High Flow Priapism Associated with Sickle Cell Disease

Ramos, Claudio Rodríguez; Park, Jin S.; Ritchey, Michael L.; Benson, George S.

doi:10.1097/00005392-199505000-00076

Cited by 15 publications

(18 citation statements)

References 10 publications

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“…7 Furthermore, although this is normally a low¯ow priapism, there have been several reports of high ow priapism in sickle patients for unknown reasons. 7,8 It has been hypothesized that high¯ow sickle priapism may result from a failure of the autonomic regulation. 9 Leukemia is the cause of less than 1% of all priapism.…”

Section: Hematologicathrombotic Causesmentioning

confidence: 99%

“…39 In addition, Ramos et al reported the successful use of bilateral pudendal artery ligation for this condition. 8 The more de®nitive therapy for high¯ow priapism which is due to penile or perineal trauma or in certain idiopathic cases is either cavernosal artery ligation or embolization. 33 ± 35,38,56 ± 61 Embolization is usually recommended and surgery is reserved for failures.…”

Section: Therapy For High¯ow Priapismmentioning

confidence: 99%

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Priapism

Melman

Serels

2000

Int J Impot Res

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Section: Hematologicathrombotic Causesmentioning

confidence: 99%

Section: Therapy For High¯ow Priapismmentioning

confidence: 99%

Priapism

Melman

Serels

2000

Int J Impot Res

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“…Hematologic diseases are usually associated with a "low flow" priapism, but some associations have also been reported between "high flow" priapism and sickle cell anemia (6). Both type of priapism are also associated with Fabry disease (7,8).…”

Section: Discussionmentioning

confidence: 99%

Priapism and glucose-6-phosphate dehydrogenase deficiency: An underestimated correlation?

Rose¹,

Mantica²,

Tosi³

et al. 2016

Arch Ital Urol Androl

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Priapism is a rare clinical condition characterized by a persistent erection unrelated to sexual excitement. Often the etiology is idiopathic. Three cases of priapism in glucose-6-phosphate dehydrogenase (G6PD) deficiency patients have been described in literature. We present the case of a 39-year-old man with glucose-6-phosphate dehydrogenase deficiency, who reached out to our department for the arising of a non-ischemic priapism without arteriolacunar fistula. We suggest that the glucose-6-phosphate dehydrogenase deficiency could be an underestimated risk factor for priapism.KEY WORDS: Non-ischemic; Glucose-6-phosphate dehydrogenase (G6PD) deficiency. obliged him to go to the emergency department. He reported a normal and spontaneous erectile function before the arising of the disease. He denied having any gender of trauma and he admitted to have a G6PD deficiency, documented by laboratory tests. He denied having taken any drugs, phosphodiesterase type 5 (PDE5) inhibitors, intracavernosal agents or any other pharmacological agents. He denied any other risk factor for priapism. At clinical examination he presented a painless erection. Systemic hemoglobin was 13.6 g/dL. Intracorporal blood resulted as arterial at gas analysis (P0 2 = 76 mmHg; PC0 2 = 44.5 mmHg; pH = 7.35). The Color Doppler ultrasonography didn't point out any arterocavernosa fistula. After a period of observation in which there wasn't the resolution of the priapism, we decided to submit him to a pelvic arteriography (Figure 1). Panoramic arteriography of the aorto-iliac and selective of internal pudendal artery showed a bilateral increase of the arterial level of the corpora cavernosa, higher in the left one, without a fistula. We performed a temporary embolization with Spongostan TM of the distal left internal pudendal artery. A complete detumescence was obtained and the next arteriography confirmed the procedure was a success. The patient was released. After 2 weeks of a state of good health, he presented a new episode of prolonged erection, after which he returned to the emergency department of our Institute.

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“…Some have contended that the blood flow pattern resembles high-flow priapism based on radiographic study, in the absence of an arterialcavernosal fistula. [37][38][39][40] High-flow priapism has been clinically assessed in priapism related to medical diseases including Fabry's disease 41 and sickle cell disease. 37 Drug-induced priapism, which as suggested implies a medication-related phenomenon, represents another variant that has resulted from use of alpha-adrenergic antihypertensives, psychotropic agents, antidepressant medications, cocaine, and pharmacotherapeutic agents for erectile dysfunction.…”

Section: Abnormal Penile Blood Flowmentioning

confidence: 99%

“…[37][38][39][40] High-flow priapism has been clinically assessed in priapism related to medical diseases including Fabry's disease 41 and sickle cell disease. 37 Drug-induced priapism, which as suggested implies a medication-related phenomenon, represents another variant that has resulted from use of alpha-adrenergic antihypertensives, psychotropic agents, antidepressant medications, cocaine, and pharmacotherapeutic agents for erectile dysfunction. [42][43][44][45][46][47][48][49][50][51][52][53][54][55][56] The mechanism of action is contended to relate to peripheral and central signaling pathways stimulated by the offending drug that produce corporal smooth muscle relaxation.…”

Section: Abnormal Penile Blood Flowmentioning

confidence: 99%

Priapism pathophysiology: clues to prevention

Burnett

2003

Int J Impot Res

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Priapism, in which penile erection persists in the absence of sexual excitation, is an enigmatic yet devastating erectile disorder. Current endeavors to manage the disorder suffer from a poor fundamental knowledge of the etiology and pathogenesis of priapism. These endeavors have remained essentially reactive, which commonly fail to avert its pathological consequences of erectile tissue damage and erectile disability, not to mention its psychological toll. The role of preventative management seems paramount with respect to priapism. As a prerequisite to formulating prevention strategies, gaining understanding of its pathogenic features and likely pathophysiologic mechanisms is viewed to be quite important. This review combined an analysis of clinicopathologic reports as well as a summary of clinical and basic science investigations on the subject to date. These assessments support the basic classification of priapism into low-flow (ischemic) and high-flow (nonischemic) hemodynamic categories, resulting from venous outflow occlusion and unregulated arterial overflow of the penis, respectively. In addition, consistent with the hypothesis that dysregulative physiology of penile erection accounts for some presentations of priapism, several plausible molecular mechanisms influencing the functional state of the erectile tissue are discussed. Current progress in the field suggests prevention possibilities using androgenic suppressive therapy, adrenergic agonist therapies, and effectors of the nitric oxide-dependent erection regulatory pathway in the penis. New ideas for prevention may emerge from targeting molecular mechanisms involved in regulating erectile tissue function.

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High Flow Priapism Associated with Sickle Cell Disease

Cited by 15 publications

References 10 publications

Priapism

Priapism

Priapism and glucose-6-phosphate dehydrogenase deficiency: An underestimated correlation?

Priapism pathophysiology: clues to prevention

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