Presentation: Association of Cigarette Smoking with Organ Damage in Primary Systemic Vasculitis (2007)

2007 Association of Cigarette Smoking with Organ Damage in Primary Systemic Vasculitis

To study the effect of cigarette smoking on the development of permanent organ damage according to Vasculitis Damage Index (VDI) in patients with Primary Systemic Vasculitis [(PSV) Wegener’s granulomatosis (WG), microscopic polyangiitis (MPA), polyarteritis nodosa (PAN), and Churg-Strauss syndrome (CSS)].
We studied 86 prevalent cases with PSV retrieved from a defined population in southern Sweden. Patients were classified according to an algorithm based on the American College of Rheumatology classification criteria 1990 and the Chapel Hill Consensus Conference definitions 1994. There were 46 patients with WG, 27 with MPA, 9 with PAN and 4 patients with CSS. Clinical, demographic, and laboratory data were collected from time of diagnosis as well as data on smoking habits prior to and at time of diagnosis. The cohort was divided according to smoking habit to: smokers (active smokers at diagnosis /ex-smokers) and non-smokers (never smoked). The assessment of organ damage according to VDI was done at 1 and 5 years after diagnosis. An additional final assessment (median follow up of 9.0 years from diagnosis, Interquartile range (IQR) 5-14.75 years) was carried out at January, 1st, 2003. In the absence of information on a given item of damage it was considered not be present.
Thirty three (38%) of patients were smokers and 53 (62%) were non-smokers. The median age of smokers at diagnosis was 58 years (IQR 39-65) and for the non-smoker was 52 years (IQR 41.5-69). There are no differences in smoking habit between the 2 largest groups of patients (WG: smokers 17, 37%, MPA: smokers 11, 40%). We find that non-smokers had significantly higher ENT damage than smokers at one year (p<0.002) and five years after diagnosis (p<0.001) as well as at final assessment (p<0.001). The most common ENT damage in non-smokers was nasal blockage /chronic nasal discharge (14 patients), followed by chronic sinusitis/radiological evidence of bone destruction (7 patients) and nasal bridge collapse/nasal perforation (5 patients).
We also found association between cardiovascular damage (myocardial infarction), but here smoking was associated with increased damage and the association was only significant at 5 years after diagnosis (P=0.021). There were no statistically significant differences in the extent of damage in other organ systems.
We found that ENT damage was significantly more prevalent in non-smokers. Considering the harmful effect of smoking in the general population there seem to be special circumstances rendering some protective effect of smoking on the development of ENT damage in patients with PSV. The association between smoking and cardiovascular damage is easier to understand. This is the first report on a possible modifying effect of cigarette smoking on the development of organ damage in PSV, and more studies are needed before any certain conclusions can be made.

 A. Mohammad, None; M. Segelmark, None.