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Short ACTH test in assessing hypothalamic-pituitary-adrenocortical function.

The adrenocortical response to the simple 30-minute ACTH stimulation test was compared with the hypothalamic-pituitary-adrenocortical (HPA) response to insulin-induced hypoglycaemia in 25 patients with various degrees of hypothalamic-pituitary malfunction. The correlations between the increase in plasma cortisol during insulin hypoglycaemia and that during ACTH stimulation (r = 0-66) and between peak plasma cortisol levels during the two tests (r = 0-90) were highly significant. Peak plasma cortisol levels in individual patients were similar on both tests, no patient showing any major discrepancy between the two test results. Thus the simple 30-minute ACTH stimulation test seems to be reliable in detecting imparied HPA function.

Adolescent↗

Adrenocortical function in old age as reflected by plasma cortisol and ACTH test during the course of acute myocardial infarction.

Adrenocortical function, as reflected by sequential analysis of plasma cortisol and adrenocorticotropin (ACTH) test, was investigated in elderly patients (greater than or equal to 65 years) with acute myocardial infarction (AMI), and compared to young patients (less than or equal to 55 years) with AMI. Further, age-matched subjects admitted with ischaemic chest pain, in whom AMI was not verified, served as controls. Following infarction, plasma cortisol peaked within 24 hours in both age groups, whereupon the cortisol level gradually decreased till day 12. Plasma cortisol during AMI disclosed no age-related difference, but was significantly correlated to the localization of infarction and lactate dehydrogenase (LDH). The development of complications, i.e. hypotension, congestive heart failure, and arrhythmia, calling for therapeutic intervention, was solely correlated to infarct size, as estimated by peak LDH. Young and elderly patients responded equally and normally to ACTH stimulation, and in both groups a significant, positive correlation between the basal and the 30-min plasma cortisol was observed. Thus, we may conclude that in patients with AMI, the hypothalamic-pituitary-adrenocortical (HPA) response to stress and ACTH test shows no repression due to age.

Adrenal Cortex Function Tests↗

Free plasma 11-hydroxycorticosteroids and the response to beta1-24-corticotrophin in regular haemodialysis patients.

The adrenocortical function of 59 patients on regular hemodialysis treatment was tested on 105 occasions by measuring the 30-min response of free plasma 11-hydroxycorticosteroids (11-OHCS) after intramuscular injection of 0.25 mg Synacthen (beta1-24-corticotrophin). The morning basal levels of 11-OHCS were within the normal range. The increase of 11-OHCS after injection of Synacthen was less than normal in 25% of the patients. In 9 patients with a low response an extended Synacthen test was performed. This caused a normal increase in plasma 11-OHCS but the response came later than in normal persons. After 0.25 mg Synacthen intramuscularly the 30-min response of 11-OHCS seemed to be lower on the first day than on the second day after dialysis. The present study supports the view that the pituitary-adrenocortical system is essentially intact in patients on regular hemodialysis treatment.

11-Hydroxycorticosteroids↗

Corticotrophin stimulation test: inverse correlation between basal serum cortisol and its response to corticotrophin.

Serum cortisol response to synthetic corticotrophin (B1-24-ACTH) was evaluated in 21 normal subjects. There was significant negative correlation (r = -0.633, P less than 0.001) between the basal serum cortisol and the increase in serum cortisol level in response to ACTH. Two subjects had an increase in serum cortisol of less than 194 nM/1 (7.0 microgram/100 ml) and two additional subjects had an increase of less than 278 nM/l (10.0 microgram/100 ml). All subjects had an absolute peak value greater than 583 nM/l (21.0 microgram/100 ml) at 30 or 60 min post-ACTH. Inverse correlation between basal serum cortisol and the increase in serum cortisol suggests that in patients who have high basal serum cortisol levels, endogenous ACTH may already have reduced the cortisol reserve of the adrenal gland.

Adrenal Cortex↗