Background The clinical evidence to support the role for bacteria in arthritogenesis has been confined to reactive arthritis (ReA) among of spondyloarthropathies. There are several bacteria associated with arthritogenesis such as Chlamydia trachomatis and enteropatogenic bacteria. However there are few reports regarding the pathogenic role of the infection with Helicobacter pylori (HP) in ReA.
Objectives The aim of the study is to investigate the possible pathogenic role of the infection with HP as a trigger of ReA.
Methods Ten patients (7 women, 3 men, aged among 19 to 57 years old) with ReA related to HP were investigated. These were identified by positive IgG and IgM antibodies agains HP using Elisa tests performed on sera obtained from one year study (01.01.1999–01.01.2000) on 18 patients with clinical picture suggestive of ReA. We also performed complex immunology investigations, x-rays and osteoarticulary scintigraphies, endoscopy, but unfortunately no IgG antibodies against CagA or serum IgG levels against heat shock protein of 60KDA (HSP60). As for the rest of 8 patients with ReA, 2 of them were induced by C trachomatis,3 by Yersinia enterocolitica serotip 03,09, 2 by Shigella flexneri and 1 by Salmonella enteritides, confirmed by specific IgM and IgG Elisa tests. All patients were HLA B27 negative.
Results The 10 HPReA patients had a female prevalence (7 women to 3 men) with young age (32 years old median), a high number of active joints 4 to 6, long duration of arthritis (3 weeks), no fever and occasionally gastroduodenal complains. However not only peripheral joint involvement but also sacroiliac one was determined by osteoarticulary scintigraphy which was concordant with the high value of erythrocyte sedimentation rate (30 up to 86 mm/h) and C-reactive protein (7 cases). 50% of the cases were ANA positive, homogenous. As for the gastroduodenal involvement only 1 case had active duodenal ulcer HP positive, 2 gastric hyperemia with HP positive tests and 7 cases with normal aspects found at endoscopy.
Conclusion HP may be considered a possible trigger of ReA beyond Chlamydia trachomatis and enteropatogenic bacteria. The homology between microbial and human HSP60 may play a role in the pathogenesis of autoimmune mechanisms/disorders. There is no strong association between gastroduodenal involvement and ReA (different CagA status?). Further studies must be performed.