Addressing Pain, Function, and Flares in Chronic Hand Eczema

“When we look at chronic hand eczema [CHE], we take a step back and look more broadly at a JAK [Janus kinase] targeting approach, as opposed to the tunnel vision that we've had for so many years now, targeting specific numbers or cytokines. Instead, you see how [CHE] can benefit from a broader approach from a cellular level,” Omar Noor, MD, said in a recent Dermatology Times Expert Perspectives custom video series.

Noor, a board-certified dermatologist, co-owner of Rao Dermatology in New York, and a Dermatology Times editorial advisory board member, reviewed the complexity of CHE, including its classic presentations compared with atopic dermatitis (AD), how he addresses severity in CHE, how he decides to initiate delgocitinib cream (Anzupgo; LEO Pharma), and his patients’ experiences with the application of delgocitinib.

Beyond Type 2 Inflammation

Noor first emphasized that CHE should not be viewed through a single inflammatory lens. “I think of [CHE] as heterogeneous pathways that just converge,” he said. Although AD is classically driven by Th2 cytokines—IL-4, IL-13, and IL-31 signaling through JAK1 and JAK3—CHE frequently reflects overlapping etiologies.

“[CHE] can be atopic in some patients,” he said, “but what we see is more complex.” Clinical presentations may reflect irritant contact dermatitis, allergic contact dermatitis, hyperkeratotic patterns, dyshidrotic disease, or mixed morphologies. In addition to type 2 inflammation, type 1 and type 3 cytokines, including IL-17–mediated pathways, along with barrier disruption and environmental irritants, contribute to disease persistence.

“All of these different types of patterns function through multiple inflammatory networks,” he said. Because these pathways converge on JAK-mediated transcription, Noor advocates for a broader JAK-targeting approach.

Clinical Presentation and Disease Burden

CHE is morphologically diverse. Unlike classic flexural AD, hand involvement can present with fingertip fissuring, palmar hyperkeratosis, recurrent vesicles, nail fold fissures, lichenification, and asymmetrical distribution involving the dorsal hands or volar wrists.

“There are a lot of different presentations of [CHE],” Noor said, “but one thing that is consistent is that it tends to flare quite often.”

Severity assessment extends beyond morphology. Clinicians must evaluate scale thickness, hyperkeratosis, fissure depth, vesiculation, crusting, and secondary infection. However, functional impairment is central to therapeutic decision-making.

“Are they a hairdresser? Are they a mechanic? Can they wash their hands? Can they even hold tools?” he asked. Even routine activities such as typing or scrolling on a smartphone may be painful. Treatment history and chronicity further inform escalation decisions.

Itch and Pain

Although pruritus dominates AD discussions, CHE frequently presents with significant pain. “Many patients will say, ‘Yes, it itches, but the pain is really what’s ruining my life,’” Noor said. Deep fissures bleed and burn with soap, sanitizers, and water exposure. “They do get intense…itch, but it can be painful, as well.”

When counseling patients, Noor focuses on both symptom domains. “It’s not just about promising less itch. I’m talking about reducing stinging and burning with everyday tasks, allowing fissures to close so that they can grip things, wash their hands without sharp pain, and improve their sleep.” Addressing both itch and pain aligns with clinical trial end points and real-world patient priorities.

Integrating Delgocitinib Cream Into Practice

In selecting therapy, Noor first evaluates functional limitation and prior treatment exposure. If patients have cycled through topical corticosteroids without sustained control, he considers delgocitinib as “a targeted nonsteroidal chronic use option” appropriate for long-term management.

Early patient feedback has been favorable. Noor reported “early reduction in itch and burning, often within the first few days, sometimes within the first couple of weeks,” followed by gradual improvement in fissuring, scaling, and vesiculation. Vehicle characteristics also influence adherence. “I was a little hesitant in the beginning, thinking that we have a product here for [CHE] to be greasy and thick,” he said. “But in fact, it’s actually a nice cream.” Patients appreciate that it is nongreasy and does not leave residue, allowing them to type or handle tools without impairment.

Improved tolerability and cosmetic acceptability translate into consistent use. “When a patient consistently uses it, they’re only going to get better,” he said.

Safety Considerations

A key counseling point involves differentiating topical from systemic JAK inhibition. “Delgocitinib is designed as a topical; it is a locally acting JAK inhibitor with minimal systemic absorption,” Noor said. This localized exposure profile distinguishes it from oral JAK inhibitors and may mitigate concerns regarding systemic immunomodulation, comorbidities, or polypharmacy.

“We get to leverage this JAK-STAT system…but with not having to worry if patients have comorbidities or multiple systemic medications,” he said. For clinicians and patients alike, the reassurance that “it’s a topical medication with very low absorption” supports its integration into chronic management algorithms.

As Noor concluded, as understanding of CHE evolves beyond a purely type 2 framework, broader pathway modulation through topical JAK inhibition offers a mechanistically aligned and function-focused option for this often recalcitrant disease.

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