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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The factors responsible for the frequent occurrence of hypertension in patients with primary hyperparathyroidism have not been elucidated. Suggested mediators have included hypercalcemia, renal insufficiency, and increased plasma renin activity. However, experimental results have not been reported in any species that test the hypothesis that sustained hypertension in this clinical syndrome is due to consequences of parathyroid hormone (PTH) excess versus unrelated factors (e.g., primary hypersecretion of other hormones, NaCl sensitivity, genetic factors). Moreover, no systematic evaluation of the renin or adrenal cortical responses to chronic PTH excess has been reported in any species. Accordingly, the present studies assessed the effects of chronic (12 days) continuous intravenous b-(1-34) PTH infusion in normal human subjects (n = 4). PTH infusion resulted in persistent hypercalcemia and hypertension, reversible during a 4-8-day recovery period. Transient but significant increases in urinary tetrahydroaldosterone excretion and plasma cortisol concentration were observed as hypercalcemia and hypertension developed. No significant changes in plasma potassium concentration or plasma renin activity were observed, suggesting that hypercalcemia-induced transient hypersecretion of ACTH was responsible for both cortisol and aldosterone responses. The present results suggest that hypertension associated with clinical primary hyperparathyroidism results from either direct or indirect effects of PTH excess, per se, and requires neither the long-term consequences/complications of the clinical disorder (e.g., severe nephrocalcinosis, renal insufficiency) nor primary hypersecretion of additional hormones. These results are consistent with the hypothesis that hypercalcemia alone or in combination with at least permissive levels of PTH can generate short-term, but persistent (12 days) hypertension in human subjects and thus may be the initiating mechanism for hypertension in clinical primary hyperparathyroidism.
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PMID:Chronic continuous PTH infusion results in hypertension in normal subjects. 354 30

Hypercalcemia is one of the most critical complications in patients with malignancy. We have used salmon calcitonin for treatment of hypercalcemia in these patients. The subjects were 49 hypercalcemic patients with various malignancies. Synthetic salmon calcitonin (SCT) was provided by Teikoku Hormone Mfg. Co. Ltd., Japan and 40 MRC units was administered twice daily i.m. or i.v. In 21 of 33 cases treated i.m. and in 8 of 16 cases treated i.v., a serum Ca decrease of more than 2 mg/dl was observed. The hypercalcemia was managed in 59% of patients within 6 days after initiation of the treatment and effective duration was 14 days. On the other hand, ineffective cases treated with a combination of SCT and glucocorticoid or SCT and mithramycin were managed in 57% and 86%. The 50% survival time was 69 days in the effective cases and 23 days in the uncontrolled cases (P less than 0.01). The main causes of death in the ineffective cases were renal insufficiency. On the other hand, in the effective cases, improvements of renal function were observed. The side effects were slight, and nausea and flushing were observed in 24% of cases. These data indicate that SCT is effective for lowering the serum Ca level in hypercalcemic patients with malignancies.
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PMID:[Synthetic salmon calcitonin as an antihypercalcemic agent for hypercalcemia in malignancy]. 374 Aug 62

Hypercalcemia has not previously been recognized as a complication of advanced chronic liver disease without hepatoma. During a five-year period, 16 patients evaluated in the liver transplantation program at the University of Pittsburgh developed hypercalcemia. All had advanced chronic liver disease with mean total bilirubin concentration of 29.5 +/- 4.6 mg/dL (50.1 +/- 78.2 mumol/L) (mean +/- SEM) and prothrombin time 16.8 +/- 0.8s. The highest serum calcium level was 17.2 mg/dL (4.3 mmol/L). The mean serum calcium level was 11.7 +/- 0.3 mg/dL (2.93 +/- 0.075 mmol/L) with an ionized calcium level of 5.41 +/- 0.35 mg/dL (1.35 +/- 0.088 mmol/L) and a phosphorus level of 4.2 +/- 0.4 mg/dL (1.4 +/- 0.1 nmol/L). Mild to moderate renal insufficiency was present in 14 (87%) patients; the mean serum creatinine level was 2.8 +/- 0.4 mg/dL (247 +/- 35 mumol/L). In five (38%) patients parathyroid hormone was completely suppressed and in an additional five (38%) patients, it was in a range most compatible with nonhyperparathyroid hypercalcemia. The 25-hydroxyvitamin D or 1,25-dihydroxyvitamin D levels were normal or low in the 11 patients in whom determinations were made. Hypercalcemia that is not due to hyperparathyroidism or hypervitaminosis D is a potential complication of advanced chronic liver disease.
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PMID:Hypercalcemia. A complication of advanced chronic liver disease. 381 45

A 42-year-old woman, with a previously resected jejunal leiomyoblastoma, was first seen with liver metastases 31/2 years after the tumor resection. Intractable malignant hypercalcemia appeared eight months later, together with renal insufficiency. No osteolytic lesions were detected. Levels of parathyroid hormone, cyclic adenosine monophosphate, and 1,25-dihydroxycholecalciferol (1,25[OH]2D) were not useful in distinguishing between the hypercalcemia of malignancy and concurrent hyperparathyroidism. Despite renal insufficiency, hypercalcemia, and subtotal parathyroidectomy, the 1,25(OH)2D levels remained elevated, consistent with the speculation that a tumor product stimulated 1-alpha-hydroxylation of 25-hydroxycholecalciferol. Phenytoin and phenobarbital (enzyme induction therapy), in combination with phosphorus and glucocorticoids, appeared to be useful in controlling the hypercalcemia.
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PMID:Leiomyoblastoma associated with intractable hypercalcemia and elevated 1,25-dihydroxycholecalciferol levels. Treatment by hepatic enzyme induction. 383 34

Forty-two patients with multiple myeloma that responded to initial treatment were observed for at least 6 months during a 2-year period. Eleven deaths occurred, seven of these being associated with hypercalcemia. None of these patients developed renal insufficiency before the serum calcium level rose, although kidney function deteriorated later in five of them. In those patients who are susceptible, hypercalcemia appears to be a good early indicator of relapse in multiple myeloma.
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PMID:Hypercalcemia, renal failure, and relapse in multiple myeloma. 396 82

A patient with IgG3 lambda plasma cell myeloma characterized by anemia, hypercalcemia, hypoalbuminemia, renal insufficiency, osteolytic bone lesions, and serum and urinary light chains inadvertently received a dose of intravenous melphalan considerably greater than standard. A complete remission ensued characterized by normal protein and bone marrow studies. Healing of bone lesions occurred. This and two somewhat similar happenstances producing rare complete remissions in myeloma may have significant chemotherapeutic ramifications.
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PMID:Multiple myeloma--complete remission with high dose melphalan chemotherapy. 397 Nov 99

The milk-alkali syndrome is the association of hypercalcaemia and renal failure, with or without alkalosis, in the presence of absorption of excessive quantities of calcium, alkali, or both. Two patients with the milk-alkali syndrome are described, one representing an acute, reversible disorder and the other demonstrating a chronic syndrome with only partially reversible renal disease. Differential diagnosis is not difficult and is usually aided by the initial clinical evaluation as well as rapid response to conservative therapy. Because the initial stages of renal insufficiency are often fully reversible, the early identification and treatment of the milk-alkali syndrome can prevent progression to irreversible, chronic renal failure. Although non-absorbable antacids, H2 blockers, and sucralphate are the basis of modern treatment of peptic ulcer disease, the syndrome may still occur, especially in patients who self-treat symptoms of dyspepsia.
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PMID:The 'milk-alkali' syndrome: two case reports with discussion of pathogenesis. 400 10

A case of sarcoidosis in a six months old male is reported. Clinical symptoms and biochemical and radiological data suggest involvement at least of three organs. Diagnosis was corroborated by pulmonary, hepatic an lymph node biopsy. Slight renal insufficiency appeared associated to hypercalcemia and hypercalciuria. Hyperaldosteronism also permits relationship with increased angiotensin-I-converting enzyme activity. Pulmonary lesions at this age, were note-worthy in this case. Finally, evolution was favorable with prednisone. Patient presents no symptoms during follow-up for four years.
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PMID:[Sarcoidosis in childhood. Presentation of a case in a very young child]. 406 74

Immunoreactive parathyroid hormone (PTH) levels and nephrogenous cyclic adenosine monophosphate (cAMP) have been reported to be useful parameters in the diagnosis of hyperparathyroidism. Measurements in hyperparathyroid patients usually give values above the normal range when PTH is measured with a carboxyterminal radioimmunoassay and when nephrogenous cAMP is related to glomerular filtration rate. We tested these two parameters in two groups of hypercalcaemic patients (twelve cases of primary hyperparathyroidism and fourteen cases of hypercalcaemia of non-parathyroid origin) and in two groups of normocalcaemic subjects (twenty-one young healthy volunteers and fourteen elderly subjects without parathyroid disease). Slight impairment of renal function caused elevated values of immunoreactive parathyroid hormone in a carboxyterminal radioimmunoassay and also of nephrogenous cAMP when related to glomerular filtration rate. We found that elevated nephrogenous cAMP without parathyroid disease could be attributed to renal insufficiency and to the mode of expression generally used for the nephrogenous cAMP.
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PMID:Nephrogenous cyclic AMP and plasma parathyroid hormone in hypercalcaemia: the influence of renal function. 608 50

Hypophosphatasia represents an inborn enzymatic deficiency characterized by a reduced activity of alkaline phosphatase in serum and tissue and an increased urinary excretion of phosphoethanolamine. 278 cases have been described until the end of 1980. Based on the age of manifestation and the predominant clinical findings the following classification is possible: The prenatal form (49 cases) with caput membranaceum, skeletal deformities and respiratory distress has a mortality of 100%. The early infantile form (94 cases) shows rickets-like osseous anomalies, dystrophy, craniostenosis, nephrocalcinosis, mortality amounting to 40%. Diagnostic features of the infantile-juvenile form (112 cases) are premature loss of deciduous teeth, bone deformities, rickets-like findings, and short stature. Mortality is only 1%. The adult form (23 cases) often remains undiscovered and has a good prognosis. It presents with pseudofractures and pains in the bones as chief symptoms. Heredity is autosomal recessive in all four types of hypophosphatasia. Possibly in the adult form there is an additional autosomal dominant inheritance. Alkaline phosphatase deficiency affects all tissues excepting the intestinal isoenzyme. Urinary excretion of phosphoethanolamine is elevated. Values for calcium and inorganic phosphorus in serum are usually normal or only slightly increased. Marked hypercalcemia is observed in severely diseased patients affected by the early infantile form. In these cases hypercalcemia often leads to nephrocalcinosis and renal insufficiency. Since alkaline phosphatase is equally active as pyrophosphatase, reduced phosphatase activity induces an accumulation of pyrophosphate in serum and its increased excretion in urine. The precise pathogenetic mechanisms of hypophosphatasia are still unknown. Possibly, the accumulation of pyrophosphate implies a disorder of calcification. Postnatal diagnosis is based on clinical findings in association with decreased alkaline phosphatase activity and increased phosphoethanolamine excretion. For the detection of heterozygotes additional biochemical markers should be tested. These include the determination of alkaline phosphatase in leucocytes and cultured skin fibroblasts, the calculation of tubular phosphate reabsorption and the analysis of pyrophosphate and pyrophosphatases. The difficulty in ascertaining the carrier state is that the measurement of a single parameter may give normal results.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Congenital hypophosphatasia]. 614 51


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