Are Selenium Status and Inflammation Linked to Cardiometabolic Risk Factors in Inborn Errors of Immunity?

Background/Objective: Patients with Inborn Errors of Immunity (IEI) are at increased cardiometabolic risk due to inflammation, immune dysfunction, and oxidative stress. Given selenium’s essential role in antioxidant defense, this study evaluated plasma selenium concentration in individuals with IEI and its associations with inflammatory and metabolic biomarkers and body mass index (BMI). Methods: A controlled cross-sectional study involved 85 patients, 22 with ataxia–telangiectasia (A-T), 32 with common variable immunodeficiency (CVI) and 31 with juvenile systemic lupus erythematosus (jSLE). The control group comprised 72 age- and sex-matched healthy individuals. Anthropometric, inflammatory, metabolic, and oxidative stress parameters were assessed, including BMI, ultrasensitive C-reactive protein (usCRP), lipid profile, fasting glucose, insulin, plasma Se concentrations, erythrocyte glutathione peroxidase (GPx) activity, and malondialdehyde levels. Results: Selenium concentrations below the reference value (46 µg/L) were observed in all groups, A-T (41%), CVI (50%), jSLE (48%) and the control group (33%). Low weight was more frequent in the A-T group (41%), whereas excess weight predominated in the CVI (47%) and jSLE (19%) groups. Multiple linear regression showed lower selenium concentrations in the jSLE (β = −10.1 ug/L) and CVI (β = −12.8 µg) groups compared with the controls (p < 0.05). Selenium concentrations were associated with age (β = 0.3 µg/L) and usCRP (p < 0.05). The GPx values were lower among all patient groups (jSLE: β = 3228 U/L, A-T: β = −2030 U/L, and CVI: β = −2060 U/L) (p < 0.05) compared with the controls. The GPx was also influenced by age (β = 56 U/L; p = 0.010). Conclusion: The present findings suggest alterations in the endogenous antioxidant defense system in patients with IEI, characterized by reduced erythrocyte GPx activity and lower plasma selenium concentrations. The inverse association between selenium and usCRP concentrations suggests a potential link between selenium status and systemic inflammation. However, these findings should be interpreted cautiously, as inflammation may influence circulating selenium concentrations, and the cross-sectional design does not establish causal inferences. Further longitudinal studies are warranted to clarify the relationship between selenium status, inflammation, and antioxidant defense in IEI.