Autoimmune Hepatitis

Autoimmune Hepatitis

    * Introduction
    * Signs and symptoms
    * Diagnosis
    * Treatment
Autoimmune hepatitis is a rare chronic disease, of unknown etiology, characterized by exaggerated autoreactivitate on a background of genetic predisposition. Patient's immune system attacks the liver causes inflammation and cell death. Although the disease is progressive and many patients have chronic hepatitis with jaundice, fever and symptoms of severe liver dysfunction. Autoimmune hepatitis occurs mainly in women-70% between age 15 and 40 years. The term "lupus-like hepatitis, had once been used for this condition, but it turned out that patients with SLE does not have an increased incidence of autoimmune hepatitis, so this name is not correct. Patients presenting with moderate or severe hepatitis associated with increased ALT, AP and increased moderately high GGT activity. The clinical picture is presented with jaundice, fever, right upper quadrant pain and occasionally extrahepatic manifestations: arthralgia, myalgia, and thrombocytopenia poliserozite. Autoimmune hepatitis is a serious disease, untreated secondary cause liver fibrosis and cirrhosis, liver failure eventually. Treatment is effective if started early in the disease. Autoimmune hepatitis can usually be controlled therapeutic trials showing a sustained response from the body to stop therapy and liver damage, even their reversibility. Basic drugs are corticosteroids and azathioprine. In almost seven out of 10 cases, the disease go into remission after 3 years of treatment. Remission begins when symptoms disappear and lab tests showed improved liver function. Some people may discontinue treatment, but shortens the period of remission, new relapses. Treatment requires careful monitoring and drug doses adjusted continuously. It is a therapy for life.
Pathogenesis
Studies show that liver lesions in a patient with autoimmune hepatitis are caused by a cell-mediated attack. This attack is directed against genetically predisposed hepatocytes. Presentations abnormal HLA class II Ag on the surface of hepatocytes facilitates the production of hepatocyte cell membrane of normal structures of Ag processing. These cells are activated, they stimulate cytotoxic T lymphocyte cloning hepatocytes sensitized to liver tissue will infiltrate, cytokine release and will help to destroy hepatocytes. Cause aberrant expression of HLA II on the surface of hepatocytes is unknown, it is considered that triggers: genetics, viral infections (hepatitis A, B, infection with Epstein-Barr) and chemical agents (interferon, melatonin, alpha-methyldopa, oxifenisatin, nitrofurantoin acid tienilic). Receptor and cytochrome P450 asialoglicoproteina autoAg are proposed as triggers. Some patients seem to develop genetically succeptibili autoimmune hepatitis. This condition is associated with HLA alleles C4AQO complement haplotype B8, B14, DR3, DR4, and Dw3. HLA DR3 predisposes to aggressive disease, unresponsive to therapy. These patients are often very young. HLA-DR4 are more likely to develop extrahepatic manifestations. Highlighting an autoimmune pathogenesis includes: -Liver histopathological lesions predominantly comprising cytotoxic T lymphocytes Circulating-autoAc: nuclear, anti smooth muscle, anti thyroid, liver and kidney antimicrosomi Ag liver soluble hepatic lectin -Association with hypergammaglobulinemia and rheumatoid factor -Association with other autoimmune diseases -Response to steroids and immunosuppressive therapy.