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The author's reply: We read with interest the comments from Dr Currie and colleagues.
It is encouraging that their group has demonstrated that rheumatoid factor (RF) is an independent risk factor for mortality in a large cohort of patients from South Wales, supporting the importance of RF as a biomarker for poor prognosis in a number of clinical situations. Our work has shown a strong association between the presence of RF and ischaemic heart disease in men from a general population.1 Previous groups have demonstrated an increased cardiovascular mortality associated with RF in the general population and among people with rheumatoid arthritis.2,3
We were also fascinated to see that the risk of all‐cause mortality associated with the presence of RF was independent of C reactive protein. This suggests that inflammation may influence mortality and ischaemic heart disease in a much more sophisticated way than previously thought. It appears that multiple different patterns of inflammation and immune activation may lead to a poor outcome. The relative balance of these different mechanisms may produce different patterns of disease and provide new opportunities for treatment. RF is strongly associated with autoimmune disease such as rheumatoid arthritis but is also present in large numbers of people in the general population and can easily be measured. It remains to be seen if RF is acting directly to cause tissue damage or is a secondary marker of a particular variety of inflammation. Further studies are needed to determine if measuring RF is a useful method of predicting poor prognosis in clinical practice.
We are also grateful for the comments of Dr Srinivasan. We agree completely that our work showing an association between the presence of rheumatoid factor (RF) and ischaemic heart disease (IHD) in men lends further support to the importance of inflammation in the aetiopathogenesis of atherosclerosis.1 We are currently measuring other markers of inflammation including highly sensitive C reactive protein in our study population. This will provide further information about whether RF has a special role in the development of atherosclerosis and IHD or whether it is merely a non‐specific marker of inflammation. Our findings that there is no association of other common autoantibodies with IHD, including antinuclear antibodies, would argue against the possibility that the association of RF is the result of non‐specific polyclonal B‐cell activation alone.