The Validity of Surrogate Markers in Rheumatic Disease

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Abstract
Although RA is an inflammatory disease primarily affecting the synovial joints it also has marked systemic consequences. Pro-inflammatory systemically active cytokines are produced within the joint, found in the serum and are capable of inducing the hepatic synthesis of acute-phase proteins. Initially it was believed that the acute-phase response was elicited by the cytokine, interleukin-1 alone. However, it is now clear that there is a complex interaction between the cytokines with inter-leukin-6 predominant, but also involving interleukin-1, tumour necrosis factor and a group of recently described cytokines including interleukin-11, leukaemia inhibitory factor and oncostatin M all of which influence the levels of acute-phase pro–teins. In clinical practice CRP is frequently used as a marker of the acute–phase response. It has a short half-life and conse–quently is a sensitive measure of cytokine-induced protein synthesis. The rate of appearance of bony erosions early in disease correlates with the mean serum concentration of CRP in some studies. It has been suggested that a weak correla–tion probably reflects the fact that joints in which erosions most frequently occur, namely the small joints of the hand, pro–duce smaller amounts of cytokine than the large joints such as the knee. A recent study examining the rate of spinal trabecular bone loss in the first year of rheumatoid disease found a strong correlation between bone loss and serum CRP concentrations. It appears that CRP concentrations reflect the level of ‘systemic osteoclast-activating factor’ and are, therefore, a good measure of the general catabolic state of the patient. Many would now consider that persistently elevated serum CRP in patients with RA is in itself an indication for CRP suppressive therapy.

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