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A Focus On: Rheumatoid Arthritis

 

Fig. 67.2
Ultrasound in rheumatoid and seronegative arthritis: (A) Proximal interphalangeal (PIP) joint synovitis in rheumatoid arthritis with hypoechoic synovial thickening and power Doppler signal on the extensor aspect of the joint (dorsal longitudinal view). (B) Flexor tenosynovitis (FT) is seen in the palmar longitudinal view of the PIP joint in panel A with hypoechoic widening of the tendon sheath and power Doppler signal in the tendon and sheath. The presence of tendon inflammation is a common feature in RA and does not differentiate seropositive from seronegative arthritis. (C) Tibialis posterior tenosynovitis in reactive arthritis shows similar hypoechoic widening of the tendon sheath (transverse view over medial ankle). (D) Panel C with power Doppler signal in the tendon sheath and tendon. Reproduced from Chapter 67: Ultrasound. In Oxford Textbook of Rheumatology, Fourth Edition. Edited by Richard A Watts, Philip Conaghan, Chris Denton, Helen Foster, John Isaacs, and Ulf Müller-Ladner. © 2011 Oxford University Press. 10.1093/med/9780199642489.001.0001
 

Rheumatoid arthritis (RA) is the most common form of destructive inflammatory arthritis. It is an autoimmune disease in which chronic systemic inflammation predominates, predisposing to cardiovascular comorbidity, increased risk of infections, and premature mortality. Rheumatoid arthritis affects 1.1% of women and 0.4% of men.  It is a costly disease on many levels. In the UK, direct costs are £560 million/year, with the cost of sick leave and work-related disability running at £1.8 billion/year.

 

Over the past 20 years there have been immense advances in our understanding of the aetiopathogenesis of RA, and modern molecular genetics has led to the recognition of increasing numbers of genes implicated in the pathogenesis of RA. Advances in medical imaging with magnetic resonance imaging and Doppler ultrasound have led to earlier diagnosis and better quantification of the extent of inflammation. The recognition of the central role of cytokines such as TNFalpha, and interleukin-6, together with T and B lymphocytes, has led to the development of targeted therapies.

 

Twenty years ago remission of disease activity was considered to be an unobtainable outcome. However, the mentioned recent developments have revolutionized the treatment and outcome for patients with RA, and have led to the concepts of a window of opportunity, ‘treat to target’, as well as established national and international RA management guidelines. Treatment within the first three months of symptoms has the greatest chance of stopping self-perpetuation of inflammation. ‘Treat to target’ refers to the aim of inducing a durable remission to avoid disease progression and disability. The current paradigm is therefore the early identification of people with RA and rapid initiation of intensive immunosuppression using both conventional immunosuppression followed by targeted therapies in those in whom remission is not achieved.

 

With these approaches it is common to see patients with little or no joint inflammation, and no progressive joint damage on imaging. Treating to specified targets is optimal evidence-based practice, but while for some patients minimal disease activity may be appropriate, aiming for remission is the ultimate goal.

Dr Richard A Watts, MA, DM, FRCP, is Consultant Rheumatologist, Ipswich Hospital NHS Trust, Ipswich, UK, and Honorary Senior Lecturer, Norwich Medical School, Norwich, UK.


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