Endocrine Abstracts

Measuring total testosterone level is the first line approach to assess androgen excess in women. Most laboratories in Europe use direct testosterone immunoassay without prior extraction. In the near future, liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) will be commonly used for measuring testosterone, providing the best accuracy with low limit of detection. In all cases, testosterone norms must be standardized for normal premenopausal women values. Where testosterone is twice the upper limit of normal, it is recommended that DHEAS assay be performed. DHEAS is primarily of adrenal origin in women. Thus, a DHEAS level of over 600 μg/dl indicates a diagnosis of androgen-secreting adrenal carcinoma (often associated with hypercorticism). In this case, abdominal scan must be performed rapidly. Where testosterone is just above the normal upper limit, the most likely diagnosis is polycystic ovary syndrome (PCOS). However, screening should be performed for the nonclassic form of 21-hydroxylase deficiency (assay of 17OH-progesterone) and depending on the clinical setting, Cushing disease must be ruled. Normal testosterone levels in patients with clear clinical symptoms of hyperandrogenism must be interpreted with care. Indeed, T circulates in the blood tightly bound to sex-hormone binding-globulin (SHBG). Low SHBG is typically observed in overweight PCOS patients, in association to inflammatory state and metabolic syndrome, and contributes to lower total testosterone by increasing its clearance from the blood. Therefore, it is recommended, to measure SHBG for correct interpretation of total testosterone by calculating free testosterone index, awaiting direct free-T assay that is still not available. Δ4-androstenedione (A) has been studied comparatively with testosterone, and dissociations exist, with isolated elevation of A but no elevation of testosterone, particularly in the incident of reduced SHBG. In unusual circumstances, dexamethasone test to suppress androgens arising from a functional adrenal source and gonadotropin-releasing hormone (GnRH) agonist in identifying ovarian androgen secreting tumor and hyperthecosis, could be helpful. All these pitfalls should not discourage endocrinologist to challenge the diagnosis of hyperandrogenic states. Decision trees for evaluating the origin of androgen excess will be suggested and discussed during the session.