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- W4291119005 endingPage "192" @default.
- W4291119005 startingPage "171" @default.
- W4291119005 abstract "Rheumatoid arthritis (RA) challenges researchers, physicians, and patients with its complexity, its impact on lives, and its refusal to respond predictably to treatment. Because we do not know what causes RA, treatment is, at this time, entirely palliative. Many environmental factors, including smoking, diet, stress, environmental chemicals, and infections, have been implicated in either the etiology or progression of RA, but none of these emerges as a distinct causative agent of RA, in general. As more data becomes available, RA appears to be a cluster of disease entities, which may have unique etiological patterns. Therefore, the best research, current and future, will subdivide RA into disease subsets based on clinical, serological, or environmental parameters. In an iterative process, once RA subsets are defined, common mechanisms may emerge that link them and help explain the complexity, thereby leading to new therapeutic or preventative approaches. This chapter attempts to set the stage for this kind of analysis, using the new paradigm of the gene/environment interaction that unites smoking and major histocompatibility complex haplotype with RA as a critical and revealing example." @default.
- W4291119005 created "2022-08-13" @default.
- W4291119005 creator A5018883043 @default.
- W4291119005 date "2012-01-01" @default.
- W4291119005 modified "2023-09-26" @default.
- W4291119005 title "Rheumatoid Arthritis" @default.
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