according to data from a large case-control study.
pmphoto/iStockphoto.com
Although smokers have shown an increased risk for ANCA-associated vasculitis (AAV), compared with nonsmokers, previous studies of the association between smoking and AAV risk have been small and the results have been inconsistent, Greg McDermott, MD, and colleagues at Massachusetts General Hospital, Boston, wrote in JAMA Internal Medicine.
The researchers reviewed data from 473 adults diagnosed with AAV between 2002 and 2017 and compared them with 1,419 matched controls without AAV who had completed a smoking history questionnaire.
Overall, the odds of having a diagnosis of AAV were significantly higher among former smokers or current smokers, compared with never smokers (odds ratios, 1.58 and 2.70, respectively). In addition, the researchers found a significant dose-response relationship between pack-years of exposure and risk of AAV. The average age of the cases and controls was 59 years, 59% were women, and 84% were white.
The association between AAV risk and former or current smoking was greater among the 147 former and 29 current smokers with AAV positive for myeloperoxidase (MPO) (OR, 1.73 and 3.54, respectively). “Proteinase 3-ANCA– and MPO-ANCA–positive AAV are increasingly recognized as distinct conditions characterized by differences in genetic risk, pathogenesis, disease manifestations, and response to treatment,” the researchers said. No stronger association was noted in patients with proteinase 3-ANCA–positive AAV, they said. However, the overall associations remained strong after adjustment for demographics and disease manifestations, they noted.
The study findings were limited by several factors including the observational design, homogeneous study population at a single center, and use of self-reports, the researchers wrote. However, the results were strengthened by the large sample size and number of patients who were MPO-ANCA positive, and the data associating smoking with AAV “expand the list of potential risk factors for AAV, including genetics and silica exposure,” they said. “Further studies to confirm these results and investigate a potential pathogenic mechanism are needed,” they concluded.
The study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. The researchers had no financial conflicts to disclose.
SOURCE: McDermott G et al. JAMA Intern Med. 2020 Apr 13. doi: 10.1001/jamainternmed.2020.0675.