Chronic active and atrophic gastritis as significant contributing factor to the development of gastric cystica profunda

Abstract

Gastric cystica profunda (GCP) is an uncommon but underestimated gastric lesion. Its precancerous potential determines its significance. In addition to previous mucosa injury due to operations, biopsy or polypectomy, chronic active and atrophic gastritis may also lead to the development of GCPs. By carefully examining the stomach and taking biopsy samples from the susceptible regions, the stage of atrophy can be determined. Chronic atrophic gastritis is a risk factor for cancer evolvement and it can also contribute to GCPs formation. GCPs frequently occur close to early gastric cancers (EGCs) or EGC can arise from the cystic glands. Endoscopic resection is an effective and minimally invasive treatment in GCP.

Key Words: Gastric cystica profunda, Chronic active gastritis, Atrophic gastritis, Operative Link for Gastritis Assessment staging, Early gastric cancer, Endoscopic resection

Core Tip: Gastric cystica profunda (GCP) is a premalignant lesion developing on basis of ischemia. Chronic active or atrophic gastritis are considered to be a significant etiological factors in the development of GCPs and carry a risk for cancer formation. GCPs, with or without early gastric cancer, can be removed effectively by endoscopic resection.

INTRODUCTION

In this editorial we comment on the article by Geng et al[1] published in the recent issue of the World Journal of Gastroenterology.

Gastric cystica profunda (GCP) is a rare gastric lesion characterized by poor clinical symptoms and mostly unremarkable endoscopic features. Therefore, the incidence of a polypoid cystic ectasia of the gastric glands is underestimated[2]. It’s pathomechanism remains obscure. A prior stomach operations, biopsy, or polypectomy can cause the development of GCP. In contrast, mucosa damage or ischaemia are factors that commonly manifest in chronic active and atrophic gastritis. Carcinoma cascade is well known since the last decade, intestinal metaplasia occurs following the loss of normal glandular tissue[3]. Helicobacter pylori (H. pylori) is frequently the cause of chronic inflammatory processes. Identification of high-risk individuals for chronic gastritis, appropriate diagnostic interventions and follow-up are critical to the prevention of invasive cancer.

It is yet not well understood how early stomach cancer development is related to GCP. The migration of stomach glands into the submucosa occurs when the muscularis mucosa is disrupted. GCP and gastric adenocarcinoma can occur simultaneously with recurrent erosion and regeneration of the mucosa if no surgical intervention was performed previously. This suggests that GCP is both a paracancerous lesion and a precancerous lesion based on the progression from dysplasia to invasive carcinoma. Mitomi et al[4] reported a case in which atypical or dysplastic epithelium in the deeper part of GCP was seen adjacent to carcinoma. In a Korean report on 39 GCP cases 16 were associated with early gastric carcinoma, 9 with adenoma and 3 with advanced adenocarcinoma[5]. If cancer cells are detected in GCPs, this may be because the submucosa provides an easier path for cancer cells to move through[6]. Data from Itami et al[6] suggest that gastric cancer (GC) has a tendency to arise in association with, linked to, above or near the GCPs, not growing from them. Xu et al[2] revealed dysplasia or intramucosal carcinoma in 50% of reported GCP cases; these were found in the glands overlying GCPs. Moreover, Kaizaki et al[7] described that EBV infection presenting together with chronic inflammation, may facilitate the development of GCPs and therefore GC. GCP may also be paracancerous or premalignant lesion. Alternatively, it might be the result of a field-effect damaging the stomach mucosa, which can result in cancer[6].

Endoscopic procedures play not only a role in adequate diagnosis of chronic inflammation, atrophy, or intestinal metaplasia, are also useful for differentiating submucosal lesions. Conventional white-light endoscopy, the most common endoscopic feature, is nonspecific in GCPs. Endoscopic ultrasonography is highly helpful in detecting the shape, size, and echoic patterns of GCP, but a definitive diagnosis should be established by histologic examination with numerous biopsy samplings to map the extent of the lesions. If GCP is discovered, according to standard protocols, endoscopic resection (ER; endoscopic mucosa resection or endoscopic submucosa dissection) depending on size, shape and location can be performed with en bloc and complete resection of the lesion[2]. According to data of the current article of Geng et al[1], ER might serve as an effective and minimally invasive treatment for GCP with or without early GCs (EGC).

CLINICAL IMPLICATION

A pathological examination is required for the diagnosis of chronic gastritis, therefore several appropriate biopsy samples are needed. Normal gastric mucosa contains only small numbers of scattered mononuclear inflammatory cells, increased infiltration of the lamina propria with mononuclear leukocytes suggest chronic inflammation while polymorphonuclear neutrophils indicate acute inflammation. Most often, they have an infectious etiology; gastritis is most commonly caused by H. pylori. The severity of inflammation depends on the H. pylori strain[3]. In order to standardize the pathological diagnosis, the updated Sydney System's recommendations are adhered to. The Operative Link for Gastritis Assessment (OLGA) and Operative Link for Gastritis Intestinal Metaplasia Assessment (OLGIM) stages allow for the identification of high-risk individuals with chronic gastritis who need special attention[8].

Active chronic inflammation can persist as non-atrophic chronic gastritis (no gland loss), or progress to multifocal atrophic gastritis, which is the initial significant step in the precancerous cascade followed by dysplasia and invasive carcinoma[3]. A different extent and topographical distribution of atrophy is associated with different cancer risk. Multiple biopsy samples should be used to map the mucosa, and the oxyntic and antral mucosa need to be examined as well. The earliest onset of atrophic–metaplastic transformation is located on the incisura angularis. The OLGA proposal recommends at least five biopsy samples from the following locations: The greater and lesser curvatures of the distal antrum, the lesser curvature at the incisura angularis and the anterior and posterior walls of the proximal corpus. The OLGA stage means the combination of the overall “antrum score” with the overall “corpus score”. The goal of this staging system is to help physicians to find high-risk patients for malignancy, develop a follow-up protocol and tailor a clinical or endoscopic management[9].

In a prospective study from Zhou et al[10], 71 patients with early GC and 156 patients with non-EGC underwent endoscopic examination and systematic biopsy. Logistic regression modeling showed significant correlations between EGC and moderate-to-severe EGA (Japanese endoscopic gastric atrophy classification) and OLGA stages III-IV, but no significant correlation between EGC and OLGIM stages[10].

Chronic inflammation due to atrophy and ischaemia are suggested to play a role in the development of GCPs, as repeated erosion and regeneration causes aberration of the gastric glands. GCP may be a risk factor for multiple GC.

CONCLUSION

According to the fact that GCPs may also be paramalignant or precancerous lesions, as was previously mentioned, its detection carries significance to prevent the precancerous cascade and invasive gastric formation, as well as identifying high risk patients for GC. Particularly in mucosal and submucosal types, the OLGA method could be used for screening. If GCP is discovered ER might serve as an effective and minimally invasive treatment even in cases when EGC exist. A prospective study is needed for better understanding the pathophysiology and to estimate incidence of GCP as well as coincidence with chronic active and atrophic gastritis. Although there are not enough data, the OLGA method may be used to screen GCPs, especially in mucosal and submucosal forms.