It refers to the chronic partial or complete obstruction of the portal vein or intrahepatic branches of the portal vein, resulting in obstruction of portal blood flow and causing increased portal pressure. To reduce portal hypertension, varices may occur in the superficial abdominal wall veins located around the umbilicus after the formation of collateral circulation around the portal vein or recanalization of the obstruction. In hepatic portal hypertension, the main manifestations are portal hypertension and secondary rupture of esophagogastric fundic varices and/or concomitant portal hypertensive gastropathy. Patients may have recurrent vomiting of blood and tarry stools with mild to moderate splenomegaly and hypersplenism; therefore, the liver function of such patients is good, so ascites, jaundice and hepatic encephalopathy rarely occur. Occasionally spongy degenerative collateral vessels may compress the superficial veins of the common bile duct located in the abdominal wall around the umbilicus. For patients with recurrent upper gastrointestinal bleeding, mild or moderate splenomegaly and basically normal liver function, the possibility of CTPV should be thought of. Confirmation of the diagnosis requires ultrasound or color Doppler examination combined with portal venography. The diagnosis can be made by physical examination. Serum antinuclear antibodies, lupus anticoagulant, C protein, S protein and antithrombin III are normal, as are the international normalized ratio (INR) and activated partial thromboplastin time. However, myocardial phospholipid antibody IgM and IgG concentrations were high, and liver function tests were normal except for albumin, serum antinuclear antibodies, lupus anticoagulant, C protein, S protein and antithrombin, and international normalized ratio (INR) and activated partial thromboplastin.