Nagoya University · Medicine
Professor Yoji Ishizu's research lab focuses on autoimmune and fibrotic diseases, particularly immunoglobulin G4-related disease (IgG4-RD) with a special emphasis on its hepatic manifestations. The lab investigates the clinical and pathological features of IgG4-related autoimmune hepatitis (AIH) and IgG4-hepatopathy, exploring their overlap with systemic IgG4-RD and associated conditions such as autoimmune pancreatitis. Research also extends to the immunological and hematological effects of antiviral therapy, particularly in hepatitis C virus (HCV)-related disorders, including changes in platelet counts linked to immune modulation and hypersplenism. The lab aims to clarify the pathogenesis and clinical course of these complex immune-mediated conditions.
Figures are computed from collected data and may differ slightly.
Immunoglobulin G4-related disease (IgG4-RD) is a systemic disease involving many organs; it includes IgG4-related sclerosing cholangitis and inflammatory pseudotumor in the hepatobiliary system. Two types of hepatic parenchymal involvement have been reported in IgG4-RD: IgG4-related autoimmune hepatitis (AIH) and IgG4-hepatopathy. Moreover, only three cases of IgG4-related AIH have been reported. Immunoglobulin G4-related AIH is clinicopathologically similar to AIH, except for an elevated serum
Immunoglobulin G4 (IgG4)-associated autoimmune hepatitis (AIH) is a new disease entity with elevated levels of serum IgG4 and marked IgG4 positive plasma cell infiltration of the liver, and its clinical course remains unknown. A patient with IgG4-associated AIH who later developed autoimmune pancreatitis (AIP) is reported. A 73-year-old man was admitted to our hospital due to elevated liver transaminase levels, hypergammaglobulinemia and positive antinuclear antibody. A liver biopsy specimen sho
Platelet counts increased at 4 weeks after starting anti-HCV treatment. Our results suggest that this rapid change was possibly caused by improvement of hypersplenism and HCV-induced myelosuppression resulting from anti-HCV therapy.
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