TY - JOUR
T1 - Impact of the Season of Birth on the Development of Juvenile Idiopathic Arthritis in the United States
T2 - A Nationwide Registry-based Study
AU - The CARRA Registry Investigators
AU - Dave, Ishaan
AU - Estroff, Brandon
AU - Gergely, Talia
AU - Rostad, Christina A.
AU - Ponder, Lori A.
AU - McCracken, Courtney
AU - Prahalad, Sampath
AU - Abel, N.
AU - Abulaban, K.
AU - Adams, A.
AU - Adams, M.
AU - Agbayani, R.
AU - Aiello, J.
AU - Akoghlanian, S.
AU - Alejandro, C.
AU - Allenspach, E.
AU - Alperin, R.
AU - Alpizar, M.
AU - Amarilyo, G.
AU - Ambler, W.
AU - Anderson, E.
AU - Ardoin, S.
AU - Armendariz, S.
AU - Baker, E.
AU - Balboni, I.
AU - Balevic, S.
AU - Ballenger, L.
AU - Ballinger, S.
AU - Balmuri, N.
AU - Barbar-Smiley, F.
AU - Barillas-Arias, L.
AU - Basiaga, M.
AU - Baszis, K.
AU - Becker, M.
AU - Bell-Brunson, H.
AU - Beltz, E.
AU - Benham, H.
AU - Benseler, S.
AU - Bernal, W.
AU - Beukelman, T.
AU - Bigley, T.
AU - Binstadt, B.
AU - Black, C.
AU - Blakley, M.
AU - Bohnsack, J.
AU - Boland, J.
AU - Boneparth, A.
AU - Bowman, S.
AU - Bracaglia, C.
AU - Brooks, E.
AU - Brothers, M.
AU - Brown, A.
AU - Brunner, H.
AU - Buckley, M.
AU - Bukulmez, H.
AU - Bullock, D.
AU - Cameron, B.
AU - Canna, S.
AU - Cannon, L.
AU - Carper, P.
AU - Cartwright, V.
AU - Cassidy, E.
AU - Cerracchio, L.
AU - Chalom, E.
AU - Chang, J.
AU - Chang-Hoftman, A.
AU - Chauhan, V.
AU - Chira, P.
AU - Chinn, T.
AU - Chundru, K.
AU - Clairman, H.
AU - Co, D.
AU - Confair, A.
AU - Conlon, H.
AU - Connor, R.
AU - Cooper, A.
AU - Cooper, J.
AU - Cooper, S.
AU - Correll, C.
AU - Corvalan, R.
AU - Costanzo, D.
AU - Cron, R.
AU - Curiel-Duran, L.
AU - Curington, T.
AU - Curry, M.
AU - Dalrymple, A.
AU - Davis, A.
AU - Davis, C.
AU - Davis, T.
AU - De Benedetti, F.
AU - De Ranieri, D.
AU - Dean, J.
AU - Dedeoglu, F.
AU - DeGuzman, M.
AU - Delnay, N.
AU - Dempsey, V.
AU - DeSantis, E.
AU - Dickson, T.
AU - Dingle, J.
AU - Donaldson, B.
AU - Dorsey, E.
AU - Dover, S.
AU - Dowling, J.
AU - Drew, J.
AU - Driest, K.
AU - Du, Q.
AU - Duarte, K.
AU - Durkee, D.
AU - Duverger, E.
AU - Dvergsten, J.
AU - Eberhard, A.
AU - Eckert, M.
AU - Ede, K.
AU - Edelheit, B.
AU - Edens, C.
AU - Edgerly, Y.
AU - Elder, M.
AU - Ervin, B.
AU - Fadrhonc, S.
AU - Failing, C.
AU - Fair, D.
AU - Falcon, M.
AU - Favier, L.
AU - Federici, S.
AU - Feldman, B.
AU - Fennell, J.
AU - Ferguson, I.
AU - Ferguson, P.
AU - Ferreira, B.
AU - Ferrucho, R.
AU - Fields, K.
AU - Finkel, T.
AU - Fitzgerald, M.
AU - Fleming, C.
AU - Flynn, O.
AU - Fogel, L.
AU - Fox, E.
AU - Fox, M.
AU - Franco, L.
AU - Freeman, M.
AU - Fritz, K.
AU - Froese, S.
AU - Fuhlbrigge, R.
AU - Fuller, J.
AU - George, N.
AU - Gerhold, K.
AU - Gerstbacher, D.
AU - Gilbert, M.
AU - Gillispie-Taylor, M.
AU - Giverc, E.
AU - Godiwala, C.
AU - Goh, I.
AU - Goheer, H.
AU - Goldsmith, D.
AU - Gotschlich, E.
AU - Gotte, A.
AU - Gottlieb, B.
AU - Gracia, C.
AU - Graham, T.
AU - Grevich, S.
AU - Griffin, T.
AU - Griswold, J.
AU - Grom, A.
AU - Guevara, M.
AU - Guittar, P.
AU - Guzman, M.
AU - Hager, M.
AU - Hahn, T.
AU - Halyabar, O.
AU - Hammelev, E.
AU - Hance, M.
AU - Hanson, A.
AU - Harel, L.
AU - Haro, S.
AU - Harris, J.
AU - Harry, O.
AU - Hartigan, E.
AU - Hausmann, J.
AU - Hay, A.
AU - Hayward, K.
AU - Heiart, J.
AU - Hekl, K.
AU - Henderson, L.
AU - Henrickson, M.
AU - Hersh, A.
AU - Hickey, K.
AU - Hill, P.
AU - Hillyer, S.
AU - Hiraki, L.
AU - Hiskey, M.
AU - Hobday, P.
AU - Hoffart, C.
AU - Holland, M.
AU - Hollander, M.
AU - Hong, S.
AU - Kitcharoensakkul, M.
AU - Schmitt, E.
AU - Syed, R.
AU - White, A.
AU - Yomogida, K.
N1 - Funding Information:
SP is supported in part by a grant from The Marcus Foundation Inc., Atlanta, and also serves on a Macrophage Activation Syndrome Advisory Committee for Novartis pharmaceuticals. This work could not have been accomplished without the aid of the following organizations: the National Institute of Health's (NIH) National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) and the Arthritis Foundation. The CARRA Legacy Registry was supported by a grant from NIH's NIAMS (award number RC2AR058934). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. The CARRA Legacy Registry was also supported by CARRA, Friends of CARRA, the Arthritis Foundation, and the Duke Clinical Research Institute. The authors would also like to thank all participants and hospital sites that recruited patients for the CARRA Registry, as well as the CARRA Registry site principal investigators, subinvestigators, and research coordinators.
Funding Information:
SP is supported in part by a grant from The Marcus Foundation Inc., Atlanta, and also serves on a Macrophage Activation Syndrome Advisory Committee for Novartis pharmaceuticals. 1I. Dave, MSPH, B. Estroff, MD, T. Gergely, BS, C. McCracken, PhD, Department of Pediatrics, Emory University School of Medicine; 2C.A. Rostad, MD, Department of Pediatrics, Division of Infectious diseases, Emory University School of Medicine, and Center for Childhood Infections and Vaccines, Children’s Healthcare of Atlanta; 3L.A. Ponder, BS, Department of Human Genetics, Emory University School of Medicine; 4S. Prahalad, MD, MSc, Department of Pediatrics, Department of Human Genetics, Emory University School of Medicine, Children’s Healthcare of Atlanta, Atlanta, Georgia, USA. I. Dave and B. Estroff contributed equally. The authors declare no conflicts of interest relevant to this article. Address correspondence to Dr. S. Prahalad, Marcus Professor and Chief of Pediatric Rheumatology, Emory University School of Medicine, 1760 Haygood Drive NE, Atlanta, GA 30322 USA. Email: 32TUsprahal@emory.edu. Accepted for publication June 7, 2021.
Funding Information:
This work could not have been accomplished without the aid of the following organizations: the National Institute of Health’s (NIH) National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) and the Arthritis Foundation. The CARRA Legacy Registry was supported by a grant from NIH’s NIAMS (award number RC2AR058934). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. The CARRA Legacy Registry was also supported by CARRA, Friends of CARRA, the Arthritis Foundation, and the Duke Clinical Research Institute. The authors would also like to thank all participants and hospital sites that recruited patients for the CARRA Registry, as well as the CARRA Registry site principal investigators, subinvestigators, and research coordinators.
Publisher Copyright:
© 2021 The Journal of Rheumatology
PY - 2021/12/1
Y1 - 2021/12/1
N2 - Objective. Autoimmune disorders result from the interplay of genetic and environmental factors. Many autoimmune disorders are associated with specific seasons of birth, implicating a role for environmental determinants in their etiopathology. We investigated if there is an association between the season of birth and the development of juvenile idiopathic arthritis (JIA). Methods. Birth data from 10,913 children with JIA enrolled at 62 Childhood Arthritis and Rheumatology Research Alliance Registry sites was compared with 109,066,226 US births from the same period using a chi.square goodness-of-fit test. Season of birth of the JIA cohort was compared to the US population estimate using a 2-sided 1-sample test for a binomial proportion and corrected for multiple comparisons. Secondary analysis was performed for JIA categories, age of onset, and month of birth. Results. A greater proportion of children with JIA were born in winter (January.March) compared to the US general population (25.72% vs 24.08%; corrected P < 0.0001). This observation was also true after stratifying for age of onset (≤ or > 6 yrs). When analyzed by the month of birth, a greater proportion of children with JIA were born in January compared to the US population (9.44% vs 8.13%; corrected P < 0.0001). Conclusion. Relative to the general population, children with JIA are more often born in the winter, and specifically in the month of January. These observations support the hypothesis that seasonal variations in exposures during the gestational and/or early postnatal periods may contribute to development of JIA.
AB - Objective. Autoimmune disorders result from the interplay of genetic and environmental factors. Many autoimmune disorders are associated with specific seasons of birth, implicating a role for environmental determinants in their etiopathology. We investigated if there is an association between the season of birth and the development of juvenile idiopathic arthritis (JIA). Methods. Birth data from 10,913 children with JIA enrolled at 62 Childhood Arthritis and Rheumatology Research Alliance Registry sites was compared with 109,066,226 US births from the same period using a chi.square goodness-of-fit test. Season of birth of the JIA cohort was compared to the US population estimate using a 2-sided 1-sample test for a binomial proportion and corrected for multiple comparisons. Secondary analysis was performed for JIA categories, age of onset, and month of birth. Results. A greater proportion of children with JIA were born in winter (January.March) compared to the US general population (25.72% vs 24.08%; corrected P < 0.0001). This observation was also true after stratifying for age of onset (≤ or > 6 yrs). When analyzed by the month of birth, a greater proportion of children with JIA were born in January compared to the US population (9.44% vs 8.13%; corrected P < 0.0001). Conclusion. Relative to the general population, children with JIA are more often born in the winter, and specifically in the month of January. These observations support the hypothesis that seasonal variations in exposures during the gestational and/or early postnatal periods may contribute to development of JIA.
KW - Juvenile idiopathic arthritis
KW - Month of birth
KW - Seasonality
UR - http://www.scopus.com/inward/record.url?scp=85121840101&partnerID=8YFLogxK
U2 - 10.3899/JRHEUM.201238
DO - 10.3899/JRHEUM.201238
M3 - Article
C2 - 34329181
AN - SCOPUS:85121840101
SN - 0315-162X
VL - 48
JO - Journal of Rheumatology
JF - Journal of Rheumatology
IS - 12
ER -