Tissue Advanced Glycation End Product Accumulation and Its Association with Clinical and Laboratory Features, Inflammatory Indices, and Comorbidities in Rheumatoid Arthritis and Ankylosing Spondylitis: A Case–Control Study

Advanced glycation end products (AGEs) accumulate under chronic inflammation and metabolic stress and may contribute to long-term tissue damage. Skin autofluorescence (SAF) enables non-invasive assessment of tissue AGE accumulation, but data in inflammatory rheumatic diseases remain limited. The present study evaluated AGE-SAF levels in patients with seropositive rheumatoid arthritis (RA) and ankylosing spondylitis (AS) and investigated their associations with disease activity, inflammatory markers, metabolic parameters, and comorbidities. Patients with RA and AS, along with healthy controls, were included. AGE-SAF was measured non-invasively. Disease activity was assessed using the Disease Activity Score in 28 joints (DAS28) and the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI). Between-group comparisons were performed both crudely and after multivariable adjustment for age, sex, and body mass index (BMI). Logistic regression and receiver operating characteristic (ROC) analyses were used to describe the exploratory discriminative performance of AGE-SAF, and propensity score analyses were conducted as sensitivity analyses to address baseline imbalance. In crude comparisons, AGE-SAF levels were higher in RA than in AS and controls, and higher in AS than in controls (p < 0.001). After adjustment for age, sex, and BMI, AGE-SAF remained significantly elevated in both RA (β = 0.440, 95% CI 0.298–0.583, p < 0.001) and AS (β = 0.304, 95% CI 0.183–0.425, p < 0.001) compared with controls; however, the difference between RA and AS was no longer statistically significant (β = 0.136, 95% CI −0.051 to 0.323, p = 0.154). Exploratory ROC analyses showed good discrimination for RA versus controls (AUC = 0.851) and moderate discrimination for AS versus controls (AUC = 0.695), whereas discrimination between RA and AS was limited (AUC = 0.670). In overlap-weighted sensitivity analysis, the RA-AS difference remained non-significant (β = 0.161, p = 0.293). AGE-SAF is elevated in inflammatory rheumatic diseases compared with healthy controls, and this elevation persists after adjustment for age, sex, and BMI. Although crude AGE-SAF values were higher in RA than in AS, this difference attenuated after confounder adjustment, indicating that a substantial part of the between-disease difference is attributable to demographic and treatment-related imbalance. AGE-SAF may therefore reflect cumulative disease-related and vascular–metabolic burden across both diseases rather than a disease-specific phenomenon.