See “Endoscopic Characteristics of Rugal Hyperplasia and Related Acid Condition in Helicobacter pylori-Infected Stomach” by Byung Chul Kim, Mi Ae Song, Sung Ho Kwon, on page 73-84.
Giant gastric rugae are often found during upper gastrointestinal endoscopic examinations. Most of these hyperplastic rugae are induced by the Helicobacter pylori infection in East Asia, which increases the risk of gastric cancer [1]. Nonetheless, data on the serum pepsinogen (PG) assay findings of rugal hyperplastic gastritis (RHG) are scarce. To resolve this issue, Kim et al. compared data between H. pylori-infected patients with and without RHG [2]. They found that the serum PG I/II ratio was lower in patients with RHG than in H. pylori-infected patients without RHG. Such differences were significant only in patients with closed-type chronic atrophic gastritis (CAG) and not in those with open-type CAG.
Notable findings of this study were the use of the serum PG assay and the strict diagnostic criteria for endoscopic diagnosis. As summarized in their figures, Kim et al. followed detailed, endoscopic criteria to diminish interpersonal variability [2]. By measuring the width of the gastric rugae with biopsy forceps after air inflation, they found a link between the low PG I/II ratio and the hypertrophic gastric rugae with a width ≥5 mm in patients with closed-type CAG. The lack of statistical significance among patients with open-type CAG might be due to the rarity of this disease and the persistently high PG II levels found in H. pylori-induced corpus gastritis [3].
Irrespective of the presence of the gastric rugae, the serum PG I and PG II levels increase with an active H. pylori infection and decrease with the progression to gastric corpus atrophy [4]. Furthermore, when there is an active H. pylori infection, PG II levels correlate more with the gastric secretory ability than with PG I levels and PG I/II ratios [5]. A high PG II level is a risk factor for diffuse-type gastric cancer [6], whereas low PG I/II ratios and PG I levels are risk factors for intestinal-type gastric cancer [7]. Giant rugae may progress to Bormann-type IV, a diffuse-type gastric cancer [8]; hence, high PG II levels are more reliable than low PG I/II ratios and PG I levels in patients with RHG.
Kim et al. analyzed H. pylori-infected patients with positive rapid urease test in their study [2]. The gastric secretory ability significantly increased in H. pylori-infected patients with RHG, as demonstrated by their high serum PG I, PG II, and gastrin levels. Nevertheless, they concluded that most patients with RHG were in a hypoacidic condition because a hypoacidic stomach was diagnosed when the PG I/II ratio was ≤2.7 [9]. It is important to exercise caution when interpreting these findings. Gastric acidity cannot be estimated solely from the PG I/II ratio in H. pylori-infected stomachs because PG levels increase during an active H. pylori infection. As demonstrated in Figure 3 by Kim et al., high PG II levels were consistently found with giant rugae regardless of the degree of CAG [2]. Moreover, most patients with RHG with a low PG I/II ratio (≤2.7) showed high PG II levels. These patients were different from those with truly hypoacidic stomachs who showed low PG I/II ratios because of the low PG I levels. In other words, most patients with RHG included in their study did not have hypoacidic stomach, but they showed low PG I/II ratios owing to their high PG II levels.
Giant rugae findings that suggest the presence of cancerous lesions include poor distention on air inflation and persistently high serum PG II levels; they may indicate scirrhous or Borrmann type IV gastric cancer (Fig. 1) [10]. Other etiologies for giant rugae include gastric large B cell lymphoma, Menetrier disease, secondary inflammatory changes due to severe extragastric inflammation, parietal cell hyperplasia, and the polyposis syndrome (i.e., the Cronkhite-Canada syndrome, the juvenile polyposis syndrome, gastric hyperplastic polyposis, and familial adenomatous polyposis with fundic gland polyps). Regardless of the etiological differences (Table 1), gastric malignancies are often missed in the giant rugae because of the false-negative biopsy findings. Hence, it should be followed up with gastroscopy and serum PG assays, especially in H. pylori-infected patients after eradication of the infection. If giant rugae with poor distention and high PG II levels are persistent even after eradication of H. pylori, abdominal computed tomography and/or endoscopic ultrasonography should be performed to exclude gastric cancer lying beneath the rugae.
In summary, giant rugae show an increased gastric secretory ability in the presence of the H. pylori infection. Nonetheless, PG I/II ratios are low because PG II levels are higher than PG I levels. Therefore, in H. pylori-infected stomachs with high PG II levels, a low PG I/II ratio may not indicate hypochlorhydria. To detect gastric cancer in these patients, the persistence of giant rugae with poor distention and high serum PG II levels should be checked after H. pylori eradication.
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