True and False Statements About Gastric Mucosa
Anatomy and Cellular Components
TRUE: The gastric mucosa contains distinct cell types with specialized secretory functions distributed across different anatomic regions. Chief and mucous neck cells in the gastric corpus and fundic glands secrete both pepsinogen I (PG I) and pepsinogen II (PG II), while PG II (but not PG I) is also produced by pyloric glands and Brunner's glands 1.
TRUE: The incisura angularis is a critical site for biopsy sampling. Atrophic gastritis and intestinal metaplasia frequently involve the incisura angularis, and providers should not skip this site when obtaining biopsies 1.
FALSE: Antral-type mucosa is normally found throughout the gastric body and fundus. In uninfected patients, antral-type mucosa at the incisura is present in only 18% of cases, whereas in H. pylori-infected patients this increases to 84% (a phenomenon called "antralization") 2. This antralization is associated with increased risk of atrophic gastritis and intestinal metaplasia 2.
Mucosal Defense Mechanisms
TRUE: The gastric mucosa maintains a sophisticated multi-layered defense system. This includes preepithelial factors (mucus-bicarbonate-phospholipid barrier), an epithelial barrier with surface cells connected by tight junctions generating bicarbonate and prostaglandins, continuous cell renewal, mucosal blood flow, and sensory innervation 3.
TRUE: The gastric mucosal barrier has regional variations in permeability. The corpus and fundus are naturally impermeable, while the antrum has normally increased permeability 4.
FALSE: The gastric mucosa is uniformly resistant to acid penetration. Mucosal injury occurs when noxious factors overwhelm intact mucosal defense or when defense mechanisms are impaired 3.
Diagnostic Considerations
TRUE: Histopathologic confirmation is required for diagnosing atrophic gastritis in the United States. The updated Sydney protocol requires 5 gastric biopsies placed in separately labeled jars: 2 from the antrum (lesser and greater curvature within 2-3 cm of pylorus), 2 from the corpus, and 1 from the incisura angularis 1.
TRUE: Serum pepsinogens reflect both functional and morphologic status of gastric mucosa. PG I levels <70 μg/L and low PG I:II ratio (<3.0) demonstrate high sensitivity and specificity for severe corpus atrophy in high gastric cancer incidence regions 1. However, PG testing is not available for routine clinical use in the United States 1.
FALSE: All H. pylori tests are equally reliable in all clinical situations. The urea breath test (UBT) can produce false-positive results when urease-producing bacterial species other than H. pylori colonize an acid-free stomach, such as in patients with pernicious anemia or atrophic gastritis 1, 5. False-negative results occur with low bacterial load due to proton pump inhibitor use, antibiotics, atrophic gastritis, bleeding peptic ulcer, or gastric cancer 5.
TRUE: Immunohistochemical staining should be utilized when H. pylori is difficult to find. When false positive tests are suspected or there is doubt about H. pylori presence, pathologists should utilize immunohistochemical staining, and one would expect to find H. pylori-associated inflammation even if the organism is difficult to identify 1.
Atrophic Gastritis and Cancer Risk
TRUE: Gastric cancer develops through a well-defined progression pathway. The sequence proceeds from chronic active gastritis to atrophic gastritis to metaplastic epithelia, intraepithelial neoplasia, and finally invasive carcinoma 1.
TRUE: Intestinal metaplasia on gastric histology almost invariably implies atrophic gastritis. The presence of intestinal metaplasia is a marker for underlying atrophic changes 6.
FALSE: H. pylori eradication completely eliminates gastric cancer risk. While eradication halts the increase of risk and reduces overall gastric cancer risk, patients with extensive or moderate to severe atrophy (OLGA/OLGIM III/IV) remain at elevated risk even after successful H. pylori eradication 1.
TRUE: The vast majority of patients with atrophic gastritis have evidence of current or prior H. pylori infection. Irrespective of etiology, patients with atrophic gastritis should be tested for H. pylori and, if positive, the infection should be eradicated 1.
Autoimmune Gastritis
TRUE: Autoimmune gastritis typically affects the fundus and body while sparing the antrum. This distribution pattern is characteristic and helps distinguish it from H. pylori-associated gastritis 6.
TRUE: Parietal cell antibodies are the most sensitive serum biomarker for autoimmune gastritis. However, false positives are common, as PCA can be elevated in H. pylori infection and other autoimmune diseases 1. Intrinsic factor antibodies should also be checked in patients with histology compatible with autoimmune gastritis 1.
FALSE: Autoimmune gastritis always presents with obvious symptoms. Atrophic gastritis is typically asymptomatic and may go undiagnosed, or present with nonspecific symptoms that occur later in the disease course 7.
Clinical Manifestations
TRUE: Iron deficiency anemia occurs in up to 50% of patients with corpus-predominant atrophic gastritis. This often presents earlier than B12 deficiency 7.
TRUE: Up to one-third of patients with autoimmune gastritis have concurrent autoimmune thyroid disease. Other autoimmune conditions including type 1 diabetes mellitus and Addison's disease may also occur 7.
FALSE: Atrophic gastritis is a rare condition. Atrophic gastritis affects up to 15% of the US population and is frequently asymptomatic in early stages, making it an underdiagnosed condition 7.
Surveillance and Management
TRUE: Endoscopic surveillance every 3 years should be considered in patients with advanced atrophic gastritis. However, optimal surveillance intervals remain to be determined, and shorter or longer intervals may be appropriate depending on individual risk assessment 1, 6.
FALSE: Routine endoscopic surveillance is recommended for all patients with gastric intestinal metaplasia. The AGA suggests against routine use of endoscopic surveillance in patients with gastric intestinal metaplasia, though patients at higher risk who value potential reduction in gastric cancer mortality may reasonably elect for surveillance 1.