We thank Graudal and colleagues for their comments. We also read with interest the preliminary data that they presented, which showed that the relative risk for development of erosive disease among patients with MBL insufficiency is higher in those with recently diagnosed RA than in those with disease of longer duration. This finding is indeed in accordance with our previous observations.
Figure 1 shows the number of patients with erosive and nonerosive RA according to serum MBL level. Because RA is a progressive disease, some patients who originally present with nonerosive disease will develop radiographically apparent erosive lesions; thus, the proportion of patients with erosive arthritis will become higher with longer duration of followup. This will further strengthen our observation that MBL insufficiency is a prognostic marker for erosive RA. Our hypothesis is supported by 2 recent studies reported by Jacobsen et al (Jacobsen S, Madsen HO, Klarlund M, Jensen T, Skjødt H, Jensen KE, et al. The influence of mannose binding lectin polymorphisms on disease outcome in early polyarthritis. J Rheumatol 2001;28:935–42) and Saevarsdottir et al (Saevarsdottir S, Vikingsdottir T, Vikingsson A, Manfredsdottir V, Geirsson AJ, Valdimarsson H. Low mannose binding lectin predicts poor prognosis in patients with early rheumatoid arthritis: a prospective study. J Rheumatol 2001;28:728–34).
We agree with Graudal and associates that an inception cohort with a long duration of followup is needed to properly delineate the association between MBL insufficiency and severity of RA. Such a cohort study is currently being set up within our unit. We believe that the data obtained from this upcoming study will further confirm our hypothesis that MBL insufficiency is associated with poor outcome in RA.