Arthritis care & research · 2015
Further Evidence Supporting a Parent-of-Origin Effect in Psoriatic Disease.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Pollock Remy A, Thavaneswaran Arane, Pellett Fawnda, Chandran Vinod, Petronis Art, Rahman Proton, Gladman Dafna D
Аннотация
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.
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.