Verrucous gastritis: also known as pockmarked gastritis or chronic erosive gastritis, is a specific type of chronic gastritis. It is an endoscopic form reported by Moutler and Corner in 1947 – a chronic gastritis with endoscopic flattened warty elevations and central umbilical-like depressed erosions of the gastric mucosa with many nodular, poxiform protrusions on the gastric mucosal surface, with lesions mostly found in the gastric sinus. It is characterized by recurrent or persistent gastric multiple erosions of unknown origin. The erosions are characteristically warty, mostly distributed within the pyloric gland area and the migratory zone, and a few are seen throughout the stomach. The lesions are round or oval in shape, mostly less than 10 mm in diameter and about 2 mm in height, but also in strips, most of which are elevated with a central trapped erosion, light red or covered with a yellow film. In typical cases of homogeneous warty lesions seen on gastroscopy, the diagnosis is usually not difficult, but if a single or two irregularly elevated lesions are encountered, they must be differentiated from type II early gastric cancer, polyps, and pseudolymphoma. In addition, superficial sinus gastritis may also present with erosions, usually flat, but also with elevated erosions, which can be difficult to differentiate from this disease. However, in general superficial sinusitis often has bile reflux, H. pylori infection, or has taken nonsteroidal anti-inflammatory and analgesic drugs, and the number of erosive foci is small. They usually subside in a few days, weeks to 3 months. The diagnosis of verrucous gastritis relies on endoscopy. The disease is not related to the currently known causes of chronic gastritis, and earlier studies have attributed it to an allergic mechanism. The natural course of the disease is long and varies from individual to individual, with some regressing in a few months and others lasting for years, with no effective treatment options, and if clinical symptoms are present, it can be treated as a peptic ulcer. Warty gastritis is most often seen in men between the ages of 30 and 60. It has a long course, some regress on their own within a few there (immature type), some can last for many years (mature type), and a few develop malignant changes. Clinically detected warty gastritis has obvious upper gastrointestinal symptoms, mostly epigastric pain, followed by acid reflux, abdominal distention, low appetite, nausea, vomiting, upper gastrointestinal bleeding and weight loss. The physical signs are mainly epigastric pain, and a few patients have wasting and anemia. The clinical manifestations are not specific. There is epigastric pain, with vague pain, and distension is mostly seen irregularly. This is followed by epigastric distention, warmth, and panacidity. One third of cases have upper gastrointestinal bleeding (manifested by vomiting blood and black stools). A small number of cases may be asymptomatic. Although there are distinctive morphological and histological changes, the clinical presentation is indistinguishable from that of the common type of chronic gastritis. With treatment or removal of the cause, the lesions may subside. In a few cases, the lesions progress to the stage of intestinal epithelial metaplasia, and the mound-like elevations do not subside easily, but the prognosis remains good. Depending on the distribution of the lesions, warty gastritis is clinically classified into sinusoidal and gastric body/diffuse types. The sinusoidal type has the same etiology as common sinusitis, most notably Helicobacter pylori (Hp) infection, and has a higher chance of coexistence with peptic ulcer and duodenal ballooning because of the common etiologic basis. In contrast, the gastric body/diffuse type is closely related to immune factors and is less associated with Hp infection. In addition, there are mature and immature types of warty gastritis, such as bulging lesions mainly due to tissue edema, the central umbilical-like depression is large and shallow, called immature; if the bulging lesions are mainly due to fibrosis, the bulge persists and does not disappear easily, as the mature type. The active phase is characterized by epithelial degeneration, necrosis, exfoliation, neutrophil infiltration and exudation of fibrous material; the repair phase is characterized by hyperplasia of the intrinsic glands around the foci of erosion, the pyloric glands or the epithelium of the gastric hollows, sometimes with fibrosis, and regenerative glandular ducts with varying degrees of atypical hyperplasia.