• Autoimmune diseases
• TaqMan assay
• genetic susceptibility
• genotyping
• single nucleotide polymorphism

• rheumatoid arthritis
• joints
• bone
• therapeutics
• biologicals
• drugs
• jaks
• noncoding rnas

• ACPA
• BMI
• MRI
• MRI-inflammation
• RA
• disease progression
• erosive progression
• obesity
• other arthritides
• radiographic progression

• Humans
• Arthritis, Rheumatoid/complications
• Arthritis, Rheumatoid/diagnostic imaging
• Arthritis, Rheumatoid/pathology
• Osteitis/etiology
• Osteitis/complications
• Synovitis/etiology
• Synovitis/complications
• Obesity/complications
• Obesity/diagnostic imaging
• Magnetic Resonance Imaging
• Disease Progression

• 714312 European Research Council
• Dutch Arthritis Foundation
• European Union’s Horizon 2020

• adipokines
• adipose tissue
• inflammation
• metabolism
• myokines
• rheumatoid arthritis
• skeletal muscle
• therapeutic targets

• No. N43/DBS/000238 Faculty of Health Sciences, Jagiellonian University Medical College, Cracow, Poland.

• adipokines
• axial spondyloarthritis
• bone erosion
• rheumatoid arthritis
• syndesmophyte

• JAK inhibitors
• adipokines
• lipids
• rheumatoid arthritis
• tofacitinib

• Humans
• Carotid Intima-Media Thickness
• Adipokines
• Resistin
• Complement Factor D
• Leptin
• Thrombospondin 1/therapeutic use
• Peroxidase
• Tumor Necrosis Factor-alpha
• Aryldialkylphosphatase
• Adiponectin
• Follow-Up Studies
• Arthritis, Rheumatoid/complications
• Janus Kinase Inhibitors/therapeutic use
• Biomarkers
• Janus Kinases
• Lipids
• Apolipoproteins A/therapeutic use
• Apolipoproteins B/therapeutic use

Adipokines may play a role in the early stages of rheumatoid arthritis. This study evaluated the performance of adipokines in a Colombian population with early rheumatoid arthritis and its relationship with disease activity.

A cross-sectional study evaluated serum adipokine levels (adiponectin, resistin, adipsin, vaspin, and leptin) in patients with early rheumatoid arthritis (eRA), evaluating demographic and clinical variables, along with a control group matched by age and gender. A factorial analysis was performed using principal components analysis (PCA), and a Spearman correlation analysis was performed. Similarly, a cut-off point for serum levels is proposed based on the receiver operating characteristic (ROC) curve between eRA and controls and sensitivity analysis.

Fifty-one eRA subjects were included; there were 41 women. The body mass index (BMI) was 25.12 ±3.8. A statistically significant correlation was identified between adipsin, BMI, and RAPID3. Vaspin and leptin were correlated with BMI. Resistin levels were higher in patients with RAPID3 near remission (p = 0.041), and adiponectin, vaspin, and leptin levels were lower in patients with DAS28 ESR in remission (p = 0.033, p = 0.012, and p = 0.017, respectively). Principal components analysis in component 1 adipokines as adipsin and leptin with BMI and RAPID3 as disease activity index are grouped. Moreover, component 2 had a strong relation between ESR and CRP with an inverse correlation with cholesterol levels and vaspin. A cut-off point was established for each adipokine, thus identifying the best performance for leptin levels greater than 0.58 ng/ml with a sensitivity of 76.5% and specificity of 74.5%.

Adipokine levels are relevant in eRA, especially with disease activity indexes. Resistin levels were higher in patients with an activity index near remission. Otherwise, adiponectin, vaspin, and leptin levels were lower in patients with low activity indexes. RAPID3 correlated with adipsin. It is complementary to the previously published analysis of adipokines.

• adipokines
• disease activity index
• rheumatoid arthritis

• arthritis
• epidemiology
• patient reported outcome measures
• physical therapy modalities

• Adipokines
• Adiponectin
• Arthritis, Rheumatoid
• Humans
• Leptin
• Metabolic Syndrome/diagnosis
• Metabolic Syndrome/epidemiology

• Adiponectin
• Adiponectin receptor 1
• Bone erosion
• Rheumatoid arthritis
• Synovial fibroblasts

• Rheumatoid arthritis
• adipokines
• leptin
• synovial fibroblasts

• DMARD
• body mass index
• disease activity
• response
• rheumatoid arthritis
• treatment

Deregulation of adiponectin is found in systemic autoimmune rheumatic diseases (SARDs). Its expression is downregulated by various inflammatory mediators, but paradoxically, elevated serum levels are present in SARDs with high inflammatory components, such as rheumatoid arthritis and systemic lupus erythematosus. Circulating adiponectin is positively associated with radiographic progression in rheumatoid arthritis as well as with cardiovascular risks and lupus nephritis in systemic lupus erythematosus. However, in SARDs with less prominent inflammation, such as systemic sclerosis, adiponectin levels are low and correlate negatively with disease activity. Regulators of adiponectin gene expression (PPAR-γ, Id3, ATF3, and SIRT1) and inflammatory cytokines (interleukin 6 and tumor necrosis factor α) are differentially expressed in SARDs and could therefore influence total adiponectin levels. In addition, anti-inflammatory therapy could also have an impact, as tocilizumab treatment is associated with increased serum adiponectin. However, anti-tumor necrosis factor α treatment does not seem to affect its levels. Our review provides an overview of studies on adiponectin levels in the bloodstream and other biological samples from SARD patients and presents some possible explanations why adiponectin is deregulated in the context of therapy and gene regulation.

• PPAR-γ
• adiponectin
• gene regulation
• interleukin 6
• systemic autoimmune rheumatic diseases
• therapy
• tumor necrosis factor α

Rheumatoid arthritis (RA), which is a chronic systemic inflammatory disease, is associated with accelerated atherosclerosis and an increased risk of cardiovascular disease (CVD), but the causal factors have yet to be completely elucidated. The studies show that the prevalence of metabolic syndrome (MtS) was significantly higher in RA patients compared to the population. In RA and MetS inflammation and atherosclerosis are closely linked. The level of chemokines and adipokines, which may play a role in the development of atherogenesis in RA with MetS patients is currently unknown. In this study, we investigated the level of chemokine C-X-C motif chemokine ligand 16 (CXCL16) and adipokine in RA with MetS patients and assessed the association of biomarkers with clinical and biochemical activity scores of RA and components of MetS.

Blood serum of 298 people (48—patients with RA and MetS, 82—with RA without MetS, 105—with MetS, 63—control group without both RA and MetS) was tested for (CXCL16), Resistin, Leptin and Fibroblast Growth Factor 21 (FGF21) levels by fluorescent antibody technique. Statistical analysis was performed using SPSS version 18.0.

The biomarker study showed the highest level in the RA with MetS patient group; but as compared with the RA group the differences were insignificant. CXCL16 (Me = 426.2 pg/ml (Q_25-75 250.5-527.6), resistin (Me = 8685.4 pg/ml (Q_25-75 6480.8-13 629.1), and FGF21 (Me = 443.6 pg/ml (Q_25-75 772.9-916.3) proved to be significantly augmented in RA with MetS patients group, and in RA without MetS patients group (Me = 312.7 (Q_25-75 199.4-517.7) pg/ml; Me = 8265.3 (Q_25-75 5779.7-13 340.5) pg/ml; Me = 412.4 (Q_25-75 300.4-497.4) pg/ml, respectively) as compared with MetS patients group (Me = 189.4 (Q_25-75 130.3-280.6) pg/ml; Me = 5364.8 (Q_25-75 2368.9-10 160.9) pg/ml; Me = 133.2 (Q_25-75 76.2-268.6) pg/ml, respectively; P = <.001). Leptin level in all groups was higher than in the control group, but there were no differences between groups. The correlation analysis found a positive relationship between the leptin level and the waist circumference (rs = 0.39; P = .007) in the RA with MetS patients, the association of biomarkers with DAS28 score and ESR did not have any statistical significance. Conclusions: The augmented chemokine, resistin and FGF21 in the RA with MetS patients proves the systemic inflammation which is the basis of RA; the augmented leptin is linked to the abdominal obesity. These data are somewhat of an explanation of the increased risk of the CVD development in RA with MetS people. A differentiated specification can be useful to assess the cardiovascular risk of patients and justify prompt personalized treatment.

• CXCL16
• FGF21
• Leptin
• Resistin
• Rheumatoid arthritis
• biomarkers
• metabolic syndrome

Psoriatic arthritis is a chronic inflammatory disease with skin and joint pathology as the dominant characteristics. Scientific evidence supports its systemic nature and relevant relationship with obesity, metabolic syndrome, and associated conditions. Metabolic syndrome and obesity share common signaling pathways with joint inflammation, reinforcing the idea that adipose tissue is a major contributor to disease development and severity. The adipose tissue is not a mere energy store but also an endocrine organ participating in the immune response. In the search for the best therapeutic strategy for a patient, we should appraise the adipose tissue as an endocrine and immune organ responsible for mild chronic inflammation. Today, our challenge is not only to achieve disease remission but to control the associated comorbidities as well. In light of the high prevalence of obesity in psoriatic arthritis patients and the importance of the adipose tissue in the development of chronic inflammation, we aimed to identify the most relevant articles in this regard published in English until June 2020 using the PubMed database. Search terms included psoriatic arthritis, in combination with metabolic syndrome, obesity, adipokines, cardiovascular disease, and treatment. This review summarizes the current evidence regarding the role of adipose tissue as an adipokine-secreting endocrine organ, discussing its influence on disease development and severity, and ultimately in meeting successful disease management.

• adipokines
• cardiovascular risk
• metabolic syndrome
• obesity
• pathophysiology
• psoriatic arthritis
• treatment

• Cranberry
• Polyphenols
• Rheumatoid arthritis
• n-3 fish oil fatty acids

• adipokines
• inflammation
• rheumatoid arthritis
• spondyloarthritis
• structural damage

• Adipokines/metabolism
• Animals
• Arthritis/metabolism
• Arthritis/pathology
• Humans
• Inflammation/metabolism
• Inflammation/pathology
• Joints/metabolism
• Joints/pathology
• Rheumatic Diseases/metabolism
• Rheumatic Diseases/pathology

Patients with rheumatoid arthritis (RA) have an increased risk of cardiovascular (CV) disease. Adiponectin is involved in the metabolism of glucose and lipids with favourable effects on CV disease, especially its high molecular weight (HMW) isoform. Body composition changes are described in RA with various phenotypes including obesity. The effects of tocilizumab on serum adiponectin and body composition, especially fat mass, in patients with RA are not well determined.

Patients with active RA despite previous csDMARDs and/or bDMARDs and who were tocilizumab naïve were enrolled in a multicentre open-label study. They were evaluated at baseline, 1, 3, 6 and 12 months. Clinical assessment included body mass index (BMI) and anthropometric measurements. Lipid and metabolic parameters, serum adiponectin (total and HMW), leptin, resistin and ghrelin were measured at each time point. Body composition (lean mass, fat mass, % fat, fat in the android and gynoid regions) was evaluated at baseline, 6 and 12 months.

One hundred seven patients were included. Both total and HMW adiponectin significantly increased from baseline to month 3, peaking respectively at month 3 (p = 0.0105) and month 1 (p < 0.0001), then declining progressively until month 6 to 12 and returning to baseline values. Significant elevation in HMW adiponectin persisted at month 6 (p = 0.001). BMI and waist circumference significantly increased at month 6 and 12, as well as lean mass at month 6 (p = 0.0097). Fat mass, percentage fat and android fat did not change over the study period. Lipid parameters (total cholesterol and LDL cholesterol) increased while glycaemia, insulin and HOMA-IR remained stable. Serum leptin, resistin and ghrelin did not change during follow-up.

Tocilizumab treatment in RA patients was associated with a significant increase in total and HMW adiponectin, especially at the onset of the treatment. Tocilizumab also induced a significant gain in lean mass, while fat mass did not change. These variations in adiponectin levels during tocilizumab treatment could have positive effects on the CV risk of RA patients. In addition, tocilizumab may have an anabolic impact on lean mass/skeletal muscle.

The ADIPRAT study was a phase IV open-label multicentre study retrospectively registered on ClinicalTrials.gov under the number NCT02843789 (date of registration: July 26, 2016).

• Adiponectin
• Body composition
• Cardiovascular risk
• Rheumatoid arthritis
• Tocilizumab

• adipsin
• inflammatory arthritis
• neutrophils

• Adiponectin
• IL-6
• Knee osteoarthritis
• Poor physical performance
• Sarcopenic obesity
• Vitamin D

Rheumatoid arthritis (RA) is a chronic inflammatory disease affecting the synovium and articular cartilage that initiates joint damage. Rheumatoid arthritis is associated with a change in many inflammatory biomarkers. The present study aims to examine the diagnostic ability of inflammatory adipocytokines (chemerin and visfatin) and their ratio for RA disease.

The study recruited 60 RA patients and 30 healthy controls. Serum visfatin and chemerin were measured using the ELISA technique. Some related parameters including body mass index (BMI), lipid profile components, C-reactive protein (CRP), and uric acid levels were also determined and correlated with the level of these adipokines.

Serum chemerin, visfatin, CRP, and uric acid (UA) levels were significantly higher (p< 0.05) in RA patients than those of the control group. The multivariate general linear model (GLM) analysis showed that 70.7% of the change in the level of measured parameters can be explained by the presence of RA disease (partial η² = 0.707, p< 0.001). To explore which parameter was affected by the diagnosis, the results of tests between subjects showed that all biomarkers were affected significantly by the diagnosis and the greater effects were on CRP (partial η² = 0.480, p< 0.001) followed by chemerin (partial η² = 0.295, p< 0.001), while visfatinshowed partial η² = 0.079 only. Chemerin showed the highest sensitivity (88.1%) and specificity (75.9%) for diagnosis of RA at cut-off concentration = 187.88 ng/ml as compared with other parameters.

Chemerin and visfatin levels are affected by RA disease when adjusted for other cofounders. The present results suggest that serum chemerin can be used as an inflammatory marker of RA patients as it has good sensitivity and specificity.

• C-reactive protein
• chemerin
• rheumatoidarthritis
• visfatin

To clarify the relationship among serum adiponectin, body composition, current disease activity and therapeutics of rheumatoid arthritis (RA).

We conducted a cross-sectional study in RA patients under treatment with agents including biological disease-modifying antirheumatic drugs (bDMARDs) and Janus kinase (JAK) inhibitors. A total of 351 subjects from the Kyoto University RA Management Alliance cohort (KURAMA) were enrolled in the analysis. We classified the participants into five body composition groups according to the cut-off points for obesity and visceral fat used in Japan: body mass index (BMI), 18.5 kg/m² for underweight and 25.0 kg/m² for obesity, and visceral fat area (VFA), 100 cm² for visceral adiposity.

Classification of body composition revealed that serum adiponectin levels and disease activity score (DAS28-ESR) in the low BMI group were significantly higher than those in the normal and overweight groups. Because both increased serum adiponectin and low BMI were previously reported as poor prognostic factors of RA, we performed multiple regression analysis to determine which factor was correlated with RA disease activity. Serum adiponectin level, but not BMI, was positively associated with DAS28-ESR (estimate = 0.0127, p = 0.0258). Subanalysis also showed that the use of bDMARD or JAK inhibitor did not have an obvious influence on circulating adiponectin.

Classification of body composition and multiple regression analysis revealed a positive and independent correlation between serum adiponectin and DAS28-ESR in Japanese RA patients. Thus, serum adiponectin may be an important marker reflecting high disease activity of RA regardless of current medications.

• adipokines
• adiponectin
• leptin
• periodontitis
• rheumatoid arthritis

• Biomarkers
• Clinical predictor
• NRDS
• Peptides
• Preterm
• Umbilical cord blood

• Biomarkers/blood
• Case-Control Studies
• Fetal Blood/metabolism
• Humans
• Infant, Newborn
• Peptide Fragments/blood
• Prognosis
• Respiratory Distress Syndrome, Newborn/blood
• Respiratory Distress Syndrome, Newborn/diagnosis

• ADIPOQ
• knee osteoarthritis
• single nucleotide polymorphisms

Rheumatoid arthritis is a chronic autoimmune disease affecting typically synovial joints and leading to progressive articular damage, disability, and reduced quality of life. Despite better recent therapeutic strategies improving long-term outcomes, RA is associated with a high rate of comorbidities, infections, malignancies, and cardiovascular disease (CVD). Remarkably, some well-known pathogenic proinflammatory mediators in RA, such as interleukin-1β (IL-1β) and tumor necrosis factor (TNF), may play a pivotal role in the development of CVD. Interestingly, different preclinical and clinical studies have suggested that biologic agents commonly used to treat RA patients may be effective in improving CVD. In this context, the contribution of adipocytokines has been suggested. Adipocytokines are pleiotropic molecules, mainly released by white adipose tissue and immune cells. Adipocytokines modulate the function of different tissues and cells, and in addition to energy homeostasis and metabolism, amplify inflammation, immune response, and tissue damage. Adipocytokines may contribute to the proinflammatory state in RA patients and development of bone damage. Furthermore, they could be associated with the occurrence of CVD. In this study, we reviewed available evidence about adipocytokines in RA, because of their involvement in disease activity, associated CVD, and possible biomarkers of prognosis and treatment outcome and because of their potential as a possible new therapeutic target.

While adiponectin is typically viewed as an anti-inflammatory mediator, such an activity of adiponectin in rheumatoid arthritis (RA) is not so obvious. In the present study we examined whether serum levels of adiponectin reflect the clinical phenotype of RA patients and/or correlate with severity of the disease and the response to anti-TNF-α therapy.

Twenty-one female RA patients qualified to receive anti-TNF-α treatment were prospectively assessed before and after 12 weeks of therapy. Patients underwent full clinical and biochemical assessment. Disease activity was assessed by the Modified Disease Activity Scores (DAS28). Serum concentrations of adiponectin were measured with an immunoassay. The individuals were divided into two subgroups according to whether their baseline serum adiponectin was below or above the median value. The subgroups did not differ in basic demographic, anthropometric, and clinical parameters.

Anti-TNF-α treatment resulted in a significant clinical (DAS28) improvement in patients from both subgroups, but no significant differences between basal and post-treatment serum adiponectin concentrations were observed. However, patients with higher baseline adiponectin experienced a significant and more pronounced improvement in laboratory parameters of inflammation (ESR, CRP, neutrophil count, neutrophil-to-lymphocyte ratio).

It is possible that adiponectin exerts systemic anti-inflammatory effects independently of the local activity of RA.

• adipocytokines
• adiponectin
• anti-TNF-α treatment
• inflammation
• rheumatoid arthritis

• body mass index
• disease activity
• inflammation
• obesity
• rheumatic and musculoskeletal diseases (RMDs)

• Axial spondyloarthritis
• Bone remodeling
• Osteoblast
• Osteoclast
• Psoriasis
• Psoriatic arthritis

• Animals
• Arthritis, Psoriatic/drug therapy
• Arthritis, Psoriatic/immunology
• Bone Remodeling/drug effects
• Bone Remodeling/immunology
• Bone Resorption/drug therapy
• Bone Resorption/immunology
• Bone and Bones/drug effects
• Bone and Bones/immunology
• Humans
• Osteoclasts/drug effects
• Osteoclasts/immunology
• Osteoprotegerin/immunology

• P30 AR069655 NIAMS NIH HHS
• R01 AR069000 NIAMS NIH HHS

• Adiposity
• Complement
• Epidemiology
• Human
• Longitudinal

Variability in response to methotrexate (MTX) in the treatment of juvenile idiopathic arthritis (JIA) remains unpredictable and poorly understood. Based on previous studies implicating an interaction between nicotinamide phosphoribosyltransferase (NAMPT) expression and MTX therapy in inflammatory arthritis, we hypothesized that increased NAMPT expression would be associated with reduced therapeutic response to MTX in patients with JIA. A significant association was found between increased plasma concentrations of NAMPT and reduced therapeutic response in patients with JIA treated with MTX. Inhibition of NAMPT in cell culture by either siRNA‐based gene silencing or pharmacological inhibition with FK‐866 was found to result in a fourfold increase in the pharmacological activity of MTX. Collectively, these findings provide evidence that NAMPT inhibits the pharmacological activity of MTX and may represent a predictive biomarker of response, as well as a therapeutic target, in the treatment of JIA with MTX.

Leptin, an adipokine responsible for body weight regulation, may be involved in pathological processes related to inflammation in joint disorders including rheumatoid arthritis (RA), osteoarthritis, and psoriatic arthritis (PsA). These arthropathies have been associated with a wide range of systemic and inflammatory conditions including cardiovascular disease, obesity, and metabolic syndrome. As a potent mediator of immune responses, leptin has been found in some studies to play a role in these disorders. Furthermore, current potent biologic treatments effectively used in PsA including ustekinumab (an interleukin 12/23 blocker) and adalimumab (a tumor necrosis factor-alpha blocker also used in RA) have been found to increase leptin receptor expression in human macrophages. This literature review aims to further investigate the role leptin may play in the disease activity of these arthropathies.

• Psoriatic arthritis
• Rheumatoid arthritis
• Leptin
• Ustekinumab
• Tumor necrosis factor-alpha

Objectives. Smoking is pathogenic for rheumatoid arthritis (RA) being tightly connected to the genetic and serological risk factors for this disease. This study aims to understand connections between cigarette smoking and serum levels of IGF1 and adipokines in RA. Methods. Serum levels of IGF1 and adipokines leptin, adiponectin, resistin, and visfatin were measured in two independent cohorts of RA patients from Gothenburg (n = 350) and Leiden (n = 193). An association of these parameters with smoking was tested in a direct comparison and proved by bivariate correlation analysis. The obtained associations were further tested in multivariate regression models where the confounders (age, gender, disease duration, and BMI) were controlled. Results. The smokers had significantly lower serum levels of IGF1, adiponectin, and leptin compared to never smokers. In regression analysis, smoking and low leptin, but not adiponectin, were associated and predicted low IGF1. Additionally, high disease activity and high BMI increased the probability of low leptin. Conclusions. The study indicates cigarette smoking as an important cause of a relative IGF1 and leptin deficiency in RA patients. This novel association between smoking and hypoleptinemia may be of importance for long-term prognosis of RA and for prediction of comorbidities.

• Actividad clínica
• Adiponectin
• Adiponectina
• Artrtitis reumatoide
• Citocinas pro-inflamatorias
• Clinical activity
• Leptin
• Leptina
• Pro-inflammatory cytokines
• Resistin
• Resistina
• Rheumatoid arthritis

• ADIPONECTIN
• CACHEXIA
• LEAN MASS
• RHEUMATOID ARTHRITIS

• Adiponectin
• Anti- inflammatory
• Biomarker
• Pro-inflammatory
• Rheumatoid arthritis

• Adipokine
• Autoimmunity
• Inflammation
• White adipose tissue

Joint destruction, as evidenced by radiographic findings, is a significant problem for patients suffering from rheumatoid arthritis and psoriatic arthritis. Inherently irreversible and frequently progressive, the process of joint damage begins at and even before the clinical onset of disease. However, rheumatoid and psoriatic arthropathies are heterogeneous in nature and not all patients progress to joint damage. It is therefore important to identify patients susceptible to joint destruction in order to initiate more aggressive treatment as soon as possible and thereby potentially prevent irreversible joint damage. At the same time, the high cost and potential side effects associated with aggressive treatment mean it is also important not to over treat patients and especially those who, even if left untreated, would not progress to joint destruction. It is therefore clear that a protein biomarker signature that could predict joint damage at an early stage would support more informed clinical decisions on the most appropriate treatment regimens for individual patients. Although many candidate biomarkers for rheumatoid and psoriatic arthritis have been reported in the literature, relatively few have reached clinical use and as a consequence the number of prognostic biomarkers used in rheumatology has remained relatively static for several years. It has become evident that a significant challenge in the transition of biomarker candidates to clinical diagnostic assays lies in the development of suitably robust biomarker assays, especially multiplexed assays, and their clinical validation in appropriate patient sample cohorts. Recent developments in mass spectrometry-based targeted quantitative protein measurements have transformed our ability to rapidly develop multiplexed protein biomarker assays. These advances are likely to have a significant impact on the validation of biomarkers in the future. In this review, we have comprehensively compiled a list of candidate biomarkers in rheumatoid and psoriatic arthritis, evaluated the evidence for their potential as biomarkers of bone (joint) damage, and outlined how mass spectrometry-based targeted and multiplexed measurement of candidate biomarker proteins is likely to accelerate their clinical validation and the development of clinical diagnostic tests.

• Adipokine
• Fat mass
• Inflammation
• Leptin
• Rheumatoid arthritis

• Chondrocytes
• Cytokines
• Knee Osteoarthritis
• Osteoarthritis
• Synovitis

• Aggrecans/metabolism
• Animals
• Arthritis, Experimental/metabolism
• Basic Helix-Loop-Helix Transcription Factors/metabolism
• Cartilage, Articular/cytology
• Cartilage, Articular/metabolism
• Chondrocytes/metabolism
• Collagen Type II/metabolism
• Humans
• Matrix Metalloproteinases/metabolism
• Menisci, Tibial/surgery
• Mice
• Mice, Inbred C57BL
• Nicotinamide Phosphoribosyltransferase/metabolism
• Osteoarthritis/metabolism
• Up-Regulation

Cardiovascular (CV) morbidity and mortality are increased in patients with rheumatoid arthritis (RA). Inflammation is thought to be an important factor in accelerated atherosclerosis in RA, whereas insulin resistance is a known risk factor for atherosclerosis in RA. We hypothesised that adipokines could be a link between inflammation, insulin resistance, and atherosclerosis in RA.

The common carotid artery (CCA) intima-media thickness (IMT), CCA resistive index (RI), and carotid plaques were measured by ultrasonography in 192 patients with RA. Insulin resistance was assessed by the homeostasis model assessment for insulin resistance (HOMA-IR). Serum adiponectin, leptin, resistin, tumor necrosis factor-α, and interleukin (IL)-6 concentrations were determined.

The CCA RI was associated with CCA IMT and the estimated total plaque volume after adjustment for conventional CV risk factors. Among adipokines, resistin and IL-6 were correlated with inflammatory parameters. Leptin and leptin:adiponectin (L:A) ratio were correlated with metabolic risk factors, including HOMA-IR. And L:A ratio was related to the CCA RI after adjustment for conventional and nonconventional CV risk factors, including HOMA-IR, erythrocyte sedimentation rate and C-reactive protein.

L:A ratio was associated with HOMA-IR and carotid RI. L:A ratio might be an independent factor for predicting cardiovascular risk in patients with RA.