ABSTRACT
BACKGROUND: The contribution of methylglyoxal (MGO) and soluble receptor for advanced glycation end products (sRAGE) in the presence of rheumatoid arthritis (RA) is still unknown. We investigated whether serum MGO and sRAGE were related to the presence of disease activity in RA. METHODS: 80 patients with RA and 30 control subjects were included in a cross-sectional study. The severity of RA was assessed using the disease activity score for 28 joints (DAS28). Serum MGO and sRAGE were measured by ELISA. RESULTS: Serum MGO levels were significantly higher in patients with RA versus control subjects (P < 0.001) and were increased in RA patients with higher disease activity versus RA patients with moderate disease activity (P = 0.019). Serum sRAGE concentrations were significantly decreased in RA patients with higher disease activity versus RA patients with moderate disease activity and versus control subjects (P = 0.004; P = 0.002, resp.). A multiple logistic regression analysis demonstrated that MGO was independently associated with the presence of activity disease in RA (OR = 1.17, 95% CI: 1.02-1.31, P = 0.01). CONCLUSION: Serum MGO and sRAGE levels are inversely related to the activity of RA, and MGO is independently associated with a higher disease activity of RA.
Subject(s)
Arthritis, Rheumatoid/blood , Biomarkers/blood , Glycation End Products, Advanced/blood , Pyruvaldehyde/blood , Adult , Cross-Sectional Studies , Female , Humans , Logistic Models , Male , Middle Aged , Severity of Illness IndexABSTRACT
Background There are limited data regarding the contribution of advanced glycation end products in the presence of rheumatoid arthritis. We investigated whether serum NÉ-carboxymethyllysine and pentosidine were related to the presence and the severity of rheumatoid arthritis. Methods Eighty patients with rheumatoid arthritis and 30 control subjects were included in a cross-sectional study. The severity of rheumatoid arthritis was assessed using the disease activity score for 28 joints. Serum NÉ-carboxymethyllysine and pentosidine were measured by enzyme-linked immunosorbent assay. Results Serum NÉ-carboxymethyllysine and pentosidine concentrations were significantly higher in patients with rheumatoid arthritis vs. control subjects ( P < 0.001). Serum NÉ-carboxymethyllysine and pentosidine concentrations were significantly higher in rheumatoid arthritis patients with high disease activity vs. rheumatoid arthritis patients with moderate disease activity ( P < 0.001, P = 0.019, respectively). A multiple logistic regression analysis demonstrated that NÉ-carboxymethyllysine was independently associated with the presence of rheumatoid arthritis (OR = 1.21, 95% CI: 1.05-1.39, P = 0.006). Furthermore, in a multivariate stepwise regression analysis, NÉ-carboxymethyllysine was independently correlated with disease activity score for 28 joints (standardized ß = 0.43, P = 0.001). Conclusion Serum NÉ-carboxymethyllysine and pentosidine were increased during rheumatoid arthritis, and NÉ-carboxymethyllysine was independently associated with the presence and the severity of rheumatoid arthritis.
Subject(s)
Arthritis, Rheumatoid/blood , Arthritis, Rheumatoid/pathology , Biomarkers/blood , Lysine/analogs & derivatives , Adult , Arginine/analogs & derivatives , Arginine/blood , Case-Control Studies , Cross-Sectional Studies , Enzyme-Linked Immunosorbent Assay/methods , Female , Humans , Lysine/blood , Male , Middle Aged , Severity of Illness IndexABSTRACT
Metabolic syndrome (MetS) is considered one of the most important public health problems. Several and controversial studies showed that the role of advanced glycation end products (AGEs) and their receptor in the development of metabolic syndrome and therapeutic pathways is still unsolved. We have investigated whether plasma pentosidine, carboxymethyl-lysine (CML), and soluble receptor for advanced glycation end products (sRAGE) levels were increased in patients with MetS and the effect of metformin in plasma levels of pentosidine, CML, and sRAGE. 80 control subjects and 86 patients were included in this study. Pentosidine, CML, and sRAGE were measured in plasma by enzyme-linked immunosorbent assay (ELISA). Plasma pentosidine, CML, and sRAGE levels were significantly increased in patients compared to control subjects (P < 0.001, P < 0.001, and P = 0.014, resp.). Plasma levels of pentosidine were significantly decreased in patients who received metformin compared to untreated patients (P = 0.01). However, there was no significant difference between patients treated with metformin and untreated patients in plasma CML levels. Plasma levels of sRAGE were significantly increased in patients who received metformin and ACE inhibitors (P < 0.001 and P = 0.002, resp.). However, in a multiple stepwise regression analysis, pentosidine, sRAGE, and drugs treatments were not independently associated. Patients with metabolic syndrome showed increased levels of AGEs such as pentosidine and CML. Metformin treatment showed a decreased level of pentosidine but not of CML. Therapeutic pathways of AGEs development should be taken into account and further experimental and in vitro studies merit for advanced research.