Adiposity, joint and systemic inflammation: the additional risk of having a metabolic syndrome in rheumatoid arthritis

Elisa Gremese, Gianfranco Ferraccioli

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

Adiposity is a predisposing condition to atherosclerosis, and rheumatoid arthritis (RA) also predisposes to accelerated atherosclerosis. Adiposity is one of the key features of the metabolic syndrome (MetS) and it is well recognised that a metabolic syndrome (and fat tissue) is a major player in this complex network. Endothelial dysfunction and carotid intima-media thickness, early pre-clinical markers of atherosclerosis which are the main determinants of cardiovascular (CV) morbidity and mortality, occur early on in RA. RA patients have an incidence of CV diseases at least two times higher than the general population. MetS and RA have a low and a severe-moderate degree of inflammation in common, respectively. Adipose tissue has emerged as a dynamic organ that releases several inflammatory and immune mediators (adipokines). In addition, fat has been recognised as a producer of B cell activating factor (BAFF) and of chemerin, an inducer at the chondrocyte level of IL1β, TNFα, IL6, IL8 and MMP13, thus possibly contributing to cartilage damage. Since fat produces inflammation, to obtain a full control of the CV risk in RA, data suggest that it is therefore mandatory to have a "tight control" of both RA and MetS-related inflammation, especially if RA presents MetS as a co-morbidity.
Original languageEnglish
Pages (from-to)w13211-w13220
Number of pages10
JournalSwiss Medical Weekly
Volume141
DOIs
Publication statusPublished - 2011

Keywords

  • Adiposity
  • Arthritis, Rheumatoid
  • Atherosclerosis
  • Cardiovascular Diseases
  • Humans
  • Inflammation
  • Metabolic Syndrome X
  • Risk Factors

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