Prostate Disease

Normal prostate growth and development requires the presence of androgens from childhood to adolescence and adulthood. In younger hypogonadal men in whom prostate diseases are uncommon, androgen replacement increases the size of the prostate from the smaller volumes at baseline to the expected range for eugonadal men (66). However, progressive increases in prostate volume do not occur with continued testosterone replacement (66,67). Serum PSA levels may increase significantly with testosterone replacement but generally remain within the normal range (15,18,55,67). In middle-aged and older men, androgen replacement has resulted, in a few instances, in lower urinary tract obstructive symptoms and increased serum PSA levels, resulting in urological referral and ultrasound-guided prostate biopsy (17,20). In most reports, prostate-related adverse events have occurred rather early in the course of androgen replacement, suggesting that such treatment may have unmasked existing latent or histological cancer. In those men, increasing serum PSA levels to values exceeding the reference range triggered an early prostate biopsy and a cancer diagnosis.

Most urologists believe that androgens do not induce BPH, but androgens should not be used in subjects with lower urinary tract obstructive symptoms until these symptoms have been treated. There is no direct evidence in hypogonadal young or older men that androgen replacement will induce the formation of prostate cancer or convert a latent, histological prostate cancer to a clinically significant or metastatic cancer (68). However, androgens should not be used in a hypogonadal man who has had prostate cancer. There are possible rare exceptions, e.g., a patient with a distant completely resected intraprostatic cancer and long-standing near-undetectable PSA levels who is suffering from severe symptoms and signs of testosterone deficiency. Treatment of such a patient may be justified but only with careful surveillance and well-documented informed consent. It is not known whether testosterone treatment, together with the 5-a reductase inhibitor finasteride or an androgen that cannot be converted to dihydrotestosterone (DHT) will have sparing effect on prostate growth. A prostate cancer primary preventive trial using a 5-a reductase inhibitor (finasteride) showed that it prevented or delayed prostate cancer but may increase the risk of high grade cancer (68a). A randomized, prospective study of androgen-replacement in androgen-deficient older men is urgently required to address the concerns of whether testosterone replacement to older hypogonadal men will increase the risk of development of clinical prostate cancer.

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