INTRODUCTION
Nummular eczema (NE) is a chronic inflammatory dermatosis marked by pruritic, coin-shaped eczematous plaques most commonly affecting the extremities and trunk.1 NE, also referred to as discoid eczema, primarily affects middle-aged and elderly men, with a reported prevalence of up to 9.1%.1 Acute lesions typically demonstrate erythema and pruritus, progressing to scaling and lichenification in chronic disease.1 Patients often experience diminished quality of life; however, many achieve clearance with proper management and avoidance of known triggers.1
While the etiology of NE remains incompletely defined, NE exhibits clinical and immunologic overlap with atopic dermatitis (AD), sharing 4.3% of differentially expressed genes.2 Immunologically, NE presents with features of Th2- and Th17-mediated inflammation, suggesting a complex inflammatory profile that converges with other eczematous and psoriasiform dermatoses.2 NE is further characterized by a distinct, multifactorial pathophysiology involving epidermal barrier dysfunction and environmental exposures.1,3 Impairment of the skin barrier may facilitate increased penetration of external irritants and allergens, contributing to immune cell activation, secondary infection, and disease exacerbation.1,4
NE has also been linked to several potential triggers, including xerosis, Staphylococcus aureus colonization, stress, and alcohol use.5 Recent evidence further suggests a notable association between NE and allergic contact dermatitis (ACD), with several studies demonstrating high rates of contact sensitization in patients diagnosed with NE.5,6 Patch testing in this patient population can be useful for identifying clinically relevant allergens.7 Despite increasing recognition of the role contact sensitization plays in NE, the most commonly involved allergens and their clinical relevance remain incompletely defined. Herein, we systematically reviewed the available clinical evidence on allergens associated with NE and characterized patterns of contact sensitization within this population.
While the etiology of NE remains incompletely defined, NE exhibits clinical and immunologic overlap with atopic dermatitis (AD), sharing 4.3% of differentially expressed genes.2 Immunologically, NE presents with features of Th2- and Th17-mediated inflammation, suggesting a complex inflammatory profile that converges with other eczematous and psoriasiform dermatoses.2 NE is further characterized by a distinct, multifactorial pathophysiology involving epidermal barrier dysfunction and environmental exposures.1,3 Impairment of the skin barrier may facilitate increased penetration of external irritants and allergens, contributing to immune cell activation, secondary infection, and disease exacerbation.1,4
NE has also been linked to several potential triggers, including xerosis, Staphylococcus aureus colonization, stress, and alcohol use.5 Recent evidence further suggests a notable association between NE and allergic contact dermatitis (ACD), with several studies demonstrating high rates of contact sensitization in patients diagnosed with NE.5,6 Patch testing in this patient population can be useful for identifying clinically relevant allergens.7 Despite increasing recognition of the role contact sensitization plays in NE, the most commonly involved allergens and their clinical relevance remain incompletely defined. Herein, we systematically reviewed the available clinical evidence on allergens associated with NE and characterized patterns of contact sensitization within this population.
MATERIALS AND METHODS
A systematic search of PubMed, Embase, and Cochrane Library was conducted on April 30, 2026, per Preferred Reporting Items for Systematic Reviews and Meta-Analyses [PRISMA] guidelines (Figure 1).
