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PubMed · 7647116

Reactive arthritis.

B Svenungsson
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Abstract

Reactive arthritis (ReA) develops after an infection elsewhere in the body, generally in the genitourinary or intestinal tract. Chlamydia trachomatis, Yersinia enterocolitica, salmonella, shigella, and campylobacter are frequent triggering agents. Between 60% and 90% of patients are positive for HLA-B27. The arthritis occurs within 4 weeks of the primary infection and is oligoarticular and asymmetric. Extra-articular manifestations include mucocutaneous symptoms, ocular inflammation, and urethritis. The average duration of arthritis is 4 to 5 months but two-thirds of patients have symptoms for more than a year. Bacterial antigens have been found in synovial specimens from patients with ReA, but cultures are sterile. The treatment of ReA comprises non-steroidal anti-inflammatory drugs, intra-articular steroid injections, and physical treatment. Short-term antibiotic treatment has no effect in manifest ReA, whereas a tendency to improvement has been seen with treatment over months, at least after chlamydia infection.

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Arthritis, ReactiveBacterial InfectionsHumansProhibitinsEditorialReview

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B Svenungsson. Reactive arthritis.. https://doi.org/10.1177/095646249500600302

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PubMed2007

Solute carrier family 11 member A1 gene polymorphisms in reactive arthritis.

To investigate the role of SLC 11A1 polymorphisms in the development of reactive arthritis, 91 patients with reactive arthritis and 163 healthy controls were enrolled in this study. The SLC 11A1 polymorphisms were determined by the method of polymerase chain reaction/restriction fragment length polymorphism. The genotype distributions of SLC 11A1 274, 823, 1703, and 1729+ 55 del 4 were significantly different between the patients with reactive arthritis and controls. The genotype frequency of SLC 11A1 274C/C was significantly decreased in the patients with reactive arthritis when compared with that of the controls. In contrast, the SLC 11A1 274C/T showed a significant association with reactive arthritis. The patients with reactive arthritis have a significantly higher frequency of SLC 11A1 823C/C than the controls. However, SLC 11A1 823T/T was resistant to the development of reactive arthritis. The allele frequencies of SLC 11A1 274T and 823C were significantly increased in the patients with reactive arthritis in comparison with those of the controls, independent of HLA-B27. On the contrary, the allele frequencies of SLC 11A1 274C and 823T were significantly decreased in the patients with reactive arthritis. The estimated haplotype frequency of SLC 11A1 274C 823T 1703G 1729+55del 4 TGTG+ was significantly decreased in the patients with reactive arthritis when compared with that of the controls. In contrast, the estimated haplotype frequency of SLC 11A1 274T 823C 1703G 1729+55 del 4 TGTG+ was significantly increased in the patients with reactive arthritis. This study shows that the SLC 11A1 274T and 823C alleles are associated with susceptibility to reactive arthritis independently of HLA-B27 in Taiwan. The SLC 11A1 274T 823C 1703G 1729+55 del 4 TGTG+ haplotype is associated with the development of reactive arthritis in Taiwan. In contrast, the SLC 11A1 274C 823T 1703G 1729+55 del 4 TGTG+ haplotype may be a protective factor.

Arthritis, Reactive↗