Internal Medicine

Ankylosing Spondylitis and the Spondyloarthropathies: A by Michael H. Weisman MD, John D. Reveille, Desiree van der

By Michael H. Weisman MD, John D. Reveille, Desiree van der Heijde

Built as a spouse textual content to the third version of the heralded Rheumatology, via Hochberg et al., this state of the art reference offers cutting-edge figuring out of the spondylarthropathies. you will find thorough examinations of the cutting edge, new remedies that problem older thoughts of therapy and administration of the disorder. famous specialists within the box additionally current the newest techniques in early prognosis utilizing complex imaging options * state-of-the-art wisdom of the pathogenetic and epidemiologic beneficial properties * crucial new advancements in immunology * and the latest realizing of the socio-demographic influence of the disease.Describes leading edge therapy and administration recommendations that show you how to offer sufferers with monstrous relief in discomfort, morbidity, and the extra dire outcomes of the illness. enables quick connection with the disease's actual manifestations via entire insurance of its scientific points. enables you to make sure the efficacy of organic brokers in line with the most recent insights on new remedies, together with anti-TNF. Assesses the advantages and boundaries of obtainable imaging modalities within the analysis and administration of spondylarthropathies.

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Extra info for Ankylosing Spondylitis and the Spondyloarthropathies: A Companion to Rheumatology 3E

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4 and 110 kb, respectively, centromeric from HLA-B, are known to be functional. MICA encodes a polypeptide of 383 amino acids with the same overall organization as an HLA class I molecule, but with only 15% to 36% sequence homology, and is the most polymorphic, with more than 50 alleles described. MIC proteins are considered to be markers of “stress” in the epithelia and act as ligands for cells expressing a common activatory NK receptor (NKG2D). 50–53 Tumor Necrosis Factor-a. With the striking proinflammatory properties of TNF and the dramatic response of AS to anti-TNF therapy, it is entirely reasonable to implicate the TNF gene complex in pathogenesis.

The link of gut inflammation to the triggering of AS is strongly suggested by data thus far but has still not been defined—this clearly is an area of promise for further investigation. REFERENCES That other genes in the MHC contribute to AS susceptibility is strongly suspected, although despite the study of a number of candidate genes, this “second” MHC gene has yet to be identified. Genome-wide scans have identified a number of regions that may contain other susceptibility genes for AS, and these are being characterized.

2002;169:4033–4038. 43. Ekman P, Kirveskari J, Granfors K. Modification of disease outcome in Salmonella-infected patients by HLA-B27. Arthritis Rheum. 2000;43:1527–1534. 44. Pimtanothai N, Rizzuto GA, Slack R, et al. Diversity of alleles encoding HLA-B40: relative frequencies in United States populations and description of five novel alleles. Hum Immunol. 2000;61:808–815. 45. Robinson WP, van der Linden SM, Khan MA, et al. HLA-Bw60 increases susceptibility to ankylosing spondylitis in HLA-B27+ patients.

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