No abstract

Rheumatoid arthritis is a systemic, inflammatory, autoimmune disorder. Enhanced understanding of molecular pathogenesis has enabled development of innovative biological agents that target specific parts of the immune system. These treatments have changed the course and face of rheumatoid arthritis and outcomes for patients and society. New knowledge has emerged of how environmental factors interact with susceptibility genes and the immune system in the pathogenesis of a major subset of rheumatoid arthritis. Research undertaken on the longitudinal disease process and molecular pathology of joint inflammation has led to new therapeutic strategies that promote early use of disease-modifying drugs with tight disease control and distinct and quantifiable treatment goals. Today, such approaches can halt most cases of joint destruction but not all instances of joint inflammation and comorbidity. Understanding the cause and pathogenesis of different rheumatoid arthritis subsets will lead not only to individualised treatments during early phases of the illness but also, possibly, to disease prevention.

Atherosclerosis occurs prematurely in patients with systemic lupus erythematosus and is independent of traditional risk factors for cardiovascular disease. The clinical profile of patients with lupus and atherosclerosis suggests a role for disease-related factors in atherogenesis and underscores the need for trials of more focused and effective antiinflammatory therapy.

Abstract-Chronic inflammatory diseases are associated with premature atherosclerosis; however, it is unknown whether arterial stiffness is increased in this setting, possibly as a manifestation of vascular disease preceding and/or independent of atherosclerosis. Carotid ultrasonography and radial applanation tonometry were performed in 101 patients with systemic lupus erythematosus, 80 patients with rheumatoid arthritis, and 105 healthy control subjects. The 3 groups were comparable in age, gender, and carotid artery absolute and relative wall thickness. Atherosclerotic plaque was more common in lupus (46%) and rheumatoid arthritis (38%) patients than in controls (23%) .001) after adjustment for differences in mean brachial pressure. In multivariate analysis involving the entire population, arterial stiffness was independently related to age, serum glucose, and the presence of chronic inflammatory disease. In multivariate analysis restricted to the patients, arterial stiffness was independently related to age at diagnosis, disease duration, serum cholesterol, and C-reactive protein (and IL-6, when substituted for C-reactive protein). When analyses were repeated in the 186 study subjects without carotid plaque, arterial stiffness remained significantly elevated in patient groups after adjustment for differences in age and mean brachial pressure. In conclusion, arterial stiffness is increased in chronic inflammatory disorders independent of the presence of atherosclerosis and is related to disease duration, cholesterol, and the inflammatory mediator C-reactive protein and the cytokine that stimulates its production, IL-6. (Hypertension. 2005;46:194-199.)