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Gastritis is defined pathologically as the presence of infiltrating inflammatory cells in the gastric mucosa. The gastric mucosa causes inflammation of the mucous membrane and regeneration of epithelial cells in response to various damages. In some cases, the gastric mucosa may be damaged without any inflammatory reaction. In general, the term gastritis is used when a gastroenterologist sees that the gastric mucosa is red when an endoscopy is performed, or when the radiologist observes irregular changes in the gastric mucosa during gastrointestinal angiography.

However, these findings of endoscopy and gastrointestinal angiography are not consistent with histopathological inflammatory findings. The term gastritis is sometimes used by patients who come to the hospital for indigestion to explain symptoms to their doctors. Therefore, what we often call gastritis is often misused in the sense of clinical dyspepsia, with or without a specific lesion.

This widely used term, gastritis, is caused by a variety of causes, including infections, drugs, or autoimmune and hypersensitivity reactions. However, no symptoms are characteristic of gastritis, and most people with gastritis usually go without symptoms.

Classification of gastritis

Gastritis can be divided into acute and chronic by the time concept it occurs. Other classifications include histological findings, anatomical distribution, and pathophysiological features.

1. Acute Gastritis

Acute gastritis is an acute inflammatory disease of the gastrointestinal mucosa, which is associated with increased gastric acid, decreased gastric mucosal blood flow, destruction of the mucous layer attached to the stomach lining, and direct damage to epithelial cells. It usually occurs immediately after exposure to various drugs or substances that damage the gastric mucosa, such as aspirin, analgesics, or alcohol, or when blood flow to the gastric mucosa decreases (trauma, burns, sepsis, etc.). At this time, endoscopic examination shows swelling of the mucous membrane and punctate bleeding, and in severe cases, mucosa and inflammatory exudates are often observed.

In general, infectious gastritis, except Helicobacter pylori, is not common because the acidity in the stomach is very high. Helicobacter pylori infection can also cause acute gastritis, with sudden symptoms such as pain, nausea and vomiting of the solar plexus.

Infectious gastritis can develop in older patients, alcoholics, or people with AIDS. Particularly in cases of bacterial gastritis or pus gastritis, gastrectomy may be necessary without proper symptomatic treatment and antibiotic treatment, and in rare cases may be life-threatening.

Other types of infectious gastritis can occur when people are less immune, such as people with AIDS or immunosuppressive treatment, which may be caused by the herpes simplex virus or cytomegalovirus.

2. Chronic Gastritis

Chronic gastritis is defined as a chronic inflammatory change in the gastric mucosa and, consequently, a condition that is accompanied by atrophy or hyperproliferation of the gastric mucosa, metabolic changes in the epithelium. Histologically, infiltration of lymphocytes and plasma cells is observed, which is initially confined to the mucosal upper layer and around the gastric glands. As inflammation progresses, the structure is destroyed, followed by atrophy and intestinal metaplasia of the mucosa.

Specifically, the stage of chronic gastritis is called superficial gastritis, where inflammatory changes are initially limited to the surface of the gastric mucosa. When this inflammation spreads to the deeper parts of the mucosal layer, it becomes “atrophic gastritis,” which gradually destroys the structure of the gastric glands. When you do an endoscopy, the mucous membrane becomes very thin and blood vessels are visible.

The gastric glands of mucous membranes undergo morphological changes due to chronic inflammation, which is similar to the small intestine glands, called intestinal metaplasia, which is thought to be a precursor to gastric cancer.

Chronic gastritis can be divided into type A and B depending on the area of โ€‹โ€‹inflammation and the mechanism of development. Type A is caused by an autoimmune mechanism and mainly affects the upper body. Type B is associated with Helicobacter pylori and mainly affects antrum.

Chronic gastritis associated with Helicobacter pylori gradually spreads from the antrum to the gastrointestinal tract as the inflammation progresses. It usually takes about 15 to 20 years for gastritis to develop in the stomach, which is common in older people and almost always occurs in people over 70 years old.

In chronic gastroenteritis caused by Helicobacter pylori infection, a number of gastric atrophy and intestinal metaplasia are observed, which is associated with an increased incidence of gastric cancer. In fact, WHO defines Helicobacter pylori infection as an independent risk factor for gastric cancer, and serologic studies have shown that people with Helicobacter pylori infection are three to six times more likely to develop gastric cancer than in the general population. However, the exact pathophysiology that causes Helicobacter pylori to cause gastric cancer is not known, and it is not recommended to prophylactic Helicobacter pylori bacterium.

There are two main ways to check for Helicobacter pylori infection: invasive and non-invasive methods of collecting and examining tissue with an endoscope. Invasive methods include fungal cultures, histological tests, and urease tests. Noninvasive methods include urea breath tests and serum antibody tests.


In acute gastritis, sudden pain, nausea and vomiting of the solar plexus area occur. In these cases, people often take medicine, alcohol, or spoiled foods before symptoms occur.

In chronic gastritis, there are no characteristic symptoms. Many patients complain of upper gastrointestinal symptoms, such as dyspepsia, and therefore are often used in combination with functional dyspepsia. Symptoms of dyspepsia include upper abdominal pain or postprandial bloating, early satiety, and nausea.


Appropriate, cost-effective approaches to simple dyspepsia (often referred to as patients with gastritis) that have not been identified are still in dispute. The idea that early endoscopy should be given to all patients with dyspepsia, and try empirical medication first, and endoscopy is more than 45 years old with high risk of malignant tumors Controversy continues among patients with weight loss, evidence of gastrointestinal bleeding, and the opinion that it should be done if there is no response to empirical medication. Early endoscopy has the advantage of accurately diagnosing diseases such as ulcers so that they can be treated appropriately, relieving the patient, reducing visits to the hospital, and identifying cancer. In fact, about two-thirds of people with indigestion endoscopy do not have a normal or major abnormality, and in these cases, a diagnosis of chronic gastritis or functional gastrointestinal disease (often using the term neurotic gastritis) is usually made.


Whether you treat gastritis depends on the symptoms you are complaining about rather than the results of an endoscopy. Often, drugs that lower the acidity of the stomach, gastrointestinal motility regulators and defensive enhancers are used.

Although there is no evidence that gastric acid secretion is excessive in chronic gastritis compared to normal people, drugs that lower the acidity of the stomach are most commonly prescribed. These drugs include antacids, H2 receptor antagonists, and proton pump inhibitors. If you have symptoms such as premature satiety or postprandial bloating, use additional gastrointestinal motility modifiers. In addition, they are also prescribed as a defensive enhancer to protect the gastric mucosa.

Frequently Asked Questions

1. The endoscopy results are called gastritis. What should I do?

Gastrointestinal findings of gastritis and when you continue treatment does not improve the symptoms of neurological gastritis is commonly used to say that the term “neuritis” is not originally used. Stomach exercise and acid secretion are controlled by autonomic nerves or cranial nerves, so the symptoms of indigestion are affected by stress or emotional stimulation that affects the physiology of the stomach. For example, this is a symptom of anorexia and indigestion when suddenly sad or worried. In these cases, the term “functional dyspepsia” is appropriate.

2. I have chronic gastritis on the endoscopy. Is there any way to cure it?

As the term chronic gastritis suggests, chronic gastritis is not a sudden but a gradual occurrence. At birth, people eat a variety of different types of foods, including spicy, salty, and burnt foods, and can be caused by irregular eating habits and Helicobacter pylori infection. As you age, your gastric mucosa also ages. Therefore, it is impossible to return this chronic gastritis to normal gastric status at birth. It’s as if it’s impossible to revert the crumpled skin of a 70-year-old grandmother to a 20-year-old firm skin.

For reference, the stomach is always stimulated by various foods and stress, so there is some degree of gastritis. This is diagnosed as physiological gastritis, which is normal.

3. Does chronic gastritis become stomach cancer?

Chronic gastritis is caused by many different causes. As far as is known, chronic atrophic gastritis and intestinal metaplasia are presumed to be a precursor to the development of gastric cancer, but not all of these patients develop gastric cancer, and in fact very rare cases of gastric cancer occur. Therefore, you do not have to worry about chronic gastritis becoming stomach cancer when it is old.

Regular endoscopy (once every 1 to 2 years) is sufficient for daily healthy living (non-smoking, regular meals, proper exercise).

4. Should I eat porridge if I cannot digest well?

It is not necessary to eat porridge for a long time, except in very special cases. In general, it is customary to tell people to eat porridge if they cannot digest it. There is no limit on how long you should eat porridge, and you are supposed to eat porridge. This is a prescription that does not help the patient.

These patients are advised to need a jogging stomach, which of course is not a jogging run but a jogging exercise. If you are severely uncomfortable with acute gastritis, etc. If you eat a few days, but if the condition improves, it is recommended to gradually strengthen the muscles of the stomach while gradually increasing the amount with a normal meal. A normal meal will be awkward at first, but the muscles of the atrophic stomach will gradually recover and digestion will return.

5. If I can’t digest myself, I have blemishes on my face. Why?

Blemishes are not directly related to digestive function. Blemishes are the original melanin pigmentation that depends on nutrition. If you have good digestion and good health condition, fat and other nutrients are stored on your face, so you won’t be able to see the blemishes.

In addition, when skin problems such as acne appear on the face when there is digestive disorder, acne may be worsened due to deteriorating health condition, and acne-like dermatitis may be caused by parasites or bacteria on the face.

When your digestive function returns to normal, your health will improve, your blemishes will lighten, and your skin acne-like skin will usually improve.

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