Gastritis should be used only for histologically documented inflammation of the stomach; it is not an interchangeable word with dyspepsia or with the presence of erythema during endoscopic investigation.
Gastritis can occur in a broad range of disorders, and it can be classified by the time course (acute or chronic), by histological features, and by the anatomical regions affected.
Acute gastritis
The most common causes of acute gastritis are infections. The most common form of acute gastritis due to infection is H. pylori, which presents in patients as a sudden onset of epigastric pain, nausea and vomiting. The limited histological studies of acute gastritis due to H. pylori show marked infiltration of neutrophils, localised edema and hyperemia.
Bacterial infection of the stomach, or phlegmonous gastritis, is a rare but life-threatening disorder characterised by acute and diffuse infiltration of immune cells with consequent necrosis of the tissue. It occurs mostly in the elderly, in patients with AIDS (caused by CMV and HSV), and in alcoholics.
Chronic gastritis
Chronic gastritis is identified by infiltration of lymphocytes and plasma cells, with a small number of neutrophils. It may be patchy without progression, and it may also progress to all parts of the stomach with severe atrophy and metaplasia.
Chronic gastritis progresses through several steps. In superficial gastritis, inflammation involves only the superficial layers, such as the lamina propria, with edema and cellular infiltrates between the intact glandular tissues. In atrophic gastritis, the inflammation deepens and the glands are destroyed. In gastric atrophy, there is complete or near-complete loss of glands, and at this stage the vessels are visible endoscopically.
Metaplasia can occur in the course of progression of chronic gastritis, in which the gastric glands change to intestinal cells with the appearance of goblet cells. The presence of goblet cells in the stomach is a predisposing factor for gastric cancer.
Chronic gastritis can be classified by the predominant location of inflammation.
Type A chronic gastritis affects the body of the stomach. It is the less common form, is autoimmune-based, and is traditionally associated with pernicious anaemia, with autoantibodies against parietal cells and intrinsic factor; because of this, type A chronic gastritis is also known as autoimmune gastritis. Antibodies against parietal cells and intrinsic factor can be found in more than 90% of pernicious anaemia and in more than 50% of patients with type A chronic gastritis. In some subsets of H. pylori, autoantibodies against parietal cells are produced, possibly owing to molecular mimicry of LPS and the hydrogen–potassium pump. Autoantibodies against parietal cells can be seen in 20% of individuals older than 60 and in more than 20% of patients with vitiligo and Addison disease. Patients with type A chronic gastritis have a low level of pepsinogen, which is used as one of the additional diagnostic values for the diagnosis, and achlorhydria in these patients can lead to hypergastrinemia.
Type B chronic gastritis affects the antrum of the stomach. It is the more common form, caused mainly by H. pylori infection. It is also named antral-predominant chronic gastritis, but this is a misnomer, because it takes time to progress to pan-gastritis, about 15–20 years; in the first stages of the disease, the total number of bacteria is much higher than when it is progressed to pan-gastritis. H. pylori is considered an independent risk factor for gastric adenocarcinoma and for low-grade MALToma of the stomach. In patients with low-grade MALToma of the stomach due to H. pylori, the bacterium should be eradicated, and the tumour followed with EUS and CT; if the B-cell tumour is stable or decreasing in size, no further intervention is needed despite eradication of H. pylori, but if it is growing it can convert to high-grade MALToma of the stomach.