Why Patients Get Psoriasis: Genetics Plus a Trigger
Recorded live from the Elevate-Derm Summer Conference in San Diego, host Lisa Weiss, PA-C, sits down with Dr. James Song to unpack the question he says patients ask most at that first encounter: why do I have this disease? Song explains that psoriasis starts with a genetic predisposition, but unlike single-gene conditions such as cystic fibrosis or Huntington's, psoriasis has no single gene. There are hundreds, and the more of those genes a patient carries, the higher the likelihood they develop psoriasis in the right context.
Genetics alone isn't enough, Song emphasizes. An environmental pull, trigger, or danger signal must activate the immune system. Common ones he names include strep throat or strep ani (often preceding an explosion of guttate psoriasis), significant physiological or psychological stress, and even everyday medications like beta blockers and lithium in predisposed patients. He frames it as a perfect storm — and warns that removing the trigger doesn't reverse the process. Once the immune system is unleashed, there's no turning back unless you actually treat it.
On a more hopeful note, Song points to the concept of intercepting psoriasis early. He notes that patients treated early—such as guttate cases or those with short disease duration—may respond better, and that a few doses of an effective IL-23 or IL-17 blocker can leave some patients clear for a long time, even after stopping the medication.
Eczematized Psoriasis and the Phenotypic Switch
Weiss asks Song to walk through the atopic dermatitis and psoriasis overlap, which he calls fairly new. In training, clinicians were taught the two couldn't coexist in the same patient—likely under-recognition, Song says —and possibly because today's highly targeted medicines can shift a patient from one phenotype toward the other. By definition, eczematized psoriasis is a patient who looks predominantly like psoriasis clinically and histologically, but carries some eczema features: more spongiosis, more eosinophils, borders that aren't as well demarcated, scale that isn't the classic silvery type, and itching that can be disproportionately high with more scratching and crusting.
Song stresses that pathology alone isn't sufficient to make the diagnosis — it has to be correlated clinically and sometimes by how the patient responds to treatment. He distinguishes eczematized psoriasis from the phenotypic switch, where a patient started on a psoriasis biologic develops eczema later (or vice versa). Rather than assuming the original diagnosis was missed, Song says clinicians should give themselves grace: it probably was that disease at one point and simply switched.
The main takeaway from his lectures: if a patient isn't responding the way they should — especially if they're getting worse — rebiopsy, even if you biopsied initially, and again and again, to confirm you're still treating the same disease. Patients appreciate the transparency, he adds, because it shows you're trying to stay on the right path rather than just cycling through medicines.
Choosing and Switching Systemic Therapy in 2026
With a full toolbox in 2026, Song leans on shared decision-making—asking patients what they prioritize among efficacy, safety, route of administration, and convenience —while acknowledging payers often dictate options. For extensive psoriasis with bad psoriatic arthritis, he reaches for a biologic with the best skin and joint data. For limited body surface area involving special sites like scalp, palms, or soles, he still considers biologics but finds oral options reasonable, noting newer orals are improving.
On non-steroidal topicals, Song uses them both as a way to delay or even prevent systemic therapy in some patients and as adjunctive therapy to mop up residual disease. He highlights the hard-to-treat patient with limited BSA but one thick, angry, red, scaly plaque who doesn't want a biologic for a single lesion — a good candidate for a safe, effective non-steroidal topical.
When a patient isn't responding, Song first classifies the non-response. No improvement at all makes him question the diagnosis. A primary non-responder (minimal improvement from the start) differs from a secondary non-responder (initial response then loss). He gives IL-23s a longer runway because of the slower onset, but uses roughly six months as his checkpoint. If there's nothing at six months and he's confident it's psoriasis, he switches classes — for example, IL-23 to IL-17. For a secondary loss of response, especially with a comorbidity like IBD, he may stay within the same class.
A Four-Question Framework for Urticaria
Song organizes urticaria visits around a short set of questions. First: is this really spontaneous urticaria, or a mimicker like urticarial vasculitis, a drug eruption, or bullous pemphigoid? Second: what type? Chronic if greater than six weeks, acute if less — and if chronic, is it reproducible (chronic inducible urticaria, or CindU) or not (chronic spontaneous urticaria, CSU)? Third: does the patient need additional workup? By and large, no, unless the history or review of systems warrants it. He limits labs, though he considers a sed rate, and tests IgE because high levels often predict good response to IgE-targeted therapy.
The fourth question is treatment. Guidelines still start everyone on second-generation antihistamines at the licensed dose, up-titrating to four times the dose if needed. Song generally gives standard dosing for about four weeks before doubling, then going to four times. Beyond antihistamines, he weighs omalizumab, dupilumab, and remibrutinib, driven by comorbidities and provider comfort. He urges listeners to think of remibrutinib's BTK selectivity the way they think about selective JAK inhibitors — highly targeted with little off-target effect compared with older oncology BTK inhibitors.
Song also counsels urticaria patients on NSAIDs, alcohol, opiates, and IV contrast, which can worsen any type of urticaria. Finally, because CSU can spontaneously remit, he's more willing to de-escalate and give these patients a break than he is with psoriasis — aiming for six to twelve months of good control, using the Urticaria Control Tool to guide whether to space out, cut, or escalate dosing.