Chronic gastritis

Abstract

Prevalence of chronic gastritis has markedly declined in developed populations during the past decades. However, chronic gastritis is still one of the most common serious pandemic infections with such severe killing sequelae as peptic ulcer or gastric cancer. Globally, on average, even more than half of people may have a chronic gastritis at present. Helicobacter pylori infection in childhood is the main cause of chronic gastritis, which microbial origin is the key for the understanding of the bizarre epidemiology and course of the disease. A life-long and aggressive inflammation in gastritis results in destruction (atrophic gastritis) of stomach mucosa with time (years and decades). The progressive worsening of atrophic gastritis results subsequently in dysfunctions of stomach mucosa. Atrophic gastritis will finally end up in a permanently acid-free stomach in the most extreme cases. Severe atrophic gastritis and acid-free stomach are the highest independent risk conditions for gastric cancer known so far. In addition to the risks of malignancy and peptic ulcer, acid-free stomach and severe forms of atrophic gastritis may associate with failures in absorption of essential vitamins, like vitamin B12, micronutrients (like iron, calcium, magnesium and zinc), diet and medicines.

Keywords: Helicobacter pylori; gastric cancer; gastritis; peptic ulcer.

Figure 1.

Corpus mucosa with “active” chronic gastritis (A): Inflammation is mononuclear but is accompanied with neutrophils and eosinophils (arrows) which penetrate into the surface epithelium. Normal (B): Normal corpus mucosa without any sign of inflammation is shown as a reference. HE stain × 500.

Figure 2.

Corpus mucosa. Normal (A): The layer of oxyntic glands is normal suggesting that the corpus mucosa is capable to secrete hydrochloric acid normally. Non-atrophic gastritis (B): Mild mononuclear inflammation is seen in upper layer (foveolar part) of the mucosa (“superficial chronic gastritis”) as indicated with arrows. The gland layer is intact suggesting that the acid secretion is normal in spite of the gastritis. Moderate atrophic gastritis in corpus (C): Intense chronic mononuclear inflammation occurs also in lower layers of the mucosa and is accompanied with a marked loss (atrophy) of normal oxyntic glands. The observation suggests that the stomach is hypochlorhydric but is not achlorhydric. Acid secretion is impaired due to loss of the parietal cells. Severe atrophic gastritis in corpus (D): Chronic inflammation is mild but all oxyntic glands are totally gone. Some foci of intestinal metaplasia occur in the lower right corner. Stomach is certainly acid free (achlorhydric). The patient is at risk for malabsorption of vitamin B12, and also the absorption of micronutrients (iron, calcium, magnesium and zinc) may be impaired. The pathologist may have difficulties to find Helicobacter pylori organisms in cases like this even though the atrophic gastritis would be of H. pylori origin. Instead, a mixed microbial flora (microbes other than H. pylori) is a common finding on the surface mucosa in cases like this. Alcian blue – PAS and modified Giemsa stains × 300.

Figure 3.

Antral mucosa. Normal (A): Normal number of antral G cells with typical “hallo” appearances occur in neck area of the pyloric glands (arrows). Non-atrophic chronic gastritis (B): Mononuclear inflammation occupies the whole mucosa giving an impression of gland loss (atrophy). Atrophic gastritis of mild to moderate degree in antrum (C): Inflammation is relative mild but there is a large area of pyloric glands lost and replaced with metaplastic glands (IM) as indicated with arrows. Severe atrophic gastritis in antrum (D): All pyloric glands are gone and the whole mucosa is “intestinalized”. Inflammation is mild, or moderate at most. Also the antral G cells are disappeared along with the loss of the normal pyloric glands. Therefore, the G-17 feedback response in physiological control of acid secretion is impaired. HE and Alcian blue – PAS stains × 300.

Figure 4.

Mean age-specific prevalence of total chronic gastritis and atrophic gastritis in biopsy samples from ∼500 consecutive endoscopy Finnish outpatients in the late 80s (Jorvi hospital, Espoo, Finland). The mean prevalences increase with age.

Figure 5.

Scheme on natural course and progression of Helicobacter pylori gastritis from a non-atrophic form to gastric malignancy (sc. “Correa cascade”). Several potentially pathogenetic factors and mechanisms, linked with carcinogenesis, play a role and are triggered stepwise on during the course and progression of the cascade.

Figure 6.

A computer simulation to demonstrate the “birth cohort phenomenon” in prevalence of Helicobacter pylori gastritis in a population consisting of cohorts with dissimilar birth years. Approximated from data on gastritis in Finland around the late 80s (see Figure 4).

Figure 7.

Relative risk of peptic ulcer disease (duodenal or gastric ulcer) or gastric cancer in various phenotypes of chronic atrophic Helicobacter pylori gastritis. The risks are presented as relative risks compared to risks in subjects with normal and healthy stomach mucosa (N/N category; yellow). The risks are extrapolated and estimated from a case-control study done in Finland in the 80s [69]. Note that the risks of peptic ulcer diseases and gastric cancer are associated with very dissimilar phenotypes of chronic gastritis.

Figure 8.

OLGA staging for risk of stomach cancer. Modified from a paper of Rugge et al [79]. The staging is a practical tool for the delineation of patients to high (stages III–IV) and low (stages 0–II) risk groups for cancer, for gastric cancer of the intestinal type in particular. The staging requires endoscopy and proper biopsy practice but can also be done non-invasively by a blood test with applying specific biomarkers (pepsinogen I and II, gastrin-17 and Helicobacter pylori serology) that reflect the function (acid secretion) and the structure of both antral and corpus mucosa in the blood plasma/serum.