Do infections trigger juvenile idiopathic arthritis?
- PMID: 20012631
- DOI: 10.1007/s00296-009-1253-4
Do infections trigger juvenile idiopathic arthritis?
Abstract
Juvenile idiopathic arthritis (JIA) is a disease that was prominent with increased inflammation response in immune system, appeared mostly with peripheral arthritis and endogenous and exogenous antigens play a role in the pathogenesis of disease. Two major reasons were thinking to be considerably important. First of them is immunological predisposition and the second one is environmental factors. Infections are considered to be the most important between environmental factors but also stress and trauma are also important in the etiology of the disease. However, the relation between JIA and infections is not clearly defined but the relation between adult chronic arthritis and infections was well-defined. A total of 70 patients, 26 with primer JIA, 20 with recurrent JIA, 24 healthy control were included in this study. Mycoplasma pneumoniae, Chlamydophila pneumoniae and C. Jejuni were detected in 4, 1 and 1 of 10 (38.46%) patients with primer JIA, respectively. Salmonella enteritidis, EBV, M. pneumoniae, C. jejuni and Borrelia burgdorferi were detected in 1, 2, 2, 2, and 1 of the 8(40%) patients with recurrent JIA, respectively. S. enteritidis were isolated in feces culture and also identified by agglutination method. Infection was detected in total 18 (39.13%) of patient groups. C. pneumoniae and C. jejuni were detected in 1 and 1 of 2(8.33) healthy control groups, respectively. Throat culture positivity was not detected in any of the patient and healthy control groups. In conclusion, etiopathogenesis of JIA is not clearly understood and suggested that various factors can trigger the disease and it is the most common rheumatoid disease of childhood. However, there are some studies focusing especially on one infectious agent but this is the first study including such a big range of infectious agents in the literature for the microorganisms that can be suggested to have a role in the etiopathogenesis of JIA. We have a conclusion in the light of our results and suggest that some microorganisms can trigger and increase the intensity of clinical situation according to the case. When we evaluate the primer and recurrent JIA groups; M. pneumoniae and C. jejuni come forward and seen common in JIA cases. We also suggest that the pre-diagnosis of microorganisms, which can play a role as primarily or by intervening in the etiopathogenesis of JIA and adding specific antimicrobial therapy to the standard JIA therapy, it is possible to perform new, extended, especially molecular based serial case studies.
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