ACR Meeting Abstracts

ACR Meeting Abstracts

Abstract Number: 2502

Contributions Of Skin and Joint Manifestations To The Parent-Of-Origin Effect In Psoriatic Disease

Remy Pollock1, Arane Thavaneswaran2, Vinod Chandran3, Art Petronis4, Al Amin P. Rahman5 and Dafna D. Gladman3, 1University of Toronto, Toronto Western Hospital, Toronto, ON, Canada, 2Rheumatology, University of Toronto, Toronto Western Hospital, Toronto, ON, Canada, 3Division of Rheumatology, University of Toronto, Toronto Western Hospital, Toronto, ON, Canada, 4The Krembil Family Epigenetics Laboratory, Centre for Addiction and Mental Health, Toronto, ON, Canada, 5Medicine, Memorial University, St Johns, NE, Canada

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords:

Session Information

Title: Spondyloarthropathies and Psoriatic Arthritis: Pathogenesis, Etiology, Animal Models II

Session Type: Abstract Submissions (ACR)

Background/Purpose:

Excessive paternal transmission has been previously documented in psoriatic disease. Our objective is to delineate the differential contributions of skin and joint manifestations to this ‘parent-of-origin’ effect, and determine whether the effect is differentially associated with psoriasis or PsA.

Methods:

Parental history of PsA and/or psoriasis without arthritis was ascertained by questionnaire or during clinical assessment of PsA and psoriasis patients from two large cohorts. Data was combined with previously-published data. Proportions of maternal and paternal transmissions were compared using a normal approximation to the binomial distribution. Parental and patient phenotypes were resolved where possible into psoriasis alone or PsA and compared by chi-square test and logistic regression. Patients with paternally and maternally-transmitted disease were compared with respect to demographic and clinical characteristics as well as carriage of risk alleles at HLA-B, -C, –DR, –DQ, and MICA, using Student’s t-test or chi-square test.

Results:

We found a preponderance of patients with affected fathers compared to affected mothers in the combined analysis (397 [56%] versus 313 [44%], p=0.002). There was a greater excess of paternal transmissions in patients with a parental history of psoriasis (223 [58%] versus 162 [42%], p=0.002) compared to patients with a parental history of PsA (75 [54%] versus 65 [46%], p=0.45), but no difference in frequencies between these patients (p=0.37). Although the parent-of-origin effect also appeared to be stronger in PsA than in psoriasis patients, paternal history of psoriasis could not predict PsA. PsA patients with paternally-transmitted psoriasis had fewer damaged joints than patients with maternally-transmitted psoriasis (mean damaged joint count 6.3 compared to 12.9, p=0.04), and PsA patients with paternally-transmitted PsA had an earlier age of PsA diagnosis than patients with maternally-transmitted PsA (mean age 32.8 compared to 37.5 years, p=0.05). In one particular cohort, PsA patients with paternally-transmitted psoriasis had lower carriage rates of HLA-B*38 (p=0.006), HLA-C*06 (p=0.03), and MICA-129Met (p=0.01).

Conclusion:

We have provided additional evidence of a parent-of-origin effect in psoriatic disease, which may be driven by paternal transmission of psoriasis without arthritis and may be characterized by an earlier-onset yet milder disease that is not associated with several known risk alleles in the MHC.

Disclosure:

R. Pollock,
None;

A. Thavaneswaran,
None;

V. Chandran,
None;

A. Petronis,
None;

A. A. P. Rahman,
None;

D. D. Gladman,
None.

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