Hepatic angiography in "alcoholic hepatitis".

Abstract

Hepatic malignant tumor is suspect in an alcoholic who shows progressive physical deterioration and poor response to medical therapy. Cirrhosis serves as a substrate for approximately 75 per cent of hepatocellular carcinoma (1). There are no reliable signs or symptoms or liver function studies, however, which differentiate cirrhosis with acute “alcoholic hepatitis” from hepatoma or metastatic carcinoma. Liver scan may show an abnormal pattern suggestive of nodular lesions of varying size in cirrhosis, neoplasm, or hepatitis (2, 3). Angiography has been extensively employed in the differential diagnosis of hepatic disease (4). The findings in acute “alcoholic hepatitis,” however, have not been emphasized. In over 200 selective celiac arteriograms at the Boston City Hospital in the past several years, 4 cases of florid “alcoholic hepatitis” have been studied. The findings were similar in all instances and form the substance of this report. Case Reports Case I: E. F., a 54-year-old white female, was admitted to the Boston City Hospital for the first time on July 1, 1965. She had been in good health until April 1965, when she noted progressive abdominal swelling and anorexia. There was a history of “heavy” alcoholic intake for several years. The patient had noted the recent onset of dark urine and light-colored stools. Physical examination showed moderately icteric sclerae, ascites, and hepatosplenomegaly. Laboratory values included a hematocrit of 29 mm and a white blood cell count of 14,200 (79 per cent polymorphonuclears and 14 per cent lymphocytes). Urine showed 4+ bile; fasting blood sugar of 140 mg per 100 cc; alkaline phosphatase of 2.3 Bodansky units; protein 6.7∕2.3 mg; amylase 38 units; cephalin-cholesterol flocculation 3+; serum glutamic oxaloacetic transaminase of 202 units; bilirubin 13.5 mg per 100 cc. Upper gastrointestinal series showed esophageal varices. On selective celiac and superior mesenteric arteriography, the right hepatic artery originated from the superior mesenteric artery. There was a large vascular area in the liver supplied by “tortuous coil-spring vessels,” and there was increased vascularity of the pancreaticoduodenal arcades (Figs. 1 and 2). The clinical and angiographic impression was “possible hepatoma.” Paracentesis showed a clear yellow fluid with no growth and no tumor cells. Liver scan with 198Au showed that the splenic uptake was much greater than normal, with diminished uptake in the liver and deposition in the bone marrow. There was an irregular deposition in the liver suggestive of a diffuse process. On conservative therapy, the patient showed progressive improvement in clinical status and liver function, and she was discharged on Sept. 29, 1965, with a clinical diagnosis of acute “alcoholic hepatitis.”