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Portal hypertensive gastropathy (PHG) is characterized as lesions caused in the inner surface of the mucous layer of the stomach. It is usually associated with gastric varices, portal hypertension, and liver cirrhosis.
Generally, this condition occurs in the upper part of the stomach and also in the gastric fundus. It may also affect the entire area of the stomach and the other regions of the gastrointestinal tract such as the colon or small intestine.
The development processes of PHG are not well defined, but they are closely associated. Although gastric antral vascular ectasia is very distinct from PHG, patients with severe PHG will acquire GAVE-like development in gastric antrum. Also, in case of severe PHG, it causes intense bleeding in the stomach. So far, the only possible treatment available for this is nonselective B-blockers.
The main cause of PHG is liver cirrhosis. Even though about 65% of patients with portal hypertension develops PHG, it occurs greatly in patients with liver diseases. Studies also reveal that occurrence of PHG is significantly more prevalent in patients suffering from esophageal varices than the ones without it.
Frequently, PHG results due to the presence of varices that are gastric or esophageal. Although the pathological process of PHG is still unclear, the most important factors involved in the progression of PHG are the excess production of prostaglandins, tumor necrosis factor, epidermal development factors, and increase in the level of gastric nitric oxide. The occurrence of PHG is also found at high levels in patients with parenchymal liver disease. PHG may result due to portal blood pressure caused by portal vein thrombosis. One other circumstance that is related to the presence and severity of PHG is Helicobacter pylori infection.
Various investigations have revealed that a higher incidence of PHG is found in high Child–Pugh score patients or patients who have undergone sclerotherapy or ligation treatment for esophageal varices.
Depending on the severity of the condition, PHG can be classified. Many classifying systems (McCormack’s, New Italian Endoscopic Club for the Study and Therapy of Esophageal Varices [NIEC], and Tanoue’s classifications) are proposed. The NIEC and Tanoue classify PHG into three categories as mild, moderate, and severe based on the endoscopic identifications, but McCormack classifies it into two. However, many researchers support the two-group classification system.
The classification of PHG in the two-grading system is as follows:
Mild: If the patient has changes only in the gastric mucosa, which appears as a snake skin-like mosaic pattern, it is categorized as mild PHG.
Severe: In addition to the mosaic-like pattern, appearance of black-brown or flat or bulging red spots along with acute bleeding is classified as severe PHG.
Severe PHG has more possibility of hemorrhage compared with mild PHG and may also lead to chronic anemia due to heavy loss of blood. Nevertheless, all the three classifications agree on the severe PHG stage with hemorrhagic spots.
Usually, PHG diagnosis is made at the time of endoscopic assessment; when the features of endoscopic identifications are noticed in the portal hypertensive patient mainly in the proximal abdomen, the PHG diagnosis is established.
Esophagogastroduodenoscopy is the simplest method for diagnosing PHG. Another type of endoscopy named capsule endoscopy is also used. It has 74% of sensitivity and 83% of specificity greater than that of esophagogastroduodenoscopy.
A case study describing 119 patients who underwent capsule endoscopy diagnosis indicates 69% sensitivity and 99% specificity. But the accuracy of diagnosis is greater in the gastric body and lesser in the fundus.
Non-endoscopy procedures such as computed tomography (CT) and magnetic resonance imaging (MRI) are alternative methods used for diagnosing PHG in the patients.
By a CT scan the enlargement of the inner membrane layer of the gastric walls can be detected, whereas an MRI scan is used to measure the diameter of the veins in the gastric part. However, these scans do not exhibit any difference between the patient with and without PHG. Hence, these approaches have been suggested for experimental purposes and endoscopic methods are considered as the key diagnostic techniques.
The PHG diagnosis through endoscopy has various entities that include lesions in gastric walls that are commonly found as a result of irritant injury due to some nonsteroids. Other considerations are GAVE or watermelon stomach. GAVE is also recognized by spots with flat red lesions but not with a mosaic pattern. However, GAVE is frequently found in the distal stomach, whereas PHG in the proximal area of the stomach. Therefore, the appurtenance of the lesions may help to distinguish the ailment.
In a few cases, red spots may appear over the entire stomach, both proximal and distal, which is very difficult for diagnosis of the disorder. Histological evaluation may support in diagnosing PHG when endoscopic results are uncertain.