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The similarity of alcoholic liver disease and nonalcoholic steatohepatitis (NASH) in terms of pathogenic mechanisms suggests that immunoglobulin A (IgA) may play an important role in the pathogenesis of NASH. We aimed to determine whether serum IgA concentrations allow a diagnosis of liver fibrosis in NASH.
We compared serum IgA concentrations between 108 patients with stages 0-2 NASH and 19 patients with stage 3 NASH.
In a univariate analysis, age (P < 0.0001), gender (P = 0.0039), serum albumin level (P = 0.0192), AST (P < 0.0001), AST/ALT ratio (P < 0.0001), platelet count (P = 0.0027), hyaluronic acid level (P < 0.0001), fasting blood sugar (FBS) (P = 0.0013), IRI (P = 0.0001), prothrombin time (%) (P = 0.0287), IgA (P < 0.0001), total sum of IgG, IgA, and IgM (P = 0.0049), and IgA/(IgG + IgA + IgM) (P = 0.0105) were significantly elevated in severe-stage NASH patients compared with the early-stage NASH group. Multiple logistic regression analysis showed that in severe-stage NASH patients, only serum IgA concentrations were significantly elevated (P = 0.0225) relative to early-stage NASH patients. The area under the curve (AUC) of serum IgA concentrations was 0.758 for detecting severe-stage NASH compared with early-stage NASH.
Serum IgA concentration could be a useful independent predictor for assessing the pre-cirrhotic progression of NASH.
Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan, firstname.lastname@example.org.
This article was published in the following journal.
Name: Digestive diseases and sciences
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A tetrameric protein, molecular weight between 50,000 and 70,000, consisting of 4 equal chains, and migrating on electrophoresis in 3 fractions more mobile than serum albumin. Its concentration ranges from 7 to 33 per cent in the serum, but levels decrease in liver disease.
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A rare inherited immunodeficiency syndrome characterized by normal or elevated serum IMMUNOGLOBULIN M levels with absence of IMMUNOGLOBULIN G; IMMUNOGLOBULIN A; and IMMUNOGLOBULIN E. It results in a profound susceptibility to BACTERIAL INFECTIONS and an increased susceptibility to OPPORTUNISTIC INFECTIONS. Several subtypes of hyper-IgM immunodeficiency syndrome exist depending upon the location of genetic mutation.
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