Objective
To determine whether the treatment of patients with testicular cancer, using cisplatin combined with etoposide and bleomycin (BEP) after orchidectomy in those with disseminated disease, causes changes in sex hormones and penile vascularization, possibly related to sexual dysfunction.
Patients and methods
Ten patients treated with BEP were compared with 11 undergoing orchidectomy alone followed by surveillance. Sex hormone levels were analysed and cavernosal artery duplex ultrasonography performed before orchidectomy and at 6 and 12 months afterward. Patients were questioned about their sexual function. After 1 year, a visual erotic stimulation (VES) test was performed to assess penile rigidity.
Results
In contrast to the surveillance group, BEP‐treated patients had higher follicle‐stimulating hormone (4.6 vs 26.5 U/L) and luteinizing hormone (1.4 vs 8.2 U/L) levels, and lower testosterone levels (21.1 vs 14.7 nmol/L) at 6 months than at baseline. At 1 year, most patients had compensated hypergonadotrophic eugonadism, but Leydig cell function had recovered. Changes in cavernosal artery peak flow velocities induced by local injection with papaverine/phentolamine showed no difference between the groups before and 6 months after orchidectomy. Loss of libido and erectile dysfunction were reported more frequently by BEP‐treated patients. However, 1 year after treatment, most reported a satisfying sex life and VES resulted in a rigid erection in nearly all patients. The reported erectile dysfunction could not be explained by changes in plasma testosterone levels or diminished blood flow velocities.
Conclusions
After being diagnosed with testicular cancer, sexual morbidity is considerable, but within 1 year some improvement may be expected. BEP induces transient testicular dysfunction but this recovers. Although BEP is related to symptoms of angiopathy, cavernosal blood flow seems to be unaffected. These findings and the normal VES‐evoked penile rigidity suggest that sexual dysfunction is more psychological than organically induced by BEP.