Alopecia areata after severe allergic contact dermatitis to a permanent hair dye

Several types of alopecia may be triggered by scalp allergic contact dermatitis (ACD) including telogen effluvium1 and scarring alopecia.2 We hereby describe an unusual case of alopecia areata (AA) activated by severe ACD to a permanent hair dye. A 24-year-old male patient with no personal/family history of autoimmune disease, but with a history of henna tattoo reaction at the age of 12, presented with acute exudative dermatitis on his scalp, ears and neck following the first self-application of a black-coloured hair dye. Two weeks later, he suddenly developed patchy non-scarring scalp and beard hair-loss compatible with AA. Hair re-growth was slowly achieved upon treatment with oral and topical corticosteroids, and topical minoxidil (Figure 1) within 5 months. Patch tests were performed 15 months after the ACD reaction with the Spanish Contact Dermatitis Research Group (GEIDAC) baseline series (TRUE Test, AllergEaze, SmartPractice), supplementary allergens (AllergEaze) and a hairdressing series (AllergEaze), on Finn Chamber (SmartPractice) occluded for 48 h. Scoring readings were conducted according to the European Society of Contact Dermatitis (ESCD) guidelines.3 We observed intense reactions to p-phenylenediamine (PPD), PPD-related substances, hydroquinone and pyrogallol (Table 1; Figure S1). Two years after the events of ACD and AA, the patient was subsequently diagnosed with multiple sclerosis (MS). No flare-ups of the AA were observed within an 8-year follow-up. The likelihood of sensitization to PPD through the exposure to temporary ‘black henna tattoos’ is high (2.5%)4 and ACD reactions elicited by PPD among patients sensitized this way are often severe. Concomitant reactions to other p-aminoaryl compounds are also more frequent among individuals sensitized to PPD through exposure to henna tattoos than among hairdressers or hair dye users.5 Our patient likely became sensitized to PPD in the ‘black henna tattoo’ as a child and rapidly developed intense ACD after the first use of a black hair dye many years later. Strong patch test reactions suggested severe sensitization to hair dye components. We observed severe sensitization to PPD-chemically-related compounds likely due to co-sensitization or cross-reactivity. AA is an autoimmune disease that targets hair follicles leading to inflammatory non-scarring hair loss. AA may improve at the areas involved by other dermatoses such as psoriasis or ACD, the latter being the basis for the immune therapy with potent allergens such as diphenylcyclopropenone (diphencyprone). This is explained by a Rënbok6, 7 (reverse Koebner) phenomenon, originally described in patients with AA and psoriasis,7 which reflects a competition between different T-cell populations leading to a switch in the local cytokine milieu. Conversely, the Koebner phenomenon has also been described to cause AA relapse, for example, after performing perilesional trichograms.8 There is one prior report on AA developing 2 weeks after the second self-application of a permanent hair dye.9 The patient noticed slight burning but no other reactions. A ‘use test’ on his arm with the dye as is performed by the patient 3 weeks thereafter, triggered intense contact dermatitis at his face, arm and hand as well as a worsening of scalp hair loss.9 The authors hypothesized that ‘irritation’ caused by the dye could have disrupted the normal hair follicle immune privilege increasing the risk of AA.9 We believe that another possible explanation is that the initially subtle burning reaction experienced by the patient was truly allergic, as in our patient. Hypothetically, interactions among overlapping inflammatory pathways underlying ACD and AA could have played a role in the AA elicitation in both cases. Interestingly, our patient was subsequently diagnosed with MS, which has rarely been described as a co-morbidity of AA. In predisposed individuals, MS may be diagnosed prior to or after AA.10 AA may also be triggered by alemtuzumab, a therapy used in MS. This case further illustrates a possible association between AA and MS. We believe ACD should be considered a trigger for AA in predisposed individuals. Interactions among inflammatory pathways may likely be involved. Maria-Elena Gatica-Ortega: Conceptualization; formal analysis; funding acquisition; investigation; methodology; supervision; validation; visualization; writing – review and editing; writing – original draft. Elena Vera-Iglesias: Investigation. Blas Gómez-Dorado: Investigation. Cristina Pérez-Hortet: Investigation. María Antonia Pastor-Nieto: Conceptualization; investigation; funding acquisition; writing – original draft; validation; visualization; methodology; writing – review and editing; formal analysis. The authors declare no conflict of interest. The authors obtained informed written consent from the patient for the photographs to be published. FIGURE S1 Patch tests with readings performed on day (D) D2 (A) and D4 (B). Strong reactions to p-phenylenediamine (PPD), p-aminodiphenylamine, p-aminophenol, toluene-2,5-diamine sulphate and o-nitro-p-phenylenediamine; moderate reactions to 3-aminophenol and hydroquinone; and, weak reactions to pyrogallol, N-isopropyl-N-phenyl-4-phenylenediamine, disperse Blue 106 and rubber mix. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.