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W Oelkers

Clinical tests of the hypothalamo-pituitary-adrenocortical axis in cases of suspected adrenocortical insufficiency are based almost exclusively on the stimulation of pituitary ACTH release or adrenocortical release of ACTH-dependent steroids. The most widely applied tests of the hypothalamo-pituitary-adrenal axis in clinical practice are the short ACTH injection test (SAT), the insulin hypoglycemia test (IHT), the short metyrapone test (SMT) and the corticotropin-releasing hormone (CRH) test (1). In this review, the reliability of these tests in special clinical settings will be discussed under the aspect of dose—response relationships between plasma ACTH and cortisol in normal man.

Problems with the conventional SAT

If a patient is suspected to suffer from primary adrenal insufficiency (Addison's disease), the test for excluding or strengthening the suspicion is the SAT, comprising the injection (im or iv) of 250 μg of ACTH (1–24) (Synacthen®, Cosyntropin® or Cortrosyn®) and the measurement of plasma or serum cortisol 30 or

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W Oelkers

In the last few years there has been increasing interest in incidentally discovered adrenal masses detected by abdominal ultrasound, computed tomography (CT) or magnetic resonance tomography in patients in whom the radiological procedure was ordered for reasons other than the suspicion of adrenal disease. Such "incidentalomas" are found in 0.6–1.3% of abdominal CTs, which is a similar percentage to the finding of adrenal nodules on necroscopy (1). Most of these nodules are 1–3 cm in diameter, but more rarely lesions up to 10 cm or larger may be discovered.

The likelihood of finding an "incidentaloma" is greater in females, in elderly people and in those with arterial hypertension. Finding an "incidentaloma" should alert the referring physician to re-examine the patient, looking for symptoms and signs of adrenocortical or adrenomedullary disease, or of a malignancy. If the patient is known to have cancer, the adrenal lesion, especially if bilateral, may be

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W. Oelkers and V. Bähr

Abstract. We attempted to answer to the question whether excessive rises in endogenous plasma angiotensin II (All) stimulate ACTH secretion by measuring PRA, All, AVP, ACTH, and cortisol in 8 patients with Addison's disease before and after withdrawal of fludrocortisone substitution. Blood was drawn at 14.30 h, exactly 6½ h after the morning dose of hydrocortisone had been taken. PRA and All were initially higher than normal in 4 patients. After withdrawal of fludrocortisone for 1 or 2 weeks, PRA and All rose markedly in 4 patients (up to 260 ng/l) without concomitant changes in plasma ACTH levels (r = −0.081, All vs ACTH). Changes in plasma cortisol could not have obscured a stimulatory effect of All on ACTH by variable feedback inhibition of ACTH release. The increase in plasma All levels in the 4 patients was larger than that observed in a previous study in normal subjects after rigorous dietary sodium restriction. In all patients, hyperkalaemia developed after fludrocortisone withdrawal, independent of changes in PRA and AII. Rises in PRA, All, and plasma potassium were partially reversed by increased sodium intake and further suppressed by resumption of fludrocortisone therapy. Plasma AVP remained in the normal range after fludrocortisone withdrawal, but was slightly elevated after increasing salt intake without fludrocortisone administration. Conclusions: 1) Rises of endogenous plasma All to levels tenfold higher than normal do not stimulate ACTH release. All is probably not a physiological modulator of ACTH secretion. 2) Mineralocorticoid substitution in Addison's disease should be monitored by plasma potassium measurement. Hyperkalaemia may coexist with normal PRA.

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W. Oelkers, H. Harendt and P. Exner

Abstract. Five normal young males on a low sodium diet received iv ACTH (1–24) infusions (10 IU/24 h) for 100 h in addition to diuretics. The aim of the study was to find out whether the biphasic effect of ACHT on aldosterone (initial stimulation followed by 'esacpe') could be prevented by keeping plasma renin activity (PRA) at a fairly constant high level. PRA was around 20 ng/kg/min before and towards the end of the ACTH infusion. Plasma aldosterone and aldosterone excretion rates were, nevertheless, only transiently stimulated, but the first was relatively more suppressed than the latter at the end of the ACTH infusion. Plasma 18-OH-corticosterone followed the same pattern. Even on the last infusion day, aldosterone and 18-OH-corticosterone levels were still higher than in normal ambulatory sodium-replete men. The fasciculata steroids cortisol, 11-deoxycorticosterone and corticosterone were continuously stimulated by ACTH.

It is concluded that the biphasic response of zona glomerulosa steroids to ACTH is basically independent of renin and angiotensin II. However, the marked suppression of aldosterone secretion observed in sodium-replete individuals during prolonged ACTH treatment was not seen in this study. Angiotensin II or a different factor associated with sodium depletion may, therefore, partly protect the zona glomerulosa from adverse effects of ACTH observed in the sodium-repelete state.