Endocrine Abstracts (2007) 14 OC7.7

Use of atorvastatin, but not simvastatin in men with Type 2 diabetes is associated with lower total testosterone levels with no effect on bioavailable or free testosterone

Roger D Stanworth1, Dheeraj Kapoor2, Kevin S Channer3 & T Hugh Jones4

1Academic Unit of Endocrinology, University of Sheffield, Sheffield, United Kingdom; 2Department of Diabetes and Endocrinology, Barnsley Hospital NHS Foundation Trust, Barnsley, United Kingdom; 3Faculty for Health and Wellbeing, Sheffield Hallam University, Sheffield, United Kingdom; 4Department of Cardiology, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, United Kingdom.

There is a high prevalence of low testosterone levels in men with type 2 diabetes (DM2) and low testosterone predates the onset of DM2. Testosterone replacement therapy for hypogonadal men with DM2 improves insulin sensitivity and glycaemic control as well as reducing central obesity. This may lead to an increase in biochemical assessment of hypogonadism in men with DM2. Androgens and other steroid hormones are produced from cholesterol and it has been postulated that treatment with HMG-Co-enzyme A reductase inhibitors (statins) could decrease testosterone levels by reducing the availability of cholesterol and/or inhibiting steroidogenesis. Low testosterone levels in men with DM2, and the widespread use of statins in DM2 mean that any such effect would be particularly important in this group.

We compared androgen status with statin use in a group of 355 Caucasian men with DM2. Data was collected in year 2002–2003. In our group, 168 patients were treated with statins (mainly simvastatin and atorvastatin) and 187 men were untreated. There were no significant differences between treated and untreated men in terms of glycaemic control, blood pressure or obesity. Statin use was associated with lower total testosterone (TT) (P=0.009) and SHBG (P=0.005) levels but bioavailable (BioT) and calculated free testosterone (cFT) were not significantly reduced. ADAM hypogonadal symptom score was not affected.

Atorvastatin was associated with reduced TT (P=0.006) and SHBG (P=0.005) compared with no treatment and there was an apparent dose response effect with the lowest levels of testosterone seen in men treated with higher doses of atorvastatin. Simvastatin did not cause a significant reduction in testosterone or SHBG levels. Our study illustrates the importance of using measured or calculated bioavailable or free testosterone in the assessment of hypogonadism in men with DM2 treated with statins, particularly atorvastatin.

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