Study Highlights Findings on Chronic Hand Eczema from Skin Tape Stripping

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New research suggests that tape stripping, along with RNA sequencing, can effectively identify distinct molecular and immune characteristics of chronic hand eczema (CHE) lesions, thus allowing for various insights into its pathogenesis.¹

These data represent the conclusion of a new study into individuals with CHE that was authored in part by Jonathan Bar, MD, of the Icahn School of Medicine department of dermatology at Mount Sinai.

Bar and colleagues noted that tape strip data related to patients with CHE have remained relatively limited. They highlighted the largest transcriptomic analysis that had been published far.²

“Thus, we aimed to investigate the molecular disease landscape of CHE,” Bar and colleagues wrote. “We acquired tape strips from lesional and location-matched non-lesional skin of 66 CHE patients who underwent a prior therapeutic washout period as well as 20 [healthy control] individuals and performed bulk RNA sequencing analyses focusing on the characterization of CHE in patients with or without concomitant [atopic dermatitis].”¹

Trial Design Details

The investigators analyzed 66 individuals and their baseline tape strips, with these patients all having CHE that had been untreated. The subjects for their analysis were recruited from various sites located throughout the US and Canada, with the participants being adults in the age range of 18 - 75 years who also had moderate-to-severe CHE.

The research team defined this diagnosis as a Physician Global Assessment (PGA) score of 3 or 4, and the disease would have to have continued for at least 6 months. It was also defined by patients’ unresponsiveness to standard topical treatments.

The investigators ruled out various subjects through their criteria for exclusion from the study, including pregnant individuals, those with a body mass index (BMI) that went over 35 kg/m², individuals showing active skin infections, or patients with recent (<4 weeks) atopic dermatitis flare-ups.

Patients were disqualified if they had implemented dupulumab, any investigational biological agents, systemic treatments within 12 weeks before the analysis, or topical agents within 2 weeks prior. The researchers would also exclude subjects who had comorbid conditions like eczema herpeticum, psoriasis, or other significant medical disorders.

For comparison, the investigative team included 20 healthy, sex-, age-, race-, and location-matched controls who did not report having hand eczema. The team gathered tape strip samples from the 66 individuals with CHE, specifically from both lesional and non-lesional skin.

They split evenly between those with and without comorbid atopic dermatitis, and subjected subjects to bulk RNA sequencing. The research team compared CHE patient data to samples drawn from the palmar skin of those in the healthy control cohort.

The investigators then looked at differentially expressed genes (DEGs) through the use of the threshold of fold change (FCH) > 1.5 as well as a false discovery rate (FDR) < 0.05. Any associations with markers for clinical severity were utilized as well, such as the hand eczema severity index (HECSI) and the modified total lesion symptom score (mTLSS).

Significant Findings

The research team’s findings at the conclusion of this analysis showed that there was a common inflammatory phenotype found within CHE lesions that was also noted as irrespective of atopic dermatitis status. They added that this phenotype was characterized by upregulated type-1 (examples being IL12RB2, IFNGR1, MX1) and type-2 (examples being CCL22, CCL24, TSLPR/CRLF2, GATA3) inflammatory mediators.

These mediators were noted along with a downregulation of epidermal barrier markers such as loricrin and filaggrin. Similar but less obvious dysregulation was observed by the research team in non-lesional skin, with the team highlighting additional suppression of type-17 pathways.

In 1 notable conclusion, the investigators reported that individuals with CHE who did not report atopic dermatitis were shown to have a stronger type-1 immune response and subjects with comorbid atopic dermatitis had a more pronounced type-2 inflammatory pattern.

Furthermore, the researchers noted correlations between gene expression biomarkers in atopic dermatitis-associated CHE that were more significant with clinical severity markers. They pointed to the role of distinct immune pathways in the disease subtypes.

“In conclusion, our study sheds new light on the transcriptomic patterns of CHE, suggests novel potential drug targets, and differentiates the expression profiles of CHE with and without [atopic dermatitis],” they wrote.¹

References

1. ^{Bar, J., Del Duca, E., David, E., Bose, S., Chefitz, G., Brunner, P.M., Bissonnette, R. and Guttman-Yassky, E. (2025), Skin Tape Stripping Reveals Distinct Biomarker Profiles in Chronic Hand Eczema of Patients With and Without Comorbid Atopic Dermatitis. Allergy. https://doi.org/10.1111/all.16466.}
2. ^{J. B. K. Solberg, A. S. Quaade, S. B. Jacobsen, et al., “The Transcriptome of Hand Eczema Assessed by Tape Stripping,” Contact Dermatitis 86, no. 2 (2022): 71–79.}