By Gideon M. Hirschfield (auth.), Gideon M. Hirschfield, E. Jenny Heathcote (eds.)
With a spotlight on sensible sufferer similar matters, Autoimmune Hepatitis: A consultant for working towards Clinicians serves as an invaluable functional, and lots more and plenty wanted, source for all these physicians offered with coping with sufferers clinically determined with autoimmune hepatitis, either acutely and over the long run. It presents a foundation for clinicians to appreciate the etiology of the affliction, in addition to detailed conditions the place administration dilemmas frequently come up. Emphasis is given to supplying administration suggestion of instant use to clinicians, whatever no longer almost immediately provided through different greater basic texts. The chapters are written through people with an services and coaching during this box and contain the hottest info. The publication should be of significant worth to Gastroenterologists, Hepatologists, and Internists in any respect degrees who see sufferers providing with autoimmune hepatitis.
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Additional info for Autoimmune Hepatitis: A Guide for Practicing Clinicians
To explore the role of autoantibodies in type 1 AIH requires identification of type 1-specific B cell autoantigenic epitopes and studies of animals immunized with the autoantigen(s). Seven human hepatocyte-specific candidate antigens were recently identified that reacted with antibodies in the sera of patients with type 1 AIH . Further characterization of these atypical “autoantibodies” should be performed. Autoantibodies in Type 2 AIH In type 2 AIH, primary and secondary B cell epitopes have been identified on the full-length CYP2D6 molecule (see above), and a potential for molecular mimicry with viral B cell epitopes has been defined [3, 4].
Part A: pathogenesis. Expert Rev Gastroenterol Hepatol. 2007;1(1):113–28. 5. Beland K, Lapierre P, Alvarez F. Influence of genes, sex, age and environment on the onset of autoimmune hepatitis.
4). At the time AIH is first diagnosed, both the quantity and function of natural Treg (CD4+CD25+FoxP3+) cells are deficient [96, 97]. Successful treatment with corticosteroids and/or azathioprine partially restored the numerical and functional deficiencies of natural Tregs [96, 97]. This observation strongly indicates that functional Treg deficiency is produced, in part, by inflammatory disease activity and the magnitude of deleterious effector cell functions. The mechanism(s) of restoration of Treg numbers and functions during immunosuppressive therapy are undefined.