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. Burnett AL, and Bivalacqua TJ. Glucose-6-phosphate dehydrogenase deficiency: An etiology for idiopathic priapism? J Sex Med 2008;5:237–240.