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tography (ERCP) is currently one of the most important tools for diagnosis and treatment of pancreatic and biliary dis− eases. Propofol is increasingly used for safe sedation in ERCP [1,2]. Despite its demonstrated safety, propofol has been associated with cases of severe side ef− fects such as pancreatitis [3] or hepatitis [4]. A 66−year−old man diagnosed 2 months previously with biliary pancreatitis with residual choledocholithiasis, had recently undergone a therapeutic ERCP under brief sedation with propofol. At 48 hours after ERCP, he was admitted because of an acute condition with abdominal pain, nausea, vomiting, and increasing liver en− zyme levels. Abdominal ultrasound and computed tomography (CT) showed nor− mal findings. Blood analysis revealed an increase to 50 times the reference value for aspartate aminotransferase (AST) and alanine aminotransferase (ALT), with a slight increase in gamma−glutamyltran− ferase (GGT) and alkaline phosphatase, and a total bilirubin of 8.9 mg/dl (normal range 0.2±1 mg/dl) with excess of conju− gated bilirubin. Serum amylase was nor− mal. An in−depth investigation ruled out other causes of acute hepatitis. The pa− tient did not want to undergo liver biop− sy. He was treated with supportive meas− ures, vitamin K, and cholestyramine. In the 2 months’ follow−up, the patient was asymptomatic and the liver enzymes were normal. Propofol is a hypnotic agent that has been widely used since its approval in 1989 [3], and is actually the agent of choice in sev− eral ambulatory surgical procedures. It has been as effective as other sedative agents, with lesser side effects [1, 2], and has been shown to provide a better recov− ery from anesthesia than other drugs [1]. The main side effect of propofol is hypo− tension [1,2], but other more important side effects have been reported, such as pancreatitis [3], transient desaturation and apnea [2], and acute hepatitis [4]. Liv− er injury secondary to the use of propofol has been associated with long−term infu− sion of the drug, rhabdomyolysis, acide− mia and bradyarrythmias [4]. The patho− physiology of propofol−induced hepatitis remains unclear. Some authors point to a immunologic mechanism as the cause of liver injury associated with the use of an− other sedative agent, pethidine [5]. In spite of these side effects, we consider that propofol remains the drug of choice for brief sedation in ERCP.

Propofol-induced acute toxic hepatitis after brief sedation for endoscopic retrograde cholangiopancreatography