Function tests

• Suspicion of secondary (hypophyseal) or tertiary (hypothalamic) adrenocortical insufficiency
• Differential diagnosis of Cushing-syndrome

The corticotropin-releasing hormone (CRH) is produced in the hypothalamus and stimulates the release of ACTH via the pituitary gland.

ACHT, cortisol

2 ml serum (for cortisol) and 2 ml frozen EDTA-plasma (for ACTH) before (0 min), as well as 15, 30, 60 and 90 min after CRH-administration. The EDTA-blood should be centrifuged within 30 min of extraction and then the EDTA-plasma should be frozen. Freezing containers will be issued on request.

• Exogenous corticoids should be discontinued at least 24 hours before the test.
• Where possible, the test should be carried out in the late afternoon (approximately 1600 hours).

1. A peripheral venous line should be inserted 30 min before test start.
2. Prior to CRH application, at 0 min, first blood collection for ACTH and cortisol
3. Slow intravenous injection, via the venous line, of 100 µg pure CRH (cortisol-releasing hormone, corticorelin, CRH-Ferring®) or 1 µg/kg body weight.
4. Further blood collections 15, 30, 60 and 90 min after CRH-administration.

Side effects: Possible mild symptoms of flushing

Adrenocortical insufficiency
Primary and secondary adrenocortical insufficiency can be excluded, if the ACTH level increases by at least 100 % (on average around 400 %) and cortisol by at least 50 % (on average around 250 %). In case of excessive ACTH reaction (> 900 % of the initial value), hypothalamic damage has to be considered. Depending on the time of its existence, there may also be excessive cortisol response (> 600 % of the initial value) or decreased response due to an already existing atrophy of adrenal cortex. The same, however, also applies to secondary adrenocortical insufficiency. Sufficient ACTH increase with a lack stimulation of cortisol secretion points towards an already existing atrophy of the adrenal cortex.

Cushing syndrome
In case of hypophyseal Cushing syndrome (Morbus Cushing), ACTH increase of at least 35 % and cortisol increase of at least 20 % can be seen. In case of ectopic cortisol production due to an endocrine active tumor (such as bronchial carcinoma), there is no increase in neither ACTH nor cortisol. In adrenal Cushing syndrome (such as adrenocortical adenoma or carcinoma, adrenocortical hyperplasia), neither the already basally suppressed ACTH nor the normal to increased cortisol can be stimulated.