Cases reported "Hypercalcemia"

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11/28. sarcoidosis-related hypercalcemia in 3 chronic hemodialysis patients.

    hypercalcemia is a frequent complication in chronic hemodialysis (CHD) patients. A rare cause of this condition is sarcoidosis, and has only been reported 6 times in CHD. Herein, we report on 3 cases of sarcoidosis-related hypercalcemia in CHD patients: an overt case, a probable case, and a recurrence of pre-dialysis sarcoidosis. hypercalcemia is a frequent complication in chronic hemodialysis patients: it is often related to uncontrollable secondary hyperparathyroidism or to the inappropriate use of calcium phosphate binders, 1alpha-hydroxylated vitamin d metabolites, high dialysate calcium concentrations, or to aluminium-related bone disease [Uach and Bover 1996]. However, other rare causes should also be considered, such as multiple myeloma, non-Hodgkin lymphoma [Uach and Bover 1996], vitamin a intoxication [Fishbane et al. 1995], or granulomatous diseases such as sarcoidosis. The latter has only been described in a total of 6 hemodialysis patient reports [Barbour et al. 1981, Barnard et al. 2002, Herrero et al. 1998, Kalantar-Zadeh et al. 1994, Kuwae et al. 2003, Naito et al. 1999]. In the present paper, we report on 3 cases of sarcoidosis-related hypercalcemia in chronic hemodialysis patients with 3 different patterns, i.e. overt sarcoidosis, probable sarcoidosis, and recurrence of pre-dialysis sarcoidosis.
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12/28. hypercalcemia complicating an industrial near-drowning.

    A 28-year-old man presented with lethargy, solmulence, and polyuria following near-drowning in a vessel of an offshore oil rig. Laboratory evaluation demonstrated severe hypercalcemia that responded to saline diuresis and nasogastric suctioning. calcium salts are used frequently in the drilling and completion of oil wells, and it is presumed that this patient's hypercalcemia represented acute intoxication from swallowed and aspirated fluid. This case highlights the need to consider the potential constituents of the drowning fluid in victims of near-drowning, particularly if unexplained clinical phenomena are evident.
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13/28. Glucocorticoid effects in vitamin d intoxication.

    calcium balance studies and measurement of 25-hydroxyvitamin D3 (25[OH]D3) levels were performed on a vitamin d intoxicated, hypoparathyroid patient before, during, and after successful management of hypercalcemia with oral prednisone therapy. prednisone effected a dramatic reduction in both mean serum calcium levels and mean 24-hour urinary calcium excretion within four days on two separate occasions. No changes were apparent in fecal calcium excretion. calcium balance became less negative with prednisone treatment. Levels of 25(OH) D3 during the same period did not change. Decreased calcium mobilization from bone best accounted for the glucocorticoid-mediated amelioration of hypercalcemia.
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14/28. Recurrent pancreatitis secondary to hypercalcemia following vitamin d poisoning.

    A 66-year-old patient had been admitted four times for recurrent episodes of acute pancreatitis. At each time, elevated serum calcium levels, between 13.5-14.5 mg/dl, were found. Surgical drainage of necrotic pancreatic tissue had to be done on one occasion. Extensive investigations failed to disclose any conventional hypercalcemic disease. At his latest admission, the serum calcium level was 13.4 mg/dl, and the serum amylase level was 440 IU/L (N, less than 85). This time, the serum 25-OH vitamin d levels were investigated using radioimmunology and proved to be raised to 330 micrograms/L (normal, 16-74 micrograms/L). Specific questioning of the patient revealed that he had been taking regularly excessive quantities of vitamin supplements as a self medication. After stopping vitamin intake, his serum amylase levels returned to normal, and he had no more episodes of pancreatitis. This case illustrates vitamin d intoxication as a cause of recurrent pancreatitis. Measuring serum 25-OH vitamin d levels is advocated in pancreatitis associated with hypercalcemia of unclear origin.
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15/28. Hyperparathyroid crisis reviewed: a role for parenteral cimetidine?

    Hyperparathyroid crisis secondary to primary hyperparathyroidism has variously been described as hypercalcemic crisis, parathyroid storm, and parathyroid intoxication as well as other equally descriptive terms. Whatever the nomenclature, all emphasize the seriousness and urgency of the condition. Although fewer than 200 cases have been described since the first report by Hanes in 1939, it is generally agreed that hyperparathyroid crisis is more prevalent than commonly appreciated. The signs and symptoms of the syndrome are believed due not only to the presence of hypercalcemia, but to the toxic effects of parathormone as well. Its wide, but nonspecific clinical spectrum makes it easily confused with other causes of rapidly fatal cardiovascular or renal disease. The mortality in untreated cases is essentially 100 per cent. With combined medical-surgical treatment, it is still reported as high as 60 per cent. Three patients with severe hyperparathyroid syndrome are reported. Effective control of both hypercalcemia and the toxic effects of acute hyperparathyroid crisis was achieved with the use of parenteral cimetidine. Definitive surgical removal of a solitary parathyroid adenoma was performed in all three patients. The intimate relationship of the bioavailability of cimetidine and its effect in primary hyperparathyroidism is clearly demonstrated. An analogy to the use of cimetidine in zollinger-ellison syndrome is made. Both are endocrinopathies that require doses of cimetidine in excess of that normally considered therapeutic for peptic ulcer disease. The signs and symptoms of hyperparathyroid crisis as well as current modalities of treatment are reviewed. It is concluded that parenteral cimetidine is an important aid in the management of acute hyperparathyroid syndromes secondary to primary hyperparathyroidism.
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16/28. Renal function in hypercalcemia after renal transplantation.

    A case of transient hypercalcemia in a 53-year-old female, who received a necro-kidney transplant, has been examined. The hypercalcemia was caused by vitamin d intoxication on three separate occasions. Each period of even moderate hypercalcemia produced a rapid fall in renal function. The effect was reversible. These findings are discussed in the light of earlier reports on stable renal function in post-transplant hypercalcemia.
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17/28. calcinosis of joints and periarticular tissues associated with vitamin d intoxication.

    We describe a patient with rheumatoid arthritis and widespread joint and periarticular calcinosis related to self-medication with vitamin d, which was aggravated by oral phosphate therapy prescribed for her hypercalcaemia. Hydroxyapatite was shown in the synovial fluid from affected joints. The role played by tissue injury in the pathogenesis of soft tissue calcification is discussed.
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keywords = intoxication
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18/28. Neonatal severe primary hyperparathyroidism and alkaptonuria in a boy born to related parents with familial hypocalciuric hypercalcemia.

    We describe a study of a boy with neonatal severe primary hyperparathyroidism (NSPHP) and alkaptonuria born to related parents of Turkish origin. The clinical and chemical courses (e.g. of mineral metabolism, of urinary excretion of amino acids and collagen metabolites) in response to various therapeutic approaches including total parathyroidectomy (PTX) are reported. Urinary excretion of calcium was unusually low before and immediately after PTX, and later during an inadvertent vitamin d intoxication. It corresponded to values typical for patients with familial hypocalciuric hypercalcemia (FHH), an autosomal dominant disorder. Both parents and one sibling had episodes of hypercalcemia with inappropriately high parathormone levels; in the father there was also relative hypocalciuria consistent with FHH. On the basis of the genetic and pathophysiologic data reported here, we speculate that homozygosity for the 'FHH-gene' is the cause of the life-threatening manifestation of NSPHP, whereas heterozygosity for the same gene leads to FHH, by comparison a mild disorder. The association of the two very rare recessively transmitted disorders, alkaptonuria and NSPHP, is unique; close linkage of the two genes, one coding for homogentisic acid oxidase, the other for the unknown gene product defective in NSPHP, can be suspected.
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19/28. Chronic vitamin a intoxication. A multisystem disease that could reach epidemic proportions.

    Two patients seen in a six-month period had a diffuse, multisystem disorder characterized by edema of the extremities and face, rash, bone pain and tenderness, symptoms of increased intracranial pressure, and hypercalcemia. Both had been receiving extraordinarily high doses of vitamin a for some time. serum vitamin a concentrations were markedly elevated, and serum vitamin d concentrations were normal. The history of excessive vitamin administration was only elicited following the detection of hypercalcemia. This is a potential complication of the administration of unregulated food supplements, stressing the need for complete dietary histories in the evaluation of multisystem disorders, with or without hypercalcemia.
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keywords = intoxication
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20/28. hypercalcemia associated with aeromonas hydrophila gastro-enteritis.

    We describe a 4 year old girl with acute aeromonas hydrophila gastro-enteritis who presented with a combination of hypercalcemia, metabolic alkalosis, and renal impairment. serum parathyroid hormone was not elevated. Both milk-alkali syndrome and intoxication of vitamins A and D were ruled out. The hypercalcemia, metabolic alkalosis, and renal impairment were improved by fluid infusion and intravenous administration of furosemide. Gastro-enteritis also improved with oral administration of the antibiotic norfloxacin. The association of A. hydrophila gastro-enteritis with hypercalcemia has not been described previously.
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