Session Type: Poster Session (Tuesday)
Session Time: 9:00AM-11:00AM
Background/Purpose: Delay in diagnosis of psoriatic arthritis (PsA) has been shown to contribute to poor radiographic and functional outcome and less successful response to treatment (Haroon et al 2015). Disease interception models are now being proposed to identify siblings at risk of psoriasis (PsC) and PsA among PsA probands, to facilitate earlier management strategies. We set out to determine genetic variants that are likely to be associated with the risk of developing PsC and PsA among siblings of PsA patients.
Methods: A total of 195 probands were identified from well-established PsA cohorts. Family history and clinical assessment of siblings was systematically evaluated, and DNA of siblings was also collected. SNP genotyping was performed using 42 PsA-weighted SNPs on the probands and siblings. 308 siblings were collected (179 unaffected siblings and 129 affected of which 71 had psoriasis without PsA (PsC), and 56 had PsA). For analysis the concordance of genes from probands to sibling pairs (PsA -PsC , PsA-PsA and PsA-PsC or PsA) were compared with PsA-unaffected sibling pair. Probandwise concordance rates were determined using the formula 2C/(2C+D), in which C is the number of concordant pairs and D is the number of discordant pairs. The concordance difference between two groups were calculated using fisher exact test with an odds ratio (OR) > 1 indicating that the concordance rate in affected siblings was greater than unaffected sibling.
Results: The mean age of the PsA probands at assessment was 48.1 yrs (±14.6) (age of onset of PsC 26.4 (±12.1) and PsA 34.4 (±10.9) yrs). The mean age of PsC siblings at assessment was 53.1 yrs (±14.3) (age onset of PsC at 27.5 (±15.7). The PsA siblings at assessment was 55.2 yrs (±13.4), with age of onset of PsC at 29.4 (±14.9) and PsA 36.1 (±12.9) yrs. Finally, the mean age of assessment of unaffected sibling was 50.2 yrs (±13.2). A differential concordance rate was noted for three genes with PsC, 4 genes with PsA, six genes for PsC or PsA, compared to the unaffected sibling (Table). In addition, when the concordance of PsA siblings were compared to PsC siblings, LCE3A was more likely (OR 2.6, p=0.015) in PsA and HLA-B*3906 was less likely (OR 0.43, p=0.038) to be shared in PsA .
Conclusion: There is greater concordance of known susceptibility genes among PsA siblings and PsC siblings of PsA probands. The genotype of the PsA probands along with the siblings is helpful in determining siblings at risk and should be considered as a potential biomarker for risk prediction.
To cite this abstract in AMA style:Badaiki W, Li Q, Burry T, Landells F, Gehue R, Penney C, Codner D, Dohey A, Smith K, Abji F, Gladman D, O'Rielly D, Chandran V, Rahman P. Predicting Risk of Developing Psoriatic Arthritis (PsA) in Siblings of Patients with Psoriatic Arthritis [abstract]. Arthritis Rheumatol. 2019; 71 (suppl 10). https://acrabstracts.org/abstract/predicting-risk-of-developing-psoriatic-arthritis-psa-in-siblings-of-patients-with-psoriatic-arthritis/. Accessed January 27, 2020.
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ACR Meeting Abstracts - https://acrabstracts.org/abstract/predicting-risk-of-developing-psoriatic-arthritis-psa-in-siblings-of-patients-with-psoriatic-arthritis/