About Gastritis

Gastritis is defined histopathologically as a condition in which inflammatory cells infiltrate the gastric mucosa. In response to various kinds of injury, the gastric mucosa undergoes inflammation and epithelial regeneration, and in some cases, mucosal damage may occur without any distinct inflammatory response. In general, the term gastritis is sometimes used by endoscopists when they observe redness of the gastric mucosa during endoscopy, and it is also used by radiologists when they observe irregular changes in the gastric mucosa during an upper gastrointestinal series.

However, these endoscopic and upper gastrointestinal series findings do not necessarily correspond to histopathological signs of inflammation. It is also used when patients who visit the hospital for dyspepsia describe their symptoms to a doctor, and conversely, when doctors explain the cause of gastrointestinal symptoms to patients. Therefore, what we commonly call gastritis is often incorrectly used clinically to mean dyspepsia, regardless of whether a specific lesion is present.

Gastritis, a term used so broadly, is caused by various factors such as infection, medication, autoimmune responses, and hypersensitivity reactions. However, there are no symptoms characteristic of gastritis, and most patients with gastritis usually live without symptoms.

Classification of Gastritis

Gastritis can be divided into acute and chronic according to the time course of onset. In addition, there are classifications based on histological findings, anatomical distribution, and pathophysiological characteristics.

1. Acute Gastritis

Acute gastritis is an acute inflammatory disease of the gastric mucosa, and increased gastric acid, decreased blood flow to the gastric mucosa, destruction of the mucus layer attached to the mucosa, and direct damage to epithelial cells are involved in the development of the disease. It often occurs soon after exposure to various drugs or substances that damage the gastric mucosa, such as aspirin, painkillers, and alcohol, or after a decrease in blood flow to the gastric mucosa (trauma, burns, sepsis, etc.). When endoscopy is performed in such cases, edema and pinpoint bleeding of the mucosa are observed, and in severe cases, mucosal erosion and inflammatory exudate are commonly seen.

In general, because the acidity inside the stomach is very high, infectious gastritis other than Helicobacter-related gastritis is uncommon. Acute gastritis can also occur due to Helicobacter infection, and in such cases, symptoms such as epigastric pain, nausea, and vomiting develop suddenly, and histologically neutrophilic infiltration and edema are seen.

In elderly patients, patients with alcohol dependence, or patients with AIDS, infectious gastritis can occur. In particular, when bacterial gastritis or suppurative gastritis develops, total gastrectomy may be necessary unless appropriate symptomatic treatment and antibiotic therapy are provided, and although rare, it can be life-threatening.

Other types of infectious gastritis can occur in people with weakened immunity, such as patients with AIDS or patients receiving immunosuppressive therapy, and in such cases, herpes simplex virus or cytomegalovirus is the cause.

In addition, common causes of acute gastritis in Korea include anisakis infection after eating raw fish, and corrosive gastritis caused by strong acid or strong alkali solutions.

2. Chronic Gastritis

Chronic gastritis is a chronic inflammatory change of the gastric mucosa and is defined as a condition accompanied by gastric mucosal atrophy or hyperplasia and metaplastic changes of the epithelium. Histologically, infiltration of lymphocytes and plasma cells is observed, and this infiltration of inflammatory cells is initially limited to the superficial layer of the mucosa and around the gastric glands. As the inflammation progresses, structural destruction occurs, followed by mucosal atrophy and intestinal metaplasia.

Looking at the stages of chronic gastritis in more detail, the early stage is 'superficial gastritis,' in which inflammatory changes are limited to the surface layer of the gastric mucosa. When this inflammation spreads to deeper parts of the mucosal layer, it becomes 'atrophic gastritis,' in which the gastric gland structure is gradually destroyed. When it becomes more severe, it becomes 'gastric atrophy,' in which the gland structure is destroyed and lost. At this point, when endoscopy is performed, the mucosa becomes very thin and blood vessels can be seen. The gastric glands of the mucosa undergo morphological changes due to chronic inflammation; when the gastric glands change to resemble small intestinal glands, this is called 'intestinal metaplasia,' which is considered a precursor lesion of gastric cancer.

Chronic gastritis can be divided into type A and type B according to the main site of inflammation and the mechanism of development. Type A occurs through an autoimmune mechanism and mainly affects the gastric body, while type B is associated with Helicobacter and mainly affects the antrum. In fact, most chronic gastritis in Korea is type B gastritis.

Chronic gastritis related to Helicobacter gradually spreads from the antrum to the gastric body as the inflammation progresses. It usually takes about 15 to 20 years for gastritis to involve the entire stomach, and such gastritis is common in older adults and appears in almost all patients over the age of 70.

In this chronic gastritis caused by Helicobacter infection, gastric atrophy and intestinal metaplasia in multiple sites are observed, and this is associated with an increased incidence of gastric cancer. In fact, the WHO defines Helicobacter infection as an independent risk factor for gastric cancer, and it is known that people with Helicobacter infection on serologic testing have a 3 to 6 times higher risk of developing gastric cancer than the general population. However, the exact pathophysiology by which Helicobacter causes gastric cancer is still unknown, and prophylactic eradication of Helicobacter is not recommended.

Methods for confirming Helicobacter infection can be broadly divided into invasive methods, in which tissue is obtained by endoscopy for testing, and noninvasive methods. Invasive methods include bacterial culture, histologic examination, and the urease test, while noninvasive methods include the urea breath test and serologic antibody testing. In Korea, histologic examination, the urease test, and serologic antibody testing are commonly used, and the urea breath test is also often used to evaluate whether the bacteria have been eradicated.

So far, I have explained the overview and definition of gastritis.

In the next part, we will look at the symptoms and treatment of gastritis.

Source: Korea Disease Control and Prevention Agency National Health Information Portal