Gastritis, chronic K29.5

Chronic gastritis has been known since the early decades of the 20th century. However, it only gained greater attention after the discovery of Helicobacter pylori (Sipponen 2015).

The link between colonization of the stomach by Helicobacter pylori and the development of gastritis was demonstrated in 1983 by a self-experiment of the first describer Barry Marshall (Trede 1994 / Hahn 1999), who received the Nobel Prize in Medicine for this together with JR Warren in 2005 (Frauenschläger 2015).

The division into acute and chronic gastritis was first established in 1947 (Kayacetin 2104).

The American pathologist Correa was the first to describe the morphological carcinogenesis of the stomach in 1992 (Correa 1992).

Chronic gastritis (CG) is defined as histologically proven inflammation of the gastric mucosa leading to atrophic (superficial) changes in the mucosa (Kasper 2015). CG is a preneoplastic disease (Shah 2021).

Chronic gastritis is chronologically divided into a:

- superficial gastritis, non-atrophic (Sipponen 2015) at the beginning of the disease

- atrophic gastritis (in the further course [Kayacetin 2014]).

Classification of chronic gastritis according to histological features (Kasper 2015) is done by the so-called ABC classification (Braun 2022):

- Type A:

The inflammatory changes with atrophy of the mucosa (Kayacetin 2104) preferentially affect cardia and corpus (Herold 2022) with typical recess of the antrum (Kasper 2015).

Antibodies against vestibular cells are found (Krams 2010), hence the name "autoimmune gastritis" (AIG). Type A occurs less frequently than type B (Kasper 2015).

- Type B:

Here, bacterial inflammation is found, predominantly caused by Helicobacter pylori (Herold 2022).

The inflammatory changes are predominantly in the antrum (Kasper 2015) and show an ascending spread with atrophy of the glandular bodies and vestibular cells. This results in hypochlorhydria in type B (Herold 2022). Type B occurs more markedly than type A. At the onset of the disease, the number of H. pylori is highest and decreases with progression of gastric atrophy (Kasper 2015)

- Type AB:

These terms, used predominantly in Anglo-Saxon countries, denote a mixed form of inflammation with respect to its localization (Kasper 2015).

- Type C:

Type C is a chemically toxic gastritis (Frühmorgen 2013). It is caused by drugs, bile reflux, etc. (Krams 2010) and induces chronic gastritis of the antrum (Herold 2022).

- Rarely occurring special forms of chronic gastritis:

These include, for example:

Crohn's- gastritis, lymphocytic gastritis, eosinophilic gast ritis (Herold 2022).

Another classification, the so-called OLGA/OLGIM classification (Operative Link on Gastritis/IM Assessment or Operative Link for Gastric Intestinal Metaplasia Assessment) is used to categorize patients in low, intermediate or high risk for developing gastric cancer (Sipponen 2015).

from: Sipponen P, Maaroos HI (2015)

Chronic gastritis is one of the most common lifelong diseases, affecting approximately half of the world's population (Sipponen 2015).

Shah (2021) estimates the prevalence of the U.S. population with respect to chronic gastritis caused by H. pylori infection at 15% and autoimmune gastritis between approximately 0.5-2%. The latter mainly affects women. The prevalence increases in the presence of other autoimmune diseases (Shah 2021).

Type-A occurs in about 5 %, type- B in about 80 %, type-C in about 15 % of patients with chronic gastritis. In Germany, however, the number of type B sufferers is now declining (Herold 2022).

There is a high infestation with H. pylori, preferably in southern and eastern Europe (Herold 2022).

B gastritis occurs with increasing age (Kasper 2015).

The main cause of chronic gastritis is an infection with Helicobacter pylori in up to 90 % (Sipponen 2015).

Chronic gastritis can be caused by untreated acute gastritis with Helicobacter pylori (Kasper 2015).

H. pylori is transmitted orally or fecally as early as infancy (Herold 2022 / Sipponen 2015). The more toxic the strain, the more active and aggressive the chronic gastritis (Sipponen 2015).

Other triggers may include:

- autoimmune diseases

It is as yet unclear whether this is a disease in its own right or whether it is primarily an infection with H. pylori that triggers an autoimmune response in appropriate individuals

(Sipponen 2015).

- Undetermined pathogens (Kasper 2015).

Type A gastritis (so-called autoimmune gastritis):

- H. pylori (in up to 50% of cases).

(Herold 2022)

Type B gastritis (also called HP gastritis):

- H. pylori

- Helicobacter heilmannii (zoonosis transmitted by cats or dogs [Herold 2022]).

Type C gastritis:

- Medications such as ibuprofen , diclofenac

- Biliary reflux (Herold 2022)

Helicobacter pylori, the main causative agent of chronic gastritis, spreads from proximally across the gastric mucosa and causes a marked change in the morphology and function of the gastric mucosa.

There are disturbances in the secretion of hydrochloric acid and intrinsic factor due to atrophy in the body area. This severely impairs the absorption of essential vitamins such as Vit. B 12 (Sipponen 2015).

In addition, disturbances in gastrin 17 synthesis and in secretion from antral G cells are found (Sipponen 2015).

As the disease progresses, the vestibular cells disappear and there is permanent hypo- or achlorhydria. However, it is equally possible that low intragastric acidity may result in spontaneous resolution of H. pylori infection (Sipponen 2015).

The development of gastric carcinoma occurs through a sequential series of histomorphologic changes in the gastric mucosa, also known as the Correa cascade:

- chronic gastritis

- atrophy

- intestinal metaplasia

- mucoid metaplasia

- dysplasia

- invasive carcinoma (Frauenschläger 2015).

Type A gastritis:

In autoimmune gastritis, antibodies are found against the parietal cells of the gastric corpus. These are recognized by CD4+ T lymphocytes as autoantigens and secrete Th1 cytokines as the onset of an autoimmune reaction. There is subsequently increased production of anti-parietal cell antibodies (APCA) and anti-intrinsic factor antibodies (AIAF) with autoimmune destruction of the gastric glands leading to atrophy (Venerito 2022).

The role of autoimmunity and genetics in the progression of chronic gastritis is not yet well understood (Sipponen 2015).

Chronic gastritis may be accompanied by the symptoms of acute gastritis (Lehmeyer 2022), such as:

- epigastric pain

- nausea

- vomiting (Kasper 2015)

- loss of appetite

- unpleasant taste in the mouth (Herold 2022)

- functional dyspepsia (Watari 2014).

If the cause of chronic gastritis is H. pylori infestation, there may be halitosis and/or nonspecific upper abdominal symptoms (Herold 2022).

However, the vast majority of patients remain asymptomatic (Siegenthaler 2005).

The diagnosis of gastritis is guided by anamnestic data and gastroscopy. Histological examination is ultimately conclusive (Herold 2022).

If type A gastritis is suspected, certain antibody tests should be performed in addition to the usual laboratory tests (see "Laboratory" for details).

- Gastroscopy:

In chronic gastritis due to H. pylori infection, a superficial gastritis with inflammatory changes of the lamina propria is found endoscopically at the beginning of the disease (Kasper 2015). The antrum is mainly affected (Sipponen 2015).

As the disease progresses, the mucosa appears very thin with visible underlying blood vessels (Kasper 2015) and expands to the corpus or fundus (Sipponen 2015).

In chronic autoimmune gastritis, the corpus and fundus are primarily affected (Li 2018).

Diagnostics for Helicobacter pylori

- Helicobacter urease test (HUT)

- 13C- breath test

- HP detection in stool

- in case of resistance: culture and PCR (Herold 2022)

Serological tests can detect antibodies to detect H. pylori infection. Cannot distinguish between acute but chronic form of gastritis (Azer 2022).

Determination of Hb, MCV, and ferritin may reveal evidence of microcytic anemia suggestive of chronic bleeding (Herold 2022).

Type A gastritis:

Detection of

- circulating antibodies against parietal cells (PCA).

- H+, K+- ATPase AK (in approximately 90%).

- Intrinsic factor (IF) antibodies (in approx. 70 %)

- Determination of vitamin B12 (Herold 2022)

Kasper (2015) additionally recommends the determination of serum biomarkers:

- Pepsinogen I and II

- Gastrin - 17

At the onset of the disease:

- inflammatory cell infiltrate of the lamina propria with lymphocytes, plasma cells and few neutrophils

- Edema and cellular infiltrates between the gastric glands

As the disease progresses, signs of atrophic gastritis with:

- deeper spread of inflammatory infiltrates

- morphological change of the glands in an ileum phenotype with goblet cells (intestinal metaplasia)

- progressive destruction of the glands

In the final stage:

- loss of the glandular structures

- only sparse infiltrates remain (Kasper 2015)

- histological detection of H. pylori

Here, the specificity is almost 100 % (Fischbach 2022).

Histologically, there are mainly inflammatory cell infiltrates of lymphocytes and plasma cells, and to a lesser extent neutrophils. The inflammatory changes are patchy, initially superficial, later there is severe destruction of the glands with atrophy and metaplasia (Kasper 2015).

- Acute gastritis

- Collagen gastritis

This is a very rare clinical picture with histologically thickened collagen band below the surface epithelium in combination with signs of inflammation of the lamina propria (Hinterberger 2014).

- Achlorhydria (anacidity).

This results from atrophy of the vestibular cells (Herold 2022). It can be seen as a mechanism of spontaneous H pylori elimination due to loss of the mucosa of the antrum (Fischbach 2022).

Type A gastritis:

- Gastric carcinoma

Seropositivity for H. pylori increased the risk of developing gastric cancer 3- to 6-fold (Kasper 2015).

- (prae)- atrophic gastritis.

- Vitamin B 12- deficiency anemia, also called " pernicious anemia " due to absence of intrinsic factor (Herold 2022).

Type B gastritis:

- Iron deficiency anemia

- Ventricular ulcer (occurs in about 1 %)

- Duodenal ulcer (occurs in about 5 %)

- Development of type A gastritis (occurs in about 5 %)

- gastric carcinoma (the risk is 1: 3,000)

- gastric B-cell or MALT lymphoma (found in 1: 40,000)

- idiopathic thrombocytopenia (ITP)

- idiopathic chronic urticaria (very rare)

- in case of existing liver cirrhosis possible painful of hepatic encephalopathy

- Guillain-Barre syndrome (Herold 2022)

Type C gastritis:

- ulcers

- gastric hemorrhage, etc. (Herold 2022)

Depending on the cause of gastritis help in healing:

- Elimination of noxious substances

- Passenger food abstinence with renunciation of solid foods

- Proton pump inhibitors (PPI)

- In case of nausea / vomiting, administration of an antiemetic such as Vomex A (Herold 2022).

Autoimmune gastritis

If type A gastritis is caused by H. pylori, eradication is indicated (see Internal Therapy).

In the case of other causes, a causal therapy is still lacking with regard to autoimmune gastritis. Only the difficulties such as vitamin B12 deficiency, iron deficiency can be treated or prevented (Venerito 2022).

Helicobacter pylori gastritis

In the case of chronic gastritis caused by H. pylori, drug therapy is always indicated

- positive H. pylori test

- histological evidence of H. pylori (Fischbach 2022)

Therapy of chronic gastritis primarily aimed at sequelae (Kasper 2015).

- First-line therapy

For Helicobacter pylori gastritis, the guideline indicates treatment with quadruple drug therapy for at least 10 days (Fischbach 2022).

The therapy consists of a proton pump inhibitor plus 2 antibiotics ( clarithromycin plus amoxicillin or clarithromycin plus metronidazole ) with additional administration of bismuth (Lehmeyer 2022).

The goal of first-line therapy for C. pylori gastritis should be an eradication rate of > 90%. The efficacy of the therapy should be verified: in uncomplicated chronic gastritis by e.g. a non-invasive stool test, in complicated form of the disease by a control gastroscopy (Fischbach 2022).

- Second-line therapy

Therapy should be based on resistance testing (Fischbach 2022).

- Third-line therapy

This should always be performed by specialists (Fischbach 2022).

Chronic gastritis begins id R. as early as infancy as simple mononuclear inflammation and progresses within years or decades to atrophic gastritis with loss of normal mucosal glands in the antrum or corpus or fundus fortress. The missing glands are replaced by immature glandular elements (so-called gut-type glands) (Sipponen 2015).

Chronic gastritis, if caused by infection with H. pylori and has not yet developed into end-stage atrophic gastritis, can be cured by eradication of H. pylori (Sipponen 2015).

In the NHANES III study from 2013 (Chen), it was shown that mortality is not increased with H. pylori infection, but that there are certainly protective effects with regard to the development of apoplexy (Fischbach 2022).

Currently, no recognized prevention is available to prevent H. pylori gastritis (Fischbach 2022). In contrast, it is known that gastric ulcers and gastric carcinomas occur very rarely without coexisting chronic gastritis (Sipponen 2015).

In autoimmune gastritis, patients should be offered an endoscopic surveillance program to detect early the development of gastric carcinoma (there is up to a threefold increased risk) (Venerito 2022).

After therapy of chronic gastritis caused by C. pylori, tests such as breath or stool tests should confirm successful eradication at the earliest 4 weeks after drug treatment or 2 weeks after discontinuation of PPI medication. Further monitoring is not required (Fischbach 2016).

Under ongoing PPI therapy, tests may be falsely negative because PPI suppresses but does not eradicate H. pylori (Braun 2022).

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