Chronic Gastritis K29.3: Symptoms and Treatment

Definition and Causes:

Chronic gastritis is a recurring and long-term inflammation of the stomach lining, leading to structural remodeling of the membrane resulting in erosion, deformity, and cellular transformation. As a consequence of these changes, there is a disruption in the secretion of gastric acid and pepsin (digestive enzymes), along with disturbances in gastrointestinal motility and the production of gastrointestinal hormones.

The prevalence of chronic gastritis is estimated to be between 80-85% in adults, according to various authors. The type of chronic gastritis associated with Helicobacter pylori bacteria predominates, accounting for 85-90% of all forms of gastritis. The prevalence of Helicobacter pylori infection reaches 80% in adult populations.

The rarest types of chronic gastritis include autoimmune gastritis (occurring three times more frequently in women). This type depends on the production of antibodies against parietal cells of the stomach (which produce digestive enzymes) and intrinsic factor (the enzyme that converts inactive B12 to active B12).

Causative Factors:
All causes of chronic gastritis development are divided into two major groups: predisposing factors and etiological factors.

Predisposing factors (which create an unfavorable background and increase the risk of chronic gastritis development) include:

  • Dietary errors (associated with irregular and incomplete nutrition)
  • Smoking
  • Genetic predisposition

Etiological factors are divided into external and internal factors.

External etiological factors for chronic gastritis include:

  • Helicobacter pylori bacterial infection (HP infection)
  • Damage to the gastric mucosa by medications (including gastritis caused by non-steroidal anti-inflammatory drugs)
  • Damage to the gastric mucosa by radiation
  • Infections other than HP
  • Alcoholic gastritis

Internal etiological factors for chronic gastritis include:

  • Obstruction (reflux) of the liver’s bile ducts
  • Continuous oxygen deficiency (oxygen starvation)
  • Autoimmune processes
  • Metabolic disorders
  • Disorders of the endocrine glands

If you notice similar symptoms, consult your doctor. Do not self-medicate, as this poses a risk to your health!

Symptoms of Chronic Gastritis:
The nonspecific symptoms of chronic gastritis can be divided into the following groups:

Pain Syndrome:

  • Often plays a leading role in the clinical picture of the disease and often prompts patients to seek medical help.
  • The location of the pain is mostly in the epigastric region (the area corresponding to the shadowing of the stomach on the anterior abdominal wall) and sometimes in other areas of the abdomen.
  • In chronic gastritis with reduced secretion, pain is associated with food intake, while pain tends to occur more frequently 1-1.5 hours after eating when there is increased secretion.
  • Digestive syndrome: characterized by decreased appetite, heartburn, nausea, belching, vomiting, and stomach discomfort after eating.

General deterioration:

  • In uncomplicated chronic gastritis, the impact on the overall condition of the body is minimal. However, as inflammatory changes progress in the gastric mucosa, this effect can change.
  • General deterioration may include:
  • Weight loss
  • Disorders in the metabolism of vitamins (B group vitamins, ascorbic acid)
  • Inability to tolerate certain foods

The liver, pancreas, and intestines are often involved in the pathological process, and with prolonged inflammation of the stomach, deviations in the psychoneurological aspect may appear. Overall, the clinical picture of chronic gastritis is determined by the nature of gastric secretion disorder, motor function, and variation in the symptoms of the mentioned syndromes above.

Classification and Stages of Chronic Gastritis Development

Classification of Gastritis:

According to Origin and Etiology (Prefix):

  • Gastritis Type A: Autoimmune atrophic gastritis, including gastritis associated with pernicious anemia (Addison–Biermer).
  • Gastritis Type B: Bacterial gastritis unrelated to infection with Helicobacter pylori bacteria.
  • Gastritis Type AB: Mixed gastritis (affecting all sections of the stomach) with a preference for the antrum or the distal part of the stomach.

According to Locations and Morphological Characteristics (Root or Nucleus):

  • Based on location:
    • Primary autoimmune gastritis (Type A).
    • Bacterial gastritis (Type B).
    • Mixed gastritis (Type AB) with a preference for the antrum or distal part of the stomach.
  • Based on morphological criteria:
    • Superficial gastritis.
    • Fundic gastritis.
    • Atrophic gastritis with mild, moderate, or severe atrophy.
    • Gastritis with intestinal metaplasia (complete or incomplete, fine or coarse).

According to Specific Morphological Features (Suffix):

  • Based on the severity of the inflammatory process in the gastric mucosa:
    • Minimal.
    • Mild.
    • Moderate.
    • Severe (depending on the degree of lymphocytic inflammatory infiltration of the mucous membrane of the stomach).
  • Based on the activity of gastritis:
    • Absence of activity.
    • Mild (I).
    • Moderate (II).
    • High (III) (depending on the presence and severity of the granulocytic component of inflammatory infiltration in the gastric mucosa).
  • Based on the presence and severity of Helicobacter pylori infection in the gastric mucosa:
    • Absence.
    • Mild (I).
    • Moderate (II).
    • High (III).

According to Clinical Characteristics:

  • Gastritis Type B with predominance of pain reflexes (gastric irritation).
  • Gastritis Type A with predominance of digestive phenomena (gastric irritation).
  • Gastritis with asymptomatic course (approximately 50%).

According to Functional Criteria (Flexion):

  • Gastritis with preserved secretion (and its increase).
  • Gastritis with decreased secretion (mild, moderate, severe, complete).

Endoscopic Criteria for Gastritis:

  • Surface oxidative gastritis.
  • Gastritis with flat erosion (acute bleeding).
  • Gastritis with protruding erosion (chronic bleeding).
  • Hemorrhagic gastritis.
  • Severe atrophic gastritis.

Chronic gastritis, like all chronic diseases, has two stages: periods of exacerbation and improvement that alternate sequentially. With each exacerbation period, greater structural changes occur in the gastric mucosa. Gastritis exacerbation and remission can be confirmed clinically or through esophagogastroduodenoscopy (EGD) and histological analysis (biopsy), which provide the most accurate confirmation.

Gastritis Resulting from Helicobacter Pylori Infection (HP Infection)

Currently, HP infection (classified as type B gastritis) plays a significant role in the development of gastritis. Most adults over the age of 60 are infected with this bacterium. Approximately 30% of children aged 5 years, 63% of those aged 15-20 years, and over 85% of adults are affected by it. The detrimental mechanism of action of this causative agent lies in the fact that chronic Helicobacter pylori infection causes changes in the gastric mucosa tissues. With time passing without symptoms appearing, as inflammation spreads to the body of the stomach and the gastric mucosa’s response increases, initial symptoms of gastritis appear. The longer the duration of the infection, the stronger the remodeling of the gastric mucosa becomes. This sequential remodeling leads to atrophy, intestinal metaplasia, congenital disorders, and eventually progresses to gastric cancer. The development of infectious atrophy is a critical step in the transformation of gastritis into gastric cancer.

Drug-Induced Gastritis (Type C)

This is the second most common form of gastritis. The impact of non-steroidal anti-inflammatory drugs (NSAIDs) on the stomach is studied extensively. They do not directly affect the stomach like acidity (gastric acid tenfold is more aggressive). Their fundamental mechanism of action on the gastric mucosa lies in blocking cyclooxygenase enzymes (COX-1 and COX-2). Blocking COX-1 inhibits the synthesis of prostaglandins (E2 and I2), which provide the quality and strength of the mucosal barrier that protects the gastric mucosa from the effects of gastric acid and pepsin. Therefore, long-term use of NSAIDs leads to thinning of the mucosal protective layer and increased effect of gastric acid on the gastric mucosa, causing chronic inflammation.

Autoimmune Atrophic Gastritis (Type A)

This is one of the rarest forms of gastritis. Its exact cause is not yet known. It is primarily characterized by the immune cells producing antibodies against gastric mucosa cells (which produce gastric acid) and intrinsic factor Castle (which participates in iron absorption in the intestines). As a result, inflammatory changes develop, leading to early hypochlorhydria (absence of acid) and, in the meantime, metabolism of vitamin B12 is impaired, exacerbating anemia.

Radiation Gastritis

Ionizing radiation is the causative factor, exerting a direct effect on the gastric mucosa layer, either through direct harmful effects or through a series of reactions with the formation of free radicals and lipid oxidation in the cellular membrane. As a result of prolonged exposure to radiation doses exceeding the maximum limit, chronic radiation gastritis develops.

Lymphocytic Gastritis

It is characterized by specific inflammation in the gastric mucosa layer, which develops in the context of gluten damage disease – celiac disease (a disorder of intestinal function, where gluten intolerance is observed). The damage occurs due to autoantibodies against the gastric mucosa layer with the development of chronic inflammation.

Transient Gastritis

Transient gastritis develops due to the projection of the stomach in the inflammatory process in Crohn’s disease (chronic inflammation in the digestive system) and intersects with damage to the mucosal layer in the form of erosion and ulcers. The chronic inflammation foci develop in its mucosal layer.

The mucosal layer is damaged due to the specific antibodies with the development of chronic inflammation. The more the stomach is exposed to allergenic stimuli, the more severe the symptoms of gastritis become.

Chronic Gastritis Development

While gastritis continues for a long period, on average, between 18 to 25 years pass before clear structural changes develop in the gastric mucosa layer. With time passing, each period of exacerbation spreads the inflammatory process, not only on the surface but also in the depth of the mucosal layer. When the impact involves the body and the fundamental part of the stomach, the production of gastric acid and pepsin decreases, leading to digestive disturbances.

Complications of Chronic Gastritis

The most common complications of chronic gastritis include:

  1. Bleeding.
  2. Gastric ulcers.
  3. Deficiency of B vitamins.
  4. Anemia resulting from intrinsic factor Castle deficiency.
  5. Digestive disorders (dyspepsia and absorption disorders).
  6. Damage to the gastric mucosa layer.
  7. Gastric cancer.
Complications of chronic gastritis

Stomach Ulcers

Currently, there isn’t a precise understanding of when gastritis turns into ulcer disease. In most cases, stomach ulcers develop as a complication of chronic gastritis resulting from prolonged infection with H. pylori and/or frequent use of nonsteroidal anti-inflammatory drugs (NSAIDs) to alleviate pain. The development of stomach ulcers may manifest as exacerbation of the main symptoms of gastritis. Often, the symptoms remain the same, but there is no response to standard treatment. Ulcers can lead to bleeding, resulting in new symptoms such as worsening pain, black stools, and vomiting with blood. If ulcers develop, the prognosis becomes less optimistic. Immediate diagnosis (upper gastrointestinal endoscopy) and adjustment of the treatment plan are required in case of the development of these complications.

Stomach Cancer
Chronic gastritis increases the risk of developing stomach cancer, especially with Helicobacter pylori infection. Uneven infection increases the risk of lower gastric cancer by 4-6 times. Eradication of Helicobacter pylori reduces the risk of stomach cancer development. Genetic factors and oncogenic mutations are also studied. Chemical and lymphoid gastritis have a lesser impact on carcinogenesis and are associated with celiac disease in some cases.

Diagnosis of Chronic Gastritis
Relies on laboratory and diagnostic tests, including upper gastrointestinal endoscopy (also known as “upper GI endoscopy”) and other tests to determine the diagnosis.

  • The “gold standard” in diagnosing chronic gastritis is endoscopic examination of the stomach with measurement of its acidity and taking samples for morphological analysis and detection of Helicobacter pylori infection. The use of methylene blue dye may increase the diagnostic value during endoscopic examination.
  • X-rays are used to examine the stomach as a secondary diagnostic method, allowing assessment of mucosal irregularities and motility function. Ulcerations and cancerous changes can also be detected.
  • Functional diagnostic methods include pH-metry and gastric electrical planning. Gastric acidity can be measured during endoscopy (pH measurement) or by measuring daily fluctuations in acidity (24-hour pH monitoring) using a special tube in the stomach. The resulting data reflect the degree of hydrochloric acid production and may indirectly indicate mucosal atrophy processes.
  • Ultrasound data for the abdomen, chemical blood analysis, and clinical blood analysis are used as complementary diagnostic methods to assist in differential diagnosis in difficult cases.

For a diagnosis of chronic gastritis, it is necessary to consult a gastroenterologist, general practitioner, or pediatrician. The doctor will provide guidance for conducting the necessary tests to determine the diagnosis.

Treatment of Chronic Gastritis

Treatment of chronic gastritis depends on excluding or reducing harmful factors on the gastric mucosa, allowing it to recover. Treatment of acute periods begins with following a mild diet.

Drug Therapy:

  • Proton pump inhibitors (PPIs): Omeprazole, Pantoprazole, Rabeprazole, Lansoprazole, Esomeprazole. The mechanism of action involves reducing gastric acid production by the proton pump. They effectively reduce gastric acid production without developing tolerance.
  • H2 receptor antagonists: Cimetidine, Ranitidine, Famotidine, Nizatidine, Roxatidine. The mechanism of action involves blocking the effect of histamine on parietal cells and the gastric mucosa, leading to reduced pepsin and gastric acid secretion. They increase prostaglandin formation, enhancing mucosal protection and stimulating regeneration processes. Prolonged use requires a continuous increase in dosage.
  • Cell protection: Bismuth preparations (Bismuth subsalicylate, Bismuth citrate, Basic bismuth nitrate), Sucralfate (Aluminum salt of sucrose sulfate), Misoprostol (synthetic prostaglandin).
  • Antibacterial therapy: It is always applied in combinations of two or three drugs (Semisynthetic penicillins, Macrolides, Tetracyclines, Nitroimidazole derivatives).
  • Motility stimulants: Metoclopramide, Domperidone, Itopride hydrochloride, Trimbutine—to reduce the frequency of bile reflux.
  • Antispasmodics: Drotaverine, Butylscopolamine bromide, Mebeverine—for relieving muscle pain syndrome.
  • Replacement therapy with enzymes and gastric acid drugs—is performed in case of atrophic gastritis and acid deficiency.

Folk Therapy
Herbal therapy and digestive drinks based on glycerin leaves, sunflower root, thyme, yarrow, and centaury are also used as adjunctive therapy. Mineral waters with low gas and mineral content are used with heating before meals at a dose of 3 ml per kilogram of body weight.

Chronic Gastritis in Children:
Chronic gastritis rarely occurs in children and increases with age. The presentation is more subtle, with symptoms less pronounced in children compared to adults. In this context, there is less complication (ulceration, bleeding, etc.), and the prognosis is better with timely therapeutic intervention. Chronic gastritis is rarely associated with Helicobacter pylori infection in children.

Treatment of Gastritis in Children:
Treatment of gastritis in children resembles that of adults, with differences in a limited range of drugs and their dosages. Children are allowed to use some basic medications, such as: Omeprazole from 1 year and Rabeprazole from 6 years, and Esomeprazole from 12 years. While intestinal protectants are allowed for children from 4 years old. Antacids (such as Ranitidine) are used from 12 years old, and coatings (such as Gaviscon) and mucolytics (from 15 years old).

Chronic Gastritis in Pregnancy:
Chronic gastritis in pregnancy generally occurs without specificity. It primarily requires following healthy dietary rules and excluding harmful factors. Treatment does not increase the risk of major congenital defects, spontaneous miscarriages, or preterm birth. Ranitidine and Esomeprazole can be safely used during breastfeeding for the breastfed infant.

Outlook and Prevention:
The outlook for chronic gastritis is often positive. The potential mucosal changes (such as metaplasia and dysplasia) in the context of gastritis leading to those changes are the only risk. Proper treatment of iron deficiency anemia, which occurs in the context of autoimmune atrophic gastritis, can prevent the development of adverse events for the patient. People with gastritis, especially the diffuse atrophic forms, should be under continuous medical care with endoscopic examinations once or twice a year, and it is preferable for them to undergo preventive treatment courses from time to time.