Gastritis:
Symptoms, Helicobacter pylori & Treatment
At a glance
Frequency
One of the most common stomach conditions; H. pylori prevalence in Germany around 30%
Most common cause
Helicobacter pylori — responsible for the majority of chronic cases
Types
Acute (mostly transient) vs. chronic — Type A (autoimmune), Type B (H. pylori), Type C (chemical)
Curable
Acute: usually yes. Type B: generally curable via eradication. Types A and C: controllable
Medications (selection)
PPIs (omeprazole, pantoprazole), bismuth quadruple therapy for H. pylori, antacids
ICD-10
K29
1. What is gastritis?
Gastritis means an inflammation of the gastric mucosa — the protective lining of the inside of the stomach. Normally, this mucosa produces stomach acid for digestion and at the same time mucus and bicarbonate to protect the stomach wall. In gastritis, this delicate balance is usually disturbed.
Gastritis ≠ heartburn ≠ stomach ulcer
In
heartburn/reflux, stomach acid rises into the esophagus. In gastritis, the gastric mucosa itself is inflamed. A stomach ulcer is generally a deeper defect — though gastritis left untreated for a long time can lead to an ulcer.
¹
Notably, the majority of people with a Helicobacter pylori infection have few or no symptoms. The gastritis often goes unnoticed in these cases — but can still have long-term consequences.¹
2. Acute vs. chronic — the three types
Acute gastritis
Acute gastritis generally comes on suddenly — often within a few hours. Common triggers are excessive alcohol consumption, certain painkillers (NSAIDs: ibuprofen, diclofenac, aspirin/ASA), severe stress (e.g. in intensive care) and acute infections (e.g. norovirus or food poisoning).
Symptoms can be intense at first but usually resolve completely once the cause is removed. The duration is generally in the range of a few days to a few weeks.
Chronic gastritis — the three ABC types
Type A
Autoimmune gastritis
A rarer form: the immune system attacks the acid-producing parietal cells of the stomach. Possible consequences: reduced stomach acid production and impaired absorption of vitamin B12 (up to pernicious anemia). The gastric body is usually affected. Not uncommonly occurs together with other autoimmune conditions — e.g. Hashimoto's thyroiditis, type 1 diabetes. Not curable, but generally well manageable — particularly with medically supervised vitamin B12 supplementation. Regular endoscopic follow-up is often recommended.
Type B
Bacterial (Helicobacter pylori) — most common form
By far the most common form of chronic gastritis. Caused by the bacterium Helicobacter pylori, which can survive in the acidic stomach environment. In Germany, H. pylori prevalence is around 30%. The gastric outlet (antrum) is typically affected. An untreated infection can lead to gastric and duodenal ulcers, MALT lymphoma and an increased risk of gastric cancer. Type B gastritis is generally considered curable — through combination antibiotic therapy (eradication, see section 6). According to the current S2k guideline, a confirmed H. pylori infection should generally be eradicated.¹
Type C
Chemical (NSAIDs, bile reflux, alcohol)
Caused by chemical irritation of the mucosa — most often by NSAID painkillers (ibuprofen, diclofenac, aspirin/ASA) or bile reflux (e.g. after stomach surgery). Therapeutically important: avoid the triggering substance where possible; in addition, a PPI is often used as gastric protection. When NSAIDs are medically necessary (e.g. for rheumatoid arthritis), a PPI is usually prescribed alongside on a long-term basis.¹
3. Symptoms and warning signs
Typical complaints
- Burning or dull pain in the upper abdomen — often after eating, sometimes also on an empty stomach
- Feeling of pressure, fullness and bloating — especially after meals
- Nausea and occasional vomiting
- Loss of appetite
- Heartburn and acidic belching
- Upper abdominal pain that can in some cases radiate to the back
- An unpleasant taste in the mouth
Warning signs — see a doctor immediately
Blood in vomit (fresh red or coffee-ground-like) · Black, tarry stool (melena) · Very severe, sudden, persistent abdominal pain · Dizziness, weakness or circulatory problems combined with stomach symptoms · Unintended weight loss over several weeks. With signs of bleeding or very severe upper abdominal pain, call 112 immediately.
4. Causes and risk factors
The three main causes
Helicobacter pylori
Responsible for the majority of chronic gastritis. Prevalence in Germany around 30% (with a downward trend). Transmission is presumed to be oral-oral or fecal-oral, mostly during childhood. Without treatment, the infection can lead to lifelong chronic-active inflammation. Relevant risk factors: lower socioeconomic status, infected family members, origin in regions with high prevalence.¹
NSAID painkillers (ibuprofen, diclofenac, aspirin/ASA)
Inhibit, among other things, the COX-1 enzyme, which is important for protecting the gastric mucosa. Risk rises with dose and duration. Combining NSAIDs with cortisone or blood thinners is considered particularly risky. Gentler alternative on the stomach in many situations: acetaminophen (paracetamol). When NSAIDs are medically necessary, a PPI is often used as gastric protection.¹
Autoimmune
The immune system attacks the parietal cells of the stomach. Rarer than H. pylori gastritis — often occurs together with other autoimmune conditions.
Other risk factors
- Alcohol — can irritate the mucosa directly, particularly high-proof drinks on an empty stomach
- Smoking — can impair mucosal regeneration
- Chronic stress — can reduce blood flow to the mucosa
- Long-term cortisone therapy — particularly in combination with NSAIDs
- Bile reflux — e.g. after stomach surgery or with motility disorders
- Older age — risk of atrophic gastritis and gastric cancer rises
5. Diagnosis: gastroscopy and H. pylori testing
Not everyone with stomach complaints needs an immediate gastroscopy. In younger patients without warning signs, a non-invasive test for H. pylori can first be considered (a so-called "test-and-treat" approach). The decision is always made by your treating doctor.¹
Gastroscopy — when is it recommended?
- Warning signs (signs of bleeding, unintended weight loss, swallowing problems)
- First onset at an older age
- Lack of treatment response
- Suspicion of a stomach ulcer or a malignant change
- Follow-up after eradication therapy in a pre-existing ulcer
Gastroscopy (gold standard)
Through a flexible endoscope, the gastric mucosa is assessed directly. Tissue samples (biopsies) for histology and a rapid urease test for H. pylori can be taken. Sedation is available on request. Important: PPIs should generally be paused for several weeks before testing for H. pylori — they can falsify the test result.¹
¹³C urea breath test
Considered the most accurate non-invasive test. The patient drinks a labeled urea solution — if H. pylori is present, the urea is split and becomes measurable in exhaled air. Also used to confirm treatment success after eradication.¹
Stool antigen test
Detects H. pylori antigens in the stool. Easy to perform and well suited for children. Accuracy comparable to the breath test.
Blood test (antibodies)
Generally only shows whether there has ever been an infection — not whether one is currently still present. Usually not suitable for follow-up monitoring.
H. pylori test only after a PPI pause!
An H. pylori test should generally only take place several weeks after stopping PPIs and several weeks after antibiotic therapy — otherwise false-negative results are possible. The exact intervals are determined by your treating doctor.
Learn more: Preparing for a doctor's appointment.