Priapism associated with concurrent use of phosphodiesterase inhibitor drugs and intracavernous injection therapy

McMahon, Chris G.

doi:10.1038/sj.ijir.3901046

Cited by 15 publications

(7 citation statements)

References 12 publications

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“…If an exogenous NO donor were administered concurrently with a PDE 5 inhibitor, there would be enhancement of the smooth muscle effects of NO but no cGMP dependent feedback on NO generation, since it does not involve NO generation through nNOS. The reports we have found in the literature on priapism with PDE 5 inhibitors involve either the use of selective PDE 5 inhibitors at a dosage above the recommended level or their use together with other pro‐erectile substances by oral or intracavernous administration ( Aoyagi et al ., 1999 ; McMahon, 2003 ; Yonessi and Saeedi, 2005 ). At least the latter are situations where a negative cGMP‐dependent feedback on NO formation might be expected to be bypassed.…”

Section: Discussionmentioning

confidence: 99%

Inhibitors of phosphodiesterase 5 (PDE 5) inhibit the nerve‐induced release of nitric oxide from the rabbit corpus cavernosum

Hallén

Wiklund

Gustafsson

2007

British J Pharmacology

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Background and purpose: Nitrergic neurons are important for erectile responses in the corpus cavernosum and impaired signalling results in erectile dysfunction, today treated successfully by oral administration of the selective phosphodiesterase 5 (PDE 5) inhibitors sildenafil, tadalafil and vardenafil. Although the importance of nitrergic neurons in urogenital function has become evident, it has not been investigated if the PDE 5 inhibitors affect the nerve-induced release of nitric oxide (NO). In a previous study we found that the soluble guanylate cyclase (sGC)/cyclic guanosine 3',5'-monophosphate (cGMP) pathway might modulate nerve-induced release of NO in isolated cavernous tissue. Experimental approach: Electrical field stimulation (EFS 5 Hz, 40 V, 0.3 ms pulse duration, 25 pulses at intervals of 2 min) of rabbit isolated cavernous tissue elicited reproducible, nerve-mediated relaxations in the presence of scopolamine (10 À5 M), guanethidine (10 À5 M) and phenylephrine (3 Â 10 À6 M). In superfusion experiments, nerve stimulation (20 Hz, 40 V, 1 ms) of the cavernous tissue evoked release of NO/NO 2 À , measured by chemiluminescence. Key results: Sildenafil, tadalafil and vardenafil decreased the muscular tone and prolonged the relaxations to nerve stimulation. The evoked release of NO decreased to 72711%, 55716% and 61714% of control, respectively after addition of sildenafil, tadalafil or vardenafil (all 10 À4 M, n ¼ 6-8, po0.05). Conclusions and Implications: Selective PDE 5 inhibitors influence the nerve-induced release of NO, probably via cGMPmediated negative feedback. This negative feedback might explain why priapism is not seen during monotherapy with the PDE inhibitors.

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Section: Discussionmentioning

confidence: 99%

Inhibitors of phosphodiesterase 5 (PDE 5) inhibit the nerve‐induced release of nitric oxide from the rabbit corpus cavernosum

Hallén

Wiklund

Gustafsson

2007

British J Pharmacology

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“…From 1999 to 2007, there have been at least nine case-based reports of oral PDE5 inhibitor dosing and adult priapism and at least one pediatric case: Aoyagi [29]; Sur [30]; Kassim [31]; Goldmeier [32]; McMahon [33]; Wilt [34]; Galatti [35]; Kumar [36]; King [37]; Wills [38]. The majority of these cases detail histories of men with increased risk for priapism: SCD, spinal cord injury, men who used PDE5 inhibitor recreationally, men who used PDE5 inhibitor with ICI, men with history of penile trauma, men on psychotropic medications, or men abusing narcotics.…”

Section: Oral Phosphodiesterase Type 5 (Pde5) Inhibitorsmentioning

confidence: 99%

Priapism: Pathogenesis, Epidemiology, and Management

Broderick

Kadıoğlu

Bivalacqua

et al. 2010

The Journal of Sexual Medicine

308

379

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Introduction Priapism describes a persistent erection arising from dysfunction of mechanisms regulating penile tumescence, rigidity, and flaccidity. A correct diagnosis of priapism is a matter of urgency requiring identification of underlying hemodynamics. Aims To define the types of priapism, address its pathogenesis and epidemiology, and develop an evidence-based guideline for effective management. Methods Six experts from four countries developed a consensus document on priapism; this document was presented for peer review and debate in a public forum and revisions were made based on recommendations of chairpersons to the International Consultation on Sexual Medicine. This report focuses on guidelines written over the past decade and reviews the priapism literature from 2003 to 2009. Although the literature is predominantly case series, recent reports have more detailed methodology including duration of priapism, etiology of priapism, and erectile function outcomes. Main Outcome Measures Consensus recommendations were based on evidence-based literature, best medical practices, and bench research. Results Basic science supporting current concepts in the pathophysiology of priapism, and clinical research supporting the most effective treatment strategies are summarized in this review. Conclusions Prompt diagnosis and appropriate management of priapism are necessary to spare patients ineffective interventions and maximize erectile function outcomes. Future research is needed to understand corporal smooth muscle pathology associated with genetic and acquired conditions resulting in ischemic priapism. Better understanding of molecular mechanisms involved in the pathogenesis of stuttering ischemic priapism will offer new avenues for medical intervention. Documenting erectile function outcomes based on duration of ischemic priapism, time to interventions, and types of interventions is needed to establish evidence-based guidance. In contrast, pathogenesis of nonischemic priapism is understood, and largely attributable to trauma. Better documentation of onset of high-flow priapism in relation to time of injury, and response to conservative management vs. angiogroaphic or surgical interventions is needed to establish evidence-based guidance.

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“…[4][5][6] Priapism may also follow simultaneous oral dose and intracavernous injection. [7] The first case report of priapism induced by oral sildenafil was due to a high dose (200 mg). [4] The initial treatment recommended is distal shunting.…”

Section: Discussionmentioning

confidence: 99%

Prolonged priapism following single dose administration of sildenafil: A rare case report

et al. 2009

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A case of priapism following the consumption of a single dose of sildenafil is reported. A 25-year-old unmarried healthy man consumed non-prescribed 50 mg sildenafil purchased over the counter. He developed painful priapism 30 min after the drug intake that had lasted for 4 days (96 h) when he sought medical advice as an emergency. The corpus spongiosum and glans was soft and the corpus cavernosa was rigid. Winter's shunt was done. Fifteen milliliters of dark blood was aspirated with 16 G needle. Detumescence was achieved within 30 min. He was discharged after 12 h. On one month follow-up, he had normal morning erections. A genetic basis with cross-reactivity of PDE-3 in addition to PDE-5 resulting in a cumulative erection effect may be possible elucidation for this unwanted side effect in rare cases. However, the number of cases reported with this side effect is still too less to draw further conclusions.

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Priapism associated with concurrent use of phosphodiesterase inhibitor drugs and intracavernous injection therapy

Cited by 15 publications

References 12 publications

Inhibitors of phosphodiesterase 5 (PDE 5) inhibit the nerve‐induced release of nitric oxide from the rabbit corpus cavernosum

Inhibitors of phosphodiesterase 5 (PDE 5) inhibit the nerve‐induced release of nitric oxide from the rabbit corpus cavernosum

Priapism: Pathogenesis, Epidemiology, and Management

Prolonged priapism following single dose administration of sildenafil: A rare case report

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