We report the case of a 36-year-old woman with a personal history of seasonal rhinitis and atopic dermatitis (AD) dating from childhood. She consulted for worsening of AD accompanied by severe lesions caused by scratching on the trunk and limbs. The initial physical examination revealed a SCORAD severity score of 47 and major involvement of the skinfolds and trunk. The results of a laboratory workup were normal, with an immunoglobulin (Ig) E levelof240IU (N<100IU). Before consulting, the patient had received various topical corticosteroids, emollients, and systemic corticosteroids (0.5-1mg/kg/d), with which she achieved a partial response. She received treatment at another center with ciclosporin 3mg/kg/d, which had to be suspended because of hypertension that was difficult to control despite the addition of amlodipine 20mg/d. Successive treatment with azathioprine 50mg/d, methotrexate 15mg/wk, and mycophenolate mofetil 1.5g/d had to be suspended because of gastrointestinal intolerance to the first 2 drugs and lack of response to the third. Treatment with narrowband UV-B was not considered, because the patient was unable to attend the sessions. During the switch to mycophenolate mofetil, the clinical expression of AD varied, with intense edema and erythema on the face and neck (Fig. 1). Therefore, the initial diagnosis proposed was head and neck dermatitis. We carried out a prick test with inhaled allergens from the standard series. The results were positive for Alternaria species, Cladosporium species, and cat dander and negative for gastrointestinal allergens, latex, and Anisakis species. The evaluation was completed with prick testing to Malassezia species and Candida species. The results were positive for the former and negative for the latter (tested with 20 healthy controls in the last 2 cases). Histopathology was consistent with AD. Treatment was started with itraconazole 100mg/12h for 1 month, which was tapered until 5 months of treatment had been completed. The patient's lesions improved considerably (Fig. 2).

Figure 1.

Erythema and edema on the face and neck at the initiation of treatment with itraconazole.

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Figure 2.

Response to therapy after 5 months of treatment.

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The prevalence of adult AD ranges from 0.3% to 14%, with the most widely accepted range being that of 1%-3%.1 In adults, pruriginous eczema affecting the face, neck, and upper thorax is known as head and neck dermatitis. It is associated with intense pruritus and a major alteration of the patient's quality of life. Curiously, the activity of AD at other sites is usually minimal or moderate. In terms of etiology and pathology, it has been associated with hypersensitivity (but not overgrowth) caused by different subspecies of the lipophilic mold Malassezia (Malassezia furfur, Malassezia restricta, Malassezia sympodialis, and Malassezia globosa). Increased colonization by Malassezia species of specific areas of the body has been observed in pubertal patients and young adults. In this case, the areas affected were the same as those affected in head and neck dermatitis, compared with healthy skin and compared with healthy persons.2

The host immune response to Malassezia species was assessed using prick testing, determination of specific IgE, and patch testing.3 Most studies have not simultaneously compared the response to Candida species, staphylococci, streptococci, and Trichophyton species. In the immune response, it seems that stimulation of B lymphocytes plays a more important role than delayed T lymphocyte–mediated hypersensitivity. Similarly, some studies correlate the severity of head and neck dermatitis with specific IgE levels to Malassezia species.4,5 This hypersensitivity is greater in patients with allergic rhinoconjunctivitis or asthma,6 as observed in the present case.

With respect to therapy, there is no well-defined protocol to enable a suitable approach to this condition. Outcome with topical antifungal agents does not seem to be satisfactory. Systemic therapy has focused on the use of ketoconazole 200mg/d or itraconazole 100-400mg/d, and it is necessary to wait a month before results appear in most patients.

Series that present a more extensive cohort of patients7,8 apply different itraconazole schedules over periods ranging from 7 days to 2 months. It seems reasonable to initiate treatment at 100-200mg/d and to evaluate the effect of therapy at 1 month in order to reduce to a minimum therapeutic dose that could be used over a longer period.9 The main reported adverse effects were flushing and headache, which resolved after interruption of treatment and enabled treatment to be reintroduced. Routine laboratory testing is not necessary in the absence of baseline liver disease or of associated contraindications. Case reports have shown that the condition can be controlled and therapy can subsequently be combined with other immunosuppressants, such as azathioprine, thus leading to a successful outcome.10