CSG is characterized by multiple linear streaks on the greater curvature side of the antrum. CSG is the most common endoscopic gastritis in Korea, followed by EG, chronic atrophic gastritis (CAG), and metaplastic gastritis (MG) [6]. Hyperemic streaks found in CSG do not require subsequent biopsy, since they are not associated with an increase in the risk of gastric cancer. CSG involves hyperacidic conditions. The secreting ability of the gastric mucosal cells remains intact.

EG presents with multiple raised erosions with hyperemic changes on the antrum. Erosions can be found in both noninfected subjects and in subjects with active H. pylori infection (Table 1). In the absence of H. pylori infection, the incidence of gastric cancer is low [7]. In EG, the intragastric conditions are hyperacidic, and the secreting ability of the gastric mucosal cells remains intact.

Endoscopic gastritis in noninfected individuals is rare areas with endemic H. pylori infections. Type A autoimmune gastritis is an initially asymptomatic disease that progresses to corpus atrophy with pernicious adenoma (B12 deficiency) or iron deficiency anemia [8]. Granulomatous gastritis is related to Crohn’s disease, tuberculosis, syphilis, sarcoidosis, anisakiasis, or reaction to a foreign body. Eosinophilic gastroenteritis presents with non-specific gastrointestinal symptoms, and may involve the esophagus or colon [9]. Others types of gastritis include collagenous gastritis, postradiation gastritis, and drug-related gastritis.

Typical endoscopic findings of acute H. pylori infection include hemorrhagic spots on the fundus and/or high-body, nodular gastritis, and hypertrophic gastric rugae (Fig. 3). The endoscopic findings of nodular gastritis are small, round, yellowish-white nodules that represent histological lymphoid follicles [10]. Endoscopic nodular gastritis is more common at the antrum than the corpus in H. pylori infection.

The secreting ability of the gastric mucosal cells is still intact during active H. pylori infection. Therefore, increased PG or acid secretion may occur upon stimulation or inflammation. Intragastric pH levels correlate well with H. pylori density and severity of gastritis [11]. H. pylori-induced gastritis can be identified using serum PG levels, because PG II levels are increased and the PG I/II ratio is decreased in patients with H. pylori infection as compared with those without infection [12,13]. Serum PG II concentration is known to be more useful in predicting active H. pylori infection than is PG I concentration.

Regardless of age, nodular gastritis increases the risk of gastric cancer [14]. Although the serum PG assay is known to be more useful for the screening of intestinal-type gastric cancer than diffuse-type gastric cancer, a high PG II level indicates an increased risk of diffuse-type gastric cancer [15-17]. Therefore, H. pylori eradication is highly recommended in this stage of active infection; cellular changes seem to be reversible before the gastric mucosal cells progress beyond the point of no return [18,19].

Decreased serum PG I levels, open-type CAG, and old age are predictors of a hypoacidic state during H. pylori infection [23]. Once the normal gastric glands are replaced by irreversible fibrosis and IM, the gastric environment becomes hypoacidic. For this reason, gastroesophageal reflux (GERD) is rare in subjects with CAG and/or MG [24]. Advanced endoscopic grading of atrophic gastritis is inversely associated with GERD.

Gastric corpus atrophy is defined as a serum PG I/II ratio of < 3.0 and a serum PG I level of < 70 ng/mL [17]. Although endoscopic, histological, and serological atrophic gastritis are well correlated, the presence of gastric corpus atrophy is not always consistent with CAG found by endoscopy [25,26]. When histological atrophic gastritis progresses, serum PG I levels and the PG I/II ratio are decreased. Similarly, when the extent of atrophy is increased, the serum PG I/II ratio decreases. Moreover, the serum PG I/II ratio is significantly decreased in subjects with severe or moderate CAG than in those with mild CAG [27].

Endoscopic changes due to gastric atrophy are consequences of long-term H. pylori infection which progress from lesser curvature side of the antrum to greater curvature side of the corpus. Endoscopic findings of CAG reveal the extent of gastric atrophy by showing an atrophic border consisting of visible transparent vessels (Fig. 4). Endoscopy is a reliable method with high reproducibility which was shown to predict histological atrophy in a multinational study [28]. Gastritis staging, so-called operative link on gastritis assessment (OLGA) staging, provides information on the gastric mucosa by integrating the atrophy score and topography [29]. More recently, the Kyoto Global Consensus Meeting developed a global consensus on the classification of chronic gastritis [30]. It is important to discriminate endoscopic findings based on their characteristics (Fig. 5).

In countries where H. pylori infection-related chronic gastritis is common, endoscopic findings or the serum PG assay are often combined to evaluate CAG and MG [31,32]. MG exhibits various endoscopic findings such as irregular whitish mucosa, a villous appearance, mucosa with an uneven-surface, and patchy redness. Notably, CAG and/or MG induce spontaneous regression of H. pylori, because it is difficult for the bacterium to survive in the hypoacidic environment produced by severe CAG and/or MG [33-36]. Greater curvature side of the upper corpus seems to be the least atrophic and metaplastic site, and is the location in which H. pylori can survive for the longest period of time before spontaneous regression.

Endoscopic and serologic findings of CAG and MG are good tools for predicting the risk of gastric carcinogenesis [37]. Subjects with a low PG I/II ratio are at an increased risk for intestinal-type gastric cancer and dysplasia [38]. One study showed the significance of the topography of histologic gastritis as a marker to identify individuals at high risk for gastric cancer; pangastritis put patients at the highest risk, followed by corpus-predominant gastritis and antrum-predominant gastritis [39]. Furthermore, MG is also a predictive marker for intestinal-type gastric cancer [40]. A study showed that IM on greater curvature side of the corpus, along with a decreased serum PG I level, indicates a high risk of intestinal-type gastric cancer and dysplasia [41].

A long-term follow-up study showed that the changes induced by mild CAG and CSG are reversible, in both histological and serological findings [42]. The degrees of inflammation and activity, and lymphoid follicle infiltration decrease after H. pylori eradication [43]. Serum PG II is a good marker of intragastric environmental changes before and after H. pylori eradication [44].

Notably, even severe gastric atrophy and IM are reversible in some patients [45]. It has been reported that some cases of MG and corpus-predominant gastritis with a low serum PG I/II ratio were reversible [46,47]. On the contrary, no significant changes were found in the molecular alterations related to carcinogenesis even after H. pylori eradication [48].

The cancer risk after eradication depends on the extent of CAG before eradication, and is highly correlated with the severity of corpus atrophy [49,50]. In subjects with irreversible damage to the gastric mucosa, serum PG I levels and PG I/II ratio continue to decrease. Therefore, periodic endoscopic screening is required [51]. Nevertheless, only 5% of patients with severe CAG develop intestinal-type gastric cancer [52]. There is no consensus in Korea on the role of eradication in the prevention of gastric cancer [53-55], but endoscopic screening is recommended for these subjects, as it is for Korean Americans with known CAG, IM, or a family history of gastric cancer [56].

Spontaneous regression occurs in the most severe, late stages of gastric atrophy and/or IM when the stomach environment is inhospitable for H. pylori growth [57]. In such advanced conditions, the serum anti-H. pylori immunoglobulin G (IgG) assay reverts to a negative finding [58]. This indicates hypoacidity of the stomach, and also provides a rationale for measuring serum PG levels as a secondary means of gastric cancer screening [59]. Subjects with gastric corpus atrophy and low H. pylori concentration show the most impaired acid secretion and the highest risk of intestinal-type gastric cancer. Taken together, the greatest risk for intestinal-type gastric cancer is found in seronegative subjects with past infections and low PG I/II ratios [60-62].