In the past, studies on seasonal variations in the onset of symptoms in patients with Wegener's granulomatosis (WG) have suggested a peak incidence in winter; however, a recent study from France reported a peak incidence in the summer (1). For some time, the investigation of seasonal variation in WG symptoms was thought to be a key to the not yet fully understood pathogenesis of the disease.
We evaluated the data of 445 consecutive patients with WG in a monocentric cohort of our third referral center. Two months after diagnosis, our patients underwent a standardized evaluation with detailed questions about the time, type, and extent of initial symptoms. The exact times of initial symptoms were then cross-checked by review of previous medical records.
We found a stable seasonal distribution of the initial symptoms over a period of 36 years without significant differences between seasons (Table 1). Similar to previous studies, the most frequent initial symptoms were ear, nose, and throat manifestations. The unique advantage of our presented data, apart from the size of the cohort and the exceptional study period, is the validity of the information; with this study protocol we can exclude a recall bias as a systemic error, which frequently limited previous studies that questioned patients years after the patients have been diagnosed.
|1966–1993 (n = 155)†||1994–1998 (n = 123)‡||1999–2002 (n = 167)‡||1966–2002 (n = 445)|
|Winter||36 (23.2)||29 (23.6)||45 (26.9)||110 (25)|
|Spring||39 (25.2)||30 (25.4)||39 (23.4)||108 (24)|
|Summer||42 (27.1)||40 (32.5)||46 (27.5)||128 (29)|
|Autumn||38 (24.5)||24 (19.5)||37 (22.2)||99 (22)|
In conclusion, we cannot support the assumption of a seasonal variation in the onset of WG symptoms. Therefore, as our data show, the time of onset of symptoms might not be the key to possible exogenous triggers of WG. In addition to some evidence for the association of silicate exposure and antineutrophil cytoplasmic antibody–associated vasculitides, the focus to collect more information about the pathogenesis of WG has been shifted to genetic associations like HLA–DPB*01 and PTPN22 (2, 3).