Psoriatic Arthritis

Spotlight article

The Association of Smoking and Psoriatic Arthritis Risk

Researchers of this large UK cohort study (THIN database; ~6.65 million adults, 1995–2015) tested the “smoking-psoriatic arthritis (PsA) paradox.” Using validated Read codes and Cox models adjusted for age, sex, body mass index, alcohol, and trauma, the authors found that current smoking increased PsA risk in the general population (adjusted HR 1.27, 95% CI 1.19–1.36), yet it appeared slightly protective among people with psoriasis (adjusted HR 0.91, 0.84–0.99). Results were consistent across multiple sensitivity analyses, including alternative smoking definitions, restricting to incident psoriasis, and a stricter PsA definition incorporating disease-modifying antirheumatic drug use.

 

Mediation analysis with marginal structural models showed the total effect of current smoking on PsA risk was 1.27, driven almost entirely by an indirect pathway via psoriasis (indirect HR 1.31), while the direct effect independent of psoriasis was about null/slightly below 1 (HR 0.96). Bias sensitivity analyses indicated that modest uncontrolled confounding could create an apparent protective association when conditioning on the “index event” of psoriasis (collider bias). Together, the data support that smoking increases PsA risk overall, while the paradox among patients with psoriasis is largely methodological. Researchers note that future studies should estimate the total effect by tracking post-psoriasis changes in smoking behavior.

 

Reference: Nguyen UDT, Zhang Y, Lu N, et al. Smoking paradox in the development of psoriatic arthritis among patients with psoriasis: a population-based study. Ann Rheum Dis. 2018;77(1):119-123. doi: 10.1136/annrheumdis-2017-211625.

Julia M. Swafford

PA-C, DFAAPA

Physician Associate, Bronson

Featured article

Systemic Lupus Erythematosus and Psoriasis/Psoriatic Arthritis: Rare Overlap, Real Management Implications

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with environmental, hormonal, and genetic contributors. It can overlap with other connective tissue disorders, and rare coexistence with psoriasis (Ps) and psoriatic arthritis (PsA) has been reported. Because clinical features may mimic each other (eg, subacute cutaneous lupus vs Ps) and anti-TNF therapy for PsA can precipitate lupus-like syndromes in a small fraction of patients, the authors retrospectively reviewed patients with SLE seen at a tertiary academic rheumatology clinic (1990-2012). SLE was defined by the 1997 American College of Rheumatology criteria; Ps was diagnosed clinically; PsA met CASPAR criteria. Demographics, labs, and radiology were abstracted, and group comparisons used chi-square tests (p<0.05).

 

Among 445 patients with SLE, 23 (5.1%) had psoriasis and 20 (4.5%) had PsA. Notably, 20 of 23 SLE+Ps patients (87%) also had PsA. Compared with SLE without Ps/PsA, those with concomitant Ps or PsA had higher frequencies of malar rash, discoid rash, photosensitivity, and arthritis, while antiphospholipid antibodies were less common. No significant differences were seen for neuropsychiatric, serosal, renal, hematologic features, anti-Sm, or anti-DNA antibodies. The findings underscore that although coexistence is uncommon, clinicians should maintain diagnostic vigilance and tailor management given overlapping cutaneous features and potential therapy-related lupus phenomena.

 

Reference: Bonilla E, Shadakshari A, Perl A. Association of psoriasis and psoriatic arthritis with systemic lupus erythematosus. Rheumatol Orthop Med. 2016;1. doi:10.15761/ROM.1000105.

Robert Laugherty

JD, MBA, PA-C

Co-Managing Uveitis: An Ophthalmology–Rheumatology Guide

Uveitis—immune-mediated inflammation of the iris/ciliary body, vitreous, choroid, and/or retina—demands tight co-management between ophthalmology and rheumatology. Etiologies span infections, malignancy “masquerades,” drug reactions, ocular syndromes, and, most commonly, systemic immune disease. Pattern recognition guides the differential: HLA-B27 disease typically causes unilateral, acute, recurrent anterior uveitis; Behçet’s is usually bilateral with retinal vasculitis; juvenile idiopathic arthritis causes insidious, bilateral chronic anterior uveitis. Collaboration is essential: ophthalmology rules out infection/masquerade; rheumatology pursues systemic causes and immunosuppression. Testing should be targeted—(eg, syphilis serology, chest imaging for sarcoid, HLA-B27 for acute unilateral anterior uveitis, urine β2-microglobulin for tubulointerstitial nephritis with uveitis) with awareness that many cases remain idiopathic.

 

Treatment is stepwise: topical steroids first. If insufficient, periocular/intravitreal steroids or short courses of oral steroids, then steroid-sparing agents. Robust trial data support adalimumab for non-infectious intermediate/posterior/panuveitis and for juvenile idiopathic arthritis-associated chronic anterior uveitis. TNF inhibitors are highly effective in Behçet’s but should be avoided in multiple sclerosis. Clinical trials are challenging given disease heterogeneity, but guidelines provide consensus care pathways.

 

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Reference: Rosenbaum JT, Dick AD. The Eyes Have it: A Rheumatologist's View of Uveitis. Arthritis Rheumatol. 2018;70(10):1533-1543. doi: 10.1002/art.40568.

Julia M. Swafford

PA-C, DFAAPA

Beyond Joints: Manage Weight to Manage Psoriatic Arthritis

A systematic review across Medline, PubMed, Scopus, and Web of Science (inception–November 30, 2024) screened 3,163 records and included 33 studies on obesity/comorbidities in psoriatic arthritis (PsA). Obesity—present in nearly half of patients with PsA—emerged as the most consistent risk factor for developing PsA from psoriasis and is linked to higher disease activity, delayed diagnosis, and poorer response to biologic disease-modifying antirheumatic drugs. Beyond adiposity, PsA commonly clusters with metabolic syndrome, dyslipidemia, hypertension, diabetes, cardiovascular disease, and mood disorders. Emerging genetic/biologic data implicate PCSK9 in psoriasis risk, though real-world effects of PCSK9 inhibitors on PsA remain untested.

 

Management should be multidisciplinary and treat both articular/skin inflammation and cardiometabolic comorbidities, with the rheumatologist coordinating care. Lifestyle interventions—dietary modification and physical activity—are foundational but show person-to-person variability. Newer anti-obesity medications can lower body mass index and improve cardiometabolic parameters, potentially enhancing overall PsA outcomes. Proactive identification and treatment of obesity and related conditions are therefore central to achieving better disease control and long-term results.

 

Reference: Maharaj AB, Eder L, Ogdie A. Obesity and Comorbidity Management in Psoriatic Arthritis. Rheum Dis Clin North Am. 2025;51(3S):e1-e18. doi: 10.1016/j.rdc.2025.07.001.

Nancy Eisenberger

DNP, FNP-BC

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