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Autoantibodies and thrombophilia in RA: TNFα and TNFα blockers
  1. G F Ferraccioli,
  2. E Gremese
  1. Division of Rheumatology, Post-Graduate School in Rheumatology, Catholic University School of Medicine, Via Moscati 31, 00168 Rome, Italy
  1. Correspondence to:
    Professor G F Ferraccioli;
    gf.ferracciolirm.unicatt.it

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The thrombophilic milieu of rheumatoid inflammation

Patients with rheumatoid arthritis (RA), an autoimmune chronic-relapsing inflammatory disease affecting joints and internal organs, present in several studies a median survival much shorter than that of the general population.1 The main cause of early premature death is cardiovascular morbidity. Solomon et al clearly showed that women with RA (aged 30–55) have an increased risk of myocardial infarction (MI), a relative risk (RR) of 2, compared with women without RA, increasing according to disease duration up to an RR of 3.1 after 10 years of disease.2 Del Rincon et al had previously recognised that the incidence rate ratio of having MI compared with patients without RA of similar age and sex was 2.65, and therefore substantially increased.3 In addition to the increased risk of MI, patients with RA have an increased risk of carotid disease and of peripheral arterial disease, only partially explained by the previous use of corticosteroids.4 More recently, data from the National Data Bank for Rheumatic Diseases confirm that patients with RA have an increased prevalence of congestive heart failure (CHF) compared with patients with osteoarthritis (3.5% v 2.2%), that their risk factors are those of the general population (male sex, hypertension, diabetes, age, body mass index), and that the Health Assessment Questionnaire, an index of overall heath, is strongly predictive of future CHF.5

“RA presents a cardiovascular risk similar to non-insulin dependent diabetes”

All these data clearly show that RA represents a population at high cardiovascular risk. Overall, the cardiovascular risk of RA has been estimated to be around 3.96,3 and therefore very similar to the overall risk of non-insulin dependent diabetes, which has been estimated by Laakso to be two- to fourfold higher than in non-diabetic subjects.6 It is very similar to …

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