LAUSR

We read with great interest the original article written by Nishino et al. Their retrospective study was performed with univariate and multivariate logistic regression analyses, demonstrating that the risk factors of portal hypertensive gastropathy (PHG) were the existence of esophageal varices, splenomegaly, severe liver cirrhosis (LC), the etiology, and the absence of atrophic gastritis (1). In Japan, there have been no reports clarifying the frequency of PHG, onset factors, prognosis, or relationship with Helicobacter pylori infection. PHG is a mucosal lesion that presents with redness, edema, and bleeding in the upper corpus of the stomach, similar to H. pylori-related gastritis, and is often observed in LC patients with portal hypertension. In their manuscript, non-viral (alcoholic) LC, liver dysfunction of Child-Pugh class >B, and splenomegaly with a spleen index of >19.5 cm were concretely shown to be independent predictors of PHG. The most interesting point in their report was the finding of a negative correlation between the appearance of redness in PHG and the existence of atrophic gastritis. PHG is endoscopically classified based on five findings according to the McCormick classification (2). Findings of fine pink speckling, superficial reddening, and a snakeskin (mosaic) pattern are considered mild PHG. Cherry red spots and diffuse hemorrhaging are considered severe PHG. Edema of the gastric mucosa and dilatation of the vessels with a significant increase in the gastric mucosal blood flow are sometimes observed (3, 4), and the incidence is reported to be around 50% to 90% in LC patients with portal hypertension (5). The endoscopic findings of redness on the body of stomach with persistent H. pylori infection are known to resemble those of PHG mentioned above. Strictly speaking, however, it is possible to distinguish between PHG and H. pylori gastritis. We previously reported that the redness (due to vasodilation) was weak in H. pylori gastritis and that the white border line at the gastric area (due to edema) were also weak compared with the snakeskin pattern of PHG, resulting in reduced contrast on the mosaic appearance of H. pylori gastritis (Figure) (6). In other words, by observing the red and white contrast of the mosaic appearance, it is possible to distinguish these entities to some extent. In cases with mild redness, identifying whether the portal hypertension potentially exist or not is important. If gastritis patients with mild redness have both portal hypertension and H. pylori infection, it may be difficult to discriminate these entities. However, severe redness, such as cherry red spots and diffuse hemorrhaging, are findings specific to PHG. Therefore, even if patients have H. pylori infection or a history thereof, these finding strongly support the diagnosis of PHG. The relationship between PHG and H. pylori infection is controversial. Balan et al. reported that the serum pepsinogen I concentrations, the ratio of polymeric to degraded gastric mucus, and the rate of gastric emptying were not significantly different between PHG patients with and without H. pylori infection. They also concluded that H. pylori infection was unlikely to be involved in the pathogenesis of PHG (7). McCormick et al. reported that H. pylori infection was identified in 26% patients with PHG and was not related to the severity of the endoscopic appearances (8). Hayashi et al. reported that the appearance rate of dot redness and mottled redness, categorized as fine pink speckling or superficial reddening, increased from 36% to 78% by H. pylori infection in the 162 patients with PHG (9). They also stated that a snakeskin (mosaic) appearance (unlike fine pink speckling and superficial reddening) was unchanged follow-