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

A case of primary hyperparathyroidism and coincidental Cushing's syndrome of hypothalamic-hypophyseal origin is reported. The hyperparathyroidism was based on an adenoma of the parathyroid glands and produced a severe hypercalcaemia (4.5 mmol/l) and calcinosis of kidneys and lungs. The Cushing's syndrome was caused by a hyperplasiogenic ACTH cell-adenoma of the pituitary which had induced a regulative hyperplasia of the ACTH-dependent zones of the adrenal cortex. The ultrastructure of the zona fasciculata and reticularis showed a conspicuous activation of the steroid hormone-producing organelles. The two endocrine diseases added together in skeleton, heart, duodenum, and pancreas. As a sign of hyperparathyroidism the osteoclastic absorption of the bone was strongly increased, whereas the bone formation was reduced due to the hypercortisolism. The pancreas showed a severe acute recurrence of chronic pancreatitis which was induced by a parathyrotoxic crisis. This was the immediate cause of death.
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PMID:[Simultaneous occurrence of primary hyperparathyroidism and pituitary Cushing's syndrome (author's transl)]. 19 Dec 34

Treatment with bromocriptine, 30-55 mg daily, in 13 acromegalics for 1-15 months, resulted in a 60% decrease in growth hormone secretion, as judged from the excretion of growth hormone in 24-h urine. Normal excretion was obtained in 10 patients, while 1 patient showed no response. The plasma growth hormone response to O-GTT was improved, but not normalized, in 4 of 7 patients treated for more than 6 months, and marked glucosuria disappeared in two diabetics. While the secretion of TSH, LH and FSH was unchanged, the prolactin secretion was inhibited. The urine excretion of free cortisol showed a 30% decrease, possibly due to a direct effect of bromocriptine on the ACTH-secretion. Hypercalcaemia was never seen, but the initial hypercalcuria showed a modest decrease without measurable changes in the creatinine clearance. The subjective relief during long-term treatment was marked in 10 of 11 patients and the dominating symptoms disappeared in 40-67%, whereas heal-pad thickness, enlarged sellae, and visual fields remained unchanged. No serious side effects were observed. Treatment with bromocriptine seems effective and should be considered as a remedy amongst others, in suitable cases of acromegaly.
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PMID:Long-term treatment of acromegaly with bromocriptine. 41 39

A radioimmunoassay for the measurement of immunoreactive parathyroid hormone (PTH) in human serum is described. The assay is based on the ability of human parathyroid hormone (h-PTH) to compete with 125I-labelled bovine parathyroid hormone (b-PTH) for binding to a guinea-pig antiserum directed against b-PTH. The linear part of the standard curve was parallel with dose response curves for anti-b-PTH serum reacting with dilutions of sera from patients with primary hyperparathyroidism and from h-PTH purified from human parathyroid adenomas, indicating that levels of immunoreactive PTH could be expressed as b-PTH equivalents. The range in 62 healthy blood donors was 1.1-2.5 ng b-PTH Eg./ml. The reproducibility was satisfactory, and the sensitivity permitted the measurement of PTH concentrations down to 0.8 ng b-PTH Eg./ml. No crossreaction with h-CT, h-STH or h-ACTH was observed. The clinical value of the assay has been considered in a number of patients with various disorders of calcium metabolism, diagnosed and treated conventionally. About 80 per cent of patients with primary hyperparathyroidism had elevated PTH levels on one or more occasions before surgery. In patients with chronic renal failure of other aetiology than primary hyperparathyroidism the levels were usually far higher. Patients with primary hyperparathyroidism and increased S-creatinine had higher PTH levels than those with normal S-creatinine. After parathyroidectomy all previously increased PTH levels became normal or low. High PTH concentrations were found in 3 patients with normocalcaemic hyperparathyroidism who at operation were shown to have parathyroid adenomas. However, in normocalcaemic patients there were also some falsely elevated PTH values which limit the diagnostic value of the assay in this group of patients. Low PTH values were observed in patients with hypercalcaemia due to malignant disorders, indicating that PTH determination may be of some value in the diagnosis of patients with hypercalcaemia of unknown origin.
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PMID:The diagnostic value of a radioimmunoassay for parathyroid hormone in human serum. 117 15

A 32-year-old woman developed myalgia, fever, consciousness disturbance, mental disorder, pyramidal tract signs and meningeal irritation signs at about 2 months after a normal labor. Laboratory examination showed hypopituitarism (decreased ACTH, TSH), renal dysfunction and hypercalcemia. A variety of antibiotics, acyclovir and gamma-globulin failed to improve her symptoms. A diagnosis of Chlamydia trachomatis infection was considered from the elevated antibody titers. In this case, minocycline was very effective. Rarely Chlamydia trachomatis infection involved general organs, including the central nervous system. It was interesting that she had endocrine disorders. We must take a look for Chlamydia trachomatis infection because this infection infrequently involves general organs, including the central nervous system and minocycline is very effective for this infection.
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PMID:[Chlamydia trachomatis infection with symptoms and signs of the central nervous system damage--a case report]. 142 47

A woman aged 62 developed a septic shock and pulmonary embolism after skin grafting for extensive burns. She was put on anticoagulants. A second shock led to renal insufficiency. Hypercalcaemia developed. A CT scan of the upper abdomen disclosed enlarged adrenal glands. An acute adrenal haemorrhage was suspected. The levels of cortisol were low in the plasma and urine and did not respond to ACTH stimulation. Cortisone replacement therapy improved the condition of the patient and normalized plasma calcium levels. The mechanisms of hypercalcaemia in acute adrenal insufficiency are discussed. Multiple factors have been proposed: haemoconcentration, an increased affinity of plasma proteins for calcium, an increase in the filtrable calcium complexes, and an enhanced calcium mobilization of skeletal origin.
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PMID:Hypercalcaemia in acute adrenal insufficiency. A case report. 216 7

Administration of pituitary extract brings important change in the cells of the corpuscles of stannius. Two variety of cells are found in the corpuscles of stannius of control group, one with dense cytoplasm while the other possess non-reactive cytoplasm. Under the influence of whole pituitary extract, there is an intense cell activity in corpuscles of stannius suggesting more synthesis of hypocalcemic factor. Other possible reasons like stimulation of interrenal, thereby activating corpuscles of stannius have also been discussed. The possible involvement of ACTH or cortisol and synergistic effect of prolactin in promotion of hypercalcemia have also been suggested.
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PMID:Effect of whole pituitary extract on the corpuscles of stannius in Notopterus notopterus (Pallas). 221 7

Bronchial carcinomas are frequently associated with ectopic secretion of hormones which may be responsible for paraneoplastic syndromes. In non small cells carcinomas, serum calcitonin levels may be raised. Hypercalcaemia can be found in squamous carcinomas and secretion of hCG (responsible for gynaecomastia) in large cells carcinomas. In small carcinomas, many hormones (ACTH, MSH, ADH, calcitonin) can be produced; however, their serial measurements as well as that of the carcino-embryonic antigen add nothing to the information available with standard staging investigations. More recent studies have identified three protein products: the BB-isoenzyme of creatine kinase, bombesin and neurone-specific enolase. The latter seems a promising marker to follow up the course of the disease.
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PMID:Role of biological markers and probes in lung carcinomas. 287 78

In a 41-year-old hirsute woman, severe hypercalcemia led to the discovery of hyperparathyroidism related to the involvement (hyperplasia/or adenoma) of the 4 parathyroid glands. Plasma and urinary DHA, plasma DHA-sulfate and delta 5 steroid precursors were elevated. Steroid hormone hypersecretion was stimulated by hCG and ACTH, and exhibited a paradoxical rise during dexamethasone administration. Computerized tomography scanning as well as arteriography disclosed bilateral adrenal hyperplasia and left adrenal adenoma. Bilateral adrenal vein catheterization indicated a left/right gradient for delta 5 steroids and delta 5 steroid sulfates. At surgery a left brown adrenal encapsulated adenoma was removed with a hyperplastic adrenal gland. Results of in vitro studies (adrenal steroid content and incubation) together with postadrenalectomy hormonal results suggest that the left brown adrenal adenoma was the main source of excessive androgen production. The infrequent association of an androgen-producing adrenal adenoma with hyperparathyroidism raises the hypothesis of multiple endocrine neoplasia syndrome. However, evidence for this diagnosis is lacking in the absence of other glandular involvement and of family history.
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PMID:Androgen producing adrenal adenoma. Report on a case associated with hyperparathyroidism. 289 90

There are a variety of water and electrolyte disorders in patients with cancer. These disorders occur during the growth of tumors, generally as a consequence of inadequate intake and absorption of electrolytes, renal failure secondary to tumor or rapid tumor destruction and production of metabolically active substances by the tumor. In this paper, the electrolyte abnormalities associated with cancer were reviewed. Hyponatremia is one of the most common clinical electrolyte abnormalities in advanced cancer. Some patients may have hyponatremia, in spite of increased total body sodium and absence of a defect in water diuresis. This status is designated as "sick cell syndrome" or "essential hyponatremia". In addition, the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in association with various tumors has been described. This syndrome is principally due to water retention, but can also be due to continuous urinary loss of sodium, and hypo-osmolality. Hypercalcemia is associated with coexistent primary hyperparathyroidism, prostaglandin (PGE2) or osteoclast-activating factor. It now seems likely that ectopic PTH is rarely the cause of hypercalcemia in nonparathyroid cancer. There are no data supporting the ectopic production of vitamin D-like substance as an important factor in the hypercalcemia of cancer. There are three general categories in which patients with hypercalcemia and cancer may be placed: those with bone metastases, those without bone metastases of solid tumors and those with hematologic malignancies. Hypokalemia is associated with ectopic ACTH- and insulin--producing tumors, and is often found in patients with mucin-secreting, potassium-losing adenocarcinoma of the colon.
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PMID:[Electrolyte abnormalities associated with cancer: a review]. 352 93

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


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