation. Continuous supplecation of calcium and vitamin d, provoked dehydration and the mechanism of the milk-alkali syndrome also contributed to this extremely high calcium level. It is concluded that hypoparathyroid patients being treated with vitamin d and calcium should be carefully monitored in the case of an intercurrent illness or a change in medication.- - - - - - - - - - ranking = 1keywords = vitamin (Clic here for more details about this article) |
2/242. hypercalcemia in an euthyroid patient with secondary hypoadrenalism and diabetes insipidus due to hypothalamic tumor.A 20-year-old Japanese man with a hypothalamic tumor (most likely germ-cell tumor) which caused secondary hypoadrenalism, hypogonadism and diabetes insipidus developed hypercalcemia and acute renal failure. The serum levels of intact PTH (iPTH), PTH-related protein (PTH-rP), 1,25-dihydroxy vitamin d (1,25- (OH)2 D), ACTH, cortisol, gonadotropins and testosterone were decreased, but his serum levels of triiodothyronine (T3) and thyroxine (T4) were within the normal range at admission, with depressed TSH and slightly increased thyroglobulin. The hypercalcemia was refractory to extensive hydration and calcitonin, but was ameliorated by pamidronate. After irradiation of the hypothalamic tumor, panhypopituitarism gradually developed. The patient has been normocalcemic for the last 2 years and is doing well under replacement therapy with glucocorticoid, L-thyroxine, methyltestosterone and 1-desamino D arginine vasopressin (dDAVP). As to the mechanism of euthyroidism at admission, transient destructive thyroiditis associated with hypopituitarism or delayed development of hypothyroidism following the hypoadrenalism was suggested. This is the first reported case of hypercalcemia in secondary hypoadrenalism due to hypothalamic tumor. hypercalcemia was most likely induced by increased bone resorption, which was probably elicited by the combined effects of deficient glucocorticoid and sufficient thyroid hormones in addition to hypovolemia and reduced renal calcium excretion. Furthermore, severe dehydration due to diabetes insipidus and disturbance of thirst sensation caused by the hypothalamic tumor aggravated the hypercalcemia, leading to acute renal failure.- - - - - - - - - - ranking = 0.5keywords = vitamin (Clic here for more details about this article) |
3/242. Symptomatic hypercalcemia in the first months of life: calcium-regulating hormones and treatment.Neonatal hypercalcemia is a rare condition often of unclear pathogenesis. If unrecognized and untreated it may result in central nervous system and renal damage. We studied three infants with symptomatic neonatal hypercalcemia pointing out pathogenetic and therapeutic aspects. One infant was found to have transient hyperparathyroidism with high intact parathyroid hormone (iPTH) levels. One infant had an incomplete form of williams syndrome with hypercalcemia and an elfin facies. The pathogenesis is unclear in this case. A reduced secretion of calcitonin or an hypersensitivity to vitamin d might be the underlying defect. The third case was found to have subcutaneous fat necrosis and hypercalcemia associated with high 1,25(OH)2D levels and suppressed iPTH levels. These findings suggest an unregulated extrarenal 1,25(OH)2D production. These infants were treated with hydratation, furosemide, corticosteroids and low calcium diet. Symptomatic neonatal hypercalcemia should be treated promptly. However blood has to be taken before starting treatment to study calcium-regulating hormones and clarify pathogenesis.- - - - - - - - - - ranking = 0.5keywords = vitamin (Clic here for more details about this article) |
4/242. hypercalcemia accompanied by hypothalamic hypopituitarism, central diabetes inspidus and hyperthyroidism.We present here a case of prominent hypercalcemia accompanied by hypothalamic tumor and Graves' disease. A 24-year-old man with hypothalamic tumor showed hypopituitarism, central diabetes inspidus (DI) and hyperthyroidism. nausea, loss of thirst and appetite, and general fatigue were found with the unveiling of hypercalcemia and hypernatremia. Parathyroid hormone (PTH) and 1alpha-dihydroxyvitamin D levels were suppressed with a normal range of PTH-related protein values. One-desamino-(8-D-arginine)-vasopressin (DDAVP) and half-saline administration normalized hypernatremia, while hypercalcemia was still sustained. Administration of cortisone acetate and thiamazole reduced the elevated serum Ca level. In the present case, concurrent hyperthyroidism was assumed to accelerate skeletal mobilization of calcium into the circulation. Hypocortisolism and central DI was also considered to contribute, to some extent, to the hypercalcemia through renal handling of Ca.- - - - - - - - - - ranking = 0.5keywords = vitamin (Clic here for more details about this article) |
5/242. 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.- - - - - - - - - - ranking = 0.5keywords = vitamin (Clic here for more details about this article) |
6/242. 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.- - - - - - - - - - ranking = 1keywords = vitamin (Clic here for more details about this article) |
7/242. hypercalcemia complicating leukemic transformation of agnogenic myeloid metaplasia-myelofibrosis.hypercalcemia is a common and potentially life-threatening metabolic derangement associated with many malignancies, especially solid tumors and multiple myeloma. hypercalcemia has been reported only rarely with acute myelogenous leukemia. We describe a patient who developed hypercalcemia in association with transformation of agnogenic myeloid metaplasia into M7 acute myelogenous leukemia. Laboratory investigation revealed low levels of serum parathyroid hormone, undetectable levels of parathyroid hormone-related peptide, and normal levels of 25-hydroxyvitamin D. These observations suggest that another mediator was responsible for hypercalcemia in this patient. awareness of this rare complication of acute myelogenous leukemia is essential for prompt diagnosis and management.- - - - - - - - - - ranking = 0.5keywords = vitamin (Clic here for more details about this article) |
8/242. hypercalcemia associated with infection by cryptococcus neoformans and coccidioides immitis.BACKGROUND: Of the 13 reported cases of hypercalcemia associated with fungal infection, 1 was caused by cryptococcus neoformans and probably mediated by increased levels of 1,25-dihydroxyvitamin D [1,25(OH)2D]. Eight others were associated with coccidioides immitis, of which only 2 had measured 1,25(OH)2D levels; in both, they were diminished. We report a patient with human immunodeficiency virus infection and simultaneous C. immitis and C. neoformans pneumonia and C. immitis fungemia associated with hypercalcemia. methods: Consecutive measurements of serum total and ionized calcium, phosphorous, blood urea nitrogen, creatinine, 25(OH)D, 1,25(OH)2D, parathyroid hormone (PTH), parathyroid hormone-related protein (PTHrp) and albumin were performed over a period of 46 months. RESULTS: While the patient was hypercalcemic, intact serum PTH and PTHrp were undetectable, serum 25(OH)D levels were normal, and serum 1,25(OH)2D levels were in the high normal range. Successful treatment of the C. immitis and C. neoformans infections resulted in resolution of the hypercalcemia and increase of PTH and PTHrp to the normal range. CONCLUSION: In some patients with hiv infection, coincident hypercalcemia, and severe fungal infection, the responsible factor may be 1,25(OH)2D. Although total serum levels of this compound may not be frankly elevated, they are inappropriately high for the circumstances. Free 1,25(OH)2D levels should be determined in this situation.- - - - - - - - - - ranking = 0.5keywords = vitamin (Clic here for more details about this article) |
9/242. 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.- - - - - - - - - - ranking = 0.5keywords = vitamin (Clic here for more details about this article) |
10/242. hypercalcemia due to talc granulomatosis.Pulmonary disease due to talc, a group of hydrous magnesium silicates, is almost exclusively encountered after occupational exposure. One form of this rare disorder is talc granulomatosis. In varying degrees, hypercalcemia is typical of granulomatous disease but has not yet been reported in talcosis. We report the case of a former mold maker who presented with hypercalcemia. Laboratory findings indicated extra-renal 1-alpha-hydroxylation of 25-hydroxyvitamin D. Pulmonary infiltrates prompted a lung biopsy that disclosed talc granulomatosis. We suggest that talc granulomatosis should be added to the list of granulomatous disorders capable of causing hypercalcemia due to increased extra-renal 1-alpha-hydroxylation of 25-hydroxyvitamin D.- - - - - - - - - - ranking = 1keywords = vitamin (Clic here for more details about this article) |
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