The impact of the metabolic syndrome on cardiovascular risk and disease in rheumatoid arthritis. Issue 4 (August 2008)

• Record Type: Journal Article
• Authors: Dessein, Patrick H; Gonzalez-Gay, Miguel A; Woodiwiss, Angela J; Joffe, Barry I; Norton, Gavin R; Solomon, Ahmed
• Is Part Of: Future rheumatology. Volume 3:Issue 4(2008)
• Page Start: 335
• Page End: 349
• Publication Date: 2008-08
• Subjects: cardiometabolic risk -- cardiovascular disease -- glucocorticoids -- high-grade inflammation -- hypothyroidism -- insulin resistance -- metabolic syndrome -- obesity -- rheumatoid arthritis; Rheumatology -- Periodicals; 616.723005
• DOI: 10.2217/17460816.3.4.335
• Languages: English
• ISSNs: 1746-0816

Abstract

The metabolic syndrome is a cluster of cardiovascular risk factors that are of metabolic origin and include atherogenic dyslipidemia, hypertension and hyperglycemia. This syndrome is generally considered to develop as a consequence of excess adiposity- mediated insulin resistance. In rheumatoid arthritis (RA), apart from excess adiposity, high-grade inflammation, routine glucocorticoid use and subclinical hypothyroidism are further implicated in insulin resistance. Several more recently uncovered metabolic risk factors including microalbuminuria, hypercoagulability, autonomic dysfunction, hyperuricemia, renin––angiotensin activation and raised aminotransferase concentrations prior to methotrexate use are also more prevalent in RA subjects as compared with non-RA subjects, linked to other metabolic syndrome components and/or related to RA characteristics. Suppression of RA disease activity improves metabolic cardiovascular risk. Systemic inflammation, glucocorticoid therapy, hypothyroidism, insulin resistance, atherogenic dyslipidemia, hypertension, hypercoagulability, hyperuricemia and raised aminotransferases are each further associated with cardiovascular disease in RA. However, the WHO and the National Cholesterol Education Program defined metabolic syndrome as less strongly associated with atherosclerosis than their components. We propose that individual metabolic risk factors should be considered in the assessment and interventions aimed at reducing cardiovascular risk in this disease. Future prospective investigations need to elucidate molecular mechanisms that account for the interactions between RA characteristics and metabolic risk factors, as well as the relative importance of altering adverse lifestyle factors and intensifying disease activity suppressant therapy in patients with controlled and uncontrolled RA disease activity.