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Unusual response to DNCB contact sensitivity in an atopic patient with alopecia areata

Some authors have shown that treatment of alopecia areata with dinitrochlorobenzene (DNCB) induces a regrowth of hair in a high % of cases (about 60--80%) (1-4). We treated a 25-year-old man suffering from alopecia areata subtotalis for 5 years, as well as from rhino-conjunctivitis and bronchial asthma for the last 3 years. The allergic nature of the respiratory disease was verified by prick tests, total serum IgE (PRIST) and IgE specific to the allergens (grass pollen) responsible for the atopic manifestations (RAST). The patient treated his rhino-conjunctivitis with antihistamine drugs and sometimes with steroids. In October 1979 he was sensitized with DNCB 2% in acetone and treated with different DNCB solutions (0.04, 0.05, 0.08 and 0.10%). After 10 weekly applications he showed a regrowth of hair; after 13 months the treatment was stopped because complete regrowth had been obtained. In spring 1980 the patient reported that he was not suffering from the classic symptoms that he had had during the preceeding years, and that he no longer used the antihistamine drugs. In spring 1981, the patient was able to give the same report, with evident satisfaction. The suggested basis of DNCB treatment for alopecia areata is antigenic competition and contact allergy. The allergic reaction to DNCB might generate some cells with suppressor activity (T-suppressor cells?). In humans, 2 distinct subsets of T-Iymphocytes have been identified, according to the presence on the cell surface of Fc receptors for IgG or IgM: TG and T1II respectively (5). These subsets exert an immuno-regulatory control over the antibody production of B-cells, as shown by the effect exerted in vitro on the T-dependent response to pokeweed mitogen (PWM). In this model system, TM cells provide help, whereas TG cells suppress B lymphocyte differentiation (6). Canonica et al. (7) have demonstrated that atopic patients (with rhinoconjunctivitis, bronchial asthma and mild rhinitis) have reduced proportions of T-cells with surface receptor for IgG (TG)' These cells are known to regulate immunoglobulin synthesis by suppressing the T-dependent B-cell differentiation in response to PWM. It is welJestablished that IgE production is regulated, like other immunoglobulin classes, by T-helper as well as T-suppressor lymphocytes (8, 9). In our case we can hypothesize that DNCB allergic contact dermatitis has induced an 'enhancement' of suppressor cells and a possible balance of T-cell sub-populations.