Outcome of reactive arthritis after an extensive Finnish waterborne gastroenteritis outbreak: a 1-year prospective follow-up study
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The purpose of the study was to assess the 1-year outcome of definitive reactive arthritis (ReA) after a waterborne outbreak. A cohort of 21 patients (15 females and 6 males, median age 54 years) with ReA related to an extensive waterborne outbreak in Finland was clinically followed-up by rheumatologists with visits at baseline, at 1 month and 3, 6 and 12 months. Although the outcome was in general favourable, 1/3 of the patients had chronic course; 7 (33 %) of the 21 patients needed disease-modifying anti-rheumatic drugs (DMARDs) and even 8 (38 %) of them used glucocorticoids at 12 months. Four (19 %) were using non-steroidal anti-inflammatory drugs and nine (43 %) other analgesics. Many patients had articular pain and impaired physical function still at 12 months, even though inflammatory parameters and the number of swollen joints were low. Only one patient (5 %) was human leucocyte antigen-B27-positive. She had the most severe ReA and also additional infectious arthritis caused by Salmonella serotype enteritidis leading to osteonecrosis of her hip joint with subsequent need for arthroplasty. ReA as observed in our study was overall fairly mild, but in many individuals, postinfectious arthralgia and DMARD use continued at least up to 1 year.
KeywordsFollow-up Gastroenteritis Outbreak Reactive Arthritis
The following investigators are members of the Pirkanmaa Waterborne Outbreak Study Group: J Antonen, P Collin, J Helenius, J Herrala, T Katto, M Korpela, E Kujansuu, A-L Kuusela, M Kuusi, J Laine, J Lumio, S Mustajoki, J Mustonen, H Oksa, P Ruutu, S Räsänen and T Uotila. This study was financially supported by the Competitive Research Funding of Tampere University Hospital (Grants 9 L002, 9 M124)
- 21.Doorduyn Y, van Pelt W, Siezen C, van der Horst F, van Duynhoven Y, Hoebee B et al (2008) Novel insight in the association between salmonellosis or campylobacteriosis and chronic illness, and the role of host genetics in susceptibility to these diseases. Epidemiol Infect 136:1225–1234CrossRefPubMedGoogle Scholar