Benign prostatic hyperplasia (BPH) is the most common prostatic disorder and is found in most intact male dogs >6 yr old as a result of androgenic stimulation or altered androgen/estrogen ratio. It is not known why some males are affected and others are not. 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. Clinical signs may be absent, 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. Medroxy-progesterone 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 BPH 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.
A new treatment for BPH, an anti-gonadotropin-releasing-factor vaccine has been conditionally licensed for use in postpubescent dogs. This product induces an immune-mediated response against GnRH, which secondarily decreases plasma testosterone concentration. In a study involving 13 dogs, 2 SC injections administered at a 4-wk interval caused a decrease in prostate volume of ~50%. The manufacturer recommends revaccination every 6 mo; however, large studies evaluating the longterm efficacy of this product have not been published. Furthermore, the effect on fertility in dogs is unknown.
Last full review/revision July 2011 by James A. Flanders, DVM, DACVS