Further Evidence Supporting a Parent‐of‐Origin Effect in Psoriatic Disease

Objective To further explore the “parent‐of‐origin” effect in a large cohort of well‐phenotyped patients with cutaneous psoriasis without arthritis (PsC) and psoriatic arthritis (PsA). Methods Self‐reported family history was obtained from PsA patients from Toronto and Newfoundland satisfying the Cl...

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Bibliographic Details
Published in:Arthritis Care & Research
Main Authors: Pollock, Remy A., Thavaneswaran, Arane, Pellett, Fawnda, Chandran, Vinod, Petronis, Art, Rahman, Proton, Gladman, Dafna D.
Other Authors: The Arthritis Society, Canadian Institutes of Health Research, Krembil Foundation, Frederick Banting and Charles Best Canada Graduate Scholarship Doctoral Research Award from the Canadian Institutes of Health Research
Format: Article in Journal/Newspaper
Language:English
Published: Wiley 2015
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Online Access:http://dx.doi.org/10.1002/acr.22625
https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1002%2Facr.22625
https://onlinelibrary.wiley.com/doi/full/10.1002/acr.22625
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Summary:Objective To further explore the “parent‐of‐origin” effect in a large cohort of well‐phenotyped patients with cutaneous psoriasis without arthritis (PsC) and psoriatic arthritis (PsA). Methods Self‐reported family history was obtained from PsA patients from Toronto and Newfoundland satisfying the Classification of Psoriatic Arthritis criteria, and PsC patients from Toronto, who were examined by a rheumatologist to exclude PsA. Proportions of probands with paternally and maternally transmitted psoriatic disease were compared by McNemar's and chi‐square tests. Baseline clinical and genetic characteristics of probands with paternally and maternally transmitted disease were compared using logistic regression. Results A total of 849 probands reported a first‐degree relative affected with psoriatic disease (PsC or PsA), of which 532 (63%) reported an affected parent. A significantly larger proportion of probands reported an affected father compared to an affected mother with psoriatic disease (289 [57%] versus 220 [43%], respectively; P = 0.003). This paternal transmission bias was evident in PsA ( P = 0.006) and PsC probands, although it did not reach statistical significance in PsC probands ( P = 0.20). Furthermore, the proportion of paternal PsC–proband PsA pairs (161 of 214 paternal transmissions [75%]) was significantly larger than maternal PsC–proband PsA pairs (103 of 161 maternal transmissions [64%]) ( P = 0.02). Newfoundland probands with paternally transmitted disease had higher HLA–B*08 carriage ( P = 0.04) and lower MICA–129Met carriage ( P = 0.03). Males had higher HLA–B*38 carriage ( P = 0.05) and a higher prevalence of nail lesions ( P = 0.01). Conclusion We have provided further epidemiologic evidence of a paternal transmission bias in psoriatic disease.