1,721,074 research outputs found
Effect of iron depletion in patients with nonalcoholic fatty liver disease without carbohydrate intolerance
No full textThe immunopathogenesis of alcoholic and nonalcoholic steatohepatitis : two triggers for one disease?
No full textAlcoholic liver disease and nonalcoholic liver disease represent a leading cause of liver disease and share similar pathogenic mechanisms among which activation of the immune system plays a key role. The main events consist in (a) activation of Kupffer cells via TLR-4 by LPS and fatty acids (b) complement activation (c) increased release of proinflammatory mediators (d) alteration in NK and NKT cell number/activity (e) activation of the adaptive immune system. At the same time, activation of intracellular pro-inflammatory pathways by cytokines and bacterial products, inhibit insulin signaling favoring lipogenesis, metabolic alterations, and cell damag
Autoantibodies and Australia antigen in acute and chronic liver
No full textSerum antinuclear (ANA), mitochondrial (AMA) and smooth muscle (SMA) antibody have been measured in 130 patients with Australia antigen a antibody, and acute and chronic hepatitis. In patients with acute hepatitis, persistent hepatitis, postnecrotic cirrhosis these indices failed to show any correlation. In the group of patients with chronic aggressive hepatitis the incidence of Au was 70%, ANA 10%, AMA 3%, SMA 33%; Au negative patients had higher incidence of autoantibodies, mainly SMA (45%) and much higher titers of SMA than Au positive patients in whom SMA was 29%. No patient with primary biliary cirrhosis was Australia positive; the incidence of AMA was 90%
Sustained virological response (SVR) to peginterferon alfa-2a (40 KD) (PEGASYS) plus ribavirin (RBV) and amantadine (AMA) Vs induction therapy with interferon alfa-2a (roferon-A) plus RBV and AMA in IFN/RBV non responders (NR) with chronic hepatitis C
No full textAspects of humoral immunity in ulcerous colitis
No full textVarious immunological indices, hitherto considered in isolation, were evaluated in a single group of 20 cases of ulcerous colitis. Immunofluorescence showed anticolon Ab in 3 cases (15%), whereas this feature was absent in a control group. Antistomach, antithyroid and non organ specific Ab's (ANA, AMA, SMA) were equally incident in both groups. One case is examined separately on account of its simultaneous presentation of human and rat antistomach and antithyroid and antismooth muscle Ab's. Rheuma test, Waaler Roose reaction, L.E. phenomenon and test, and direct and indirect Coombs test results were negative in nearly all cases. Slight quantitative changes in serum proteins revealed by electrophoresis and immunodiffusion were indicative of inflammation with a immunogenic tendency. The data are not sufficient to support the attribution of an autoimmunizational etiology to ulcerous colitis, though simultaneous evaluation of reaction indices serves to strengthen this view
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