Andropause

Prostate growth, whether malignant or benign, is highly dependent on steroid hormones. A major concern is that testosterone replacement will stimulate the onset or hasten the development of prostatic carcinoma. The inhibitory effect of removing androgens on clinically diagnosed prostate cancer is well known. Whether replacing testosterone in hypogonadal men promotes development of de novo malignancies or progression of sub-clinical carcinomas is not known. To date, the small and short-term studies have not demonstrated an increased risk (Morales et al.). However, the level of experience at this time is insufficient to conclusively rule out a causal relationship (Morales et al.). For this reason, careful monitoring of these patients with serum prostate-specific antigen (PSA) and digital rectal exams are recommended.

The effect of testosterone on benign prostatic enlargement has also been a concern. The most recent data from placebo-controlled trials of testosterone replacement in hypogonadal men suggests that the changes in PSA, prostate volume, and lower urinary tract symptoms are clinically insignificant (Tenover, 1998). Current recommendations suggest serum PSA and digital rectal exam before instituting testosterone replacement, then yearly thereafter.

The effects of hypogonadism and testosterone replacement on lipid profiles and risk of cardiovascular disease are unclear. Interestingly, low serum testosterone levels appear to be associated with increased triglycerides and decreased levels of high-density lipoprotein (HDL) cholesterol; testosterone replacement appears to restore these to more favorable levels (Zmuda et al.). Several recent studies have suggested that hypogonadism may be a risk factor for coronary artery disease, although this remains to be fully explained (Philips et al.; Uyanik et al.). The impact of testosterone therapy on cardiovascular risk is not entirely clear, however; most current data suggest it does not induce an atherogenic profile (Vermeulen and Kaufman). Careful lipid monitoring should be provided for patients on testosterone replacement, particularly those with risk factors for coronary artery disease.

Current injectable, oral, and transdermal testosterone preparations (available in the United States only) without methyltestosterone are believed not to cause the liver toxicity described with previously used methylated forms of testosterone (Morales et al.).

Testosterone stimulates erythropoiesis (production of red blood cells) through an unclear mechanism and can result in increased hematocrit, increased hemoglobin, and hypercoagulability in as many as 24 percent of patients (Jockenhovel et al.; Winkler). For this reason hematocrit assessment on a three-month basis has been recommended for men on testosterone replacement.