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Войти в исследования The journal of sexual medicine · 2007
Glucose-6-phosphate dehydrogenase deficiency: an etiology for idiopathic priapism?
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Burnett Arthur L, Bivalacqua Trinity J
Аннотация
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.
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.