
Gastritis stands out as one of the most prevalent stomach ailments. Often, the inflammation proceeds without pain, which can be misleading. Gastroenterologist Natalia Igorevna Trofimovskaya shared with “Rambler” insights on the causes of gastritis development, its treatment methods, and the required dietary approach.
What Gastritis Is
The diagnosis of “gastritis” encompasses a range of conditions sharing a common feature: inflammation of the stomach’s mucosal lining. According to the Ministry of Health data, there are 462 reported cases per 100,000 individuals. This equates to roughly one affected person in every subway car during peak hours.
Gastritis can manifest as acute (persisting for under three months) or chronic.
Causes
Several factors, or combinations thereof, can trigger this inflammation.
Infection
Most frequently, the inflammation is initiated by the bacterium Helicobacter pylori. This is an extremely common pathogen. The World Gastroenterology Organisation estimates that half the global population is infected. Russian statistics, per a study in the journal Helicobacter, indicate that 38.8% of the population carries the infection. However, not all carriers necessarily develop gastritis. Certain individuals are more susceptible to H. pylori, raising their likelihood of inflammation. Genetic predispositions and lifestyle choices play a role here.
Helicobacter pylori is not the sole cause of infectious gastritis. Other bacteria (Helicobacter heilmannii, Enterococcus, Mycobacteria), viruses (Enterovirus spp., Human cytomegalovirus, Epstein-Barr virus), fungi (Mucorales, Candida, Histoplasma capsulatum), and parasites (Cryptosporidium, Strongyloides stercoralis) can also induce inflammation, although these instances are rarer in clinical practice.
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Alcohol and Smoking
Alcohol renders the stomach vulnerable to digestive juices. Frequent and heavy consumption can lead to alcoholic gastritis.
Nicotine impairs blood supply to the stomach lining and compromises its defense mechanisms. Consequently, gastritis progresses more rapidly in smokers, and atrophic gastritis—considered a risk factor for stomach cancer—is more common.
“Atrophy is a consequence of years of inflammation, resulting in a reduction of functional cells in the gastric mucosa, which are partially replaced by intestinal epithelium. This condition is termed intestinal metaplasia. The extent of atrophy and metaplasia can vary. The risk of stomach cancer is determined based on the type of metaplasia, the severity of the atrophy, family history, and coexisting conditions.”
Important Note: While food may provoke gastrointestinal symptoms, diet itself does not cause gastritis. Even spicy dishes do not induce inflammation; in fact, they can sometimes suppress gastric acid secretion.
“Substances found in ginger and chili peppers, such as capsaicin, exhibit beneficial properties for mucosal healing and overall GI tract motility. Whether to include them is a matter of personal habit and preference,” the gastroenterologist notes.
Medications
Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, nimesulide, and diclofenac, irritate the stomach’s epithelium. Prolonged and regular use can damage the mucosa, leading to gastritis and the formation of ulcers. This risk escalates if the person is infected with H. pylori and is taking NSAIDs.
Stress
In high-risk individuals, gastritis can develop following physiological stress. This can occur after major trauma or surgery, where the body initiates a cascade of reactions that leave the gastric lining vulnerable to ulcer formation.
It is specifically physiological stress being referred to, although some studies on mice suggest that emotional shocks and prolonged depression might also impact the GI tract.
Other Illnesses
Gastritis can arise as a complication of other diseases. For instance, inflammation of the gastric lining is observed in patients with Crohn’s disease, vasculitis (blood vessel inflammation), or sarcoidosis (an autoimmune inflammatory disorder).
Autoimmune gastritis is recognized separately, occurring when the body mistakenly attacks its own gastric mucosal cells. This most often happens in patients who already have other autoimmune conditions, such as Hashimoto’s disease or type 1 diabetes.
Gastritis Symptoms
Since the stomach lining lacks pain receptors, gastritis frequently presents without any symptoms. However, H. pylori infection can trigger dyspepsia (digestive disorders) and manifest with symptoms such as:
upper abdominal pain;
nausea and vomiting;
heartburn;
a sensation of stomach fullness.
Important: Not every patient with H. pylori infection and digestive upset has gastritis. Therefore, the Kyoto Consensus on Gastritis classifies dyspepsia caused by this bacterium as a distinct condition.
“Gastritis strictly implies inflammation of the gastric mucosa confirmed via morphological examination—that is, studying samples of this lining under a microscope. Discomfort after eating, belching, bloating, and even areas of mucosal redness noted by an endoscopist do not, in themselves, confirm gastritis,” the gastroenterologist clarifies.
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Diagnosis
Not all stomach pain signifies inflammation, and not every H. pylori carrier suffers from gastritis. Consequently, diagnosis requires undergoing several assessment stages.
Laboratory Tests
The objective of lab tests is to detect H. pylori infection. Results can be influenced by external factors, such as medication use. Thus, the choice of testing method must be decided by a physician.
¹³C-Urea Breath Test. The patient consumes a fluid containing carbon-14. They then exhale into a sealed bag. The presence of radioactive carbon traces in the breath determines the presence or absence of the bacterium. This is the most accurate non-invasive test. A Cochrane review and meta-analysis indicated a sensitivity (ability to correctly identify the sick) of 94% and a specificity (ability to correctly identify the healthy) of 90%.
Antigen Tests. This method detects the infection via a stool sample. The specificity mirrors that of the breath test, but sensitivity is lower at 83%.
Blood Tests. Serological methods are better suited for epidemiological statistics. They confirm prior exposure to the bacterium but cannot definitively indicate a current infection. Therefore, they are of limited value for clinical diagnosis.
Endoscopy
A positive test for H. pylori is insufficient for diagnosis; a visual inspection of the stomach walls via esophagogastroduodenoscopy (EGD or simply gastroscopy) is mandatory. An endoscope (a flexible tube with an optical device) is passed down the esophagus into the stomach. This allows the physician to assess the lining and take a biopsy—a tissue sample for microscopic examination.
“Paradoxically, individuals who suspect they have gastritis, or are even convinced they’ve lived with it for years, often do not receive a formal diagnosis upon closer inspection. Conversely, patients reporting no complaints may be diagnosed with gastritis during routine check-ups. Therefore, everyone over 40–45 years of age should undergo gastroscopy. Ignoring this recommendation because nothing bothers you would be a significant error,” the doctor warns.
Treatment
The therapeutic strategy hinges on the cause of the gastritis. In some cases, no treatment is necessary; for instance, acute medication-induced or viral gastritis may resolve once the patient recovers or stops taking the offending drugs.
“Chronic gastritis is most often linked to Helicobacter pylori infection or autoimmune processes. Autoimmune gastritis is incurable; such patients require routine monitoring. However, Helicobacter pylori and its associated gastritis can be eradicated using an adequate and current combination of medications,” comments Dr. Natalia Trofimovskaya.
Medication
All patients diagnosed with chronic gastritis who test positive for the infection are prescribed 14 days of eradication therapy (eradication meaning elimination or eradication of the bacterium). Several regimens exist. The standard triple therapy involves taking two types of antibiotics along with a proton pump inhibitor (which blocks the production of hydrochloric acid).
The Russian Ministry of Health and the American College of Gastroenterology recommend incorporating tripotassium dicitrato bismuth into the regimen to boost treatment efficacy. This substance acts as a gastroprotector, safeguarding damaged areas of the gastric lining.
Important: This specific regimen is not universally applicable. Patients who have already undergone eradication therapy require a different treatment approach. Consequently, medications and dosages must be tailored by a doctor.
One month later, it is vital to re-test the infection to confirm the therapy’s effectiveness. If standard treatment fails, a new protocol using different agents is initiated.
Diet
Mucosal inflammation is unrelated to food intake. Therefore, there is no specific “gastritis diet.”
However, if gastritis is accompanied by dyspepsia, certain foods might trigger nausea, belching, pain, or heartburn. In such instances, the American College of Gastroenterology suggests eating smaller, more frequent meals and limiting hard-to-digest foods, carbonated drinks, certain vegetables (beans, cauliflower, broccoli), and starchy products (oats, wheat, potatoes). These items do not affect the inflammation but increase gas production and can cause bloating.
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Alternative Methods
Phytotherapy and homeopathy lack proven efficacy. Using these treatments is not only ineffective but potentially dangerous. Left untreated, chronic gastritis can progress to ulcers or stomach cancer. The sooner effective therapy is started, the greater the chances of recovery and the lower the long-term risks.
Prevention
The primary driver of chronic gastritis is Helicobacter pylori infection. As there is no vaccine against it, gastritis prevention boils down to maintaining a balanced diet (generally beneficial for healthy GI function), abstaining from alcohol and cigarettes, and using painkillers moderately. Furthermore, regular gastroscopy after the age of 40–45 is essential to catch potential disease early.