7166 Gallbladder wall thickening in acute hepatitis : what is the cause?

Abstract

Background/Aims: During ultrasonographic examination of patients withacute hepatitis, we can often see thickening of the Gallbladder(GB) walland contraction of the GB. However, there is rarely an opportunity for thehistological analysis of these structural changes. Endoscopic ultrasonographycan delineate the GB wall structure accurately, thus it is helpful inobserving the changes of GB wall in patients with acute hepatitis. Hence,we attempted to disclose any detailed structural changes of GB wall inpatients with acute hepatitis using endoscopic ultrasonography. Methods:The subjects were 15 patients diagnosed as having acute hepatitis usinglaboratory and clinical data. We estimated the severity of the GB wallthickening and the change of each layer composing the wall of the GBusing endoscopic ultrasonography. Results: We observed a thickened GBwall in all the patients and the mean wall thickness was estimated to be5.6mm. In seven patients, hypertrophy of the muscular and serosal layerswas visualized with a mean thickness of 4.3mm, and each layer of the GBwall was well defined. A diffuely thickened GB wall without delineation ofeach layer was observed in 8 patients in which the mean wall thicknesswas 6.8mm. There was no significant relationship between the level ofserum AST/ALT and the degree of GB wall change. Conclusions: GB wallthickening in acute hepatitis results from the hypertrophic changes of themuscular and serosal layers, and the distinction between each layer of GBwall becomes difficult to delineate as the thickening progresses. Background/Aims: During ultrasonographic examination of patients withacute hepatitis, we can often see thickening of the Gallbladder(GB) walland contraction of the GB. However, there is rarely an opportunity for thehistological analysis of these structural changes. Endoscopic ultrasonographycan delineate the GB wall structure accurately, thus it is helpful inobserving the changes of GB wall in patients with acute hepatitis. Hence,we attempted to disclose any detailed structural changes of GB wall inpatients with acute hepatitis using endoscopic ultrasonography. Methods:The subjects were 15 patients diagnosed as having acute hepatitis usinglaboratory and clinical data. We estimated the severity of the GB wallthickening and the change of each layer composing the wall of the GBusing endoscopic ultrasonography. Results: We observed a thickened GBwall in all the patients and the mean wall thickness was estimated to be5.6mm. In seven patients, hypertrophy of the muscular and serosal layerswas visualized with a mean thickness of 4.3mm, and each layer of the GBwall was well defined. A diffuely thickened GB wall without delineation ofeach layer was observed in 8 patients in which the mean wall thicknesswas 6.8mm. There was no significant relationship between the level ofserum AST/ALT and the degree of GB wall change. Conclusions: GB wallthickening in acute hepatitis results from the hypertrophic changes of themuscular and serosal layers, and the distinction between each layer of GBwall becomes difficult to delineate as the thickening progresses.