Histological changes of esophageal and gastric mucosa in hiatal hernias

Abstract

Background. Morphological changes in the esophageal mucosa depend on the duration of reflux esophagitis. In type I hiatal hernia (HH), morphological changes are pronounced, the transition of the pathologi­cal process from inflammation to metaplasia/dysplasia is observed, while in HH type II, changes in the esopha­geal mucosa are less significant. Another associated pathology is inflammation of the gastric mucosa, which affects the stages and duration of treatment. Purpose: to investigate histological and morphometric differences of the esophageal and gastric mucosa depending on the type of HH. Materials and methods. The study was conducted on biopsy material of the esophageal and gastric mucosa in patients with HH (n = 34) who were divided by its types: type I — axial HH (n = 24) and type II — paraesophageal HH (n = 10). To study the histological structure, biopsy sections 5–7 µm thick were cut using a rotary microtome РM60-EКA, and staining was carried out using the standard method with hematoxylin-eosin. To obtain morphometric data, the sections were photographed with a light microscope XSZ-21 (Ukraine) and measured using Image J.45S software (USA). Results. Morphological study has shown that the development of pathological changes in the esophageal mucosa on the background of HH type I was accompanied by an increase in the height of the basal layer in 62.5 % of cases, an increase in the height of the papillae in 66.7 %, an expansion of the intercellular space in 83.3 %, the presence of eosinophils in the infiltrate in 20.8 %, lympho-plasmacytic inflammatory infiltration in 75.0 % (with HH type II, in 70.0 %), ballooning degeneration — in 33.3 % of cases (with HH type II, in 50.0 % of cases). Barrett’s esophagus was observed in 23.5 % of patients with HH type I: 14.7 % had intestinal metaplasia of the small- and large-intestine type, and 8.8 % had high-grade dysplasia. In HH type I, chronic non-atrophic gastritis (CNG) was diagnosed in 66.7 % of cases and chronic atrophic gastritis (CAG) — in 33.3 %, whereas in HH type II, CNG was diagnosed in all cases. According to morphometric studies of the gastric mucosa in case of CAG and CNG against the background of HH type I, a significant difference was found in the depth of the pits (p < 0.05), the length of fundic glands (p < 0.05), the height of the surface epithelium (p < 0.05) and the foveolar epithelium (p < 0.05). Significant changes between HH type I and type II were found regarding the thickness of the gastric mucosa (p < 0.05). The highest number of cells of the inflammatory infiltrate of the gastric CO was observed in CAG against the background of type I HH (p < 0.05). Conclusions. HH is accompanied by the development of esophagitis, the histological examination of which revealed an increase in the height of the papillae, basal layer, expansion of the intercellular space, ballooning degeneration, lymphocytic-neutrophilic and eosinophilic infiltration of the esophageal mucosa. The height of the basal layer in HH type I exceeds the norm morphometrically by 86.9 % (p < 0.01), in HH type II — by 68.8 % (p < 0.01), and the height of the papillae — by 56.7 and 46.6 %, respectively (p < 0.01). In HH type I, 23.5 % of patients were histologically diagnosed with Barrett’s esophagus. In HH type I, CNG was diagnosed in 66.7 % of cases, CAG — in 33.3 % of cases, and in HH type II, all patients had CNG.