The incidence of thrombocytopenia in patients with viral hepatitis is very common and is higher in patients with all types of chronic hepatitis and cirrhosis and severe hepatitis and fulminant liver failure, and it has long been natural to think that splenomegaly and hypersplenism are the main causes of thrombocytopenia in liver disease. In fact, the mechanism of thrombocytopenia in viral hepatitis is more complex and is the result of a combination of factors, which are briefly described here: I. Role of the spleen: more than 1/3 of the whole body platelets are retained in the spleen, which can exchange freely with the peripheral blood platelets, about 7 5% aging; platelets are destroyed in the spleen and liver. It has long been believed that the spleen plays an important role in platelet destruction, which is related to the enlarged spleen due to portal hypertension in liver cirrhosis. This is consistent with the fact that thrombocytopenia is often the earliest and most pronounced in hypersplenism, and the platelet count is also significantly higher after clinical splenectomy than before surgery. Bone marrow suppression: Hepatitis virus can affect the bone marrow, ranging from mild bone marrow abnormalities to bone marrow failure. HBV-DNA was found to inhibit the proliferation and differentiation of hematopoietic cells in an in vitro test with HBV, and the inhibitory effect was clearly dependent on the viral serum concentration. Platelet-associated immunoglobulin-mediated immune mechanisms: In recent years, many studies have found that platelet-associated immunoglobulin is increased in patients with chronic liver disease, and there is a negative correlation between platelet count and platelet-associated immunoglobulin, so it is believed that platelet reduction in patients with chronic liver disease may be related to autoimmune disorders. Platelet-associated immunoglobulins can have two components, a true anti-platelet antibody, or platelet-specific antibody, and an immune complex. True anti-platelet antibodies can be adsorbed by human platelets, combine with platelet glycoproteins, and travel with the bloodstream to the spleen, liver, and other mononuclear macrophage systems to be phagocytosed and destroyed, resulting in thrombocytopenia. The mechanism of thrombocytopenia in patients with chronic hepatitis and cirrhosis may be different. Patients with chronic hepatitis usually do not have splenomegaly, and their thrombocytopenia may be mainly related to immune destruction, while patients with cirrhosis have a high incidence of splenomegaly, and their thrombocytopenia may be caused by pathological enlargement of the spleen, increased retention of platelets, and subsequent destruction of platelets in the spleen by platelet-associated immunoglobulin-mediated immune mechanisms. The result is that platelets are destroyed in the spleen by platelet-associated immunoglobulin-mediated immune mechanisms. In recent years, with the continuous research on platelet thrombopoietin, it was found that the decrease of serum platelet thrombopoietin level in chronic liver disease with impaired liver function is directly related to the decrease of platelet count. In summary, the causes of viral hepatitis platelet reduction are multifaceted, the mechanism is more complex, for patients with thrombocytopenia, feasible bone marrow aspiration, thrombopoietin, platelet-related immunoglobulin-mediated examination, to make the correct etiological diagnosis, do not blindly splenectomy or splenic embolism.