RNL26 Report: Psoriatic Arthritis Save
Audrey Gibson, PA-C, reports from RheumNow Live 2026 in Dallas, Texas, on two talks: "Why Do Plain X-Rays in Psoriatic Arthritis" by Dr. Arthur Kavanaugh and "Paradoxical Psoriasis and Strange Reactions" by Dr. Joseph Merola.
Transcription
Hi everyone, I'm Audrey Gibson, physician assistant reporting live from Dallas, Texas. We just finished with the afternoon lectures and two talks really challenged how we think about psoriatic disease in everyday practice — how we image it and how we manage unexpected inflammatory consequences of targeted therapy.
Let me start with imaging in psoriatic arthritis. Dr. Arthur Kavanagh walked us through an important question: why do we perform plain X-rays in psoriatic arthritis? Historically, radiographs were foundational. They taught us about erosions, joint space narrowing, and pencil-and-cup deformities and the irreversible nature of structural damage. But recent studies have shown radiographic progression in modern PsA cohorts is uncommon, slow, and seen in a minority of patients, particularly those with ongoing active synovitis.
What still matters, though, is what X-rays represent. Joint space narrowing more than erosions correlates with long-term functional loss. Damage contributes to disability that inflammation control alone cannot reverse. So while plain films may no longer be sensitive for early disease, they still capture something clinically meaningful — accumulated damage that predicts function years down the road.
My personal takeaway is this: X-rays still have a role. Baseline films can help with prognosis, documentation of damage, and difficult conversations about treatment urgency. I think X-rays are most useful in patients with long-standing disease and persistently active symptoms between symptoms and exam. But for early disease activity, ultrasound, MRI, and emerging imaging technologies are where the field is headed.
That brings us to the second talk from Dr. Joseph Merola, where he reviewed paradoxical and off-target inflammatory reactions to biologic and targeted therapies — reactions that we are seeing more often simply because we are using these drugs more.
Dr. Merola discussed TNF inhibitors inducing psoriasis; IL-17 or IL-23 blockade leading to eczematous eruptions; dupilumab unmasking inflammatory arthritis. Several patterns stood out. Paradoxical psoriasis with TNF inhibitors occurs more often in women, often without personal or family history of psoriasis, and commonly presents as pustular pustulosis. Histology frequently shows overlapping psoriasiform and spongiotic features with eosinophils, reminding us that these are immune shifts, not classic disease flares.
Similarly, eczema developing on IL-17 or IL-23 inhibitors appears to be driven by a shift away from TH17 towards TH2 pathways. And with dupilumab blocking IL-4 and IL-13, it may release TH1 and TH17 activity, occasionally resulting in inflammatory arthritis even in patients with no prior rheumatic disease.
So a few of my main takeaways: first, don't ignore or dismiss these symptoms. Second, rule out alternative diagnoses such as new PsA, RA, lupus, or even infection before assuming it's a drug reaction. And third, management should be proportional to the severity of the disease. Mild cases may be treated through with topicals, NSAIDs, or short steroid courses. Moderate disease often requires co-management and combination strategies — adding methotrexate or apremilast, for example. Severe or persistent cases may require holding the offending agent and switching mechanism, with growing evidence supporting oral JAK inhibitors as effective rescue options that can cover both skin and joint inflammation.
The unifying message from both talks is this: psoriatic disease is not static, and neither is our management. Structural damage is still important and can directly impact our patients, and immune modulation is powerful but not always predictable. Our job increasingly is pattern recognition, thoughtful imaging, and early intervention in hopes of preserving function and improving quality of life long term.
RheumNow Live in Dallas has exemplified the practical application of scientific knowledge with careful consideration directly relevant to clinical practice. I'm looking forward to an exciting day tomorrow covering axial spondyloarthritis, myositis, highlights in autoimmune disease, as well as vasculitis. Thanks for tuning in and stay tuned for more updates.
Let me start with imaging in psoriatic arthritis. Dr. Arthur Kavanagh walked us through an important question: why do we perform plain X-rays in psoriatic arthritis? Historically, radiographs were foundational. They taught us about erosions, joint space narrowing, and pencil-and-cup deformities and the irreversible nature of structural damage. But recent studies have shown radiographic progression in modern PsA cohorts is uncommon, slow, and seen in a minority of patients, particularly those with ongoing active synovitis.
What still matters, though, is what X-rays represent. Joint space narrowing more than erosions correlates with long-term functional loss. Damage contributes to disability that inflammation control alone cannot reverse. So while plain films may no longer be sensitive for early disease, they still capture something clinically meaningful — accumulated damage that predicts function years down the road.
My personal takeaway is this: X-rays still have a role. Baseline films can help with prognosis, documentation of damage, and difficult conversations about treatment urgency. I think X-rays are most useful in patients with long-standing disease and persistently active symptoms between symptoms and exam. But for early disease activity, ultrasound, MRI, and emerging imaging technologies are where the field is headed.
That brings us to the second talk from Dr. Joseph Merola, where he reviewed paradoxical and off-target inflammatory reactions to biologic and targeted therapies — reactions that we are seeing more often simply because we are using these drugs more.
Dr. Merola discussed TNF inhibitors inducing psoriasis; IL-17 or IL-23 blockade leading to eczematous eruptions; dupilumab unmasking inflammatory arthritis. Several patterns stood out. Paradoxical psoriasis with TNF inhibitors occurs more often in women, often without personal or family history of psoriasis, and commonly presents as pustular pustulosis. Histology frequently shows overlapping psoriasiform and spongiotic features with eosinophils, reminding us that these are immune shifts, not classic disease flares.
Similarly, eczema developing on IL-17 or IL-23 inhibitors appears to be driven by a shift away from TH17 towards TH2 pathways. And with dupilumab blocking IL-4 and IL-13, it may release TH1 and TH17 activity, occasionally resulting in inflammatory arthritis even in patients with no prior rheumatic disease.
So a few of my main takeaways: first, don't ignore or dismiss these symptoms. Second, rule out alternative diagnoses such as new PsA, RA, lupus, or even infection before assuming it's a drug reaction. And third, management should be proportional to the severity of the disease. Mild cases may be treated through with topicals, NSAIDs, or short steroid courses. Moderate disease often requires co-management and combination strategies — adding methotrexate or apremilast, for example. Severe or persistent cases may require holding the offending agent and switching mechanism, with growing evidence supporting oral JAK inhibitors as effective rescue options that can cover both skin and joint inflammation.
The unifying message from both talks is this: psoriatic disease is not static, and neither is our management. Structural damage is still important and can directly impact our patients, and immune modulation is powerful but not always predictable. Our job increasingly is pattern recognition, thoughtful imaging, and early intervention in hopes of preserving function and improving quality of life long term.
RheumNow Live in Dallas has exemplified the practical application of scientific knowledge with careful consideration directly relevant to clinical practice. I'm looking forward to an exciting day tomorrow covering axial spondyloarthritis, myositis, highlights in autoimmune disease, as well as vasculitis. Thanks for tuning in and stay tuned for more updates.
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