Arthur L Burnett1, Trinity J Bivalacqua. 1. Department of Urology, The James Buchanan Brady Urological Institute, The Johns Hopkins Hospital and The Johns Hopkins University School of Medicine, Baltimore, MD, USA. aburnett@jhmi.edu
Abstract
INTRODUCTION: Efforts to identify the health risk associations for priapism may reveal pathophysiologic mechanisms for the disorder and suggest a scientifically rational approach for correcting it. AIM: We describe a clinical presentation of idiopathic recurrent priapism in a patient with glucose-6-phosphate dehydrogenase (G6PD) deficiency and consider a possible nitric oxide (NO)-dependent mechanistic basis from which the medical condition causes priapism. METHODS: The case report profiled a 35-year-old African-American man with G6PD deficiency who presented with a rapid progression of recurrent priapism episodes. He was outwardly healthy and did not have sickle cell disease or trait by hematologic screening. His management featured use of a long-term, continuous phosphodiesterase type 5 (PDE5) inhibitor therapeutic regimen. MAIN OUTCOME MEASURES: Clinical history data and response to PDE5 inhibitor therapy. RESULTS: After a 3-month duration of PDE5 inhibitor therapy, priapism recurrences were sufficiently resolved and the patient discontinued therapy. At 18-month clinical follow-up, he experienced only minor priapism recurrences and retention of full erectile ability. CONCLUSIONS: G6PD deficiency offers an explanation for idiopathic priapism. The medical condition generates a pathophysiologic milieu consistent with aberrant NO signaling and heightened oxidative stress in the penis.
INTRODUCTION: Efforts to identify the health risk associations for priapism may reveal pathophysiologic mechanisms for the disorder and suggest a scientifically rational approach for correcting it. AIM: We describe a clinical presentation of idiopathic recurrent priapism in a patient with glucose-6-phosphate dehydrogenase (G6PD) deficiency and consider a possible nitric oxide (NO)-dependent mechanistic basis from which the medical condition causes priapism. METHODS: The case report profiled a 35-year-old African-American man with G6PD deficiency who presented with a rapid progression of recurrent priapism episodes. He was outwardly healthy and did not have sickle cell disease or trait by hematologic screening. His management featured use of a long-term, continuous phosphodiesterase type 5 (PDE5) inhibitor therapeutic regimen. MAIN OUTCOME MEASURES: Clinical history data and response to PDE5 inhibitor therapy. RESULTS: After a 3-month duration of PDE5 inhibitor therapy, priapism recurrences were sufficiently resolved and the patient discontinued therapy. At 18-month clinical follow-up, he experienced only minor priapism recurrences and retention of full erectile ability. CONCLUSIONS:G6PD deficiency offers an explanation for idiopathic priapism. The medical condition generates a pathophysiologic milieu consistent with aberrant NO signaling and heightened oxidative stress in the penis.
Authors: Jiaming Wen; Xianzhen Jiang; Yingbo Dai; Yujin Zhang; Yuxin Tang; Hong Sun; Tiejuan Mi; Rodney E Kellems; Michael R Blackburn; Yang Xia Journal: J Sex Med Date: 2010-09 Impact factor: 3.802
Authors: Trinity J Bivalacqua; Biljana Musicki; Lewis L Hsu; Mark T Gladwin; Arthur L Burnett; Hunter C Champion Journal: J Sex Med Date: 2009-06-11 Impact factor: 3.802