Rheumatoid Arthritis: Thompson R

Giles JT, Bartlett SJ, Andersen R, Thompson R, Fontaine KR, Bathon JM. · Johns Hopkins University School of Medicine, Baltimore, Maryland. · Arthritis Rheum. · Pubmed #18759279 links to  free full text

Abstract: OBJECTIVE: The serum C-reactive protein (CRP) concentration is commonly used in rheumatoid arthritis (RA) as a surrogate marker of systemic inflammation, presumably induced by synovitis. However, other tissues, such as adipose tissue, can induce CRP production. This study was undertaken to explore the associations between measures of adiposity and CRP levels in RA. METHODS: One hundred ninety-six men and women with RA underwent anthropometric assessment and total body dual-energy x-ray absorptiometry for measurement of total and regional body fat and lean mass. The associations between measures of fat and lean mass and serum levels of CRP and interleukin-6 (IL-6) were determined in analyses stratified by sex, with adjustment for pertinent demographic, lifestyle, and RA disease and treatment covariates as well as for the potential modifying effects of articular activity and biologic pharmacotherapeutic agents. RESULTS: All measures of adiposity were significantly associated with the level of CRP in women, but not in men. In women, the measure of adiposity that showed the strongest association with the CRP level was truncal fat, in which, in adjusted analyses, each kilogram increase was associated with a 0.101-unit increase in the logarithmically transformed CRP level (P < 0.001). Neither the level of articular activity nor the use of biologic agents significantly modified this association in women. However, in men, elevated articular involvement was associated with a decreasing CRP level as truncal fat increased. For all analyses, substitution of IL-6 for CRP produced similar findings. CONCLUSION: Adiposity is independently associated with CRP levels in women with RA, and thus may confound the estimation of RA disease activity when serum CRP concentration is used as a surrogate for systemic inflammation.

Severs GA, Lawlor TH, Purcell SM, Adler DJ, Thompson R. · Lehigh Valley Hospital-Muhlenberg, Bethlehem, Pennsylvania, USA. · Cutis. · Pubmed #17956013 No free full text.

Abstract: Infliximab is a chimeric immunoglobulin G1kappa monoclonal antibody against tumor necrosis factor alpha (TNF-alpha), a proinflammatory cytokine that participates in both normal immune function and the pathogenesis of many autoimmune disorders. Treatment with infliximab reduces the biologic activities of TNF-alpha and thus is indicated in the treatment of rheumatoid arthritis, Crohn disease, ankylosing spondylitis, psoriatic arthritis, plaque psoriasis, and ulcerative colitis. To our knowledge, there have been 13 case reports of new-onset psoriasis, psoriasiform dermatitis, and palmoplantar pustular psoriasis that developed during treatment with infliximab. We report 3 additional cases of biopsy-proven new-onset psoriasis that developed while the patients underwent treatment with infliximab for inflammatory bowel disease. Although the mechanism for the development of psoriasis in these patients is unclear, several possible explanations are proposed. With increasing use of infliximab and other TNF-alpha inhibitors in clinical practice, more cases of similar reactions to these drugs probably will be reported and are necessary to determine the importance of this eruption.

Chakravarty K, Kuttikat A, Saeed I, Thompson R. · Haroldwood Hospital, Gubbins Lane, Romford, Essex RM3 OBE, UK. · Rheumatology (Oxford). · Pubmed #16449372 links to  free full text

This publication has no abstract.