Impact of disease activity on impaired glucose metabolism in patients with rheumatoid arthritis

Abstract

Objective To explore glucose metabolism in rheumatoid arthritis (RA) and its association with insulin resistance (IR) risk factors and disease activity indicators, including matrix metalloproteinase-3 (MMP3). Methods This single-center study included 127 non-diabetic subjects: 90 RA patients and 37 matched controls. IR-related risk factors, disease activity (DAS28-ESR/CRP), concentrations of inflammation markers, MMP3, glucose, specific insulin, and C-peptide (a marker of β-cell secretion) were determined. Homeostasis Model Assessment was used to establish insulin resistance (HOMA2-IR) and sensitivity (HOMA2-%S). Associations of HOMA2 indices with IR-related risk factors, inflammation markers, and RA activity were tested using multiple regression analyses. Results RA patients had significantly increased HOMA2-IR index than controls. In the RA group, multivariate analysis revealed DAS28-ESR, DAS28-CRP, tender joint counts, patient’s global assessment, and MMP3 level as significant positive predictors for HOMA2-IR (β = 0.206, P = 0.014; β = 0.192, P = 0.009; β = 0.121, P = 0.005; β = 0.148, P = 0.007; β = 0.075, P = 0.025, respectively), and reciprocal negative for HOMA2-%S index. According to the value of the coefficient of determination (R2), DAS28-ESR ≥ 5.1 has the largest proportion of variation in both HOMA2-IR indices. DAS28-ESR ≥ 5.1 and ESR were independent predictors for increased C-peptide concentration (β = 0.090, P = 0.022; β = 0.133, P = 0.022). Despite comparability regarding all IR-related risk factors, patients with DAS28-ESR ≥ 5.1 had higher HOMA2-IR than controls [1.7 (1.2–2.5) vs. 1.2 (0.8–1.4), P = 0.000]. There was no difference between patients with DAS28-ESR < 5.1 and controls [1.3 (0.9–1.9) vs. 1.2 (0.8–1.4), P = 0.375]. Conclusions RA activity is an independent risk factor for impaired glucose metabolism. DAS28-ESR ≥ 5.1 was the main contributor to this metabolic disturbance, followed by MMP3 concentration, outweighing the impact of classic IR-related risk factors.

Association between skeletal muscle mitochondrial dysfunction and insulin resistance in patients with rheumatoid arthritis: a case–control study

“…Our data confirm previous studies that show a higher level of insulin resistance among RA participants compared to controls [ 41 ]. Insulin resistance in RA is multifactorial, with corticosteroid treatment and systemic inflammation likely playing a major role [ 41 ].…”

“…Our data confirm previous studies that show a higher level of insulin resistance among RA participants compared to controls [ 41 ]. Insulin resistance in RA is multifactorial, with corticosteroid treatment and systemic inflammation likely playing a major role [ 41 ]. Skeletal muscle mitochondrial dysfunction has been implicated in insulin resistance [ 9 , 12 , 42 ], but this has not been previously reported in RA.…”

Serum Adiponectin and Insulin Resistance in Systemic Lupus Erythematosus and Rheumatoid Arthritis Patients

“…In SLE and RA patients, Cpeptide demonstrated a statistically significant positive connection with ESR and HOMA-B (P=0.004, P=0.000, and P=0.019, P=0.041, respectively). Additionally, according to Risti et al (34) , ESR was a standalone predictor of elevated C-peptide concentration (P= 0.133, P = 0.022). According to a recent study Martín-González et al (35) on RA patients, hyperglycemia brought on by insulin resistance causes beta-cell malfunction, which manifests as increased insulin and C-peptide production.…”

Characteristics of atherosclerotic plaque and the thickness of the carotid artery intima-media complex in patients with rheumatoid arthritis

“…Furthermore, compared to RA patients in remission, RA patients with active disease seem to have less stable and more vulnerable plaques which increases the probability of an acute CV event 40 . RA activity represents an independent risk factor for impaired glucose metabolism which is known to be an independent risk factor for cardiovascular diseases 41 . In contrast, Jonsson et al 42 , Roman et al 35 and Cuomo and colleagues 43 have shown in their researches that there is no correlation between IMT and disease activity, while Semb et colleagues stated that there is a positive correlation of CP vulnerability and RA disease activity assessed with CDAI but not with DAS28 40 .…”