GastritisK29.7

Gastritis was first described by autopsy in the 1800s (Kayacetin 2104).

Phlegmonous gastritis was first described by Fränkl in 1889 (Trum 2014).

It was first classified as acute and chronic gastritis in 1947 (Kayacetin 2104).

The association 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).

The most common classification of gastritis is the Sydney classification, which was presented at the World Congress of Gastroenterology in Sydney in 1990 (Krams 2010).

Gastritis is defined as a histologically proven inflammation of the gastric mucosa and is not synonymous with dyspepsia (Kasper 2015). Gastritis thus represents a purely histological diagnosis (Labenz 2020).

There are different classifications of gastritis (Krams 2010).

The most common classification comprises 5 different categories in the so-called Sydney classification:

- 1. severity of inflammation (measurable by the density of lymphocytic / plasma cell infiltrates).

- 2. activity of the inflammatory process (measurable by the density of granulocytes)

- 3. occurrence and density of Helicobacter pylori

- 4. occurrence and expression of atrophic mucosal inflammation

- 5. occurrence and expression of metaplastic mucosal changes

Each of the categories is assigned a point value between 0 - 3. Mild changes are found at level 1, marked changes at level 2, and severe changes at level 3 (Krams 2010).

In addition, gastritis is differentiated between various forms of progression:

- I. Acute gastritis

Acute gastritis histologically shows a marked infiltrate of neutrophils, hyperemia and edematous swelling (Kasper 2015). Superficial epithelial defects to larger erosions are found. The latter is also referred to as "erosive gastritis" (Herold 2022).

Acute gastritis can be triggered by infections with:

- H. pylori (main pathogen)

- H. heilmannii

- Phlegmonous

- mycobacteria

- syphilis

- viral

- parasites

- Mycoses (Kasper 2015)

Bacterial infection of the stomach is also known as phlegmonous gastritis and is a rare but potentially life-threatening condition (Kasper 2015).

However, acute gastritis can also result from other noxious agents such as:

- alcoholic excess

- Alimentary excess

- stress due to e.g. trauma, postoperative, shock, intracranial diseases

- medications, e.g. especially acetylsalicylic acid, NSAIDs, corticosteroids, cytostatics

- Food poisoning due to e.g. toxin-producing staphylococci, streptococci, etc. (Herold 2022)

- II. chronic gastritis (Kasper 2015)

- II a. superficial gastritis

- II b. atrophic gastritis (Kayacetin 2104).

Chronic gastritis can be caused by untreated acute gastritis (Kasper 2015), provided that it is caused by Helicobacter pylori (Sauerbruch 2021).

Triggers of chronic gastritis can be:

- Helicobacter pylori

- autoimmune diseases

- undetermined pathogens (Kasper 2015).

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, and later there is severe destruction of the glands with atrophy and metaplasia (Kasper 2015).

The classification of chronic gastritis is based on histological features (Kasper 2015) by the so-called ABC- classification (Braun 2022):

- Type A:

In this case, antibodies against vestibular cells are found (Krams 2010), also referred to as "autoimmune gastritis" (AIG). There are preferentially in the fundus inflammatory signs with atrophy of the mucosa (Kayacetin 2104).

- Type B:

Here, bacterial inflammation due to e.g. Helicobacter species is found (Krams 2010).

- Type C:

Type C is a chemical toxic gastritis (Frühmorgen 2013). It is caused by drugs, bile reflux, etc (Krams 2010).

- III. unusual forms of gastritis (Kasper 2015)

- Lymphocytic gast ritis: Presumably autoimmune, lymphocytic gastritis occurs in approximately 0.2-0.4% of affected individuals (Krams 2010).

- Eosinophilic gastritis: This represents a rarely occurring form and is found especially in patients with milk and soy allergy (Verdaguer 1993).

- M. Crohn's gastritis

- Sarcoidosis gastritis

- isolated granulomatous gastritis

- Russell body gastritis

- Cytomegalovirus (CMV) Intranuclear inclusions are found in CMV- gastritis (Kasper 2015).

- Herpes simplex (Kasper 2015).

Other forms of gastritis include:

- Collagenous gastritis

This represents the counterpart of collagenous colitis (Krams 2010) and is characterized by subepithelial thick acellular collagen bands with damage to the surface epithelium and inflammatory changes. The involvement may be diffuse or in the form of patches. The cause is unknown. It occurs clustered with other collagenous bowel diseases or with autoimmune diseases (Kayacetin 2104).

- Radiation gastritis

It is rare. In this case, necrosis, edema, mononuclear inflammatory cell infiltrates are found in the glands of the gastric fundus. This form of gastritis is reversible (Kayacetin 2104).

- Phlegmonous gastritis (PG).

The cause of phlegmonous gastritis is as yet unknown (Trum 2014). It is clustered in extensive ulceration, gastric carcinoma, and after gastric surgery (Siewert 2006) and is also seen after routine esophagogastroduodenoscopy biopsies (Jenssen 2014).

It is an acute clinical picture that is not infrequently lethal (Kayacetin 2104).

In this case, histologically pronounced acute inflammatory infiltrates of the entire gastric wall (especially the submucosa [Siewert 2006]) are found. Sometimes necrosis is also detectable (Kasper 2015).

Pathogens are predominantly:

- Streptococci

- staphylococci

- E. coli

- Proteus

- Haemophilus species (Kasper 2015).

Phlegmonous gastritis particularly affects:

- elderly people

- alcoholics

- AIDS patients

- Mucosal injections with India ink

- Polypectomy (Kasper 2015)

- Type A gastritis:

The prevalence is between 2 - 5 %. However, it is often underdiagnosed (Coati 2015).

- Type B gastritis:

It represents the most common variant with up to 80% (Krams 2010).

- Type C- Gastritis:

This occurs in up to 15% of those affected by gastritis (Krams 2010).

- Phlegmonous gastritis:

This is extremely rare. So far, only 140 cases have been described worldwide (Trum 2014).

An imbalance of mucosa-damaging versus mucosa-protecting factors results in mucosal injury. In gastritis caused by alcohol or NSAIDs, for example, there is suppression of endogenous prostaglandin production (Braun 2022).

The bacterium Helicobacter pylori, for example, invades gastric glands, causing atrophy of the glands with a decrease in acid production and increasing metaplasia of the epithelium (Braun 2022).

In autoimmune gastritis, autoimmune processes against the parietal cells occur with formation of autoantibodies against the proton pump of the parietal cells. In up to 80% of cases, parietal cell antibodies are detectable. This in turn also causes reduced acid production (Braun 2022).

In acute gastritis, the following symptoms are found:

- sudden onset of epigastric pain

- nausea

- vomiting (Kasper 2015)

- loss of appetite

- unpleasant taste in the mouth (Herold 2022)

Chronic gastritis:

If acute gastritis is not treated, the picture of chronic gastritis develops (Kasper 2015).

Chronic gastritis may present with the symptoms of the acute form (Lehmeyer 2022), but the vast majority of patients are asymptomatic (Siegenthaler 2005).

Hematemesis may also occur as the disease progresses (Braun 2022).

Phlegmonous Gastritis:

Phlegmonous gastritis manifests clinically as

- severe epigastric pain

- fever

- defensive tension of the abdomen (Siewert 2006)

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

Gastroscopy

During gastroscopy, biopsies should always be taken from the antrum and corpus. If hematemesis is present, gastroscopy should be performed immediately or within 24 h at the latest (Braun 2022).

- Acute gastritis:

In the erosive course, the substance defect is limited to the lamina propria, in contrast to the substance defect in ulcer, which always involves the muscularis mucosa (Braun 2022).

- Autoimmune gastritis:

Here, the changes are usually limited to the fundus and corpus (Braun 2022).

- Helicobacter- pylori gastritis:

Antrum- dominant gastritis with typical erosions is seen. Sometimes there is corpus- dominant gastritis without erosions but with erythema and edema (Braun 2022).

- Chronic gastritis:

In chronic gastritis, a very thin mucosa with visible underlying blood vessels is found endoscopically (Kasper 2015).

ECG

To rule out posterior wall infarction as a differential diagnosis, a resting ECG should be performed in the presence of epigastric symptoms (Lehmeyer 2022).

Histologically, conclusions can be drawn about the form of gastritis.

- In case of inflammation of the lamina propria:

- diffuse:

- autoimmune gastritis

- lymphocytic gastritis

- eosinophilic gastritis

- collagenous gastritis (Kayacetin 2104)

- focal: mixed lymphohistiocytic or neutrophilic granules are found, such as after transplantation and inflammatory bowel disease (Kayacetin 2104)

- granulomatous: granulomatous gastritis such as in Crohn's disease, sarcoidosis, parasitic gastritis, mycobacteria, etc. (Kayacetin 2104)

- Lamina propria with mild or absent inflammation:

- acute gastritis

- reactive gastritis

- GAVE- syndrome (Gastric antral vascular ectasia)

- portal hypertensive gastropathy (PHG)

- Graft versus host disease (GVHD)

(Kayacetin 2104)

Differential diagnosis may include other diseases of the stomach or duodenum or diseases of the pancreas or gallbladder (Herold 2022).

In addition, a posterior wall infarction must be excluded as a differential diagnosis (Lehmeyer 2022).

- Ulcers

Gastritis may result in the development of a stress ulcer or gastric hemorrhage (especially in erosive gastritis) (Herold 2022).

- Gastric carcinoma

Helicobacter pylori has been considered a major cause of gastric carcinoma for 30 years (Waldum 2021).

Similarly, autoimmune gastritis (also known as type A- gastritis) and atrophy increase the risk of carcinoma (Labenz 2020).

- MALT- lymphoma (mucosa-associated lymphoid tissue).

This is not infrequently associated with type B gastritis (Siegenthaler 2005).

Depending on the type of gastritis help in healing:

- elimination of noxious substances

- temporary abstinence from food with renunciation of solid meals

- Proton pump inhibitors (PPI)

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

Type B gastritis:

In Helicobacter pylori gastritis, complete eradication with triple drug therapy - consisting of proton pump inhibitor plus 2 antibiotics(clarithromycin plus amoxicillin or clarithromycin plus metronidazole) - for 7 - 14 days is required. If necessary, bismuth may also be prescribed for 10 days as quadruple therapy (Lehmeyer 2022).

Phlegmonous gastritis:

Here, therapy with antibiotics is initially indicated. If there is no improvement, gastrectomy may be necessary (Kasper 2015).

Uncomplicated gastritis usually heals spontaneously (Herold 2022).

Phlegmonous gastritis

This is lethal in up to 70%, as it is a systemic toxicity (Trum 2014).

For mild gastrointestinal complaints (after clarification) also herbal relief:

Althaeae radix, Althaeae folium, Liquiritiae radix, Malvae folium, Menthae piperitae folium, Matricariae flos

without monograph: Lythri herba, Mentzeliae cordifoliae stipites, Anethi fructus, Calami rhizoma, Anethi fructus

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