Can Gastritis Cause Elevated IgA Levels?
Yes, gastritis—particularly H. pylori-associated gastritis—causes elevated IgA levels both systemically (serum) and locally in the gastric mucosa, with the magnitude of elevation correlating with disease severity and bacterial density.
Mechanism of IgA Elevation in Gastritis
H. pylori-Induced IgA Response
H. pylori infection triggers a robust mucosal IgA response in the gastric mucosa, with 76 of 78 patients (97%) with chronic gastritis demonstrating positive IgA responses in gastric biopsy supernatants 1
The gastric mucosa shows massive accumulation of IgA-secreting cells during H. pylori infection, driven by increased production of CCL28 (mucosa-associated epithelial chemokine), which specifically recruits IgA-secreting cells to the gastric tissue 2
CCL28 protein and mRNA levels are significantly elevated in H. pylori-infected gastric tissue compared to uninfected individuals, providing the chemotactic signal for IgA cell recruitment 2
Correlation with Disease Severity
Serum IgA antibody levels against H. pylori correlate significantly with the severity of gastritis, as measured by the Whitehead score and Sydney system classification 3
IgA antibody absorbance index correlates with the density of H. pylori colonization in the gastric corpus, though this relationship is less consistent than for IgG antibodies 3
The pattern of immune response (IgG, IgA, or IgE predominance) influences oxidative stress markers in chronic gastritis, with elevated IgA responses associated with increased lipid peroxidation and antioxidant enzyme activity 4
Clinical Significance of IgA Elevation
Diagnostic Implications
Mucosal IgA responses to specific H. pylori proteins (particularly 120 kDa, 90 kDa, 61 kDa, and 31 kDa proteins) are present in 75-97% of patients with chronic gastritis, making IgA a sensitive marker of active infection 1
IgA-secreting cells from H. pylori-infected tissues demonstrate specific migration toward CCL28 but not CCL25, distinguishing them from IgG-secreting cells which migrate toward CXCL12 2
Relationship to Gastritis Type
In autoimmune gastritis, the primary serologic markers are parietal cell antibodies (PCA) and intrinsic factor antibodies (IFA), not IgA elevation 5
H. pylori-associated gastritis is the most common form of atrophic gastritis and the primary driver of IgA elevation in gastritis patients 6, 7
Important Clinical Caveats
Limitations of IgA Testing
While IgA levels correlate with gastritis severity, serum IgA testing cannot replace endoscopic examination to evaluate the degree of macroscopic gastrointestinal damage 8
IgG antibodies show stronger correlation with antral gastritis severity and bacterial density than IgA antibodies, making IgG a more reliable serologic marker for antral disease 3
Differential Diagnosis Considerations
Elevated IgA can occur in other conditions beyond gastritis, so the finding must be interpreted in clinical context with endoscopic and histologic confirmation 5
Parietal cell antibodies can be falsely elevated in H. pylori infection and other autoimmune diseases, so IgA elevation alone does not distinguish between autoimmune and H. pylori-associated gastritis 5
Practical Approach to Elevated IgA in Suspected Gastritis
Test for H. pylori infection using non-invasive methods (urea breath test or monoclonal stool antigen test) when elevated IgA is found in the context of dyspeptic symptoms 7
Confirm gastritis diagnosis with endoscopy and histopathology using the updated Sydney protocol (5 topographically separated biopsies) 5
If H. pylori is detected, eradicate the infection and confirm successful eradication with subsequent non-serologic testing 5
In patients with histology compatible with autoimmune gastritis, check parietal cell antibodies and intrinsic factor antibodies rather than relying on IgA levels 5