A simple technique for maximal tip deflection of an upper endoscopy.
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Biomedical subjects
Publications and source records attributed to Tatsuro Yanagawa.
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Anti-mitochondrial antibodies (AMA) are frequently detected in sera from patients with primary biliary cirrhosis (PBC). Major autoantigens for AMA have been identified as members of the 2-oxoacid dehydrogenase enzyme complex family, with pyruvate dehydrogenase complex (PDC)-E2 showing strongest reactivity to AMA in PBC patients. Recently, anti-PDC-E2 has been found in patients with other diseases. Since frequency and significance of anti-PDC-E2 in patients with autoimmune hepatitis (AIH) remain obscure, we measured anti-PDC-E2 in sera from well-defined AIH cases by Western blotting using bovine heart mitochondrial protein and recombinant PDC-E2 protein as antigen sources. All 55 enrolled patients fulfilled the international diagnostic criteria for definite or probable AIH. Anti-PDC-E2 positivity showed concordance between native and recombinant antigens. Anti-PDC-E2 was detected in nine of 55 sera from AIH patients (16%). Variables including alkaline phosphatase (ALP) and IgM concentrations, effects of prednisolone, and pathologic findings concerning bile ducts showed no significant differences between anti-PDC-E2-positive and anti-PDC-E2-negative AIH patients. These data indicate that detection of anti-PDC-E2 is not rare in defined AIH, but anti-PDC-E2-positive AIH does not represent an intermediate entity in a clinical spectrum between AIH and PBC.
A patient with hepatitis C virus (HCV)-related liver cirrhosis and hepatocellular carcinoma (HCC) was treated successfully with an orthotopic liver transplantation (OLT) followed by interferon therapy. The 36-year-old Japanese man was diagnosed as having liver cirrhosis in 1983. HCC was detected in 1991, and by 1994, jaundice and ascites had developed. The patient underwent OLT in June 1995, after which hepatitis C recurred, with elevated aminotransferases. His liver biopsy specimen showed chronic active hepatitis. He was given interferon-alpha three times weekly for 24 weeks in 1999. Six months after the end of the interferon treatment, the patient's serum HCV RNA became negative, with normalization of aminotransferases, and his liver histology exhibited amelioration of fibrosis and inflammation. At the present time, he remains free of HCC (more than 6.5 years after the OLT) and free of HCV RNA (more than 2.5 years since interferon therapy was completed). This is the first Japanese patient whose HCC was cured by OLT and HCV was eradicated by interferon therapy.