We report the case of a seventy year-old type 2 diabetic man presenting with a fifteen year history of erectile dysfunction. He had micro- and macrovascular complications of diabetes and liver cirrhosis secondary to Hepatitis C infection. Investigations showed a high total testosterone of 32.3 nmol/l, raised SHBG at 127 nmol/l with elevated LH 20.4 IU/l and FSH 14.9 IU/l. Initial calculated free testosterone was 281 pmol/l with a bioavailable testosterone of 1.67 nmol/l, both of which were normal. His liver function tests reflected a hepatitic picture. Alpha subunit was measured and found to be raised at 1.85 IU (normal <1). A presumptive diagnosis of gonadotrophinoma was made.
Subsequent pituitary MRI scanning was normal. In the absence of a mass the patient was monitored with serial testosterone measurements. His erectile dysfunction was managed successfully with intracorporeal prostaglandin injection (caverject).
Over 18 months testosterone production declined. Total testosterone levels fell to 16.4 nmol/l with free testosterone of 127 pmol/l and bioavailable testosterone of 1.12 nmo/l both of which are subnormal. He has now been commenced on testosterone replacement and is responding well to therapy.
The diagnosis is therefore primary gonadal failure with increased SHBG levels falsely increasing the plasma testosterone levels.
An elevated serum concentration of alpha-subunit is often felt to be diagnostic of gonadotrophinoma in secondary hypergonadism. This case demonstrates that it can be raised in compensated hypogonadism and in this situation alpha subunit measurement may not be a good indicator of gonadotrophinoma. This case also stresses the importance of estimating free testosterone levels in patients with liver disease to define their true gonadal status. An elevated alpha subunit may be a useful predictor of subsequent frank gonadal failure in compensated hypogonadism and this warrants further investigation.
06 - 07 Nov 2006
Society for Endocrinology