In addition to esophageal and fundic varices, there are also non-variceal diseases in the upper gastrointestinal tract due to portal hypertension, the common one being portal hypertensive gastropathy (PHG), in which patients have dilated small blood vessels in the gastric mucosal tissue without significant inflammation. Some intestinal lesions similar to PHG are called portal hypertensive enteropathy (PHE), which is also a cause of portal hypertensive gastrointestinal bleeding. I. PHG 1. Diagnosis and endoscopic classification: PHG is an endoscopic term, and the diagnosis is based on what is seen endoscopically. There are various methods of classifying endoscopic PHG, of which the McCormack classification is the most widely used, classifying endoscopic PHG as mild or severe: (1) mild: pale pink-like spots or scarlet fever-like rash, striated redness on the surface of mucosal folds, erythematous exfoliation-like or mosaic pattern-like appearance, similar to snakeskin-like manifestations; (2) severe: diffuse cherry red-like spots or diffuse fused hemorrhagic gastritis. This classification method is simple and easy to use, and it can also effectively predict the risk of hemorrhage occurrence. 2, histological features of PHG: Studies have shown that the histological features of the gastric mucosa in PHG are dilated mucosa and submucosa capillaries, focal thickening of the lining, which can be accompanied by inflammatory cell infiltration, and changes in the vasculature are often more significant than inflammation. viggian et al. proposed that the gastric mucosa and submucosa vessels in PHG are not only dilated, but more importantly, the changes in the structure of the mucosal vessel wall in the lamina propria of the gastric pits lead to thickening of the vessel wall and dilation of the lumen. Therefore, vasodilation and mucosal congestion and edema are considered to be the characteristic injuries of PHG, with inflammatory infiltration and glandular atrophy as secondary signs. It has also been shown that the endoscopic findings of PHG patients are not completely consistent with the histological lesions of the gastric mucosa. 3. Pathogenesis: It is not well understood that elevated portal pressure is the most important factor for its occurrence. In portal hypertension, the hemodynamic changes of gastric mucosa are high blood volume and low perfusion, relatively reduced effective blood flow, tissue hypoxia, and local gastric mucosal tissue damage.Merkel et al. showed that the severity of PHG was correlated with portal pressure, and the condition of PHG improved significantly after treatment with transjugular intrahepatic portosystemic shunt (TIPS) or surgical shunt. It has been suggested that abnormal opening of the arteriovenous shunt in the gastric wall is the most basic cause of PHG complicating the course of portal hypertension in liver cirrhosis. In PHG, the gastric mucosal defense mechanism is disrupted, the mucus layer is reduced, the level of gastrin is increased, and the number of mural cells is reduced. The capillaries within the gastric mucosa are significantly dilated and distorted, the lamina propria and submucosa are edematous, nutrients are lost and metabolism is impaired, and the gastric mucosa is prone to erosion and bleeding. It is now well established that patients with PHG have increased susceptibility to damage caused by nonsteroidal anti-inflammatory drugs. Increased NO production has also been considered as a possible pathogenesis of PHG, and as a potential vasodilator, NO is elevated in both cirrhotic and PHG patients. expression levels of transforming growth factor (TGF) and epidermal growth factor (EGF) are elevated in PHG rat models. Studies have confirmed that patients with portal hypertension have strong positive expression of various growth factors such as TGFa and EGF in the walls of gastric coronary veins, which promote the release of various vasoactive substances from smooth muscle cells in the vessel walls, leading to decreased vascular compliance and increased resistance to blood flow. Most scholars now believe that there is no significant correlation between H. pylori infection and the development of PHG. 4, treatment: PHG can lead to severe upper gastrointestinal bleeding. It was found that 13% of patients with mild PHG and 75% of patients with severe PHG can have gastric bleeding. Currently, the treatment of PHG is mainly focused on reducing portal pressure. It mainly includes: (1) β-blockers: It is still an important treatment for PHG, and studies have shown that propranolol can reduce the risk of initial bleeding and rebleeding in PHG and reduce the formation of PHG after esophageal variceal ligation treatment. (2) Growth inhibitors and their analogues: A controlled study on the efficacy of upper gastrointestinal bleeding due to PHG showed that bleeding was 100% controlled in the octreotide group after 48 h of administration, compared with 64% and 59% in the vasopressin and omeprazole groups, respectively. (3) Other drugs: vasopressin and terlipressin can reduce gastric blood flow and are also effective in the treatment of PHG bleeding. (4) Surgical and interventional treatment: Various portal shunts and TIPS are effective in bleeding caused by PHG by reducing portal pressure, but they are limited by the patient’s liver function condition. Liver transplantation can completely cure portal hypertension and is also effective in the treatment of PHG. Second, PHE PHE mainly manifests as intestinal mucosal vasodilatation, spider nevus-like changes and varicose veins. The pathogenesis of PHE is still unclear, but it is mostly thought to be closely related to the intestinal hemodynamic changes caused by portal hypertension. In addition, endotoxemia, NO, prostaglandins, etc. can also be involved in the occurrence of PHE. 1, endoscopic manifestations and pathological changes: endoscopic manifestations and pathological changes of PHE have not yet reached a consensus, most scholars believe that the following characteristics can diagnose PHE: (1) varicose veins: endoscopic manifestations of submucosal tortuous, significantly dilated cystic venous plexus, which can occur in various parts of the intestine, with the highest incidence of rectal varicose veins; (2) vasodilatation: the number of visible vessels under the mucosa The incidence is slightly higher than that of varicose veins; (3) capillary dilation: capillary dilation in the intestinal mucosa is the pathological basis of PHE, and the capillary bed of the entire GI mucosa from the stomach to the anus is almost dilated, with an increase in the diameter and cross-sectional area of capillaries. Except for submucosal vascular changes, other lesions of the intestine lack characteristics, including intestinal mucosal atrophy, mild inflammation, ulceration, and mucosal punctate red sign. 2.Diagnosis: The diagnosis of PHE is mainly made by various endoscopic examinations, and local or diffuse submucosal vasodilatation and varicose veins can be observed, and sometimes “red signs” can be seen in the mucosa. Mucosal biopsy can show capillary dilation and mucosal atrophy. Ultrasound endoscopy, barium enema, CT, MRI, etc. are also helpful for the diagnosis of PHE. 3. Treatment: There are many reports about bleeding caused by PHE, but the exact incidence is unclear. Sudden increase in portal pressure, food friction, surface mucosal erosion or ulceration, decreased ability of mucosa to repair damage and the presence of coagulation mechanism disorders in patients are all factors affecting bleeding. The amount of bleeding can be large or small, with the highest incidence of variceal bleeding. Therefore, patients with portal hypertension who present with positive fecal occult blood, black stool and anemia should consider the possibility of PHE. (1) Diet: Diet is important to improve the nutritional status of patients and prevent gastrointestinal bleeding, and it is advisable to eat a vitamin-rich diet with less residue and soft texture, and to ensure a certain amount of high-quality protein intake; (2) Drugs: The main purpose is to reduce portal pressure to improve PHE and prevent bleeding and rebleeding, including p-receptors blockers, growth inhibitors and their analogues, vasopressin, etc.; (3) other: including interventional and surgical treatment, etc.