Gastritis refers to inflammatory lesions of the gastric mucosa or gastric wall caused by various physical, chemical, or biological damaging factors. It can be classified into acute and chronic types based on the course of the disease, with chronic gastritis being more common.
Etiology and Pathogenesis
Acute Gastritis
Acute gastritis is often secondary and results from stress responses caused by severe infections, shock, intracranial injuries, severe burns, respiratory failure, and other critical illnesses (also known as acute gastric mucosal lesions or acute stress-induced mucosal disease). Acute inflammation of the gastric mucosa may also result from accidental ingestion of toxic or corrosive substances, consumption of food contaminated with bacteria or bacterial toxins, use of medications that damage the gastric mucosa (e.g., aspirin or other NSAIDs), food allergies, the presence of foreign objects in the stomach, emotional fluctuations, and mental strain.
Chronic Gastritis
Chronic gastritis is the result of long-term, repeated damage to the gastric mucosa by harmful factors. Non-atrophic (previously referred to as superficial) gastritis accounts for approximately 90%–95% of cases in children with chronic gastritis, while atrophic gastritis and special types of gastritis are less common. The exact etiology remains unclear, but several factors are believed to contribute to its development:
Helicobacter pylori (Hp) Infection
Gastric infection with H. pylori has been confirmed as a major cause of gastritis. The prevalence of H. pylori is particularly high in active and severe gastritis. The familial clustering of chronic gastritis suggests that H. pylori may spread among family members.
Bile Reflux
Gastric motility disorders due to various causes may lead to duodenogastric reflux. Refluxed bile salts reduce the barrier function of the gastric mucosa to ion permeability, allowing hydrogen ions in gastric juice to diffuse back into the mucosa, resulting in inflammation.
Long-Term Consumption of Irritating Foods or Medications
Chronic use of coarse, overly hard, extremely cold or hot, and spicy foods, frequent overeating, heavy consumption of tea or coffee, and prolonged use of NSAIDs like aspirin or corticosteroids may contribute.
Neurological and Psychological Factors
Persistent psychological stress or excessive pressure may lead to abnormal secretion of digestive hormones.
Chronic Systemic Diseases
Chronic kidney disease, uremia, severe diabetes, liver and biliary system diseases, rheumatoid arthritis, and systemic lupus erythematosus are potential contributors.
Other Factors
Environmental, genetic, immune, and nutritional factors are also associated with the pathogenesis of gastritis.
Clinical Manifestations
Acute Gastritis
Acute gastritis presents with a sudden onset. Mild cases may involve anorexia, abdominal pain, nausea, and vomiting, while severe cases may result in hematemesis, melena, dehydration, and disturbances in electrolyte and acid-base balance. Cases involving infections often manifest with fever and systemic toxic symptoms.
Chronic Gastritis
Symptoms include recurrent and irregular abdominal pain. Pain typically occurs during or after eating, most commonly in the epigastrium or periumbilical region, but the location may vary in some patients. Pain may range from intermittent, mild dull pain to severe colicky pain. Symptoms are often accompanied by anorexia, nausea, vomiting, and abdominal distention, which can subsequently affect nutritional status and growth. Erosive mucosal bleeding may present with hematemesis or melena.
Auxiliary Examinations
Gastroscopy
Gastroscopy is the most valuable and reliable diagnostic modality. It allows direct observation of gastric mucosal lesions and their severity, including mucosal hyperemia, edema, erosion, and hemorrhage. Mucus plaques or refluxed bile on the mucosal surface may occasionally be observed. In cases of H. pylori infection, the gastric mucosa may exhibit small nodules (also known as antral nodules or lymphocytomatous nodular hyperplasia). Biopsies from the affected areas can be used for H. pylori testing and histopathological evaluation.
Helicobacter Pylori Testing
Tests for H. pylori can be divided into invasive and non-invasive categories:
Invasive Tests
These are performed using gastric mucosal tissue obtained during gastroscopy, including:
- Rapid urease testing
- Histological examination
- H. pylori culture
Non-invasive Tests
These primarily include:
- 13C-urea breath tests
- Fecal H. pylori antigen detection
- Serological detection of anti-H. pylori IgG antibodies
Pathology
Acute Gastritis
Pathological features include degeneration and necrosis of epithelial cells, infiltration of large numbers of neutrophils into the lamina propria, and few or no lymphocytes or plasma cells. Glandular cell degeneration and necrosis are observed at varying levels.
Chronic Gastritis
Non-atrophic gastritis is characterized by degeneration of epithelial cells, hyperplasia of foveolar epithelial cells, and lymphocyte and plasma cell infiltration in the lamina propria.
Atrophic gastritis is marked by atrophy of glandular structures in the lamina propria, intestinal metaplasia, and inflammatory cell infiltration.
Diagnosis and Differential Diagnosis
A diagnosis can generally be established based on medical history, physical examination, clinical manifestations, gastroscopy, and pathological examination. Given the many potential causes of abdominal pain in children, acute abdominal pain requires differentiation from surgical acute abdomen as well as organic diseases of intra-abdominal organs, such as the liver, gallbladder, pancreas, and intestines, as well as abdominal-type Henoch-Schönlein purpura. Chronic, recurrent abdominal pain necessitates differentiation from peptic ulcer disease, eosinophilic gastroenteritis, intestinal parasitic infections, and functional abdominal pain.
Ascariasis
Symptoms often include nonspecific abdominal pain, eating preferences or pica, nausea, vomiting, and other signs of digestive dysfunction. Systemic allergic symptoms may sometimes occur. A history of expelling or vomiting worms, the detection of ova in stool, and a favorable response to antiparasitic treatment are diagnostic clues. With improvements in hygiene, the incidence of ascariasis has significantly decreased.
Eosinophilic Gastroenteritis
This is a gastrointestinal disorder caused by eosinophilic infiltration of the gastrointestinal mucosa. In its mucosal type, the clinical symptoms closely resemble those of gastritis, but standard treatment for gastritis is typically ineffective.
Functional Abdominal Pain Associated with Psychological Factors
This is a common psychosomatic disorder during childhood. Its cause is not well understood and is believed to relate to emotional changes, stressful life events, and excessive anxiety within a family. It is characterized by diffuse, episodic abdominal pain lasting from several minutes to several hours, which resolves spontaneously. Symptoms such as nausea and vomiting may occur, but they typically disappear during sleep. Clinical and auxiliary examinations generally do not reveal positive findings.
Treatment
Acute Gastritis
Treatment involves removing the underlying cause and actively managing the primary disease while avoiding all irritative foods and medications. Water and electrolyte imbalances are corrected promptly. For cases involving upper gastrointestinal bleeding, bed rest is recommended, along with maintaining a quiet environment and monitoring vital signs as well as instances of vomiting and melena. Acid-suppressing medications and gastric mucosal protectants may be utilized. In cases of bacterial infection, effective antibiotics are introduced.
Chronic Gastritis
Dietary Therapy
Emphasis is placed on establishing healthy eating habits and maintaining a regular lifestyle. Meals should adhere to a fixed schedule and quantity. Irritative foods and medications harmful to the gastric mucosa are avoided.
Pharmacological Therapy
Mucosal Protectants
Examples include bismuth subcarbonate, sucralfate, and montmorillonite powder.
Acid-Suppressing Medications
Commonly used drugs include cimetidine, ranitidine, and famotidine.
Prokinetic Agents
Domperidone, cisapride, or mosapride may be added in cases of abdominal distension, vomiting, or bile reflux.
Treatment for Helicobacter pylori (Hp)
Standardized treatment for H. pylori infection is recommended (refer to the section on peptic ulcer treatment).
The duration of pharmacological therapy depends on the patient's condition.