**4. Diagnostic evaluation**

cases portosystemic shunts. Thus, it is important to differentiate GAVE and PHG as their

GAVE accounts for approximately 4% of all upper gastrointestinal bleeding [1]. Approximately 40% of GAVE patients have cirrhosis of the liver, and 1 in 40 patients require liver transplantation [2]. Cirrhotic GAVE patients are predominantly males (75%; mean age 65 years), whereas noncirrhotic GAVE patients are predominantly females (71%; mean age of 73 years). GAVE has been associated with autoimmune disorders such as autoimmune connective tissue disorders (62%), Raynaud's phenomenon (31%), and sclerodactyly (20%) [3]. GAVE have also been reported in other medical conditions including scleroderma, bone marrow transplantation, chronic renal failure, ischemic heart disease, hypertension, valvular heart disease, familial

The prevalence of PHG varies from 20 to 75% in portal hypertensive patients, and from 35 to 80% in patients with cirrhosis [7]. According to the HALT-C trial, approximately 37% of patients (364 of 1011) with biopsy confirmed cirrhosis or bridging fibrosis from hepatitis C had PHG [8]. While PHG can present at any age, its severity can vary from mild to severe. The severity of liver disease and severity of portal hypertension greatly influences the natural

The pathophysiology of GAVE remains unknown; however, several mechanisms have been proposed including gastric dysmotility or autoimmune reactivity to gastric blood vessels [10–12]. A study on antral motility revealed an increase in antral area transit time with cirrhosis and GAVE when compared to controls [10]. Chronic recurrent trauma can lead to fibromuscular hyperplasia and vascular ectasia. Reduced gastrin levels have also been identified in GAVE patients when compared to patients with severe PTH and normal controls [13]. Prostaglandins E2 (PGE2) levels were found significantly elevated when compared to controls [14]. GAVE is not associated with portal hypertension and treatments aimed to decrease

The pathogenesis of PHG is related to increased resistance to portal blood flow in patients with liver disease, and concomitant elevation in portal pressure [16]. In patients with portal hypertension, approximately 70% develop PHG [17]. Resolution of PHG and its recurrence has been observed in patients with cirrhosis posttransjugular intrahepatic portosystemic shunt (TIPS) placement, and in noncirrhotic patients with postsurgical decompression of the portal system [17–19]. However, the linear correlation between the severity of portal hypertension and that of PHG is controversial. In a prospective study of 331 patients, it was reported that severe PHG showed a significantly shorter expected survival time than mild PHG (median survival

management options are different.

Mediterranean fever, and acute myeloid leukemia [3–6].

portal pressure have no role in treatment of GAVE [15].

**2. Epidemiology**

44 Stomach Disorders

progression of PHG [9].

**3. Pathophysiology**

GAVE and PHG can be encountered during upper endoscopy in both symptomatic and asymptomatic patients with liver cirrhosis. GI bleeding is the common significant complication of GAVE and PHG. PHG is responsible for about 8% of nonvariceal upper GI bleeding, while GAVE accounts for up to 4% [27, 28]. Both GAVE and PHG may have similar endoscopic appearances and require further histological analysis. In 1995, Payne et al. established that portal hypertensive gastropathy (PHG) and GAVE are distinct clinical entities that require different forms of treatments [13]. Thus, it is incumbent on clinicians to be able to differentiate both diseases.

GAVE is a disease limited to the stomach and is almost exclusively noted in the gastric antrum on endoscopy [29]. GAVE was first reported in 1984 and initially termed 'watermelon' stomach in three patients with iron deficiency anemia [30]. In their report, they described visible convoluted and tortuous columns of ectatic vessels along rugal folds of the antrum, which converged at the pylorus, resembling stripes of a watermelon. In more severe cases, GAVE can present as more punctate lesions or more diffusely, extending to the gastric body, which is most commonly associated with GAVE in cirrhotics than other etiologies [31]. Interestingly, GAVE patients have been reported to have more severe liver disease, greater blood loss, lower serum gastrin levels, and a higher incidence of previous sclerotherapy [13].

Histologically, GAVE is characterized by dilated mucosal capillaries and venules with intimal thickening, fibrin thrombi, spindle cell proliferation, and fibromuscular hyperplasia of the lamina propria [13, 32]. The presence of these histological features is used to calculate a GAVE score which has 80% diagnostic accuracy. This can be used to distinguish GAVE from PHG with a GAVE score equal or greater than three [13].

PHG lesions are typically seen in the gastric fundus unlike GAVE which is commonly found in the antrum. Endoscopically, PHG appears as a mosaic-like pattern or a diffuse, erythematous, and reticular cobblestone pattern of gastric mucosa consisting of small polygonal areas with superimposed red punctate lesions >2 mm in diameter and a depressed white border [33–35]. Severe PHG is associated with flat or bulging red spots, resembling a scarlatina rash with friability or diffuse hemorrhagic gastropathy [36–38].
