Abstract

RHEUMATOID ARTHRITIS (RA) is known to occur worldwide but not with the same frequency or degree of severity among various population groups. These differences have been related to the uneven distribution of the rheumatoid epitope and the HLA-DR alleles carrying it, although other genes acting alone or in conjunction with the rheumatoid epitope (polymorphisms of tumor necrosis factor alpha, T-cell receptors, Fcgamma receptor IIIA, and interferon gamma, for example) as well as nongenetic factors may be important determinants of the predisposition to RA and to its severity (1-7). Some populations with a relatively low frequency of the rheumatoid epitope are known to have a relatively mild disease; such is the case for Caucasians from the Mediterranean basin and their descendants elsewhere in the world (8-15). In contrast, African descendants from North America, who also have a low frequency of the rheumatoid epitope, have a disease as severe as that of the Caucasians from the same geographic area (16,17). The study by Anaya et al in this issue of the journal (18) includes 2 Colombian subpopulations, one of African descendants from Quibdo and the other of Mestizos (an admixture of the original inhabitants of the region and Spanish conquistadors) from Medellin. The investigators studied with some detail the Quibdo patients, characterizing their clinical and immunogenetic features. The Medellin patients, attending a rheumatology clinic at a general hospital, served as a frame of reference to indicate that in fact patients with erosive RA are being seen in Colombia. There are 2 obvious angles to this report: the first is the comparison between the RA patients from the 2 Colombian ethnic groups and the second is the comparison between the Quibdo African descendants (“African Colombians”) and the African descendants from North America (“African Americans”). In both cases the report posits more questions than provides answers. Given the different methodologies used to study the 2 Colombian populations (case ascertainment and clinical and immunogenetic characterization), I have chosen to concentrate my comments on the 2 populations of African ancestry, the one from Quibdo reported in the Anaya article (18) and the one from the United States studied by McDaniel et al several years ago (16). The African Colombian patients had in general a relatively mild disease as evidenced by the paucity of erosions and low levels of IgM-rheumatoid factor (18). These findings are in clear contrast with the patients from the U.S. whose disease was as severe as that of Caucasians from the same geographic area (16). The African Colombian patients also carried the rheumatoid epitope sparingly (as did a small number of local controls); the investigators then concluded that the infrequency of the rheumatoid epitope was probably the reason for the mild disease observed in their Africandescendant patients, pointing out that this is probably not the sole explanation. I concur with their assessment, as the rheumatoid epitope also was found to be infrequent among the African Americans studied by McDaniel et al (16). If in fact African descendants in South America had a much milder disease than those in North America (granted, this is only 1 study in a relatively small community of African descendants in 1 South American country), were the phenotypic differences observed real or artifactual (since the methods used to study these 2 populations are different and thus not directly comparable)? (19).

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