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Abstract Background Celiac disease (CeD) is a prevalent disorder due to an immunologic reaction to the ingestion of gluten. CeD is characterized by inflammation, antibodies to transglutaminase, small intestinal villous atrophy, and subsequent malabsorption. Studies have indicated an increased risk of cardiovascular disease (CVD) in patients with CeD, potentially mediated by inflammation, yet the results are inconsistent. Studies assessing the impact of CeD on the heart and CVD risk are thus warranted. Subclinical myocardial injury can be assessed as increased concentrations of cardiac troponin I (cTnI) and is associated with an increased risk of CVD. Purpose To assess the association between CeD, systemic inflammation, and subclinical myocardial injury, expressed as increased C-reactive protein (CRP) and circulating concentrations of cTnI, respectively. Methods We cross-sectionally measured CRP and cTnI in 37 559 participants (mean age 55 years, 45% male) in the fourth wave of the population-based cohort, the Trøndelag Health Study (HUNT4). Study participants were serologically screened for CeD with transglutaminase 2 (TG2) IgA and IgG antibodies, and all seropositive participants without known CeD were invited to endoscopy with duodenal biopsies during 2019-2023 for verification of a potential CeD diagnosis (clinicaltrials.gov identifier: NCT04041622). Participants were categorized into no CeD, potential CeD, known CeD prior to the study, and newly diagnosed CeD following the current study. The association between the categories of CeD diagnosis, CRP, and cTnI concentrations, were assessed using linear regression analysis. Results In total, 336 (0.89%) of the participants in the current study were diagnosed with a new CeD diagnosis, an additional 268 (0.71%) had a known CeD diagnosis prior to the study, 170 (0.45%) were categorized as potential CeD, and 36 785 (97.94%) did not have CeD. Participants with a new CeD had lower median CRP concentrations than participants without CeD (1.0mg/L, 25th-75th percentiles, 0.6-2.2mg/L versus 1.3mg/L, 0.6-2.8mg/L; p < 0.01). Median cTnI concentrations were also lower in participants with a new or known CeD diagnosis compared to participants without CeD (1.5ng/L, 0.6-3.1ng/L, and 1.5ng/L, 0.6-3.1ng/L, respectively, versus 1.7ng/L, 0.6-3.5ng/L; all p < 0.05) (Table 1). In the fully adjusted regression models, CRP was not associated with CeD. Only a known CeD diagnosis was associated with lower cTnI concentrations compared to no CeD (B -0.154, 95% Confidence Interval -0.260, -0.049; p = 0.004) (Table 2). Conclusions In this large, contemporary general population study, a known CeD diagnosis, but not a new CeD diagnosis, was associated with lower cTnI concentrations, potentially suggesting a cardioprotective effect of gluten free diet in patients with CeD. However, no association between CeD and CRP concentrations was observed, suggesting that systemic inflammation may not be a prominent feature of CeD.
