By Barend J. van Royen, Ben A. C. Dijkmans
The 1st and in basic terms interdisciplinary advisor devoted to the topic, this reference leads readers in the course of the pathogenic, genetic, medical, and biomechanical points of ankylosing spondylitis (AS) and addresses matters with regards to results review, clinical therapy, surgical problems, illness administration, and genetics.
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Additional resources for Ankylosing Spondylitis: Diagnosis and Management
Studies with full matching for B27 are required to conclusively demonstrate the existence of further MHC loci independent of B27. Non-MHC Genes Two whole genome studies in British Caucasians have been published, involving a total of 188 families with 255 affected sibling pairs (130,131). These screens provide strong evidence as to the loci encoding the non-MHC genetic susceptibility to AS. Regions on chromosomes 1, 2, 6, 9, 10, 16, and 19 were identiﬁed with at least moderate linkage to the disease.
Independent support of this ﬁnding has been reported in a preliminary report on a further genome-wide screen (133). The region of linkage is very broad, with the 3-LOD conﬁdence interval extending from 84 to 114 cm, and contains numerous Epidemiology, Pathogenesis, and Genetics of AS 35 potential candidate genes. Further reﬁnement of this interval by high density association/linkage disequilibrium mapping will be required to identify the actual genes involved. The magnitude of the genetic effect observed in affected sibling pair linkage screens is measured by the statistic k, which is the ratio of the observed/expected number of pairs sharing zero alleles identical by descent.
69%) (71). B27 homodimers are expressed on the cell surface, but do not appear to be derived from intracellular sources; rather they are produced from B27 heterodimers either at the cell surface or in endocytic compartments (66). High afﬁnity peptide-binding by B27 heterodimers appears to reduce the homodimer formation (66). Further, high afﬁnity binding of a B27-speciﬁc peptide in B27-transgenic rats reduces the incidence of spondyloarthritis, perhaps by effects on homodimer formation (72). It has therefore been postulated that bacterial triggering infections may promote homodimer formation by interference with the peptide-loading complex, or by changing the intracellular oxidative conditions promoting disulﬁde bond formation (66).
Ankylosing Spondylitis: Diagnosis and Management by Barend J. van Royen, Ben A. C. Dijkmans