Contact dermatitis is a rising environmental and occupational health problem. It generates high costs for health care systems and the economy due to loss of productivity. Moreover, it possesses a huge impact on the quality of life of the individual patient.

The immune system generates a complex response to contact allergy, which is still unclear. Recent years have provided interesting insights into the pathogenesis of allergic contact dermatitis (ACD) by identifying distinct immune pathways and explaining the activation of these pathways by different allergens. 

Itch is a major symptom in ACD, causing a relevant burden on a patient′s quality of life. The precise mechanisms that cause the development of itch in ACD remain poorly defined. 

In many itch conditions, antihistamines remain ineffective, suggesting a nonhistaminergic itch. Targeting nonhistaminergic itch-sensory pathways is a big step forward for patients with chronic itch disorders such as ACD. These discoveries about the pathogenesis of ACD and the development of itch in ACD patients create perspectives. 

Topical steroids are effective in the short-term for the majority of patients. While difficult to treat and/or chronic cases require topical calcineurin inhibitors, light therapy and systemic agents such as steroids and cyclosporine. Antihistamines remain largely ineffective for the associated itch. The innovative topical or systemic drugs that target single specific itch mediators (anti-cytokine monoclonal antibodies such as anti-IL-31, anti-IL-33 and anti-thymic stromal lymphopoietin) or inhibit multiple pruritogenic cytokines by blocking common signal transduction pathways (anti-JAKS) are either already used or under investigation in atopic dermatitis. They seem plausible candidates for difficult-to-treat patients. The discovery of the Mrgpr circuit and the preferential role of Mrgprb2 in ACD and associated pruritus make it a novel therapeutic target.

Source: Lambert J. Itch in allergic contact dermatitis. Front Allergy. 2021;2:702488.