Do genetic and environmental factors play a role in Psoriatic arthritis?
Yes. Twin studies, family studies, and genome-wide association studies (GWAS) suggest a genetic predisposition to PsA.
Concordance among monozygotic twins ranges from 35% to 70%, versus 12% to 20% for dizygotic twins. Epidemiologic studies have found that first-degree relatives of PsA patients are 27 to 50 times more likely to develop arthritis.
Up to 40% of patients with PsA have a family history of psoriasis.
PsA is a polygenic disorder. GWAS have identified numerous possible associated genes. HLA-Cw6 is associated with severe, early-onset skin psoriasis. HLA-B38 and HLA-B39 are associated with PsA, and HLA-B27 is associated with sacroiliitis and spondylitis. Notably, only 50% of patients with psoriatic sacroiliitis/spondylitis are HLA-B27-positive. Major histocompatibility complex class I polypeptide-related sequence A and other genes in linkage disequilibrium with additional susceptibility loci have been found to be associated with peripheral PsA. HLA-DR∗04 is associated with worse radiographic progression.
Evidence suggests that trauma and infection may play a role in PsA. Trauma to a joint (deep Koebner phenomenon) is reported in 25% of patients before the onset of a patient’s PsA. Subclinical trauma may explain distal interphalangeal (DIP) involvement. Bacterial agents such as streptococcal pharyngitis have been reported before the onset of guttate psoriasis. Obesity increases the risk of PsA in psoriasis patients.