BACKGROUND: Psoriasis is a chronic T-cell-mediated immunological skin disease with a complex pathogenesis where both genetic and environmental factors are involved. OBJECTIVE: To study the conditional and relative risk of developing psoriasis in identical and fraternal twins whose co-twin has a positive history of the disease and to estimate the relative contribution of genetic and environmental factors on the liability for psoriasis in Norway. METHODS: Self-reported history of psoriasis in twins from the population-based Norwegian Twin Panel (N = 8045) was studied. Absolute and relative risks of developing psoriasis conditioned on the positive history of psoriasis in a co-twin were calculated by Kaplan-Meier survival analysis and Cox regression, respectively. Structural equation modelling was used to estimate genetic and environmental variance components. RESULTS: Altogether, 334 (4.2%) of the twins reported having psoriasis. No difference in prevalence of the disease across sexes and zygosity groups was found. Identical twins were more likely to develop psoriasis than fraternal twins if a co-twin reported having the disease. The best-fitting model showed that additive genetic effects could explain 66% of the variation in liability for psoriasis in this population, and the remaining 34% was due to non-shared environmental influences. CONCLUSIONS: High heritability due to additive genetic effects together with considerable environmental contribution to the liability of psoriasis support the current opinion on the multifactorial aetiology of the disease. No sex-specific patterns of heritability of psoriasis were found.
BACKGROUND:Psoriasis is a chronic T-cell-mediated immunological skin disease with a complex pathogenesis where both genetic and environmental factors are involved. OBJECTIVE: To study the conditional and relative risk of developing psoriasis in identical and fraternal twins whose co-twin has a positive history of the disease and to estimate the relative contribution of genetic and environmental factors on the liability for psoriasis in Norway. METHODS: Self-reported history of psoriasis in twins from the population-based Norwegian Twin Panel (N = 8045) was studied. Absolute and relative risks of developing psoriasis conditioned on the positive history of psoriasis in a co-twin were calculated by Kaplan-Meier survival analysis and Cox regression, respectively. Structural equation modelling was used to estimate genetic and environmental variance components. RESULTS: Altogether, 334 (4.2%) of the twins reported having psoriasis. No difference in prevalence of the disease across sexes and zygosity groups was found. Identical twins were more likely to develop psoriasis than fraternal twins if a co-twin reported having the disease. The best-fitting model showed that additive genetic effects could explain 66% of the variation in liability for psoriasis in this population, and the remaining 34% was due to non-shared environmental influences. CONCLUSIONS: High heritability due to additive genetic effects together with considerable environmental contribution to the liability of psoriasis support the current opinion on the multifactorial aetiology of the disease. No sex-specific patterns of heritability of psoriasis were found.
Authors: Philip E Stuart; Rajan P Nair; Lam C Tsoi; Trilokraj Tejasvi; Sayantan Das; Hyun Min Kang; Eva Ellinghaus; Vinod Chandran; Kristina Callis-Duffin; Robert Ike; Yanming Li; Xiaoquan Wen; Charlotta Enerbäck; Johann E Gudjonsson; Sulev Kõks; Külli Kingo; Tõnu Esko; Ulrich Mrowietz; Andre Reis; H Erich Wichmann; Christian Gieger; Per Hoffmann; Markus M Nöthen; Juliane Winkelmann; Manfred Kunz; Elvia G Moreta; Philip J Mease; Christopher T Ritchlin; Anne M Bowcock; Gerald G Krueger; Henry W Lim; Stephan Weidinger; Michael Weichenthal; John J Voorhees; Proton Rahman; Peter K Gregersen; Andre Franke; Dafna D Gladman; Gonçalo R Abecasis; James T Elder Journal: Am J Hum Genet Date: 2015-11-28 Impact factor: 11.025
Authors: Lam C Tsoi; Sarah L Spain; Jo Knight; Eva Ellinghaus; Philip E Stuart; Francesca Capon; Jun Ding; Yanming Li; Trilokraj Tejasvi; Johann E Gudjonsson; Hyun M Kang; Michael H Allen; Ross McManus; Giuseppe Novelli; Lena Samuelsson; Joost Schalkwijk; Mona Ståhle; A David Burden; Catherine H Smith; Michael J Cork; Xavier Estivill; Anne M Bowcock; Gerald G Krueger; Wolfgang Weger; Jane Worthington; Rachid Tazi-Ahnini; Frank O Nestle; Adrian Hayday; Per Hoffmann; Juliane Winkelmann; Cisca Wijmenga; Cordelia Langford; Sarah Edkins; Robert Andrews; Hannah Blackburn; Amy Strange; Gavin Band; Richard D Pearson; Damjan Vukcevic; Chris C A Spencer; Panos Deloukas; Ulrich Mrowietz; Stefan Schreiber; Stephan Weidinger; Sulev Koks; Külli Kingo; Tonu Esko; Andres Metspalu; Henry W Lim; John J Voorhees; Michael Weichenthal; H Erich Wichmann; Vinod Chandran; Cheryl F Rosen; Proton Rahman; Dafna D Gladman; Christopher E M Griffiths; Andre Reis; Juha Kere; Rajan P Nair; Andre Franke; Jonathan N W N Barker; Goncalo R Abecasis; James T Elder; Richard C Trembath Journal: Nat Genet Date: 2012-11-11 Impact factor: 38.330
Authors: Kristina Gervin; Magnus D Vigeland; Morten Mattingsdal; Martin Hammerø; Heidi Nygård; Anne O Olsen; Ingunn Brandt; Jennifer R Harris; Dag E Undlien; Robert Lyle Journal: PLoS Genet Date: 2012-01-19 Impact factor: 5.917