This study reports the clinical and radiologic findings in seven patients infected with HIV who had 10 consecutive episodes of symptomatic cholecystopathy induced by infusion of interleukin-2. Ten episodes of right upper quadrant pain associated with gallbladder wall thickening were seen in seven of 29 HIV-infected patients who received IV interleukin-2. Patients received 6-18 million IU/day of continuous interleukin-2 infusion for 5 days. Patients with right upper quadrant pain underwent sonographic examinations, which were interpreted prospectively. Medical records and previous sonographic studies were reviewed retrospectively. Follow-up was obtained through outpatient visits and sonography. Right upper quadrant pain during these 10 episodes of cholecystopathy usually developed 4-5 days after starting infusion of interleukin-2. Sonography during that time showed gallbladder wall thickening (mean thickness, 12.4 mm; range, 5-18 mm) and a wide variety of sonographic appearances. Tenderness during sonography was focal in six episodes, diffuse in one, and absent in three. Sludge was identified in one episode; calculi were not seen. Findings on radionuclide biliary scans were normal in three cases. Symptoms abated rapidly in every case after infusion of interleukin-2 was reduced or stopped. No surgery was necessary. When treatment was repeated, three patients had recurrent episodes, with clinical courses and sonographic aberrations showing little variance from the initial episodes. Follow-up sonography in three episodes showed a maximal thickness of the gallbladder wall of 4 mm. No patient had a history or laboratory evidence of intrinsic biliary disease. Symptomatic thickening of the gallbladder wall during infusion of interleukin-2 can exactly mimic other forms of acalculous cholecystitis, except that when associated with interleukin-2 the thickening is rapidly reversible and surgery is not required. Radionuclide scans can be useful in clinical decision making. The process appears to be benign, and cessation of interleukin-2 therapy, along with close clinical observation, appears to be the appropriate treatment.