A possible explanation for the high frequency of contact sensitisation in chronic venous ulcers

Dear Editors, A 62-year-old woman was referred to our department for an itchy eruption on the left leg that had appeared 2 weeks into a bandage treatment with Iruxol ointment (a mixture of collagenase clostridiopeptidase A and proteases) (Figure 1A). Based on patient history and vesicular appearance of lesions, a diagnosis of contact dermatitis to Iruxol, confirmed by patch testing (Figure 1B), was made. Suspension of the causative ointment and a 2-week therapy with topical corticosteroids induced remission of the condition (Figure 1C). Allergic contact dermatitis is a T-cell-mediated inflammatory reaction (delayed-type hypersensitivity reaction) to a contact allergen (hapten), occurring at the site of challenge in sensitised individuals. Classically, its pathophysiology consists of two distinct phases: the sensitisation and the elicitation phases, which are considered to be temporally and spatially dissociated (1). Patients with venous ulcers are often treated with a large variety of dressings and ointments to which they frequently acquire contact sensitisation. A high incidence of allergic contact dermatitis in patients with venous ulcers or even with simple stasis dermatitis has been well-documented (2). These patients often have multiple sensitivities to a large series of medications, including lanolin and rubber, although the pattern of allergens appears to be changing, and this change is likely to be determined by local wound care practice (2). Many influencing factors have been hypothesised to be involved in the pathogenesis of this phenomenon: intrinsic genetic predisposition, lipophilic galenics, use of occlusion and the disrupted skin barrier, with an increased permeability