Primary biliary cirrhosis (PBC) is a chronic non-suppurative granulomatous cholangitis, mainly affecting the intrahepatic interlobular bile ducts, which is more prevalent in women, with a median age of 50 years. Cholestatic liver function changes, AMA and/or AMA-M2 titers >1:40 and corresponding histopathological features are present to make a “definite” diagnosis of PBC, while the presence of any two of them is a “probable” diagnosis. IgM levels may be elevated in 95% of PBC patients, but may be normal in a small number of patients. Patients with asymptomatic PBC with normal liver function can be followed for 3-4 months without medication. The effect of UDCA on clinical symptoms, histological changes and long-term survival of patients with PBC is controversial. It is generally believed that UDCA has a significant benefit on long-term survival only in patients with histological stage I and II, with relatively poor efficacy in patients with progressive disease, which emphasizes the importance of early diagnosis of PBC. On the other hand, patients who respond poorly to UDCA have a poor prognosis. adverse reactions to UDCA are rare, with gastrointestinal reactions and weight gain being the most common. A study showed that budesonide combined with UDCA treatment for 3 years significantly improved histological lesions in patients with PBC. Primary sclerosing cholangitis (PSC) is a chronic progressive disease of unknown cause characterized by progressive inflammation, fibrosis, and narrowing of the intra- and extrahepatic bile ducts in large and medium sized livers.PSC predominantly affects men and is associated with inflammatory bowel disease in 70% (40-98%) of patients.PSC can lead to destruction of intra- and extrahepatic bold ducts, causing intrahepatic cholestasis liver fibrosis and cirrhosis. The risk of bile duct cancer is elevated at all stages of the disease. psc also shows some genetic susceptibility, mainly associated with three HLA-II molecular haplotypes. The autoantibody most associated with PSC, PANCA, is present in more than 85% of PSC cases and is only a non-specific indicator, with no definitive significance for PSC. The diagnosis of PSC relies on unique bile duct imaging changes, which show intra- and extrahepatic bile duct involvement, typically in the form of bead-like changes. The goal of PSC treatment is to slow down or reverse the disease process and to control the complications of PSC including cholestasis and progressive liver disease. However, PSC treatment is not ideal. Convenient doses of UDCA may result in improvements in abnormal biochemical parameters, but have no effect on histology, manifestations of biliary disease, or survival. The efficacy of high-dose UDCA for PSC needs to be further evaluated. Endoscopic bile duct dilatation is feasible in severe bile duct strictures. Liver transplantation can be successfully used for end-stage liver disease referred to PSC and may improve survival. Recurrent PSC can occur after liver transplantation, but the latter rarely progresses progressively. Overlap syndrome Three states may exist: the coexistence of two diseases; the presence of one major disease accompanied by some features of the other; and a sequential progression of both diseases with changes in the level of diagnosis and treatment. The study showed that 18% of 225 patients with self-exempt liver? There is overlap, including AIH/PBC (7%), AIH/PSC (6%), and AIH/autoimmune cholangitis (AIC) overlap (11%).AIH/PBC overlap signs are usually divided into two categories, one of which is patients with the histological features of AIH but serologically exhibit the typical features of PBC, i.e. AMA(+) AIH, whose clinical development and treatment The clinical development as well as response to treatment is almost exactly similar to that of type I AIH; the second is that the patient may have histological features suggestive of PBC, but usually AMA (-), cut ANA (+) and/or SMA (+). The above may be referred to as autoimmune cholangiopathy. Patients with AIH/PBC overlap usually respond to corticosteroids and are initially treated with hormones as in typical type I AIH patients, and can be treated with UDCA maintenance when remission is achieved. Autoimmune cholangitis (AIC), also known as AMA-negative PBC . Patients also respond to hormones when serum aminotransferases are at high levels. AIH/PSC overlap syndrome is relatively uncommon in the PSC variant. Hormones alone may have little effect on clinical symptoms, biochemical parameters and histological remission. Immunosuppressive + UDCA therapy is effective in AIH/PSC overlap syndrome and has a better survival rate than in “classic” PSC patients. Sixty-five percent of HCV-infected patients may develop low-titer ANA, SMA, or antithyroid antibodies. About 7% of patients with AIH may have low titers of anti-LKM-1 antibodies, and false positives for anti-HCV antibodies can be detected, which need to be determined by testing for HCV RNA. Three conditions may exist: AIH with false-positive anti-HCV; chronic hepatitis C, which may have low levels of autoantibodies (+); and AIH and chronic hepatitis C together. The incidence is recognized as 10% and 6% in children. AIH/HCV syndrome is recommended to be treated first with immunosuppressive agents and closely monitored for changes in the condition.