Endocrine Abstracts

A 26 year old lady under investigation for infertility was referred to our endocrine clinic for raised testosterone levels at 6.6 nmol/l (0.5–2.8).she had regular period with no features of hirsutism. Her past medical history included common acute lymphoblastic leukaemia on chemotherapy, liver cirrhosis with portal hypertension secondary to chemotherapy, Trans jugular intrahepatic portosystemic shunt (TIPS) insertion for bleeding gastric varices.

Clinical examination she has no features of hirsutism.

Endocrine Investigations: Plasma Testosterone- 6.6 nmol/l, SHBG 139 nmol/l, Androstenedione 35 nmol/l were high. DHEAS, Dihydrotestosterone, TSH, Prolactin, gonadotropins and oestrdiol were within reference range. Baseline and post synacthen 17-hydroxypregestrone were normal. The repeat short synacthen test showed normal cortisol response and follicular phase 17 OHP was not raised making congenital adrenal hyperplasia unlikely. Low dose dexamethasone suppression test showed supressed cortisol, testosterone, androstadiene and DHEA which excludes adrenal/ovarian androgen producing tumours.

Her day 21 progesterone was reasonable but still she was unable to conceive. A urine steroid profile showed low virilising androgen metabolites but increased androstenetriol and normal a-cortlone levels. CT adrenals excluded ovarian and adrenal pathology.

Discussion The high testosterone level in this patient was likely to be due to portal hypertension secondary to liver cirrhosis. The majority of patients with liver cirrhosis have raised SHBG concentrations which in fact will protect them from virilising symptoms. This accounts for the less free plasma testosterone concentrations. As per our literature search we could find only one another case with similar condition. We do not believe her high testosterone is contributing to her infertility especially when she does not have any signs of androgenisation and we suspect virilisation risk of the foetus is extremely low if she conceives. However foetus is completely protected by placental aromatase which inactivates maternal androgens.