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The ACTH test (also called the cosyntropin, tetracosactide, or Synacthen test) is a medical test usually requested and interpreted by endocrinologists to assess the functioning of the adrenal glands' stress response by measuring the adrenal response to adrenocorticotropic hormone (ACTH; corticotropin) or another corticotropic agent such as tetracosactide (cosyntropin, tetracosactrin; Synacthen ...
A cosyntropin stimulation test may be needed in mild cases, but usually the random levels of 17OHP are high enough to confirm the diagnosis. [ 92 ] [ 93 ] [ 94 ] Elevated 17OHP may activate androgen "backdoor" pathway, that leads to excess of 5α-dihydrotestosterone and other potent androgens.
To determine the origin of dysfunction, the ACTH stimulation test is the best initial test as it can differentiate between primary and secondary adrenal insufficiency. [2] If cortisol levels remain low following ACTH stimulation, then the diagnosis is primary adrenal insufficiency. [2]
A low-dose ACTH stimulation test has been suggested as a sensitive test for secondary adrenal insufficiency diagnosis. [10] When compared to insulin tolerance testing [11] and the high-dose ACTH test, this test allows for a more accurate identification of patients with secondary adrenal insufficiency. [12]
The activity of 11β-hydroxylase can be determined by observing the basal 11-deoxycortisol level. A level over 10 ng/mL, indicates followup with ACTH stimulation test. The 60th minute post-stimulation 11-deoxycortisol levels higher than 18 ng/mL are diagnostic of LOCAH. [45]
The exact dose of ACTH remains a matter of debate. [18] In the CORTICUS study, ACTH stimulation testing predicted mortality whereas baseline cortisol levels did not. [19] However, possible benefits of corticosteroid therapy do not seem to be completely predicted by ACTH stimulation testing.
Inefficient cortisol production results in rising levels of ACTH, because cortisol feeds back to inhibit ACTH production, so loss of cortisol results in increased ACTH. [28] This increased ACTH stimulation induces overgrowth (hyperplasia) and overactivity of the steroid-producing cells of the adrenal cortex. The defects causing adrenal ...
3β-HSD II mediates three parallel dehydrogenase/isomerase reactions in the adrenals that convert Δ 4 to Δ 5 steroids: pregnenolone to progesterone, 17α-hydroxypregnenolone to 17α-hydroxyprogesterone, and dehydroepiandrosterone (DHEA) to androstenedione. 3β-HSD II also mediates an alternate route of testosterone synthesis from androstenediol in the testes. 3β-HSD deficiency results in ...