Lack of association between infection and onset of polymyalgia rheumatica.

J Rheumatol

Department of Rheumatology, Hospital Príncipes de España, Ciudad Sanitaria y Universitaria de Bellvitge, Hospitalet de Llobregat, Barcelona, Spain.

Published: April 2000

Objective: The etiology of giant cell arteritis (GCA) is unknown, but its sudden onset and the wide variation in incidence reported from various parts of the world suggest a genetic predisposition and/or the influence of environmental factors, such as infectious agents or a seasonal effect. We analyzed 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 1997. To evaluate seasonal variation in disease onset, the month of onset of the first symptoms related to GCA was used to calculate season-specific incidence rates. Differences between season incidence rates were assessed by chi-square test. To test for an association between infection and GCA onset, we considered only infections that occurred within 2 months before the onset of disease. Because of the difficulty in determining whether an infection was present using only the clinical and laboratory data recorded in patients' medical charts, we categorized the likelihood of patients having infection into 3 groups: no infection, probable infection, and definite infection.

Results: Between 1985 and 1997 (both years included), a total of 143 patients (88 women, 55 men) were diagnosed with GCA. Of these, 85 had isolated polymyalgia rheumatica (PMR), 22 had temporal arteritis (TA) without PMR, and 36 had PMR associated with TA. The main clinical features in our population were similar to those reported in other studies. We found no seasonal variation 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.

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