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Benign Prostatic Hyperplasia |  |
| Benign prostatic hyperplasia is the most common prostatic disorder and is found in most intact male dogs >6 yr old. It is a result of androgenic stimulation or altered androgen/estrogen ratio, but why some males are affected and others are not is unknown. In some dogs, hyperplasia may begin as early as 2.5 yr of age and, after 4 yr of age, cystic hyperplasia tends to develop. There may be no clinical signs, or tenesmus, persistent or intermittent hematuria, and bleeding may
occur. The diagnosis is suggested by physical and historical findings and by a nonpainful, symmetrically enlarged prostate. Radiology can confirm prostatomegaly. Ultrasonography should show diffuse, relatively symmetric involvement with multiple, diffuse, cystic structures. Cytologic examination of massage or ejaculate specimens reveals hemorrhage with mild inflammation without evidence of sepsis or neoplasia. Definitive diagnosis is only possible by biopsy. Castration is the
treatment of choice; prostatic involution is usually evident within a few weeks and is often complete in several months. |
| For males intended for use in breeding, medical therapy may be feasible. Estrogens have been used to reduce prostatic hyperplasia but cannot be recommended because of potential side effects. Whenever estrogenic stimulation is present (eg, exogenous administration or endogenous production by Sertoli cell tumor), squamous metaplasia of the prostate can develop. Squamous metaplasia can cause prostatic enlargement and worsen the clinical signs. It may also enhance the risk of cystic
changes and infection within the prostate. In addition, estrogens can cause negative feedback to the hypothalamus and pituitary (thereby diminishing spermatogenesis) and are potentially toxic to the bone marrow with resultant anemia, thrombocytopenia, and leukopenia. Medroxyprogesterone acetate has been used to treat prostatic hypertrophy in dogs, but testosterone concentration decreased, testicular degeneration occurred, and only 53% of dogs had a detectable decrease in prostatic size. |
| Perhaps the most effective medical agent for treatment of benign prostatic hypertrophy in dogs is finasteride, which blocks the action of 5 α-testosterone reductase, an enzyme that converts testosterone to dihydrotestosterone. Dihydrotestosterone is considered to be the key hormone for promoting prostatic hypertrophy in both humans and dogs. Giving 1 mg/kg of finasteride, PO, sid for 16-21 wk, to laboratory beagles resulted in a
50-70% reduction in prostatic hypertrophy with no negative effect on semen quality. Lower doses of finasteride (0.1 mg/kg, PO, sid for 16 wk) reduced hypertrophied prostate volume by 43%, resolved clinical signs, reduced dihydrotestosterone concentration by 58%, maintained normal testosterone levels, and had no deleterious effect on semen quality, fertility, or libido in a group of 9 dogs with prostatic hypertrophy. However, prostatic hypertrophy returns if finasteride
administration is discontinued. The low dose (0.1-0.5 mg/kg) of finasteride correlates to convenient dosing of one 5-mg capsule of finasteride sid, for dogs weighing 10-50 kg. |
