Upadacitinib is feasible for patients with palmoplantar pustulosis, according to David Gleeson, BM BCH, PhD, whose remarks frame the oral JAK inhibitor as a treatment option worth serious consideration in one of dermatology's most therapy-resistant presentations.

Palmoplantar pustulosis presents a distinct clinical problem. Pustules and scale confined to the palms and soles impair walking, gripping and working, and patients frequently fail topical therapy, phototherapy and classic systemic agents. The condition carries a heavy quality-of-life burden precisely because lesions sit where patients cannot spare skin function. Any oral agent that clears those sites changes the daily reality of the disease.

Upadacitinib, a selective JAK1 inhibitor, already holds regulatory approvals across immune-mediated diseases, including psoriatic arthritis, atopic dermatitis and several rheumatologic indications. Dermatologists therefore know its dosing, its laboratory monitoring requirements and its labeled safety profile from existing prescribing experience. Gleeson's assessment extends that familiarity into palmoplantar pustulosis, a setting where the treatment arsenal remains thin and consensus guidelines offer few definitive answers.

Why does feasibility matter for this condition?

Feasibility — tolerability combined with a workable monitoring burden — often decides real-world treatment success in palmoplantar disease more than raw efficacy percentages do. Patients with palmoplantar pustulosis tend to stay on therapy for years, so an oral agent that patients can sustain matters as much as one that clears skin quickly.

JAK inhibitors as a class carry boxed-warning considerations, and clinicians prescribing upadacitinib already follow the labeled precautions applicable to the class. Gleeson's commentary positions the drug as practical within that established safety framework rather than as an experimental leap.

The route of administration also works in the drug's favor here. Palmoplantar skin is thick, hyperkeratotic and notoriously poorly penetrated by topicals, which partly explains why corticosteroids and vitamin D analogues underperform at these sites. An oral small molecule bypasses that barrier entirely.

What could this change in practice?

For dermatologists managing refractory palmoplantar pustulosis, upadacitinib now enters the shortlist of systemic options that merit discussion during shared decision-making. Gleeson's expert perspective gives clinicians a reference point when conventional agents have failed or produced unacceptable responses.

The broader signal matters for the JAK class. As dermatology continues to map where selective JAK inhibition delivers value beyond atopic dermatitis and psoriatic arthritis, palmoplantar phenotypes represent a logical frontier — inflammatory, driven by cytokine pathways the drug targets, and starved of alternatives.

Insurance coverage will shape access, as it does for all JAK inhibitors in off-indication dermatologic use, and clinicians should expect prior-authorization friction when prescribing outside approved indications. Documentation of failure on standard therapies will likely remain the practical gateway to treatment.

What comes next?

Gleeson's feasibility assessment sets the stage for structured evaluation — longer-term follow-up, larger cohorts and formal efficacy endpoints would convert expert clinical experience into evidence suitable for treatment algorithms. Until then, upadacitinib stands as a credible, practically deployable option that dermatologists can weigh when palmoplantar pustulosis resists everything else on the shelf.