Endocrine Abstracts

A 24-year-old woman complained about secondary amenorrhoea after stopping oral contraceptive whereas she wanted to be pregnant. Physical examination showed an android obesity with a non-progressive but major hirsutism. Endocrinological investigations eliminated pregnancy but revealed on different samples a high plasma testosterone level (from 2.15 to 2.77 ng/ml), in the tumoral range whereas DHEA-sulfate, delta4-androstendione, sex binding protein and prolactine were normal. Stimulation test eliminated a 21-hydroxylase block. Further investigations suggested polycystic ovaries: LH hyperpulsatility, typical microfollicular ovaries aspect on pelvic MRI, metabolic syndrome with glucose intolerance and hypertriglyceridemia. Tomography scan of the adrenal glands showed a unilateral hypertrophy. In order to prove that ovaries were responsible of hyperandrogenism, a diagnostic treatment with long-acting gonadotrophin releasing hormone (GnRH) was performed. GnRH administration produced only a partial decrease in serum testosterone levels (0.77 ng/ml). Because of this absence of testosterone normalisation under GnRH and the presence of an unilateral adrenal hypertrophy, an adrenal and ovarian venous catheterism was performed. There was no gradient in testosterone secretion to suggest hyperandrogenia was from an ovarian or adrenal origin. We concluded that high testosterone levels were the results of a benign ovarian hyperandrogenism. A glitazone treatment was initiated associated with hypocaloric diet and physical exercise. Evolution of the adrenal morphology will be performed. This case is an example that polycystic ovaries can produce high levels of testosterone that can remind of a tumoral secretion. Nevertheless, testosterone levels up to 2 ng/ml must lead to eliminate a tumoral origin, even when the metabolic and endocrinological context suggests a polycystic ovary syndrome.