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 blind prospective study was undertaken to determine the use of calcitonin (CT) as a tumor marker. After final diagnosis, results revealed elevated plasma CT (greater than 150 pg/ml) in common cancers as follows: lung, 38%; colon, 24%; breast, 38%; pancreas, 42%; and gastric, 30%. Fifty-eight percent of oat cell carcinomas were associated with elevated plasma CT. CT immunoreactivity was detected in 14% of tumor extracts and was not detectable in normal tissue other than thyroid. Hypercalcemia was not the cause of hypercalcitonemia. Incubation studies of [125I]human CT in cancer plasma and tumor extracts demonstrated that measurements were not an artifact of label degradation. In a survey of control patients with nonneoplastic disease, elevated CT was noted in renal failure, acute gastrointestinal bleeding, and in some patients with chronic obstructive lung disease. In conclusion, plasma CT is elevated in a substantial proportion of common neoplasms and is useful as a tumor marker.
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PMID:Calcitonin in nonthyroidal cancer. 46 77

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

9 patients with advanced renal failure and renal osteodystrophy documented by iliac crest biopsy were treated with 1,25-dihydroxycholecalciferol (average dose 0.53 micrograms per day) for 6 months. Under 1,25-DHCC there was a statistically significant increase in serum calcium and decrease in serum alkaline phosphatase and immune parathyroid hormone. Histomorphometric evaluation of posttreatment bone biopsies showed reduction of osteoclastic resorption and endosteal fibrosis. Osteoid volume decreased in most cases. In 3 patients with predominant fibroosteoclasia, bone turnover practically normalized. Bone mineral content of the radius (photoabsorptiometry) did not change with treatment. Transient hypercalcemia occurred in 5 patients and was easily corrected by adjustment of 1,25-DHCC dosage.
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PMID:[Effect of 1,25-dihydroxycholecalciferol in renal osteopathy]. 53 67

Plasma calcium was measured routinely as a part of profile screening of patients admitted to a geriatric department. Pathological hypercalcaemia was found in 1.33% of those screened, the cause being bone metastases (29%), hyperparathyroidism (21%), bronchial carcinoma without bone metastasis (18.5%), lymphosarcoma without bone metastasis (8%) and multiple myeloma (2.5%). There remained a further group of patients with hypercalcaemia and renal failure (21%) in whom diagnosis was often obscure. Where renal function was normal, discriminant analysis showed that the four main diagnostic groups were biochemically distinguishable. Discriminant analysis thus seems likely to be of practical value in the differential diagnosis of hypercalcaemia in elderly patients with normal renal function, but requires prospective validation.
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PMID:Hypercalcaemia in elderly hospital in-patients: value of discriminant analysis in differential diagnosis. 57 68

Between 1972 and 1976 15 patients with chronic renal failure of different aetiology and varying severity were observed who developed 23 hypercalcaemic phases during treatment with calcium-containing drugs. 12 instances of hypercalcaemia occurred during conservative treated during conservative treatment (serum creatinine 177-1061 mumol/l, equivalent to 20-120 mg/l) and 11 during chronic haemodialysis (serum creatinine 707-1061 mumol/l, equivalent to 80-120 mg/l). In 15 cases hypercalcaemia was caused by a hexacalciumhexasodium-heptacitratehydrate complex (Acetolyt), in 6 cases by the combined use of this drug with calcium ion-exchange resins on a calciumpolystyrolsulfonate base, and in two cases by the use of calcium tablets and calciumpolystyrolsulfonate, respectively. The daily doses of these drugs were in the usual therapeutic range in most cases. Deterioration of renal function was observed in two cases and coma in a further two cases. In 5 cases gastric ulcers were demonstrated. Three patients died. In no patient was there evidence of florid hyperparathyroidism. Treatment with calcium-containing drugs in patients with renal failure should only be carried out under regular control of calcium concentrations.
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PMID:[Hypercalcaemic crises in patients with chronic renal failure caused by ion-exchange resins, antacidotics and other calcium-containing drugs (author's transl)]. 59 99

Acute renal failure may be a contributory cause of death in patients with acute leukemia. The purpose of this study was to define the causes and course of acute renal failure in group of patients with acute leukemia in order to identify preventive measures and reversible aspects of the renal insufficiency. Among 88 patients with acute leukemia whose courses were followed to the time of death, ten developed acute renal failure. Etiologic factors of the renal failure were uric acid nephropathy, sepsis with complicating hypotension and hypovolemia, and the administration of nephrotoxic antibiotics. In one patient ureteral obstruction from clots was responsible for renal failure, while in another patient disseminated aspergillosis led to renal failure. Other causes of acute renal failure in persons with acute leukemia, but not observed in this patient group, are hypercalcemia and leukemic infiltration of the kidneys.
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PMID:Acute renal failure in patients with acute leukemia. 63 12

The authors studied the presence of visceral calcification as evidenced by the visceral uptake of bone-seeking radionuclides during the course of a bone scan among 22 patients with terminal renal failure maintained on dialysis, nine patients with hypercalcemia secondary to malignancy, and nine patients with primary hyperparathyroidism. Uptake by the lungs or stomach was observed in 11 renal failure patients (50%) and in four of those with malignancy and hypercalcemia (44%). None of the patients with primary hyperparathyroidism had evidence of visceral calcification. The serum CaXP product was significantly higher among those with visceral calcification than those without. The results of this study indicate that a CaXP product of 60 represents the saturation product of calcium phosphate in serum above which spontaneous precipitation of this salt may occur in such viscera as stomach and lungs.
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PMID:Visceral calcification and the CaXP product. 71 4

Hypercalcemia occurred in 4 dogs with renal failure. Primary causes of hypercalcemia previously described in the dog (primary hyperparathyroidism, pseudohyperparathyroidism, vitamin D toxicosis) were not identified. Increased concentrations of circulating immunoreactive parathormone were found in 2 dogs, and thyroparathyroidectomy of 1 dog resulted in decreased serum concentrations of that hormone as well as of calcium. The latter observations indicated that hypercalcemia was related to increased parathormone activity, but the possibility of other homeostatic imbalances was not excluded. It was concluded that renal failure should be considered as a primary cause of hypercalcemia, along with other causes previously identified.
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PMID:Hypercalcemia secondary to chronic renal failure in the dog: a report of four cases. 72 83

Hypercalcemia was induced in 5/6 nephrectomized rats fed a low calcium diet by administering pharmacologic doses of vitamin D. The degree of hypercalcemia was greater in uremic rats than in sham-operated rats both of which were given vitamin D. Bone resorption was marked in both groups but differed in distribution. Increased osteoclasis in uremic rats was limited to diaphyseal cortical bone while metaphyseal trabeculae were relatively unaffected compared to sham-operated rats administered vitamin D. Ultrastructurally thyroid C cells were degranulated and in an active stage in both groups of rats receiving vitamin D. Urinary calcium excretion was greater in sham-operated rats given vitamin D than in uremic rats. The greater renal retention of calcium in uremic rats given vitamin D was felt to contribute to the development of hypercalcemia. These studies suggest that although trabecular bone was resistant to pharmacologic levels of vitamin D in renal failure, hypercalcemia developed due to selective resorption of cortical bone and impairment of renal calcium excretion.
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PMID:Vitamin D-induced hypercalcemia in experimental renal failure. 84 25


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