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Identifying risk factors for onset of Psoriatic Arthritis (PsA) is a major unmet need. Comparing potential risk factors for the diagnosis of PsA, rheumatoid arthritis (RA), and ankylosing spondylitis (AS) is of interest. Such studies may help us identify shared and unique risk factors of onset of chronic inflammatory arthritis. Meer E et al compared potential risk factors for the diagnosis of PsA, psoriasis, RA, and AS. They conducted four parallel case-control studies using data collected between 1994 and 2015 in The Health Improvement Network, an anonymized longitudinal patient dataset collected at primary care clinics throughout the United Kingdom. PsA was associated with obesity, pharyngitis, skin infections, moderate alcohol intake, gout, and uveitis. As expected, PsA and AS were associated with uveitis. Interestingly, PsA and RA were associated with preceding gout. Smoking was a risk factor for all disease and statin use was inversely associated with all 4 diseases. This study has identified potential risk factors for inflammatory diseases including PsA and may help in early identification as well as risk mitigation.
Most patients develop psoriatic arthritis (PsA) after or simultaneously with cutaneous psoriasis. The mechanisms underlying progression from cutaneous psoriasis to arthritis psoriasis are currently unclear. An important question is whether modern targeted treatment of cutaneous psoriasis reduces the risk of developing PsA. To address this, Acosta Felquer ML et al conducted a retrospective cohort study to compare the incidence of PsA in 1719 patients with psoriasis (14,721 patient/years of follow up) grouped according to different treatments for their skin psoriasis: topicals, phototherapy or no treatment (n= 1387), conventional disease-modifying antirheumatic drugs (cDMARDs) or biological DMARDs (bDMARDs). During follow-up, 239 patients (14%) developed PsA. The risk of developing PsA in patients treated with bDMARDs was significantly lower (incidence rate ratio (IRR)=0.26; 95% CI 0.03 to 0.94), compared with topicals, but not compared with cDMARDs (IRR=0.35; 95% CI 0.035 to 1.96). Male sex, nail involvement and higher body mass index were associated with increased risk of developing PsA, while bDMARD use was protective. Thus, this study provides some evidence that systemic treatment might ‘protect’ against development if PsA. Appropriately designed prospective studies are required.
One important clinical question is whether patients with oligoarthritis (involvement of <5 joints) progress to polyarthritis. In an observational study Gladman DD et al reported that in 407 patients evaluated within 12 months of diagnosis, 192 (47%) presented with oligoarthritis. More patients with polyarthritis presented with dactylitis, enthesitis, higher HAQ and lower SF-36 scores. Of the 192 patients with oligoarthritis, 75 (39%) progressed to polyarthritis. Lower SF-36 mental component summary score was the predictor for progressing to polyarthritis. Thus, except for the burden of musculoskeletal involvement, oligoarticular PsA resembles polyarticular PsA and therefore the two PsA subclasses should simply be classified together as peripheral arthritis.
Identifying risk factors for onset of Psoriatic Arthritis (PsA) is a major unmet need. Comparing potential risk factors for the diagnosis of PsA, rheumatoid arthritis (RA), and ankylosing spondylitis (AS) is of interest. Such studies may help us identify shared and unique risk factors of onset of chronic inflammatory arthritis. Meer E et al compared potential risk factors for the diagnosis of PsA, psoriasis, RA, and AS. They conducted four parallel case-control studies using data collected between 1994 and 2015 in The Health Improvement Network, an anonymized longitudinal patient dataset collected at primary care clinics throughout the United Kingdom. PsA was associated with obesity, pharyngitis, skin infections, moderate alcohol intake, gout, and uveitis. As expected, PsA and AS were associated with uveitis. Interestingly, PsA and RA were associated with preceding gout. Smoking was a risk factor for all disease and statin use was inversely associated with all 4 diseases. This study has identified potential risk factors for inflammatory diseases including PsA and may help in early identification as well as risk mitigation.
Most patients develop psoriatic arthritis (PsA) after or simultaneously with cutaneous psoriasis. The mechanisms underlying progression from cutaneous psoriasis to arthritis psoriasis are currently unclear. An important question is whether modern targeted treatment of cutaneous psoriasis reduces the risk of developing PsA. To address this, Acosta Felquer ML et al conducted a retrospective cohort study to compare the incidence of PsA in 1719 patients with psoriasis (14,721 patient/years of follow up) grouped according to different treatments for their skin psoriasis: topicals, phototherapy or no treatment (n= 1387), conventional disease-modifying antirheumatic drugs (cDMARDs) or biological DMARDs (bDMARDs). During follow-up, 239 patients (14%) developed PsA. The risk of developing PsA in patients treated with bDMARDs was significantly lower (incidence rate ratio (IRR)=0.26; 95% CI 0.03 to 0.94), compared with topicals, but not compared with cDMARDs (IRR=0.35; 95% CI 0.035 to 1.96). Male sex, nail involvement and higher body mass index were associated with increased risk of developing PsA, while bDMARD use was protective. Thus, this study provides some evidence that systemic treatment might ‘protect’ against development if PsA. Appropriately designed prospective studies are required.
One important clinical question is whether patients with oligoarthritis (involvement of <5 joints) progress to polyarthritis. In an observational study Gladman DD et al reported that in 407 patients evaluated within 12 months of diagnosis, 192 (47%) presented with oligoarthritis. More patients with polyarthritis presented with dactylitis, enthesitis, higher HAQ and lower SF-36 scores. Of the 192 patients with oligoarthritis, 75 (39%) progressed to polyarthritis. Lower SF-36 mental component summary score was the predictor for progressing to polyarthritis. Thus, except for the burden of musculoskeletal involvement, oligoarticular PsA resembles polyarticular PsA and therefore the two PsA subclasses should simply be classified together as peripheral arthritis.
Identifying risk factors for onset of Psoriatic Arthritis (PsA) is a major unmet need. Comparing potential risk factors for the diagnosis of PsA, rheumatoid arthritis (RA), and ankylosing spondylitis (AS) is of interest. Such studies may help us identify shared and unique risk factors of onset of chronic inflammatory arthritis. Meer E et al compared potential risk factors for the diagnosis of PsA, psoriasis, RA, and AS. They conducted four parallel case-control studies using data collected between 1994 and 2015 in The Health Improvement Network, an anonymized longitudinal patient dataset collected at primary care clinics throughout the United Kingdom. PsA was associated with obesity, pharyngitis, skin infections, moderate alcohol intake, gout, and uveitis. As expected, PsA and AS were associated with uveitis. Interestingly, PsA and RA were associated with preceding gout. Smoking was a risk factor for all disease and statin use was inversely associated with all 4 diseases. This study has identified potential risk factors for inflammatory diseases including PsA and may help in early identification as well as risk mitigation.
Most patients develop psoriatic arthritis (PsA) after or simultaneously with cutaneous psoriasis. The mechanisms underlying progression from cutaneous psoriasis to arthritis psoriasis are currently unclear. An important question is whether modern targeted treatment of cutaneous psoriasis reduces the risk of developing PsA. To address this, Acosta Felquer ML et al conducted a retrospective cohort study to compare the incidence of PsA in 1719 patients with psoriasis (14,721 patient/years of follow up) grouped according to different treatments for their skin psoriasis: topicals, phototherapy or no treatment (n= 1387), conventional disease-modifying antirheumatic drugs (cDMARDs) or biological DMARDs (bDMARDs). During follow-up, 239 patients (14%) developed PsA. The risk of developing PsA in patients treated with bDMARDs was significantly lower (incidence rate ratio (IRR)=0.26; 95% CI 0.03 to 0.94), compared with topicals, but not compared with cDMARDs (IRR=0.35; 95% CI 0.035 to 1.96). Male sex, nail involvement and higher body mass index were associated with increased risk of developing PsA, while bDMARD use was protective. Thus, this study provides some evidence that systemic treatment might ‘protect’ against development if PsA. Appropriately designed prospective studies are required.
One important clinical question is whether patients with oligoarthritis (involvement of <5 joints) progress to polyarthritis. In an observational study Gladman DD et al reported that in 407 patients evaluated within 12 months of diagnosis, 192 (47%) presented with oligoarthritis. More patients with polyarthritis presented with dactylitis, enthesitis, higher HAQ and lower SF-36 scores. Of the 192 patients with oligoarthritis, 75 (39%) progressed to polyarthritis. Lower SF-36 mental component summary score was the predictor for progressing to polyarthritis. Thus, except for the burden of musculoskeletal involvement, oligoarticular PsA resembles polyarticular PsA and therefore the two PsA subclasses should simply be classified together as peripheral arthritis.