Association between autoimmune thyroid disease and presence of CagA and gastric intestinal metaplasia among patients with H. pylori: a cross-sectional endoscopic study

Autoimmune thyroid disease (AITD), specifically Graves’ disease and Hashimoto’s thyroiditis, has been seen to co-occur with Helicobacter pylori (H. pylori) infection. Some evidence suggests that the link is particularly strong with the H. pylori virulence factor cagA, though findings remain inconclusive. We sought to evaluate whether the presence of cagA and the pre-cancer lesion gastric intestinal metaplasia (GIM) differed by AITD status among patients with current H. pylori infection confirmed by histological assessment of endoscopic tissue biopsy. In a retrospective cohort of 478 Black and White adults with confirmed H. pylori infection on histological assessment from endoscopic gastric biopsy, AITD status was determined through electronic health records and patients were categorized into one of four mutually exclusive groups (no autoimmune disease, Graves’, Hashimoto’s, and other autoimmune disease). cagA status was identified using droplet digital PCR on gastric tissue samples. Logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for the association between AITD and cagA, and GIM, separately. Graves’ patients had an over 5-fold increased likelihood of cagA-positivity compared to individuals with no autoimmune disease (OR, 5.47; 95% CI: 1.06, ∞, p = 0.04). In contrast, Hashimoto’s thyroiditis patients had a suggestive 63% decreased likelihood of having a cagA-positive H. pylori strain compared to individuals with no autoimmune disease (OR, 0.37; 95% CI: 0.12, 1.06; p = 0.07). Neither AITD was associated with the presence of GIM. The seven cagA-positive Graves’ patients were grouped by treatment type, which revealed patterns showing that after eradication of H. pylori, patients who had thyroidectomy or those treated with RAI had stable thyroid hormone levels, while patients without definitive treatment had decreased thyroid stimulating hormone levels. These findings suggest a higher prevalence of positivity to the virulence factor cagA in H. pylori-infected patients with Graves’ disease compared to H. pylori-infected patients without autoimmune conditions. This suggests a need for assessing H. pylori presence and the effect on eradication on thyroid antibody levels and management of Graves’, to determine if incorporation of H. pylori screening into Graves’ care, as done in other autoimmune diseases, improves outcomes. Not applicable.