Postmenopausal
hyperandrogenism can be tumour- or non-tumour-related, with pathology residing either in the ovary or adrenal gland(s). The
tempo of investigation is determined by the clinical severity of
hyperandrogenism (presence/absence of actual virilisation) and degree of serum
testosterone elevation. When clinical or biochemical
hyperandrogenism is severe, rapidly developing, or associated with
hypercortisolism, screening for adrenocortical or ovarian
carcinoma with cross-sectional imaging should be prioritised over detailed biochemical evaluation. Adrenal
hyperandrogenism is readily characterised, both biochemically and radiologically. By contrast, even a combination of high-resolution imaging with laboratory evaluation, including dynamic endocrine testing, often cannot distinguish between ovarian hyperthecosis (
OH) and virilising ovarian tumour (VOT); a definitive diagnosis usually emerging only after histological examination of excised ovaries. VOTs are typically below the resolution-limit of current imaging modalities and exhibit suppression of
gonadotropin-dependent
androgen secretion with
GnRH-analogue
therapy. Thus, for well-characterised ovarian
hyperandrogenism, laparoscopic bilateral
salpingo-oophorectomy may serve both as a diagnostic and therapeutic procedure. Nevertheless, women unable or unwilling to undergo ovarian surgery can be reassured that malignant VOTs are exceedingly rare and that long-term medical
therapy with oral
antiandrogens or
GnRH-analogues is safe and well-tolerated.
OH is strongly associated with
insulin-resistance, with hyperinsulinaemia acting synergistically with raised
gonadotropin levels to stimulate thecal cell
hyperplasia and
androgen secretion by the postmenopausal ovary, which lacks granulosa cell
aromatase activity and thus cannot convert
testosterone to
17 beta estradiol. Thus, features of
metabolic syndrome may indicate
OH, and significant reductions in
androgens can thereby potentially be achieved with lifestyle measures and/or
insulin-sensitising drugs.