SULT2A1 and polycystic ovary syndrome: Hyperandrogenemia in patients with CPSS occurs secondary to impaired hepatic sulfation of DHEA to its less active form DHEAS because of the bypass of DHEA into systemic circulation.21,22 The production of more potent downstream androgens is upregulated by increased levels of DHEA in the setting of normal or low DHEAS, which results in premature adrenarche.22