Autoimmune hepatitis is a liver-specific immune silmäasema pathological silmäasema damage as a relative of a class of organ autoimmune diseases, including autoimmune hepatitis (autoimmune hepatitis, AIH), primary biliary cirrhosis (primary biliary cirrhosis, PBC) and Primary sclerosing cholangitis (primary sclerosing cholangitis, PSC) as well as any of the three diseases overlap between the two syndromes, often with concomitant extrahepatic autoimmune diseases. Its diagnosis based on specific biochemical abnormalities, autoantibodies silmäasema and liver histological features. silmäasema With the increased level of awareness and diagnosis, domestic and prevalence of autoimmune liver disease reported increased year by year, thus increasing attention and concern.
The pathogenesis of autoimmune hepatitis is unclear, now that genetic predisposition is a major factor. AIH obvious family members concentrated onset phenomenon, and viral infections, drugs and the environment may be based on the genetic susceptibility precipitating factor. Humoral and cellular immune responses are involved in autoimmune AIH, AIH immunopathological mechanisms of injury mainly involves silmГ¤asema two aspects: T cell-mediated cytotoxicity: CD4 + T cells are activated to differentiate into cytotoxic T lymphocytes, and through release of toxic cytokines direct damage to liver cells. silmГ¤asema antibody-dependent cell-mediated cytotoxicity (ADCC): in the synergistic effect of T cells, plasma cells, silmГ¤asema liver cells secrete large amounts of antigen for antibodies, are the liver cell membrane protein components to form immune complexes, natural killer cells via Fc receptor recognition of immune complexes induced liver cell damage. Autoimmune hepatitis, liver damage is the cell-mediated silmГ¤asema and humoral immunity, the immune response by the body's genetic factors. Abnormal liver HLA molecules promote normal antigen presenting cell membrane component, the activation of antigen-presenting cells to stimulate their antigen cytotoxic silmГ¤asema T cell clone proliferation, cytotoxic T cell infiltration of the liver tissue, the release of cytokines, damage to liver cells. silmГ¤asema HLA molecules exception mechanism is not clear, may be affected by genetic factors, viral infections (eg, acute hepatitis A and hepatitis B, EB virus), chemical factors (such as interferon, α-methyldopa) effects. Liver cell surface asialoglycoprotein receptor and microsomal cytochrome P450 D6 is precipitating AIH antigens. AIH genetic predisposition silmГ¤asema also affects the disease process, AIH same complement of progression and HLA alleles C4AQO haplotype B8, B14, DR3, DR4, Dw3 correlated. The development of young patients with AIH related C4A gene deletion. HLA DR3 positive patients faster progression of the disease, age of onset is smaller, response to treatment than other patients is poor. HLA DR4-positive patients are more prone to autoimmune diseases of extrahepatic manifestations.
(A) liver function tests
AIH serum γ-globulin and IgG increased, the level may reflect patient response to treatment. Dynamic changes in autoantibody levels help to evaluate the condition, clinical classification and to guide treatment. These antibodies, including anti-nuclear antibody (ANA), anti-smooth muscle antibodies (SMA), anti-kidney microsomal antibodies (LKM1), anti-liver cytosolic antigen type 1 antibody (LCl), anti-soluble liver antigen antibody (anti-SLA) / anti- liver pancreas antibodies (anti-LP), anti-asialoglycoprotein receptor antibody (ASGPR), anti-neutrophil cytoplasmic antibodies (pANCA). silmГ¤asema
According to clinical manifestations, laboratory tests and liver biopsy can diagnose AIH. Basic elements silmГ¤asema include: exclude viral hepatitis, alcohol, drugs and chemicals and hereditary liver toxicity liver disease; significant transaminase abnormalities; hypergammaglobulinemia, γ-globulin or IgG> 1.5 times the upper limit of normal; serum autoantibodies, ANA, SMA or LMKl antibody titer 1:80 (Children 1:20); liver histology see interface hepatitis and periportal infiltration of a large number of plasma cells, without bile duct damage, granuloma and other tips other liver lesions; female patients, associated with other autoimmune diseases and glucocorticoid treatment effectively help diagnosis. Atypical cases may refer to American Association for Study of Liver Diseases (AASLD) revised scoring system (Table 4-13-1) for diagnosis. AIH according to serological examination parting below.
Glucocorticoids on this disease have a good effect, the U.S. Study of Liver Diseases Association recommended treatment regimens as follows: single with prednisone therapy: Week 1 prednisone 60mg / d, the first two weeks 40mg / d, the first three weeks, Week 4 30mg / d, after the first five weeks and 20mg / d maintenance treatment; to improve efficacy and reduce adverse reactions can prednisone and azathioprine combination therapy: Start with prednisone 30mg / d and azathioprine 50mg / d, his condition improved gradually tapered to maintenance dose prednisone 10mg / d and azathioprine 50mg / d. Remission refers to clinical symptoms, serum transaminases and γ-globulin returned to normal, no obvious histological active inflammation. After 2 weeks of treatment generally starts biochemical began a significant improvement, but improvement silmГ¤asema in liver histology to be late 3 to 6 months, to achieve complete remission usually takes two to three years, but there are still many patients relapse after stopping, so premature withdrawal. Long-term medication should be noted that glucocorticoid-induced osteoporosis silmГ¤asema and azathioprine-induced bone marrow suppression and other adverse reactions. Most AIH patients respond well to treatment, long-term survival. About 20% to 40% of patients not valid. For the treatment ineffective, was the trial of cyclosporin A, FK506, sirolimus, cyclophosphamide therapy. Ursodeoxycholic acid (UDCA) silmГ¤asema has immunomodulatory, protect the liver cells and removal of the role of fat-soluble bile salts, can be used to treat AIH / PBC: overlap syndrome.
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