Adiponectin and Leptin as Biomarkers of Disease Activity and Metabolic Disorders in Rheumatoid Arthritis Patients

Abstract

Background Rheumatoid arthritis (RA) is an autoimmune disease, characterized by inflammation of multiple joints, resulting in irreversible cartilage and bone destruction. Chronic disease activity may be associated with metabolic disorders and premature atherosclerosis. Adipokines are involved not only in metabolism regulation, but also in inflammatory and immune response. Aim This study is designed to explore relationships between adipokines (adiponectin, leptin) and metabolic parameters, as well as disease activity, in patients with chronic RA. Methods This cross-sectional study enrolled 109 patients with RA. The clinical assessment was performed including tender and swollen joint counts, Disease Activity Score 28 (DAS28), body mass index (BMI). The following laboratory parameters were performed: erythrocyte sedimentation rate, C-reactive protein, glucose, lipid profile, creatinine. Serum levels of adiponectin and leptin were assessed by enzyme-linked immunosorbent assay (ELISA). Results The mean adiponectin and leptin serum concentrations remained within normal ranges. Both, adiponectin and leptin levels were not associated with current disease activity markers (clinical and laboratory), and type of treatment. Significant relationships were found between adipokines and metabolic parameters, as well as with coexistent conditions and RA characteristics. Higher leptin levels were noticed in patients with hypertension. In the multiple linear regression analysis, correlations were confirmed. Adiponectin was positively correlated with HDL-C (b = 0.37, p < 0.001), age (b = 0.39, p < 0.001), and negatively with glucose (b = −0.17, p = 0.03). Leptin was positively correlated with BMI (b = 0.58, p < 0.001), and negatively with estimated glomerular filtration rate (eGFR) (b = −0.30, p < 0.001). Conclusion The results of this study show the value of adipokines as indicators of metabolic disorders, rather than inflammatory markers in patients with chronic RA, treated with immunosuppressive or biological drugs. High leptin level may indicate poor prognostic factors, kidney and cardiovascular complications. Adiponectin seems to be protective against metabolic disorders in chronic RA.

Metabolic Effects of Anti-TNF-α Treatment in Rheumatoid Arthritis

“…Comparable results were reported in a study focused on the role of adipokines in RA [8]. Unchanged concentrations of leptin and adiponectin remains unchanged even after two years of observation [54]. One of the limitations of this study is that participating patients had a healthy glucose or lipid metabolism even before bDMARDs treatment initiation, at least based on the parameters measured.…”

Adipokines in Rheumatoid Arthritis: Emerging Biomarkers and Therapeutic Targets

“…However, recent studies in human chondrocytes have shown that these cells can produce leptin and express its long receptor, suggesting that this molecule may have a local function [208]. While some studies have reported a correlation between circulating leptin levels and disease activity markers such as C-reactive protein (CRP) and DAS28 [82,205,209,213,218,223,[226][227][228][229][230][231][232][233], not all investigations support these associations [220,222,224]. In their metaanalysis, Lee et al [82] concluded that a modest yet statistically significant correlation exists between leptin levels and disease activity parameters such as DAS28 and CRP.…”

Correction of Hormonal Disorders Induced by Chronic Cold Stress Using Synthetic Neuropeptide

“…Leptin is one of the key markers of adipose tissue metabolism and energy metabolism [5]. At the same time, it is regarded as a proinflammatory adipokine since it stimulates the production of proinflammatory cytokines (TNF-α, IL-6), CC-chemokines, favors the Th1 phenotype in the Th1/Th2 balance, and correlates with the C-reactive protein level [5,6]. The results showed that chronic cold stress leads to a significant increase in leptin serum level (Table 1).…”