Abstract

It is still debated whether clinical and/or biological indices of hyperandrogenism (HA) should be present to qualify a patient as having polycystic ovary syndrome (PCOS). We hypothesized that excessive follicle number (FN) assessed by ovarian ultrasonography and/or serum anti-Müllerian hormone (AMH) concentrations may be used as surrogates for the classical markers of HA. Data were obtained from a database of clinical, hormonal, and ultrasound features that were consecutively recorded in 270 women with PCOS (defined using the Rotterdam Criteria) and 217 infertile nonhyperandrogenic normoovulatory women. These variables were submitted to principal component analysis, a multivariable statistical procedure that transforms a number of possibly correlated variables into a smaller number of uncorrelated variables called principal components (PC). Variables that aggregate in the same PC capture the same information. In the control group, as expected, three independent PCs were identified: 1) the markers of the metabolic (i.e. insulin resistance) status; 2) those of the androgen status; and 3) those of the follicle status. In the PCOS group, the metabolic variables also aggregated in a first PC. Ovarian androgen and follicle markers aggregated in a second independent PC, with FN and serum AMH having the strongest correlation coefficients. A third PC summarized the adrenal contribution to the HA of PCOS. In both groups, the free androgen index correlated equally to the first and second PCs. The similarity of the first PC between controls and PCOS supports the hypothesis that the metabolic anomaly of PCOS is neither intrinsic nor specific. Conversely, by gathering the androgen and follicle variables, the second PC in PCOS may be viewed as summarizing a specific ovarian anomaly. Because both FN and/or serum AMH were strongly correlated to the second PC along with androgens, they may be used equally as surrogates for the classical markers of ovarian HA. This reconciles the Rotterdam Consensus and other definitions for PCOS, especially in women having the Rotterdam PCOS phenotype without HA. We thus propose a simple strategy for the diagnosis of PCOS in clinical practice.

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