M J Zelefsky1, J F Eid. 1. Department of Radiation Oncology, Memorial Sloan-Kettering Cancer, New York, NY 10021, USA.
Abstract
PURPOSE: To determine the etiology of treatment-induced erectile dysfunction among patients who underwent surgery or radiotherapy for prostatic cancer. METHODS AND MATERIALS: Ninety-eight patients were evaluated for erectile dysfunction after definitive therapy for prostate cancer with Duplex ultrasonography before and after intracorporal prostaglandin injection. Patients were classified as having arteriogenic, cavernosal, mixed (arteriogenic/cavernosal), or neurogenic impotence based upon the results of the Duplex studies. RESULTS: Among patients who underwent radical prostatectomy (RP), 31 (52%) had cavernosal dysfunction, 19 (32%) had arteriogenic dysfunction, 3 (5%) were classified as mixed, and 7 (12%) as neurogenic dysfunction. Among patients treated with radiotherapy (RT), 24 (63%) had arteriogenic dysfunction, 12 (32%) had cavernosal dysfunction, 1 (2.5%) were classified as mixed, and 1 (2.5%) as neurogenic dysfunction. A multivariate analysis identified prior RT as the only predictor of an arteriogenic etiology (p < 0.001) and prior RP as the only predictor of a cavernosal etiology (p < 0.04) for erectile dysfunction among these patients. In the RP and RT groups, the median erectile responses were 70 and 65%, respectively. Arterial peak flows < 25 cc/min predicted for a suboptimal erectile response with intracavernosal prostaglandin injections. Among 47 patients with arterial peak flows < 25 cc/min, 21 (55%) had erectile responses of < 70%, while for 51 patients with arterial peak flows > or = 25 cc/min, 31 (39%) had erectile responses of < 70% (p < 0.039). CONCLUSIONS: While the etiology of erectile dysfunction after definitive therapy for prostatic cancer is likely a multifactorial phenomenon, these data suggest that the predominant etiology among patients who undergo RT is arteriogenic and among patients who undergo RP is veno-occlussive/cavernosal pathology. This information may have implications for the design of more effective therapies to address erectile dysfunction in this patient population.
PURPOSE: To determine the etiology of treatment-induced erectile dysfunction among patients who underwent surgery or radiotherapy for prostatic cancer. METHODS AND MATERIALS: Ninety-eight patients were evaluated for erectile dysfunction after definitive therapy for prostate cancer with Duplex ultrasonography before and after intracorporal prostaglandin injection. Patients were classified as having arteriogenic, cavernosal, mixed (arteriogenic/cavernosal), or neurogenic impotence based upon the results of the Duplex studies. RESULTS: Among patients who underwent radical prostatectomy (RP), 31 (52%) had cavernosal dysfunction, 19 (32%) had arteriogenic dysfunction, 3 (5%) were classified as mixed, and 7 (12%) as neurogenic dysfunction. Among patients treated with radiotherapy (RT), 24 (63%) had arteriogenic dysfunction, 12 (32%) had cavernosal dysfunction, 1 (2.5%) were classified as mixed, and 1 (2.5%) as neurogenic dysfunction. A multivariate analysis identified prior RT as the only predictor of an arteriogenic etiology (p < 0.001) and prior RP as the only predictor of a cavernosal etiology (p < 0.04) for erectile dysfunction among these patients. In the RP and RT groups, the median erectile responses were 70 and 65%, respectively. Arterial peak flows < 25 cc/min predicted for a suboptimal erectile response with intracavernosal prostaglandin injections. Among 47 patients with arterial peak flows < 25 cc/min, 21 (55%) had erectile responses of < 70%, while for 51 patients with arterial peak flows > or = 25 cc/min, 31 (39%) had erectile responses of < 70% (p < 0.039). CONCLUSIONS: While the etiology of erectile dysfunction after definitive therapy for prostatic cancer is likely a multifactorial phenomenon, these data suggest that the predominant etiology among patients who undergo RT is arteriogenic and among patients who undergo RP is veno-occlussive/cavernosal pathology. This information may have implications for the design of more effective therapies to address erectile dysfunction in this patient population.
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