ArticleBiomedical journal2019
Incidence and effect of insulin resistance on progression of atherosclerosis in rheumatoid arthritis patients of long disease duration.
Article in Biomedical journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- The Liver-Heart Axis in Rheumatoid Arthritis: Associations of Liver Fibrosis, Organokines, Endothelin-1, and Cardiovascular Risk.International journal of molecular sciences · 2026Article
- Article
- Cardiometabolic risk and vascular changes in rheumatic diseases.Rheumatology international · 2026Review
- Association between different triglyceride-glucose index combinations with obesity indicators and arthritis: results from two nationally representative population-based study.European journal of medical research · 2024Article
- Association between metabolic score for insulin resistance and cardiovascular disease mortality in patients with rheumatoid arthritis: evidence from the NHANES 1999-2018.Frontiers in endocrinology · 2024Article
- Role of Inflammatory Cytokines in Rheumatoid Arthritis and Development of Atherosclerosis: A Review.Medicina (Kaunas, Lithuania) · 2023Review
- A novel visceral adiposity index predicts bone loss in female early rheumatoid arthritis patients detected by HR-pQCT.Scientific reports · 2023Article
- Systemic complications of rheumatoid arthritis: Focus on pathogenesis and treatment.Frontiers in immunology · 2022Review
- The Effect of TNF-Cardiology research and practice · 2022Review
- Review
- The body's integrated repair kit: Studying mesenchymal stem cells for better ligament repair.Biomedical journal · 2019Article
- Puzzling mRNA: Alternative splicing fine-tunes specificity and function.Biomedical journal · 2019Article
- Circulating TNF-α levels in rheumatoid arthritis: a systematic review and meta-analysis and comparison to TNF-α levels in sepsis.Therapeutic advances in infectious diseaseReview
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe continued atherosclerotic risk in rheumatoid arthritis (RA) has been inadequately explained by conventional factors. Chronic inflammation and endothelial activation seems responsible for developing insulin resistance (IR). The study was aimed to assess the role of inflammation and endothelial activation causing IR in long term RA patients leading to increased atherosclerotic risk.
methodsFifty (25 long-duration and 25 short-duration) RA patients and twenty-three healthy controls were recruited excluding potential confounding co-morbidities. Fasting insulin, proinflammatory cytokines, endothelial stress markers and adipokines were quantified by ELISA. Homeostasis Model Assessment (HOMA)-IR calculated using glucose and insulin values. Atherosclerotic indices were measured using ultrasound.
resultsLipid profile was comparable among groups. Mean carotid intima media thickness (cIMT) was significantly higher in both RA groups (p = 0.0062) compared to controls. HOMA-IR was significantly higher in long-duration RA (p = 0.005); it showed significant associations with DAS 28 (p = 0.01) and hsCRP (p = 0.03) in this subset. Mean cIMT for short-duration RA (p = 0.02) and long-duration RA (p = 0.0006) respectively was also significantly associated with HOMA-IR. Pro-inflammatory markers like TNF-α, resistin and leptin were highest in long-duration RA, higher in short-duration RA when compared to control group respectively. HOMA-IR was significantly dependent on TNF-α (p = 0.008), resistin (p = 0.031), leptin (p = 0.0054). Mean cIMT showed association with all parameters mainly with TNF-α (p = 0.001), iNOS (p = 0.001), resistin (p = 0.008) and leptin (p = 0.04).
conclusionsPersistent inflammation leads to altered adipokine secretion promoting IR in RA patients with long disease duration. Treatment with conventional disease modifying anti-rheumatic drugs (DMARDs) is incomplete to control chronic inflammation and limit progression of atherosclerosis.
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