Marked atrophy of the right lobe seen in idiopathic portal hypertension confirmed by laparoscopy

Abstract

cigarettes. His past medial history consisted of pulmonary tuberculosis in 1963 and gastric ulcer in 1990. He had not received blood transfusion. He had been treated as an outpatient with gastric ulcer since 1990 by a doctor in practice. A physical examination on admission revealed an alert and well-nourished elderly man. No anemia or jaundice was noted on the conjunctivas. The chest findings were unremarkable except for moist rales on the bilateral lung bases. The lung-liver border was located at the 7th intercostal space. The liver was palpable 3 cm on the median line, showing a dull edge with increased consistency. The spleen was not palpable. There were no engorged veins on the abdominal wall, ascites, leg edema, spider angioma, or palmar erythema. No flapping tremor was elicited.Laboratory data on admission is given in Table 1. A complete blood count revealed a mild decrease in platelet count. Blood chemistry revealed increases in levels of biliary enzymes and g-globulin. The indocyanine green (ICG) test was 25% at 15 min. The hepatitis virus markers were negative for hepatitis B surface antigen and hepatitis C antibody, and autoimmune antibodies including antinuclear antibody and antimitochondrial antibody was also negative.Upper GI endoscopy (Fig. 1) showed five winding, blue-colored esophageal varices with RC signs at 25 cm from the incisors. There were no gastric varices (LmF2CbRC(+)Lg(-)).Abdominal ultrasound showed an enlarged left lobe of the liver, without detection of the right lobe. No mass lesions were noted in the liver.A 70-year-old-male was hospitalized for the treatment of esophageal varices and close examination of the liver. Blood chemistry tests revealed mild liver dysfunction. Abdominal ultrasound and computed tomography scan revealed marked atrophy of the right and quadrate lobes of the liver without abnormalities of the biliary system. Abdominal angiography revealed marked atrophy of the right lobe of the liver, without obliteration in the portal venous system, but it could not be determined whether the atrophy was congenital or secondary. Subsequently performed laparoscopy revealed marked atrophy of the anterior segment of the right lobe and quadrate lobe with the whitish scarred edge demarcating the border between the edge and neighboring liver parenchyma. The liver surface appeared to be undulant, but non-cirrhotic. These findings suggest secondary lobar atrophy of the liver, without cirrhosis. Liver biopsy of the left lobe showed the findings to be compatible with idiopathic portal hypertension (IPH), and we diagnosed IPH based on these findings and hepatic lobar atrophy was attributable to IPH. There have been few reports of cases with hepatic lobar atrophy associated with IPH, and the mechanism of atrophy is unclear. We report a case of IPH with marked liver atrophy in which laparoscopy is a decisive means whether liver atrophy is congenital or secondary.