Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In-vitro and in-vivo studies have suggested a role for the adrenergic system in the regulation of secretion of parathyroid hormone (PTH). In the present study the effects of insulin induced hypoglycaemia on serum concentrations of PTH, cortisol, calcium and phosphate were evaluated in ten healthy subjects. Maximum hypoglycaemia occurred 25 to 35 min after administration of insulin at a standard dose of 0.15 U/kg body weight. All this time there was a slight and transient increase of the serum calcium concentrations whereas there was a marked drop in the serum phosphate levels with a nadir 15 min after maximum hypoglycaemia. Cortisol levels were below baseline when blood glucose was as lowest but increased to a maximum level of 200% 60 minutes after maximum hypoglycaemia. Serum PTH levels increased significantly and reached a maximum of 130% of baseline values concomitant with maximum hypoglycaemia, whereafter they returned to pre-insulin-injection levels within 15 minutes. These findings indicate that during stress endogenous catecholamines affect the secretion of PTH which could be of physiologic importance. In five patients with primary hyperparathyroidism there was, however, no increase in the PTH levels, although they displayed the same response to hypoglycaemia for cortisol and phosphate. This supports previous suggestions that these patients have an impaired capacity to respond to circulating catecholamines.
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PMID:Insulin-induced hypoglycaemia stimulates secretion of parathyroid hormone. 639 99

Cortisol secretion has been reported to be increased in primary hyperparathyroidism (PHPT). Our aim was to evaluate circulating and urinary cortisol levels and the relationships with biochemical and bone parameters in patients with PHPT at the time of diagnosis. We studied 180 consecutive patients with PHPT (mean age +/- SD 60.0 +/- 13.2 years; F/M 140/40, BMI 25.8 +/- 4.8 kg/m(2)) and 56 subjects with incidentally discovered adrenal adenoma who served as controls (age 56.2 +/- 12.8 years, F/M 40/16, BMI 25.7 +/- 3.9 kg/m(2)). Serum morning and midnight cortisol and urinary free cortisol were measured in both groups. In PHPT patients bone mineral density was measured at the lumbar spine, femur, and forearm. Serum morning cortisol and urinary cortisol were similar in PHPT patients and controls, whereas midnight cortisol was higher in PHPT patients (5.3 +/- 4.7 vs. 2.9 +/- 0.9 microg/dL, P = 0.001). In this group, midnight cortisol correlated positively with age (r = 0.27, P = 0.008) and negatively with forearm (r = -0.36, P = 0.003) and total-femur T score (r = -0.30, P = 0.02). Multivariate regression analysis, including age, calcium, parathyroid hormone (PTH), and midnight cortisol as independent variables and forearm T score as dependent variable, indicated that age (beta = -0.29, P < 0.0001), PTH (beta = -0.33, P < 0.0001), and midnight cortisol (beta = -0.14, P < 0.04) were independently associated with forearm T score. Our findings show increased midnight cortisol levels in patients with PHPT, indicating a subtle alteration of the hypothalamo-pituitary-adrenal axis dynamics that is unrelated to the degree of disease activity; further data are needed to demonstrate the supplementary effect of this subtle alteration to bone damage in this condition.
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PMID:May an altered hypothalamo-pituitary-adrenal axis contribute to cortical bone damage in primary hyperparathyroidism? 1938 29