Abstract Introduction Priapism is a urologic emergency with devastating long-term consequences if left untreated. Some cases of priapism are recurring, requiring patients to have multiple visits to the emergency room for drainage and possible creation of penile shunts. Priapism has been historically classified into three categories: nonischemic, ischemic, and “stuttering” (also known as “recurrent”). The etiologies and management of patients with stuttering priapism remain somewhat perplexing, with many patients requiring trials of several medications including phosphodiesterase inhibitors and/or anti-androgens or surgery to prevent relapse of their condition. Apart from patients with sickle cell disease and other hematological conditions, most cases of stuttering priapism are idiopathic. The underlying pathophysiological basis for some causes, such as sickle cell disease, is believed to be due to depletion of nitric oxide and resulting dysfunction of cGMP-induced vasodilation of corporal smooth muscle. Objective After analyzing a case series of three cases of stuttering priapism at our institution, we propose a potential mechanism for stuttering priapism in patients with obstructive sleep apnea (OSA). Methods We constructed a case series of three patients with stuttering priapism with OSA at our institution. A thorough query of our institution’s electronic medical record was performed from January 1st, 2023 to January 1st, 2024 through the use of an existing IRB approval. Results A total of three patients were identified with a history of OSA who were treated for stuttering priapism. The mean patient age was 43 years old. Two of the three patients also had a history of hypertension and diabetes. All three patients were not consistently treating their OSA (i.e., inconsistent CPAP use, lack of regular pulmonology follow up). However, patients did report less priapism episodes during periods when they were adherent to their CPAP machine. Interestingly, two of three patients were hypogonadal (with testosterone <150) and the third patient had low-normal testosterone at 344. Conclusions OSA is a risk factor for multiple conditions, such as coronary artery disease, type 2 diabetes, stroke, and cerebrovascular diseases. One hypothesis for the increased risk of a variety of cardiovascular conditions in OSA is due to decreased NO. Oxidative stress due to repetitive hypoxemic episodes in OSA induces apoptosis and dysfunction of endothelial cells, which are responsible for production and regulation of NO. Given that there is low nitric oxide both in patients with sickle cell disease and in those with OSA, we hypothesize that this results in extremely down-regulated PDE5. Thus, through alternative non-nitric oxide pathways, there can be episodic uncontrolled cGMP-induced vasodilation of penile smooth muscle thereby resulting in prolonged erection time. Non-nitric oxide mediated pathways including vasoactive peptide and acetylcholine release have been described in producing erections. Previous studies have also shown that the consistent use of CPAP for more than 12 weeks is associated with improvement or normalization of nitric oxide levels in patients with OSA. In our case series, our patients reported less episodes of priapism when using their CPAP consistently. Disclosure No.
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