Functional classification of polycystic ovary syndrome according to source of androgen excess

PCOS functional type	Source of androgen	GnRHa test: 17OHP response	DAST testosterone response	ACTH test: DHEA response	Prevalence among PCOS
Typical PCOS (PCOS-T)	Primary FOH (typical FOH)	High^¶	High in 92.5%	High in 28% (associated FAH)	67%^Δ
Atypical PCOS (PCOS-A)	Primary FOH (atypical FOH)	Normal^¶	High	High in 30% (associated FAH)	20%
	Isolated primary FAH (isolated FAH)	Normal	Normal	High	5%
	PCOS without FOH or FAH (atypical PCOS of obesity or idiopathic atypical PCOS)	Normal	Normal	Normal	8%

The FOH seen in two-thirds of PCOS cases is distinguished by 17OHP hyperresponsiveness to stimulation testing with GnRHa. However, in one-third, it is detected only by an elevated testosterone in response to a DAST. FAH is distinguished by DHEA hyperresponse to ACTH, which correlates with the DHEAS level. FAH occurs most often concomitantly with FOH, but it can also occur in the absence of FOH (isolated FAH). Text (high versus normal) indicates defining characteristics; percentages indicate experimentally determined prevalence of abnormality.

PCOS: polycystic ovary syndrome; GnRHa: gonadotropin-releasing hormone agonist; 17OHP: 17-hydroxyprogesterone; DAST: dexamethasone androgen-suppression test; ACTH: adrenocorticotropic hormone (corticotropin); DHEA: dehydroepiandrosterone; FOH: functional ovarian hyperandrogenism; FAH: functional adrenal hyperandrogenism.

* Based on data of Rosenfield RL, et al. Determination of the source of androgen excess in functionally atypical PCOS by a short DAST and a low-dose ACTH test^[1].

¶ "High" versus "normal" denotes defining characteristics; percentages indicate experimentally determined prevalence of abnormality.

Δ Prevalence determined from an age-matched subgroup (n = 60) of an original cohort (n = 99) in which 69% had PCOS-T.

Reference:

Rosenfield RL, Mortensen M, Wroblewski K, et al. Determination of the source of androgen excess in functionally atypical polycystic ovary syndrome by a short dexamethasone androgen-suppression test and a low-dose ACTH test. Hum Reprod 2011; 26:3138.

Modified from: Rosenfield RL, Ehrmann DA. The pathogenesis of polycystic ovary syndrome (PCOS): The hypothesis of PCOS as functional ovarian hyperandrogenism revisited. Endocrine Reviews 2016; 37:467. By permission of Oxford University Press on behalf of The Endocrine Society. Copyright © 2016.

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Functional classification of polycystic ovary syndrome according to source of androgen excess