82 Case lism, serum levels of assorted drugs can vary greatly often resulting in serious adverse affects [1–3]. Pharmacokinetic interactions among antiretroviral agents may influence the potency or toxicity of co-administered drugs, such as the addition of new antipsychotics to this patient’s regimen. This case of low-flow priapism, a urologic emergency, required immediate and aggressive management and may prove to cause lasting urologic and sexual dysfunction. Prior cases of antipsychotic-induced priapism have been reported; however, this is the first reported case of priapism associated with a likely drug interaction between antipsy- chotics and protease inhibitors (PIs). A 50-year-old African-American man presented to the emergency department (ED) in acute pain due to a protracted case, approximately 42 h, of untreated priapism. The patient has been HIV positive since 1996. He stated he has taken HIV medications for many years and is extremely adherent to his regimen. Current medications included a multi-drug antiretroviral regimen including the combination PI, lopinavir/ritonavir (Kaletra®, Abbott Labs) 200/50 mg two tablets twice daily and the combination reverse transcriptase inhibitor abacavir/lamivudine/zidovudine (Trizivir, GlaxoSmithKline) 300/150/300 mg two tablets daily. The patient was diagnosed with schizoaffective disorder and was started on a regimen including two antipsychotics, quetiapine (Seroquel®, AstraZeneca) 300 mg, three tablets at bedtime, and perphenazine (Trilafon®, Schering-Plough) 8 mg by mouth nightly administered two days prior. His prescribing physician also added benztropine (Cogentin®, Merck) 1 mg by mouth twice daily to abate extrapyramidal symptoms secondary to antipsychotic therapy. The patient began taking these new antipsychotic medications 48 h prior to presenting. Five to six hours after taking his new medication the patient stated the occurrence of a lasting non-stimulated erection. The patient did not attempt to self-treat, seek medical advice, or take any medications for his condition until he presented to the hospital. The ED work-up verified the patient’s history. He had no record of prior erectile disturbances or priapism, sickle cell disease, oncologic malignancies, blood dyscrasias, or pelvic injury. Physical examination revealed an erect shaft with soft glans, indicating a low-flow priapism. The patient expressed that he had been on various medications over the years with no history of priapism. He is compliant with his current regimen and recently started new medications for his psychological issues. The patient denied use of any illicit drugs, over-the-counter (OTC) products, herbal medications, and/or vasoactive medications for erectile Int J Emerg Med (2010) 3:81–84 dysfunction. Medication history was verified by a call to the patient’s local retail pharmacy where medications, doses, and frequencies were verified. The patient verbalized that the erection began approximately 5–6 h after the initial dose of his new medications. He did not attempt to seek care or treatment until the pain became unbearable. No other antipsychotic-related side effects were present. Initial laboratory work-up included a basic metabolic panel (BMP) and complete blood count (CBC) both of which were unremarkable. He was treated with intravenous hydromorphone (Dilaudid®) and ondansetron (Zofran®) to treat pain and nausea. He was later given oral hydrocodone with acetaminophen (Lortab®) for pain. A urology consult was ordered. Upon arrival the urologist examined the patient and determined a course of action. The corpus cavernosum was locally anesthetized with lidocaine 1% with epinephrine and irrigated with dilute ephedrine and saline. Due to the extended period of engorgement, multiple attempts at irrigation and drainage with non-heparinized saline and dilute ephedrine were made to reduce the blood volume. Eventually detumescence was achieved after aspiration of over 60 ml of blood. A post-procedure urine sample was obtained before the patient was discharged home. Urine toxicology test determined the patient was positive for opiates and tricyclic antidepressants, while negative for any recreational or drugs of abuse. Opioid metabolites were most likely from the hydromorphone and hydrocodone given for pain. Tricyclic metabolites in the urine confirm the use of quetiapine. No other records of possible medications for these positives results were obtained from the patient’s local retail pharmacy. Discussion There is no way to foresee which patients will develop priapism. The only predictor of it may be a history of previous prolonged painless erections, which can lead to a painful, damaging event. Priapism can occur with initial doses of antipsychotics, after years of use, or with the addition of new medications to a patient’s regimen [4]. Low-flow priapism, although rare (less then 1% occur- rence), can be an adverse event of antipsychotic agents resulting from a proposed blocking action at α-adrenergic receptors. This α-blockade causes venous constriction and prevents blood return to circulation [5–12]. Previous management of patients with priapism due to antipsychotics involved reducing the dose of the offending agent or changing the medication to one with a lower α-adrenergic affinity. This management style assumes that priapism can be a dose-related function of the prescribed medication. CYP450 enzymes are proteins produced in the liver, responsible for the oxidative metabolism of drugs. Various