Gastritis is a medical term defining inflammation of the inner lining of the stomach, known as the gastric mucosa. This condition is not a single disease but a descriptor for cellular change triggered by various factors. The term encompasses several distinct conditions, meaning the question of whether gastritis is an autoimmune disease does not have a simple answer. Only one specific form is classified as an autoimmune disorder; the vast majority of cases result from external irritants or infections.
Gastritis: The Common Causes That Are Not Autoimmune
The most frequent causes of gastritis involve an external agent that compromises the stomach’s natural defense mechanisms. The stomach lining is normally protected by a thick layer of mucus, which shields the tissue from highly corrosive hydrochloric acid. When this protective layer is breached or overwhelmed, the underlying tissue becomes inflamed.
The single most common cause of chronic gastritis is infection with the bacterium Helicobacter pylori (H. pylori). This bacteria colonizes the stomach lining, releasing substances that weaken the protective mucus layer and cause long-term inflammation. The resulting inflammation is the body’s immune system reacting to an external pathogen, not an attack on the body’s own healthy cells.
Chemical injury, often called reactive gastropathy, is another prevalent cause. This commonly occurs from the chronic use of Nonsteroidal Anti-inflammatory Drugs (NSAIDs), such as ibuprofen or naproxen. These medications directly damage the surface cells of the stomach lining and interfere with the production of protective mucus. Excessive alcohol consumption or the backflow of bile from the small intestine can also cause direct chemical irritation and subsequent inflammation.
In these non-autoimmune forms, inflammation is a protective measure initiated by the body to neutralize or repair damage caused by an external source. Once the external irritant is removed or the infection is treated, the stomach lining typically has the potential to heal. The underlying issue is environmental or infectious, distinguishing these common forms from a genuine autoimmune response.
The Specific Mechanism of Autoimmune Gastritis
While most cases of gastritis are non-autoimmune, Autoimmune Gastritis (AIG) is a distinct form where the immune system mistakenly attacks its own stomach cells. This condition develops when the immune system launches an attack specifically against the parietal cells in the upper regions of the stomach lining. Parietal cells are specialized cells responsible for producing hydrochloric acid and a protein called intrinsic factor.
The immune response in AIG involves the production of autoantibodies that target the parietal cells or the intrinsic factor itself. The primary target of the autoantibodies is the H+/K+-ATPase (the proton pump), which parietal cells use to secrete acid. The resulting destruction of the parietal cells leads to a progressive thinning and wasting away of the stomach lining, known as atrophic gastritis.
The loss of parietal cells has two significant consequences. First, reduced hydrochloric acid production leads to hypochlorhydria, which can impair the absorption of iron from food. Second, the lack of intrinsic factor prevents the body from properly absorbing Vitamin B12. Intrinsic factor is required to bind to dietary Vitamin B12, forming a complex absorbed later in the small intestine.
Without this binding protein, Vitamin B12 cannot be absorbed, leading to a deficiency over time. Since Vitamin B12 is essential for red blood cell formation and nerve function, this deficiency eventually results in a type of megaloblastic anemia known as pernicious anemia. Unlike other forms of gastritis, AIG is a systemic disorder causing a specific nutritional deficiency and is often associated with other autoimmune conditions, such as Hashimoto’s thyroiditis.
How Doctors Differentiate the Types of Gastritis
Distinguishing Autoimmune Gastritis from the more common H. pylori or NSAID-induced forms requires diagnostic tests focused on identifying the specific cause. Definitive diagnosis of any gastritis requires a visual examination and tissue sampling via an upper endoscopy. During this procedure, a flexible tube with a camera is passed down the esophagus to view the stomach lining.
During the endoscopy, a physician takes small tissue samples for a biopsy, which a pathologist examines under a microscope. The biopsy is crucial as it reveals the pattern of inflammation, the extent of cellular damage, and the specific location of the atrophy. For instance, AIG atrophy is typically confined to the body and fundus of the stomach, while H. pylori-related atrophy often affects the antrum (the lower part of the stomach).
To identify infection, specific tests for H. pylori are performed, such as a urea breath test, a stool antigen test, or special stains on the biopsy sample. For AIG, blood tests are the primary means of confirmation. These tests look for autoantibodies directed against the parietal cells and the intrinsic factor, which are the definitive markers of the autoimmune process.
Blood tests also measure Vitamin B12 levels, which are typically low in AIG patients due to malabsorption. Doctors may also check levels of the hormone gastrin, which is often significantly elevated as the body attempts to compensate for the lack of stomach acid. The combination of histological findings from the biopsy and the presence of specific autoantibodies allows doctors to accurately differentiate the types of gastritis.