Background-Peripheral arthropathy is a well-recognised complication of inflammatory bowel disease (IBD). Little is known of its natural history, but a variety of joint involvement has been described, from large joint pauciarticular arthropathy to a rheumatoid pattern polyarthropathy. Aims-To classify the peripheral arthropathies according to pattern of articular involvement, and study their natural history and clinical associations. Methods-The case notes of all patients attending the Oxford IBD clinic were reviewed, and information on general disease characteristics, extraintestinal features, and arthropathy extracted. This was confirmed by direct patient interview using questionnaires at routine follow up.Patients with recorded joint swelling or eVusion were classified as type 1 (pauciarticular) if less than five joints were involved and type 2 (polyarticular) if five or more were involved. Patients without evidence of swelling were classified as arthralgia. Results-In total, 976 patients with ulcerative colitis (UC) and 483 with Crohn's disease (CD) were reviewed. Type 1 occurred in 3.6% of patients with UC (83% acute and self-limiting) and in 6.0% of those with CD (79% self-limiting); 83% and 76%, respectively, were associated with relapsing IBD. Type 2 occurred in 2.5% of patients with UC and 4.0% of those with CD; 87% and 89%, respectively, caused persistent symptoms whereas only 29% and 42%, respectively, were associated with relapsing IBD. Conclusion-Enteropathic peripheral arthropathy without axial involvement can be subdivided into a pauciarticular, large joint arthropathy, and a bilateral symmetrical polyarthropathy, each being distinguished by its articular distribution and natural history. (Gut 1998;42:387-391)

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Objective-To compare the TCR repertoire of peripheral blood CD8 enriched (CD8+) and depleted (CD8−) T cells in rheumatoid arthritis (RA) patients and controls using CDR3 length analysis (spectratyping). Methods-CD8+ and CD8− T cells were separated from 14 RA patients and 12 controls, using magnetic beads coated with anti-CD8 monoclonal antibodies. cDNA was prepared as the template for amplification with 22 V -C primer pairs. The products were resolved by electrophoresis in an ABI373 sequencer using GENES-CAN software. Expansions were identified as dominant CDR3 lengths, where the area underlying the corresponding peak exceeded the sum of the areas of the two adjacent peaks. This method was validated by sequencing 10 samples displaying dominant peaks. The expansion frequencies in RA patients and controls were compared using the 2 test statistic. Results-Dominant peaks were evident in several V families. They were more frequent in RA patients in both the CD8+ subset (RA normalised frequency 10.6; control normalised frequency 8.0; p=0.03) and the CD8− subset (RA normalised frequency 2.9; control normalised frequency 1.5; p=0.02). Sequencing of 10 samples exhibiting dominant peaks revealed an unequivocal clonal expansion in nine (90%). Conclusions-RA patients exhibited a significantly increased frequency of T cell expansions both in the CD8+ and CD8− subsets. This phenomenon may reflect the proliferation of autoreactive cells, a nonspecific expansion of memory T cells in response to pro-inflammatory cytokines or a defect of T cell regulation that predates the onset of RA and may itself predipose to disease. (Ann Rheum Dis 1998;57:319-322) A pivotal role of T cells in the initiation of rheumatoid arthritis (RA) has been inferred from the prominence of CD4+ T cells in the synovium early in disease, the association of RA with particular HLA-DR4 and DR1 antigens, the eYcacy of treatments that deplete or suppress CD4+ cells, and animal models of chronic arthritis. The T cell receptor (TCR) endows this cell with its discriminatory properties. In developing T cells, functional genes for the and chains of the TCR chain are produced by rearranging selected V /J or V /D /J segments and joining them to their respective constant regions. Unlike the CDR1 and CDR2 loops, which are encoded in the germline, the CDR3 loops are determined by the V J or V D J junctional region and diversity is further enhanced by trimming the germline segments and insertion of nongermline encoded nucleotides. The resulting variation in length of the CDR3 loop is the basis for the "spectratyping" technique, in which the CDR3 region is amplified and the distribution of CDR3 lengths can be used as a readout of TCR repertoire.