Endocrine Abstracts

A 55-year-old post-menopausal female presented with hirsutism and increased libido. Testosterone was elevated at 9.7 (RR <1.8 nmol/l). LH/FSH were appropriate post-menopause (LH 28.8; FSH 54.1U/l). DHEAS, androstenedione and 17-hydroxyprogesterone were unremarkable. GnRH analogue suppression testing (GnST) appropriately suppressed LH/FSH and testosterone (testosterone 0.2 nmol/l), suggesting an LH-dependent source of testosterone. Pelvic MRI suggested a left ovarian tumour. This was felt by gynaecology to require urgent resection and, also noting a presumed likely ovarian source for her excess testosterone production, bilateral salpingo-oophorectomy was performed. Histology demonstrated bilateral stromal hyperplasia without hyperthecosis and hilar Leydig cells but no tumour. At the time of oophorectomy, LH and FSH remained suppressed post-GnRH analogue. As this suppression wore off, LH/FSH increased. Unexpectedly, testosterone also rose, to 5.3 nmol/l, with a return of hyperandrogenic symptoms. Repeat GnST again demonstrated suppression of testosterone, continuing to suggest LH-driven production. Low-dose-dexamethasone-suppression testing did not affect testosterone (while appropriately suppressing cortisol). The pelvic MRI had suggested a left adrenal mass. Dedicated adrenal CT demonstrated a 14mm nodule. No other radiological abnormality was seen to suggest ectopic ovarian tissue. 11C-metomidate PET/CT demonstrated tracer avidity within the adrenal lesion, suggesting adrenocortical tissue. Suppression testing excluded autonomous production of cortisol or aldosterone. Urine steroid profiling was unremarkable. Adrenal vein sampling demonstrated markedly higher testosterone levels from the left adrenal vein than either IVC or the right adrenal vein, raising the possibility of a left adrenal source for the testosterone. Interestingly, the size of the adrenal nodule changed on serial CT (14mm – 10mm – 12mm), with the size reduction occurring after the two GnSTs (12 and 6 months prior to scan). The subsequent re-enlargement was seen 9 months later. This is an intriguing case of LH-dependent female testosterone production, persisting after bilateral oophorectomy, suggesting a rare LH-responsive adrenal source.