Priapism secondary to hypertriglyceridemia.

Various etiologies of priapism have been described, including sickle-cell disease, cocaine abuse, hematological malignancies, penile metastases, trauma, intracavernous injection therapy for erectile dysfunction and oral medications. Nevertheless, many cases of priapism are classified as idiopathic. We report a case of priapism secondary to hypertriglyceridemia, and recommend screening patients with a serum lipid profile if an obvious etiology cannot be identified. CASE REPORT A 33-year-old black male with diet controlled diabetes mellitus presented with a painful erection 18 hours in duration. The patient had woken in the morning with an erection unrelated to sexual stimulation. He denied a history of sickle cell anemia, cocaine abuse or penile trauma, and he was not taking any medications. The patient reported occasional marijuana and heavy alcohol use. He described a previous episode of priapism approximately 3 months prior that had lasted 8 hours but resolved without intervention. Physical examination confirmed classic low flow priapism that was extremely tender to palpation. Laboratory evaluation revealed a serum white blood count of 10.8 10 9 /l., hematocrit 42.4% and platelet count 248 10 9 /l., all of which were within normal limits. A sickle cell screening panel was negative. Blood glucose level was 109 mg./dl. (normal 65 to 110) and serum creatinine 1.3 mg./dl. (0.7 to 1.4). Urine toxicology screen was positive only for cannabinoids. It is noteworthy that during the blood collection process the phlebotomist observed a thick white layer on top of the blood drawn in the chemistry tube. This finding prompted measurement of serum triglyceride, which was increased to 2,041 mg./dl. (normal 40 to 160). Liver function tests were within normal limits. Corporeal blood gas demonstrated a pH of 6.95, partial carbon dioxide pressure 93 mm. Hg and partial oxygen pressure 16 mm. Hg. The patient was treated with multiple intracavernous injections of 250 to 500 g. phenylephrine, cavernous aspiration and cavernous irrigation with saline. Aspiration of corporeal blood showed a fatty layering similar to that seen in the blood collection tube. Complete detumescence was achieved with these treatments. Endocrinology consultation for evaluation of hypertriglyceridemia was obtained, and treatment was started with gemfibrozil. Serum lipid profile was obtained the next day, and revealed total cholesterol 393 mg./dl. (normal 80 to 220), high density lipoprotein 41.6 mg./dl. (35.0 to 68.0) and repeat triglyceride level 856 mg./dl. (40 to 160). DISCUSSION Previous reports have described an association of priapism with total parenteral nutrition.1, 2 It is hypothesized that the lipid emulsion is the precipitating factor. To our knowledge this case of priapism secondary to hypertriglyceridemia unrelated to total parenteral nutrition represents the first such case reported in the English literature. Hypertriglyceridemia may cause sludging of blood, hypercoagulability and fat embolus leading to venous outlet obstruction of the corpora cavernosa. Investigators have demonstrated distortion of erythrocyte morphology, increased erythrocyte aggregation and adhesiveness, and decreased capillary flow associated with the intravenous infusion of fat.3 Our patient presented with a serum triglyceride level more than 12 times the upper limit of normal. It was postulated that the hypertriglyceridemia was related to pancreatic insufficiency secondary to alcohol abuse, although the patient might have had an undiagnosed familial disease. Urine toxicology screen confirmed the use of marijuana but we do not believe that marijuana use is an etiological factor in priapism. In addition, we are unaware of any case reports associating marijuana with priapism. Since many cases of priapism have an unidentifiable etiology, we believe a serum lipid profile screen is indicated in the diagnostic evaluation. REFERENCES