**2. History**

blood flow, thus if the pressure gradient anywhere along the portal venous system (between the portal vein, and hepatic veins or the inferior vena cava (IVC)) is increased,

The normal portal venous pressure ranges from 5 to 10 mm Hg, therefore, if the hepatic venous pressure gradient (HVPG) is ≥10 mm Hg, significant portal hypertension is consid‐

The causes of portal hypertension are classified into three categories related to anatomical consideration. First, are causes originating in the portal venous system before it reaches the liver (pre‐hepatic), e.g. portal vein thrombosis, schistosomiasis, primary biliary cholangi‐ tis/primary sclerosing cholangitis, or congenital hepatic fibrosis. Second, are causes within the liver (intrahepatic) e.g. cirrhosis as a result of viral, non alcoholic fatty liver disease (NAFLD), or autoimmune. Finally, are causes between the liver and the heart (post‐hepatic) e.g. Budd‐Chiari syndrome, inferior vena cava obstruction, or hepatic veno‐occlusive dis‐

ered, but if the HVPG is ≥12 mm Hg, severe portal hypertension is diagnosed [2].

ease (**Table 1**). The most common cause of PH is cirrhosis [3].

**Prehepatic Hepatic Posthepatic**

alcoholic, autoimmune, NAFLD, biliary atresia, etc.

Arteriovenous fistula Primary biliary cholangitis Hepatic vein thrombosis Splenomegaly Primary sclerosing cholangitis Budd‐Chiari syndrome

Granulomatous or infiltrative diseases (Gaucher,

Toxicity (from arsenic, copper, methotrexate,

Schistosomiasis Right sided heart failure, e.g. from

Inferior vena cava obstruction

constrictive pericarditis

Portal vein thrombosis Cirrhosis of any cause, e.g. chronic viral hepatitis,

Congenital hepatic fibrosis

Nodular regeneration hyperplasia

sarcoidosis, amyloid deposition

amiodarone, ….)

NAFLD, non alcoholic fatty liver disease.

**Table 1.** Condition associated with portal hypertension.

Veno‐occlusive disease

portal hypertension develops.

58 Stomach Disorders

**1.2. Essentials to diagnose PHG**

• Characteristic endoscopic findings.

• Portal hypertension with or without cirrhosis.

In 1984, Sarfeh et al. recognized a distinct form of gastric mucosal hemorrhage in patients who had portal hypertension, they called it "portal hypertensive gastritis". They reported that this mucosal lesion in patients with portal hypertension was reversed after the portacaval shunt, in contrary to the mucosal lesion of patients without portal hypertension. Therefore, they concluded that there is a unique mucosal change excited with portal hypertension. 1 year later, it was discovered that this mucosal change was not a form of gastritis as there is no evidence of inflammation in the mucosa. Specific histopathological findings described this change, and the term "portal hyper‐ tensive gastropathy" was introduced by McCormack et al. in 1985 as a separate entity. However, there was no grading system of the endoscopic findings to put an accurate score for this condition. Several grading systems like the three‐ category system, and the two‐category system have been proposed in 1994. The clinical importance of grading classification system resides in the fact that patients with severe PHG have a higher chance to bleed than patients with mild PHG [4].

The overall mortality from gastrointestinal bleeding is up to 25% of the mortality in patients with cirrhosis. In recent years however, PHG has been recognized as a distinct entity of gastrointestinal bleeding in patients with cirrhosis and portal hypertension. While variceal hemorrhage and peptic ulcer disease are known as significant causes of GI bleeding in cir‐ rhosis, PHG and gastric antral vascular ectasia (GAVE) should also be considered as impor‐ tant causes. However, PHG should be differentiated from GAVE, GAVE occurs in patients with cirrhosis and portal hypertension, in addition to other conditions, such as chronic renal failure, connective tissue disorders, and bone marrow transplantation. On the other hand, PHG occurs only in patients with portal hypertension, whether with or without cirrhosis. In patients with cirrhosis, PHG is more common than GAVE [5].

However, although the endoscopic, histological and hemodynamic features of PHG mucosa have been extensively studied, the pathogenesis of PHG is still poorly understood, its natural history is not clearly documented and its treatment needs to be improved [6].
