Takeo Imanishi

Clinical and experimental studies on the profiles of serum proteins in acute hepatic injury

SummaryThe change with time in profiles of five serum proteins in acute hepatitis were studied. Prealbumin (Pre) decreased in the initial stage and made a peak to be normal thereafter. α1 antitrypsin (α1AT) showed a slight increase in the initial stage but no remarkable change thereafter. Haptoglobin (Hp) decreased in the initial stage and then increased gradually to be normal. α2HS glycoprotein (α2HS) and β1CA globulin (β1CA) showed no decrease, but they later increased in the 2nd or 3rd week. In fulminant hepatitis, α1AT was somewhat high in the initial stage but decreased gradually to the lower normal limits; Pre and Hp decreased markedly; and α2HS and β1C/A decreased from the initial stage. α2HS and β1C/A were found useful for estimation of the severity of acute hepatitis in the initial stage. It was found that when Hp showed a marked decrease, especially ahaptoglobinemia, the hepatic injury was serious.Various degrees of hepatic injury were produced by Gal-N in rats and mice were compared with the amount of these proteins. The level of albumin (A1), transferin (Tr), α1AT and Hp was inversely proportional to the amount of liver cell necrosis. Particularly, Hp showed a marked decrease in submassive or massive necrosis, while a moderate decrease in minimal change of focal necrosis. Al and Tr showed a slight decrease of about the same degree, and the decrease of α1AT was somewhat greater. β1C/A decreased in inversely proportion with the amount of liver cell necrosis and its decrease in massive necrosis was more pronaunced than the other proteins.

Does the diagnosis of primary biliary cirrhosis or autoimmune cholangitis depend on the 'phase' of the disease?

Abstract: Background: It is unclear whether autoimmune cholangitis (AIC) is a separate disease entity or primary biliary cirrhosis (PBC) without antimitochondrial antibodies (AMA) since fluctuation of AMA titres by immunofluorescence (IF) is often observed during the course of PBC. The aim of this study was to determine the serial changes in AMA profiles during the course of initially diagnosed PBC or AIC.

Interferon Alfa-2a Treatment for Chronic Hepatitis C without Cirrhosis and Its Effects on the Incidence of Hepatocellular Carcinoma

The aim of interferon treatment for chronic hepatitis C is eradication of the hepatitis C virus during the early stages of the disease to prevent progression to liver cirrhosis or hepatocellular carcinoma. However, the effects of interferon on preventing the development of hepatocellular carcinoma for chronic hepatitis C without cirrhosis remain obscure. We wished to study these effects. In this retrospective study, we followed up 66 patients with chronic hepatitis C who were treated with interferon alfa-2a (total dose 324 to 792 MIU) for an average period of 3 years after treatment. Of these 66 patients, 3 patients developed hepatocellular carcinoma during the follow-up period (range, 0.3 to 2.8 years; yearly incidence 1.5%). All 3 patients were among 27 patients who did not respond to interferon treatment. Of these 3 patients, 1 patient developed liver cirrhosis after interferon treatment, and the histologic staging of the remaining 2 patients before interferon treatment was F3, according to the new Inuyama classification. None of the 18 patients who were complete responders to interferon treatment or the 21 patients with incomplete responses developed hepatocellular carcinoma. Our results suggest that patients with chronic hepatitis C who have no response to interferon treatment and histologically advanced disease should be closely followed up after interferon treatment, although the mechanism of malignant transformation to hepatocellular carcinoma in patients with chronic hepatitis C virus infection is still obscure.

Laparoscopic and Histopathologic Features of the Liver in Severe Chronic Active Epstein‐Barr Virus Infection Syndrome: A Case Report

Abstract: A 40‐year‐old man was admitted to our hospital with persistent fever, generalized lymphadenopathy and hepatosplenoamegaly. Immunological examination demonstrated high titers of several anti‐Epstein‐Barr virus (EBV) antibodies, including anti‐viral capsid antigens 1gG‐antibody 1: 20, 480, anti‐early antigens‐DR IgG‐antibody 1: 5, 120, and reduced activity of EBV‐specific cytotoxic T lymphocytes. Laparoscopic features resembled those of chronic active viral hepatitis, including an uneven surface appearance and diffuse hepatic enlargement. Histopathological examination of a liver biopsy specimen showed inflammatory cell infiltration along sinusoidal surfaces (single file appearance) and enlarged portal areas with intralobular punched‐out necrosis. The diagnosis was confirmed by detecting the EB viral genome in serum. Despite treatments with natural alpha‐interferon, adenosine arabinocide and recombinant human interleukin‐2, the patient died of progressive hepatic failure.