Primary desiccation syndrome is a systemic autoimmune disease with dry mouth and eyes as the main clinical manifestation, and the liver is one of the main organs involved. The incidence of liver injury due to this disease has been reported in the literature to range from 5-35%. Currently, liver injury due to pSS is gradually gaining attention. Diagnostic criteria for liver injury: ①alanine aminotransferase (ALT) > 40 U/L; ②aspartate aminotransferase (AST) > 40 U/L; ③total bilirubin (TBIL) > 18.8 mol/L, direct bilirubin (DBIL) > 5.9 mol/L; ④alkaline phosphatase (AKP) > 90 U/L; ⑤transpeptidase (r-GT) > 40 U/L. At least two of the above abnormalities, and excluding factors such as drugs, infection, hemolysis, myositis or hepatobiliary tumors. The pathogenesis of liver involvement in SS patients is unclear, and it is generally believed that the infiltration of lymphocytes and plasma cells into the hepatic confluent area causes abnormalities in humoral and cellular immunity and releases various inflammatory mediators causing tissue inflammation and destruction, which may be related to genetics, gender, disease course, autoantibodies, and T-cell function and regulation. The pathological processes of autoimmune liver injury and dry syndrome are similar in that they are immune inflammation and lymphocytic infiltration of the ductal epithelium of the liver and the ductal epithelium of the salivary glands, respectively, and Abraham et al. The lymph that infiltrates the ducts and salivary gland epithelium of the liver are CD4-positive T cells. pSS patients have excessive immune inflammation that gradually leads to liver damage over the course of the disease. I summarized 144 hospitalized cases with a clear diagnosis of pSS in our hospital from January 2004 to February 2008 and analyzed the clinical and laboratory characteristics of their liver injury. 17 of 149 pSS patients (11.4%) presented with liver injury. The patients with liver injury were all female, with a mean age of 54.9 ± 13.5 years and a mean disease duration of 13.7 ± 10.5 years. 10 of them were diagnosed with autoimmune hepatitis and 7 with primary cholestatic cirrhosis. The clinical manifestations of SS patients varied, and 8 of 17 patients with liver involvement were first diagnosed with liver-related disorders, which could manifest as non-specific symptoms such as jaundice, nausea and poor appetite, abdominal distension, discomfort in the liver area, ascites, upper gastrointestinal bleeding, and hepatosplenomegaly, while dry mouth and eyes and parotid enlargement were not obvious, and rarely accompanied by arthritis and purpura of both lower limbs. Dry syndrome is likely to cause specific damage to the liver through some mechanism such as M2 mitochondrial antibodies. Clinical studies have shown that 14-18% of patients with PBC and AIH have combined autoimmune diseases such as rheumatoid arthritis and dry syndrome. In the present study, all 17 patients with liver injury showed alterations in liver enzymes before diagnosis, and clinical attention should be paid to patients with elevated transaminases of unknown cause for the diagnosis and differentiation of immune diseases and immune liver diseases. Studies excluding the effects of drugs, hepatitis viruses and common infections have found that the longer the duration of the patient’s disease, the greater the chance of concurrent liver injury, and serum hyperglobulin levels are also an independent risk factor for autoimmune injury to the liver. Therefore, timely early diagnosis and early treatment of pSS, application of immunosuppressants to improve patients’ excessive immunoglobulins, and correction of B-cell hyperactivity may be instructive in preventing liver injury. In addition, we compared serum abnormalities in patients with combined liver injury and without liver injury, showing that M2-type mitochondrial antibody IgG, hyperglobulinemia and elevated IgG and IgM were significantly higher in patients with liver injury than in patients without liver injury, and this immune abnormality seems to parallel liver injury, suggesting the significance of immune intervention therapy to reduce liver complications.M2-type mitochondrial antibody was significantly higher in patients with liver injury Patients also have significantly more M2 mitochondrial antibodies in patients with liver injury, showing that this antibody is not only a serum signature antibody but also has a predictive function for disease progression. A 5-year follow-up study of foreign patients with positive M2 mitochondrial antibodies showed that patients with positive M2 mitochondrial antibodies progressively develop autoimmune liver injury, but whether this is one of the causative factors needs to be further investigated. Ursodeoxycholic acid becomes the major bile acid in serum and bile by stimulating the secretion of bile acids from damaged hepatocytes and competitively inhibiting the uptake of endogenous hydrophobic bile salts by the ileum, preventing direct damage to hepatocytes and bile duct cells from toxic bile acids by competitively replacing toxic bile acid molecules on cell membranes and organelles, and maintaining membrane by binding to membrane nonpolar structural domains stabilization of membrane polarity and organization of membrane damage by hydrophobic bile acids. Although ursodeoxycholic acid is currently the drug of choice for the treatment of PBC, most scholars believe that it is effective for early-stage PBC and poor for late-stage. When TBIL is greater than 34.2 mol/L, glucocorticoids and/or immunosuppressants can be used to improve the condition. In our department, ursodeoxycholic acid has been applied to 16 patients with dry syndrome combined with liver damage for 1-4 years, and the enzymatic abnormalities of the liver were basically corrected and the clinical symptoms were greatly improved. Therefore ursodeoxycholic acid is effective in the treatment of autoimmune liver disease, and the drug needs to continue to expand its clinical application and follow up patients for clarification.