Acalculous Cholecystopathy Publications (7)
Acalculous Cholecystopathy Publications
Studies with GBEF ≤40 % and SS >4 were considered to have cholecystopathy and SOD respectively. Three of the 13 patients with PCS had SS of 6 each, suggestive of SOD. Delayed biliary visualization (>15 min) and activity in common bile duct 60 min > liver 15 min were the specific features in these cases. Opioid induced SOD patients had SS >4 with retrograde refilling of GB in one patient and normalization of the SS parameters after nifedipine challenge in the other patient. Patients with RP and biliary pain were stratified into four groups, normal (GBEF >40 % and SS ≤4), cholecystopathy (GBEF ≤40 % and SS ≤4), normal with SOD (GBEF >40 % and SS >4) and cholecystopathy with SOD (GBEF ≤40 % and SS >4). Four patients with intact GB had cholecystopathy with scintigraphic features of SOD. Quantitative cholescintigraphy with fatty meal and SS scoring identified biliary dyskinesia and SOD in patients with biliary pain, recurrent pancreatitis and post-cholecystectomy syndrome.
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.
Significant differences were observed in the age of patients with gallstones when compared to subjects without gallstones or with acalculous cholecystopathy. Although, in the last years, the high transfusional regimen has decreased the incidence of cholelithiasis, the frequent liver disease could be a cause of acalculous cholecystopathy in younger thalassemic patients.
The half emptying-time of the gallbladder after cholecystokinin injection was 104.36 +/- 43.93 minutes in the first group, 17.92 +/- 23.57 minutes in the second and 20.42 +/- 23.67 minutes in the third group (p less than 0.005). After 6 weeks of ursodeoxycholic acid treatment, regression of pain and a significant reduction in the half emptying-time from 104.36 +/- 43.93 to 74.35 +/- 52.79 minutes (p less than 0.01) was observed in the first group. These results, which need to be confirmed by further studies, show that in acalculous gallbladder disease there is a delay in gallbladder emptying which could explain the formation of cholesterol crystals by bile stasis as described by various authors.
Radiological study showed a stenotic process in the first, second and third duodenal portion, later on confirmed by endoscopy. This was confirmed at surgery, when a gastrojejunostomy with truncal vagotomy, cholecystectomy, besides duodenum and liver biopsies were performed. The patient is asymptomatic four years after surgery. It is considered that bile reflux, resulting from involvement of Vater papilla by CD, is responsible factor of the biliary pathology.