Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 36-year-old man with sarcoidosis had four episodes of hypercalcaemia in seven years, all of them during the summer months. Measurement over three years showed that hypercalcaemia was associated with small seasonal increases in serum-25-hydroxycholecalciferol within the normal range. These changes could be mimicked by the administration of 3000 units of vitamin D3 daily. Serum 1, 25-dihydroxycholecalciferol concentrations ranged between 26--62 pg/ml when serum calcium was normal, but were strikingly high, up to 137 pg/ml, when the patient was hypercalcaemic. These studies show for the first time that hypercalcaemia in sarcoidosis is associated with abnormally high circulating concentrations of 1, 25-dihydroxycholecalciferol, probably as a result of overproduction of this, the hormonal form of vitamin D.
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PMID:1, 25-dihydroxycholecalciferol in the pathogenesis of the hypercalcaemia of sarcoidosis. 8 69

Urinary cyclic AMP (UcAMP) appropriate for the serum calcium concentration was determined in normal subjects during the base-line state and during alteration in their serum calcium concentrations by saline and calcium infusions. This was compared to the UcAMP in 76 patients with hypercalcemia and 5 patients with hypocalcemia. In 54 of 56 patients with primary hyperparathyroidism, the UcAMP was inappropriately high for their serum calcium concentration, the 2 exceptions having renal failure. In four patients with vitamin D intoxication, sarcoidosis, milkalkali syndrome, and thiazide-induced hypercalcemia and in five patients with hypocalcemia due to hypoparathyroidism, the UcAMP was appropriately low for their serum calcium concentration. In 16 patients with nonparathyroid neoplasms, 10 had UcAMP levels that were inappropriately high suggesting ectopic parathyroid hormone (PTH)-mediated hypercalcemia and 6 had UcAMP levels that were appropriately low suggesting that their hypercalcemia was due to osteolytic factors other than PTH. Correlations between UcAMP, serum calcium concentration, and carboxyl-terminal immunoreactive PTH suggest that random UcAMP is a sensitive accurate reflection of circulating biologically active PTH. If there is adequate renal function (serum creatinine concentration less than 2.0 mg/dl), a random UcAMP expressed as mumol/g creatinine and analyzed as a function of the serum calcium concentration completely separates patients with PTH and non-PTH-mediated hypercalcemia.
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PMID:Urinary cyclic AMP analyzed as a function of the serum calcium and parathyroid hormone in the idfferential diagnosis of hypercalcemia. 18 21

Mean plasma 1(alpha),25-dihydroxyvitamin D[1(alpha),25(OH)(2)D] was significantly increased and serum parathyroid hormone was suppressed in three patients with sarcoidosis and hypercalcemia. Prednisone lowered the mean plasma 1(alpha),25(OH)(2)D to normal range and corrected the hypercalcemia. To elucidate the mechanism for the increased sensitivity to vitamin D in this disorder, the effects of orally-administered vitamin D(2) were determined in seven normal subjects, four patients with sarcoidosis and normal calcium metabolism and three patients with sarcoidosis and a history of hypercalcemia who were normocalcemic when studied. Serum and urinary calcium, serum 25-hydroxyvitamin D (25-OHD), plasma 1(alpha),25(OH)(2)D and, in some studies, calcium balance were measured. Vitamin D(2), 250 mug a day for 12 d, produced little, if any, change in mean plasma 1(alpha),25(OH)(2)D and in urinary calcium in the normals and in the patients with normal calcium metabolism. In contrast, vitamin D(2) produced increases in plasma 1(alpha),25(OH)(2)D from concentrations which were within the normal range (20-55 pg/ml) to abnormal values and increased urinary calcium in two patients with abnormal calcium metabolism. In an abbreviated study in the third patient, vitamin D(2), 250 mug a day for 4 d, also increased plasma 1(alpha),25(OH)(2)D abnormally from a normal value. There was a highly significant correlation between plasma 1(alpha),25(OH)(2)D and urinary calcium. Serum 25-OHD and serum calcium remained within the normal range in all subjects and patients. These findings provide evidence that the defect in calcium metabolism in sarcoidosis probably results from impaired regulation of the production and(or) degradation of 1(alpha),25(OH)(2)D. Prednisone may act to correct the abnormal calcium metabolism by reducing circulating 1(alpha),25(OH)(2)D.
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PMID:Evidence that increased circulating 1 alpha, 25-dihydroxyvitamin D is the probable cause for abnormal calcium metabolism in sarcoidosis. 31 11

Current concepts concerning the mechanisms, diagnosis and means of treatment of a number of the major causes of hypercalcemia and hypocalcemia are reviewed. In particular, the role of abnormalities in metabolism of vitamin D including (1) excessive hepatic production of 25-hydroxyvitamin D (vitamin D intoxication), (2) increased production of 1 alpha, 25-dihydroxyvitamin D (hyperparathyroidism and sarcoidosis), (3) impaired production of 1 alpha, 25-dihydroxyvitamin D (hypoparathyroidism, renal failure, vitamin-D-dependent rickets type I, pseudohypoparathyroidism) and (4) resistance to 1 alpha, 25-dihydroxyvitamin D; the use of vitamin D and its metabolites therapeutically is discussed.
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PMID:Hypercalcemic and hypocalcemic disorders: diagnosis and treatment. 44 May 8

Hypercalcemia is most commonly seen in normal infants as the result of normal rapid bone growth. The most common causative diseases are malignant disease and hyperparathyroidism. A variety of pharmacologic agents, especially vitamin D and its metabolites and thiazide diuretics, can elevate serum calcium levels. Hypersensitivity to vitamin D appears to be a cause of hypercalcemia in infants and in patients with granulomatous disease, such as sarcoidosis. Ingestion of escessive amounts of calcium, especially with alkali, may also cause hypercalcemia, as may prolonged immobilization, particularly under conditions of rapid bone turnover.
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PMID:Causes of hypercalcemia. 48 79

A diagnosis of systemic lupus erythematosus (SLE) was established in a 54-year-old woman with a compatible history, as well as patchy alopecia, anemia, arthralgias, and a positive LE cell preparation. Sixteen months later bilateral hilar and mediastinal lymph nodes appeared on chest roentgenogram. Sarcoidosis was diagnosed when hypercalcemia and noninfectious, noncaseating epithelioid granulomas were found in the skin and liver. The sarcoidosis remitted with corticosteroid therapy, but slowly advancing renal failure ultimately resulted in the patient's death. We believe the concurrence of SLE and sarcoidosis had not been previously reported in the English literature. Immune mechanisms are discussed.
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PMID:Acute sarcoidosis occurring during the course of systemic lupus erythematosus. 50 69

Six patients with biopsy-proven renal sarcoidosis presented with renal failure of unknown origin; in none was the diagnosis of sarcoidosis initially considered. The serum creatinine concentration at the time of presentation ranged from 265 to 1380 mumol/l (3.0 to 15.6 mg/dl), with a mean of 787 mumol/l (8.9 mg/dl). Although only two patients were hypercalcemic at the time of presentation, the 24-hour urinary excretion of calcium was increased in three of the four patients in whom it was measured, and renal calculi were present in one case. Renal biopsy revealed interstitial nephritis and tubular atrophy in all cases, as well as nephrocalcinosis in three cases and noncaseating granulomas negative for acid-fast bacilli in four cases. In each patient steroid therapy led to a rapid improvement in renal function (mean post-treatment serum creatinine level 274 mumol/l [3.1 mg/dl]). The follow-up period ranged from 8 months to 8 years (mean 3.0 years). In three patients renal function remained stable with low-dose steroid therapy. In two cases recurrent hypercalcemia and deteriorating renal function accompanied steroid withdrawal but resolved with its reinstitution. In one additional case reversible deterioration in renal function accompanied tapering of the steroid dose; however, there was no hypercalcemia.This report emphasizes the importance of considering sarcoidosis in the differential diagnosis of acute renal failure of unknown origin. Long-term follow-up of such patients is essential, as relapse is common.
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PMID:Clinical and pathological features of six cases of sarcoidosis presenting with renal failure. 51 62

Lymphomatoid granulomatosis was diagnosed in a 60-yr-old woman 2 yr after presentation with a multi-system disorder resembling sarcoidosis. Five months later autopsy revealed malignant lymphoma. Large aggregates of intracytoplasmic tubular structures resembling nucleocapsid material of the paramyxovirus group were found within cells of lymphoma deposits in the liver. Sequential immunological studies over more than 2 years demonstrated a relatively stable T-cell deficiency associated with variable B-cell dysfunction. The latter was characterized by the production of immunoglobulins of restricted electrophoretic mobility. Intermittent hypercalcaemia was associated with increases in serum IgG and appeared to be due to the presence of Ca-binding paraproteins. It is suggested that lymphomatoid granulomatosis may be a pre-malignant lymphoproliferation, with immune deficiency as a predisposing cause. The pattern of immunological abnormalities suggests that the lymphoma may have been due to B-cell malignant transformation.
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PMID:Pulmonary lymphomatoid granulomatosis with immunodeficiency terminating as malignant lymphoma. 52 88

A 56-year-old man with a three-month history of fever, malaise, anorexia, mental confusion, and weight loss had hypercalcemia and azotemia. The chest roentgenogram was normal. Biopsy material removed 2 1/2 years previously showed noncaseating granulomas. Sarcoidosis was diagnosed, and prednisone was administered. Fever persisted, and the patient died 49 days after admission. Postmortem examination showed evidence of extensive disseminated histoplasmosis, interstitial nephritis, and papillary necrosis. This communication emphasizes the difficulty in diagnosing the etiology of disseminated, noncaseating granulomatous disease.
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PMID:Histoplasmosis with hypercalcemia, renal failure, and papillary necrosis. Confusion with sarcoidosis.. 57 82

The influence of hypercalcemia on renal function was studied retrospectively in 13 patients suffering from primary hyperparathyroidism, sarcoidosis, vitamin D intoxication, malignant lymphoma or chronic lymphatic leucemia. Different kinds of treatment, depending upon the primary disease, often induced a rapid fall in the serum calcium concentration. The serum creatinine concentration always fell simultaneously. The serum phosphate concentration fell in all but two patients. Changes in serum calcium and serum creatinine correlated significantly (p less than 0.001), as did changes in serum calcium and serum phosphate concentrations (p less than 0.05). Serum calcium/serum creatinine and serum calcium/serum phosphate ratios were significantly higher in patients with primary hyperparathyroidism than in patients with hypercalcemia of non-hyperparathyroid origin (p less than 0.01, p less than 0.001). This suggests a different effect of calcium on the glomerular filtration rate in hyperparathyroid and non-hyperparathyroid patients, the latter group being more sensitive to the influence of hypercalcemia. Possible explanations for this difference, such as a protective effect of PTH on the glomerular filtration, are discussed.
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PMID:Reversible renal failure caused by hypercalcemia. A retrospective study. 64 44


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