Gastritis: Symptoms, Helicobacter pylori & Treatment
At a glance
Frequency
One of the most common stomach diseases; H. pylori prevalence in Germany around 30%
Most common cause
Helicobacter pylori — responsible for a large share of the chronic cases
Forms
Acute (mostly temporary) vs. chronic — type A (autoimmune), type B (H. pylori), type C (chemical)
Curable
Acute: mostly yes. Type B: generally curable through 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 refers to an inflammation of the gastric mucosa — the protective layer that lines the inner wall of the stomach. Normally this mucosa produces stomach acid for digestion and at the same time mucus and bicarbonate to protect the stomach wall. With gastritis, this delicate balance is usually disturbed.
Gastritis ≠ heartburn ≠ stomach ulcer
With
heartburn/reflux, stomach acid rises into the esophagus. With gastritis, the gastric mucosa itself is inflamed. A stomach ulcer is usually a deeper defect — a gastritis left untreated for a longer time can, however, lead to an ulcer.
¹
Interesting: a large proportion of people with a Helicobacter pylori infection have no or hardly any symptoms. In these cases the gastritis often remains unnoticed — but can nevertheless have long-term consequences.¹
2. Acute vs. chronic — the three types
Acute gastritis
Acute gastritis usually occurs suddenly — often within a few hours. Common triggers are excessive alcohol consumption, certain painkillers (NSAIDs: ibuprofen, diclofenac, ASA), severe stress (e.g. in the intensive care unit) as well as acute infections (e.g. noroviruses or food poisoning).
The symptoms can be severe at first, but mostly subside completely after the cause is removed. The duration is usually 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 disturbed absorption of vitamin B12 (up to pernicious anemia). Usually the body of the stomach is affected. Not rarely occurs together with other autoimmune diseases — e.g. Hashimoto's thyroiditis, type 1 diabetes. Not curable, but generally well controllable — especially through medically supervised vitamin B12 supplementation. Regular endoscopic checks are 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, the H. pylori prevalence is around 30%. Typically the stomach outlet (antrum) is affected. An untreated infection can lead to stomach and duodenal ulcers, a MALT lymphoma and an increased risk of gastric carcinoma. Type B gastritis is generally considered curable — through a combined antibiotic therapy (eradication, section 6). According to the current S2k guideline, a detected H. pylori should generally be eradicated.¹
Type C
Chemical (NSAIDs, bile acid reflux, alcohol)
Caused by a chemical irritation of the mucosa — most often by NSAID painkillers (ibuprofen, diclofenac, ASA) or bile acid reflux (e.g. after stomach surgery). Therapeutically important: avoid the triggering substance as far as possible; in addition, a PPI is often used as stomach protection. When NSAIDs are medically necessary (e.g. with rheumatoid arthritis), a PPI is usually prescribed alongside on a permanent basis.¹
3. Symptoms and warning signs
Typical symptoms
- Burning or dull pain in the upper abdomen — often after eating, sometimes also on an empty stomach
- A feeling of pressure, fullness and bloating — especially after meals
- Nausea and occasional vomiting
- Loss of appetite
- Heartburn and acid regurgitation
- Upper abdominal pain that can partly radiate into the back
- An unpleasant taste in the mouth
Warning signs — have them evaluated by a doctor immediately
Blood in the vomit (fresh red or coffee-ground-like) · Black, tarry stool (melena) · Very severe, sudden, persistent abdominal pain · Dizziness, weakness or circulatory problems in combination with stomach complaints · Unintentional weight loss over several weeks. With signs of bleeding or very severe upper abdominal pain, call 112 immediately (in the US: 911).
4. Causes and risk factors
The three main causes
Helicobacter pylori
Responsible for the majority of chronic gastritis. Prevalence in Germany around 30% (tending to decline). Transmission probably oral-oral or fecal-oral, mostly in childhood. Without therapy, the infection can lead to a lifelong chronically active inflammation. Relevant risk factors: lower socioeconomic status, infected family members, origin from regions with high prevalence.¹
NSAID painkillers (ibuprofen, diclofenac, ASA)
Inhibit, among others, the enzyme COX-1, which is important for the protection of the gastric mucosa. The risk rises with dose and duration. The combination of NSAIDs with cortisone or blood thinners is considered particularly risky. A more stomach-friendly alternative in many situations: paracetamol (acetaminophen). When NSAIDs are medically necessary, a PPI is often used as stomach protection.¹
Autoimmune
The immune system attacks the parietal cells of the stomach. Rarer than H. pylori gastritis — often occurs in combination with other autoimmune diseases.
Further risk factors
- Alcohol — can directly irritate the gastric mucosa, especially high-proof on an empty stomach
- Smoking — can impair the regeneration of the mucosa
- Chronic stress — can reduce the blood supply to the mucosa
- Long-term cortisone therapy — especially in combination with NSAIDs
- Bile acid reflux — e.g. after stomach surgery or with motility disorders
- Older age — the risk of atrophic gastritis and gastric carcinoma increases
5. Diagnosis: gastroscopy and H. pylori test
Not every person with stomach complaints needs a gastroscopy right away. In younger patients without warning signs, a non-invasive test for H. pylori can first be considered (so-called "test-and-treat"). The decision is always made by the treating doctor.¹
Gastroscopy — when recommended?
- Warning signs (signs of bleeding, unintentional weight loss, difficulty swallowing)
- First manifestation at an older age
- A lack of treatment success
- Suspicion of a stomach ulcer or a malignant change
- Follow-up check after eradication therapy with a pre-existing ulcer
Gastroscopy (gold standard)
Via a flexible endoscope, the gastric mucosa is assessed directly. Tissue samples (biopsies) for histology and a rapid test for H. pylori (urease test) can be taken. Sedation is possible on request. Important: PPIs should generally be paused a few weeks before an H. pylori detection — 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 the breath. Also used to check success after eradication.¹
Stool antigen test
Detection of H. pylori antigens in the stool. Simple to carry out, also well suited for children. Informative value comparable to the breath test.
Blood test (antibodies)
Generally only shows whether an infection ever existed — not whether one is currently still present. For a follow-up check it is mostly not suitable.
H. pylori test only after a PPI pause!
An H. pylori test should generally be done only a few weeks after stopping PPIs and a few weeks after antibiotic therapy — otherwise false-negative results are possible. The exact time intervals are determined by the treating doctor.
More: Preparing for a doctor's appointment.