@article {Cao292, author = {Yali Cao and Kuo Liu and Zhigang Tian and Susan L. Hogan and Jiajin Yang and Caroline J. Poulton and Ronald J. Falk and Wenge Li}, title = {PTPN22 R620W Polymorphism and ANCA Disease Risk in White Populations: A Metaanalysis}, volume = {42}, number = {2}, pages = {292--299}, year = {2015}, doi = {10.3899/jrheum.131430}, publisher = {The Journal of Rheumatology}, abstract = {Objective. No clear consensus has been reached on the PTPN22 R620W polymorphism and anti-neutrophil cytoplasmic antibody (ANCA) disease, especially when stratified by ANCA specificity and disease phenotypes. Methods. A metaanalysis was conducted on the PTPN22 R620W polymorphism across 4 studies in 1399 white patients with ANCA disease and 9934 normal control subjects. Results. Overall, metaanalysis showed a statistically significant association between the A allele and ANCA disease in all subjects (OR 1.44, 95\% CI 1.26{\textendash}1.64, p \< 0.00001), and stratification by disease category indicated the A allele was associated with granulomatosis with polyangiitis (Wegener{\textquoteright}s; GPA; OR 1.72, 95\% CI 1.35{\textendash}2.20, p \< 0.0001) and microscopic polyangiitis (MPA; OR 1.53, 95\% CI 1.08{\textendash}2.15, p = 0.02) as compared to controls. However, when stratified by ANCA specificity, the association of the A allele was statistically evident among those with proteinase 3 (PR3) ANCA disease (OR 1.74, 95\% CI 1.25{\textendash}2.430, p = 0.001), with the same trend but not statistically associated with myeloperoxidase ANCA disease (OR 1.94, 95\% CI 0.64{\textendash}5.85, p = 0.24). The marked associations were also demonstrated between this allele with lung (OR 1.69, 95\% CI 1.21{\textendash}2.36, p = 0.002), ENT (OR 2.03, 95\% CI 1.45{\textendash}2.84, p \< 0.0001), skin (OR 2.55, 95\% CI 1.69{\textendash}3.84, p \< 0.0001), and peripheral neuropathy involvement (OR 2.12, 95\% CI 1.39{\textendash}3.22, p = 0.0005). Conclusion. The PTPN22 620W allele confers susceptibility to the occurrence and development of ANCA disease in whites, with specific evidence among subsets with GPA, MPA, and PR3 ANCA.}, issn = {0315-162X}, URL = {https://www.jrheum.org/content/42/2/292}, eprint = {https://www.jrheum.org/content/42/2/292.full.pdf}, journal = {The Journal of Rheumatology} }