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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 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

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

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

A study is reported of the estimation of plasma chloride concentration and acid-base status in the differentiation of primary hyperparathyroidism from all other causes of hypercalcaemia. In the two groups of patients studied, all of whom had hypercalcaemia, there was complete separation between the two groups on the basis of plasma chloride concentration and acid-base status. In 16 patients with primary hyperparathyroidism the increase in plasma chloride concentration and associated metabolic acidosis could have been accounted for by the known renal tubular effects of parathyroid hormone. In 13 patients with hypercalcaemia due to various other causes the decrease in plasma chloride concentration and associated metabolic alkalosis could be accounted for either by the known effects of an excess of calcium-ion on the renal tubules, or perhaps by suppression of endogenous parathyroid hormone secretion. In patients with hypercalcaemia and hypophosphataemia of ;pseudohyperparathyroidism' associated with non-endocrine tumours it is postulated that the low plasma chloride concentrations and metabolic alkalosis found in these patients were due either to a differing biological activity of the parathyroid-hormone-like polypeptide secreted by the tumour cells, or possibly to simultaneous secretion by these cells of an ACTH-like polypeptide.
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PMID:Value of plasma chloride concentration and acid-base status in the differential diagnosis of hyperparathyroidism from other causes of hypercalcaemia. 557 36

Parathyroid hormone is concerned with urolithiasis, and regulated by serum ionized calcium concentration. We thought that parathyroid hormone might also be regulated by a hormone. 1 mg of ACTH injection was given intramuscularly to 6 patients with primary hyperparathyroidism, 6 patients with urolithiasis, and 5 control subjects. Serum calcium significantly increased 2 h after ACTH injection in primary hyperparathyroidism. However in the other two groups, an increase of serum calcium was not observed. Parathyroid hormone increased after ACTH injection in most subjects of all three groups. Calcium concentration in a culture medium of parathyroidectomy increased in 4 cases, and the parathyroid hormone concentration in the culture medium increased in 3 cases after ACTH addition. From these data, we believe that ACTH directly influences the parathyroid glands, and that calcium is released from the parathyroid cells. Therefore, the decrease in calcium concentration in the parathyroid cells activates the excretion of parathyroid hormone. The fact that serum parathyroid hormone increases in most subjects in all groups supports our hypothesis, namely that ACTH acts directly on the parathyroid gland.
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PMID:Relation between parathyroid hormone and adrenocorticotropic hormone in primary hyperparathyroidism. 632 18

This study deals with the setting up of human serum calcitonin radioimmunoassay (hCT-RIA) using the high titer and specific antibody which was prepared by our own laboratory. The final dilution of the antibody titer was 1:1,200,000 when the binding rate of Bo/T was 30%. The antibody's affinity constant (Kd) was 2.25 x 10(11) L/M. No cross reaction was found between the antibody and the following eight different peptide hormones and proteins, viz.: TSH, T3, T4, ACTH, PTH, BGP, Insulin and Gastrin. The coefficients variation of intra and inter assay were 3.2% and 9.0%, respectively. The mean recovery rate of CT was 99.8%. The sensitivity of this assay was 9.4 pg/ml. The examination of this methodology showed that all its indices met the demands of RIA. There was no difference in the mean value of serum CT between the two sexes in 232 normal subjects, but the serum CT concentration in those aged of sixty and over of men and women, were much lower than those aged of fourty group. Mean CT concentration was low in the patients with primary osteoporosis, but were significantly higher in those suffering from medullary thyroid carcinoma, primary hyperparathyroidism crisis and chronic renal failure.
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PMID:[The setting up of human serum calcitonin radioimmunoassay and its clinical application]. 1045 98

Thymic carcinoid in multiple endocrine neoplasia type 1 (MEN 1) is previously reported as a non-ACTH producing tumor. The present case is a 39-year-old man with mortal outcome from thymic carcinoid and Cushing's syndrome with high plasma ACTH. The symptom was first observed at age 29 and was relieved after extended thymectomy, with reduction of ACTH level. The tumor was positive for ACTH, Grimelius silver staining and Chromogranin A. The finding of primary hyperparathyroidism, pituitary adenoma, and a novel germline nonsense mutation (W423X) established the diagnosis of MEN 1. Cushing's syndrome due to ACTH producing thymic carcinoid should be also considered as one phenotype of the MEN 1 spectrum.
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PMID:Multiple endocrine neoplasia type I and Cushing's syndrome due to an aggressive ACTH producing thymic carcinoid. 1648 44

We report a rare case of ACTH-independent macronodular adrenal hyperplasia (AIMAH) with primary hyperparathyroidism (PHPT). A 57-year-old woman was admitted to our hospital for further examination of secondary hypertension and bilateral adrenal macrotumors. Midnight serum cortisol elevation with undetectable plasma ACTH, increased 24-hour urinary free cortisol excretion, and loss of the normal circadian rhythm in cortisol secretion established the diagnosis of Cushing's syndrome. Total resection of the enlarged left adrenal gland was performed with subsequent steroid replacement. Her general condition improved but serum calcium level increased 3 weeks after surgery. PHPT was diagnosed on the basis of endocrinological examination, although imaging studies failed to detect parathyroid lesion. In summary, we believe this to be the first report of a case of AIMAH with PHPT.
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PMID:A case of adrenocorticotropin-independent bilateral adrenal macronodular hyperplasia (AIMAH) with primary hyperparathyroidism (PHPT). 1654 80