Atopic dermatitis and allergic reactions to individual fragrance chemicals

Background:  Allergic contact dermatitis prevalence is reported as equal in atopic and nonatopic dermatitis. Atopic dermatitis is under‐represented in those with allergic contact dermatitis to agents having cutaneous and dietary exposure. We compared rates of atopic dermatitis between patients with allergic contact dermatitis arising out of individual fragrance chemicals with known oral/cutaneous exposure against exclusively cutaneous exposure. Methods:  Between 1982 and 2007, 37 065 dermatitis patients were tested with Fragrance mix I. Those who were positive were tested for individual fragrance allergy. Chemicals were categorized according to whether their exposure pattern was solely cutaneous, oral or mixed. Current and past atopic dermatitis rates were compared between the whole population and groups allergic to individual fragrances. Age and gender were controlled. Results:  Cinnamic alcohol and cinnamal allergy groups had reduced rates of both ‘current’ [24/266 (9.0%) P = 0.0008, 38/364 (10.4%) P = 0.0005] and ‘past’ atopic dermatitis [44/266 (16.5%) P = 0.009, 70/346 (19.2%) P = 0.037]. Atopic dermatitis rates in groups allergic to Evernia prunastri and hydroxycitronellal (cutaneous exposure only) were not reduced [120/597 (20.1%) and 41/153 (26.8%)]. Groups allergic to cinnamic alcohol (P < 0.0001, P < 0.0001) and cinnamal (P < 0.0001, P < 0.004) had reductions in ‘current’ and ‘past’ atopic dermatitis, compared with Evernia prunastri. Conclusions:  Patients allergic to individual fragrances with dietary exposure have reduced rates of atopic dermatitis. This suggests that patients with atopic dermatitis have heightened oral tolerance to dietary haptens, in contrast to the known close association of atopic dermatitis with food‐protein allergy. Haptens may interfere with food protein tolerance by binding to soluble protein to alter its configuration and immunogenic profile.     

Contact allergy to budesonide contained in a nasal spray

We describe a case of contact allergic sensitization to budesonide in a nasal spray used in the treatment of allergic rhinitis. No cross-sensitivity to other topical corticosteroids was found.     

Diagnostic approach in allergic and irritant contact dermatitis

Contact dermatitis is a highly frequent disease with a significant impact on the quality of life of the affected patients and a relevant socioeconomic impact. According to the pathophysiological mechanisms involved, two major types of contact dermatitis may be recognized: irritant contact dermatitis (ICD) and allergic contact dermatitis (ACD). The two types may, and often do, coexist. Differentiating between ICD and ACD is often difficult in the clinical setting. The basis for a diagnosis of either ICD or ACD is mainly established by a comprehensive clinical history and physical examination, as well as by performing appropriate diagnostic patch testing. The only useful and reliable method for the diagnosis of ACD remains the patch test. Positive patch test results, the current and/or past relevance of which has to be assessed, are confirmative of contact sensitization. Additional tests, such as the repeated open application test or the provocative use test, are sometimes necessary to confirm a causal relationship. This algorithmic diagnostic approach will allow the adoption of rational measures of allergen or irritant avoidance and the implementation of realistic patient information and education.     

A case of autoimmune progesterone dermatitis misdiagnosed as allergic contact dermatitis

Autoimmune progesterone dermatitis is a rare autoimmune response to endogenous progesterone that usually occurs in fertile females. Cutaneous or mucosal lesions develop cyclically during the luteal phase of the menstrual cycle when progesterone levels are elevated. Symptoms usually start 3-10 days before menstruation and resolve 1-2 days after menstruation ceases. We report the case of a 48-year-old woman with intermittent eczematous skin lesions of the legs, forearms, and buttocks. She was diagnosed with allergic contact dermatitis, and topical steroids were prescribed. Her skin eruptions waxed and waned for 6 years and were associated with her menstrual cycle. We performed an intradermal test using progesterone, which was positive, and prescribed gonadotropin-releasing hormone analogues monthly for 3 months. The patient's skin lesions improved, confirming the diagnosis. Autoimmune progesterone dermatitis should be included in the differential diagnosis of recurrent eczema that is refractory to treatment in women of child-bearing age.     

Vitamin D in atopic dermatitis,chronic urticaria and allergic contact dermatitis

Vitamin D influences allergen-induced pathways in the innate and adaptive immune system, and its potential immunomodulatory role in allergic skin disorders has been explored. This comprehensive review article provides an overview of the role of vitamin D in three common dermatologic conditions: atopic dermatitis (AD), chronic urticaria, and allergic contact dermatitis (ACD). Whereas the literature regarding vitamin D and AD has resulted in mixed findings, several studies have described an inverse relationship between vitamin D levels and AD severity, and improvement in AD with vitamin D supplementation. Similarly, several studies report an inverse relationship between vitamin D levels and severity of chronic urticaria. Although current research in humans remains limited, an increased likelihood of ACD has been demonstrated in vitamin D-deficient mice. Additional well-designed clinical trials will be necessary to determine whether vitamin D supplementation should be recommended for prevention or adjuvant treatment of these common dermatologic conditions.     

Contact sensitizer 2,4‐dinitrochlorobenzene is a highly potent human TRPA1 agonist

2,4‐Dinitrochlorobenzene (DNCB) is widely used in human clinical studies and in experimental animal studies to evoke allergic contact dermatitis. 2,4‐Dinitrochlorobenzene is a potent immunogen capable of inducing contact sensitization in all humans exposed. However, the mechanism by which DNCB evokes such symptoms is presently unknown. TRPA1 is a nonselective cation channel that is expressed in peptidergic sensory neurons and fibroblasts. TRPA1 activation was recently implicated in the pathophysiology of atopic dermatitis especially in transducing cutaneous itch signals. Here, we test the hypothesis that DNCB acts as a TRPA1 agonist and thereby evokes allergic symptoms. We found that DNCB activates human TRPA1 dose dependently in FLIPR experiments with an EC₅₀ of 167 nM, an effect that was fully blocked by selective TRPA1 antagonists Chembridge‐5861528 and A‐967079. Similarly, DNCB activated nonselective TRPA1 current in patch clamp studies. Neutralization of 3 critical cysteines in TRPA1 resulted in a loss of DNCB agonism.