Lack of association between infection and onset of polymyalgia rheumatica

Citation
J. Narvaez et al., Lack of association between infection and onset of polymyalgia rheumatica, J RHEUMATOL, 27(4), 2000, pp. 953-957
Citations number
30
Categorie Soggetti
Rheumatology,"da verificare
Journal title
JOURNAL OF RHEUMATOLOGY
ISSN journal
0315162X → ACNP
Volume
27
Issue
4
Year of publication
2000
Pages
953 - 957
Database
ISI
SICI code
0315-162X(200004)27:4<953:LOABIA>2.0.ZU;2-9
Abstract
Objective, The etiology of giant cell arteritis (GCA) is unknown, but its s udden onset and the wide variation in incidence reported from various parts of the world suggest a genetic predisposition and/or the influence of envi ronmental factors, such as infectious agents or a seasonal effect. We analy zed the influence of season on GCA in our area over the period 1985-97, as well as the possible association between infection and onset. Methods. Retrospective study of 143 cases of GCA diagnosed from 1985 to 199 7. To evaluate season al variation in disease onset, the month of onset of the first symptoms related to GCA was used to calculate season-specific inc idence rates. Differences between season incidence rates were assessed by c hi-square test. To test for an association between infection and GC:A onset , we considered only infections that occurred within 2 months before the on set of disease. Because of the difficulty in determining whether an infecti on was present using only the clinical and laboratory data recorded in pati ents' medical charts, we categorized the likelihood of patients having infe ction into 3 groups: no infection, probable infection, and definite infecti on. Results. Between 1985 and 1997 (both years included), a total of 143 patien ts (88 women, 55 men) were diagnosed with GCA. Of these, 85 had isolated po lymyalgia rheumatica (PMR), 22 had temporal arteritis (TA) without PMR, and 36 had PMR associated with TA. The main clinical features in our populatio n were similar to those reported in other studies. We found no seasonal var iation in disease onset during the 13 year period. Moreover, only one (0.7% ) of 143 patients was categorized as a probable infection, whereas definite infection was not observed in any case. From these results, the hypothesis of an infectious cause for GCA seems highly improbable. Conclusion. We were unable to observe a seasonal pattern or an association between infection and the onset of GCA.