S3359 A Restless Drug: Ropinirole-Induced Pancreatitis in a RLS Patient

Introduction: Acute pancreatitis (AP) is typically caused by gallstones or alcohol, with drug-induced cases comprising just 1–2%. Dopamine agonists are an extremely rare cause, and to date, ropinirole-induced AP has only been described in Parkinson’s disease patients. This is the first known case implicating ropinirole in an individual with restless legs syndrome (RLS). Case Description/Methods: A 42-year-old woman with a history of RLS presented with sudden epigastric pain radiating to the back, accompanied by nausea and vomiting. She denied alcohol, tobacco, or NSAID use. Exam showed epigastric tenderness without peritonitis. Lipase was 1,354 U/L. Computed tomography abdomen revealed interstitial pancreatitis with peripancreatic fat stranding. right upper quadrant ultrasound showed no cholelithiasis, and HIDA scan confirmed normal gallbladder ejection fraction of 42%. Serum calcium, fasting triglycerides, liver enzymes, and autoimmune markers were unremarkable. She initially denied regular medications but later reported using ropinirole 1 mg nightly for 2 months, last dose taken 2 days prior to symptom onset. She was managed with intravenous fluids, analgesics, and diet as tolerated. Lipase normalized by day 5. Ropinirole was discontinued, and she was discharged with complete symptom resolution and remained well at 2-month follow-up. Discussion: This case highlights a rare example of ropinirole-induced pancreatitis in an RLS patient. Diagnosis was supported by the exclusion of other causes and a clear temporal association with drug use. While the exact mechanism remains unclear, dopamine receptors in pancreatic tissue may influence inflammatory or enzymatic pathways. As ropinirole is a first-line RLS therapy, this report underscores the importance of clinician awareness for this potential adverse effect. Timely identification and withdrawal of the offending agent can prevent recurrence and complications. Further pharmacovigilance and mechanistic research are needed to clarify the true incidence and pathophysiology of dopamine agonist–associated pancreatitis.