Rheumatology Vol. 44 No. 1 © British Society for Rheumatology 2005; all rights reserved
LETTER TO THE EDITOR |
Poststreptococcal reactive arthritis (PSRA): a plea for diagnostic criteria
Medical Centre Leeuwarden, Department of Rheumatology, POB 888, 8901 BR Leeuwarden, The Netherlands
Correspondence to: T. L. T. A. Jansen. E-mail: T.Jansen{at}znb.nl
SIR, With great interest we read the paper by Mackie and Keat on poststreptococcal reactive arthritis (PSRA) [1]. In their study they try to tackle the intriguing problem of defining PSRA, which is appreciated. However, one may question whether their objective, to find if PSRA is a discrete homogeneous syndrome, is methodologically answered properly by reviewing recent literature. One may consider first that the inclusion criteria of case reports, mainly characterized by presentation of arthritis and positive streptococcal (often only antistreptolysin-O) serology, induced heterogeneity. Another problem may well be publication bias. Some case reports are lacking in their study, even one paper from Rheumatology [2].
Additionally, we fully agree that there is a need for a homogeneous group of PSRA. One may start trying to homogenize the patient group by applying a set of criteria as proposed before [3]: Ayoub and Ahmed have proposed a set of clinical and serological PSRA criteria which may be used as a starter to find a set of criteria applicable for making a diagnosis of PSRA due (probably) to group A streptococci (GAS) [3]: (i) arthritis with acute onset and of non-migratory type; (ii) arthritis with a protracted course or of a recurrent type; (iii) arthritis with poor responsiveness to salicylates/non-steroidals; (iv) evidence of antecedent streptococcal infection; (v) not fulfilling Jones's criteria on acute rheumatic fever; and (vi) absence of any of Jones's major manifestations. In an attempt to separate GAS-induced from non-GAS-induced PSRA, one may apply (vii) lower antistreptolysin-O/antiDNase-B ratios as an additional tool [4]. Clearly, we need a homogeneous group of PSRA patients meeting validated diagnostic criteria. Future prospective studies are warranted to find out what proportion of a more homogeneous group of GAS-induced PSRA patients should or should not strictly adhere to penicillin prophylaxis for purposes of potentially recurrent arthritis or cardiac involvement. Could the authors explain their statement on the aforementioned application of diagnostic criteria, and possibly clarify the fulfilment within these criteria of the case reports they studied?
References
- Mackie SL, Keat A. Poststreptococcal reactive arthritis: what is it and how do we know? Rheumatology 2004;43:949–54.
[Abstract/Free Full Text] - Jansen TLTA, Hoekstra PJ, Bijzet J, Limburg PC, Griep EN. Elevation of D8/17 positive B lymphocytes in only a minority of Dutch patients with poststreptococcal reactive arthritis. A pilot study. Rheumatology 2002;41:1202–3.
[Free Full Text] - Ayoub EM, Ahmed S. Update on complications of group A streptococcal infections. Curr Prob Pediatr 1997;27:90–101.[Medline]
- Jansen TLTA, Janssen M, Traksel R, de Jong AJL. A clinical and serological comparison of group A versus non-group A streptococcal reactive arthritis and throat culture negative cases of post-streptococcal reactive arthritis. Ann Rheum Dis 1999;58:410–4.
[Abstract/Free Full Text]
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