This case report examines the first known case of cannabis-associated priapism in a patient where all other known causes of priapism have been excluded. While cannabis use has already been noted in educational sources and textbooks as a potential cause of priapism, an electronic literature review was only able to identify four distinct cases of cannabis use coinciding with priapism, none of which were convincingly able to prove cannabis was the sole cause (Reichman, 2013). In the first two papers, the patients had cannabis use and concurrent sickle cell trait (Matta et al., 2014; Birnbaum and Pinzone, 2008). Sickle cell disease itself is the number one cause of secondary priapism in children ages five to ten years old (Banos et al., 1989). The third report notes cannabis and 3,4-methylenedioxymethamphetamine (MDMA or ecstasy) use prior to the episode of priapism, with MDMA already having been proven a cause of priapism (Tran et al., 2008). The fourth case report notes concurrent insulin dependent diabetes mellitus, cocaine use, and anabolic steroid use, with cocaine and diabetes each previously described causes of priapism (Evans et al., 2016). An additional report gives supporting evidence that synthetic cannabinoids, which are 100 times more potent activators of the same cannabinoid type 1 receptor (CB1R) as THC, can cause priapism (Ortac et al., 2018; Wiley et al., 2014). If synthetic cannabinoids can cause priapism, plant cannabis, affecting the same CB1R, would also be capable to potentiate this reaction.
In total, there are over 400 psychoactive compounds in cannabis. Of these, delta-9-tetrahydrocannabinol, or THC, is both found in the highest quantities and the primary psychoactive compound (Atakan, 2012). THC interacts with the two primary cannabinoid receptors, Cannabinoid type 1 receptor and cannabinoid type 2 receptor (CB2R). THC primarily interacts with CB1R, with its major psychoactive effects due to CB1R’s presence in the central nervous system’s basal ganglia, limbic system, hippocampus, and cerebellum; however, CB1R can also be found throughout the peripheral body, notably in the peripheral nervous system, uterus, testicular tissues, and vasculature (Russo and Guy, 2006; Pagotto et al., 2006; Pertwee, 2006). It is possible that the sympathetic blockage thought to occur as a result of cannabinoid activity limits the ability of the thoracolumbar sympathetic pathway to cause detumescence or that the now unopposed sacral parasympathetic activity that initiated the erection increases the risk for priapism (Dean and Lue, 2005). Alternatively, cannabinoids direct vascular effects could potentiate the unrelenting erection notable in priapism.
A third possible effect of more chronic cannabis use involves the thrombogenic effects caused by increased platelet activation (Randall, 2007). There is noted expression of CB1R and CB2R on platelets and during THC use there is a measurable increase in platelet expression of glycoprotein IIb-IIIa and P-selectin, resulting in greater platelet activation (Deusch et al., 2004). This culminates in a 4.8-fold increase in myocardial infarction in the 60 min after THC use (Mittleman et al., 2001). These factors together could lead to thrombotic causes of priapism, similar to that noted in sickle cell patients. Our patient has a direct, albeit circumstantial, connection between his recurrent (stuttering) priapism and cannabis use. He notes recurrent priapism when heavily using cannabis at age sixteen and seventeen. These episodes each lasted under four hours and resolved without medical intervention or medical examination. When the patient stopped using cannabis at age eighteen, his priapism resided, with no notable episodes in his twenties. He once again resumed his use of cannabis over six months ago and noted at least a dozen episodes that self-resolved in under four hours at home. The abstinence and subsequent use of cannabis were the only appreciable factors in this patient’s battle with recurrent unwanted erections.
