Riehl\'s melanosis: Pigmented contact dermatitis caused by fragrances

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Riehl's melanosis: Pigmented contact dermatitis caused by fragrances Gabriel Serrano, MD, Conrad Pujol, MD, Jesfls Cuadra, MD, Sofia Gallo, MD, and Adolfo Aliaga, M D Valencia, Spain We report a case of a 27-year-old woman with a patchy, dark brown hyperpigmentafion on the face. Patch tests were positive to lemon oil, geraniol, and hydroxycitronellal. A compact face powder that the patient used contained two of these chemicals. Hyperpigmentation disappeared within 6 months after the patient avoided contact with cosmetics containing these fragrances. (J AM ACADDERMATOL1989;21:1057-60.)

Riehl's melanosis is a nonpruritic pigmented dermatitis characterized by a brownish gray pigmentation that develops rapidly over the face, being most intense on the forehead and the temples. Its incidence is greater in women, but it also has been described in men and children. Histopathologically, Riehl's melanosis is characterized by liquefactive degeneration of the basal cells accompanied by the formation of melanophages in dermis. A moderate cellular infiltration of lymphoid cells and histiocytes also is usually present in the papillary dermis. 1 Although the cause has not been clarified completely, nutritional factors and sensitizing chemicals in cosmetics have been suggested. 1 According to recent reports from Japan, 25 patients frequently show positive patch test results to cosmetics or their ingredients and the disease is called pigmented cosmetic dermatitis. These patients' pigmented dermatitis was cured or greatly improved by avoiding cosmetics containing these allergens. We report a case of a patient with Riehl's melanosis secondary to a contact hypersensitivity reaction to the fragrances contained in a compact face powder. CASE REPORT

A 27-year-old woman came to the department of dermatology in October 1986 with a patchy pigmentation on From the Department of Dermatology, Unit of Photobiology, General Hospital. Reprint requests: Gabriel Serrano, MD, Department of Dermatology, Unit of Photobiology, General Hospital, Valencia, Spain. 16/4/15794

the face, particularly on the cheeks. This hyperpigmentation had developed gradually in the spring of 1980, just 2 months after the patient started to use a compact face powder. The patient was not taking any medication and, in particular, was not taking birth control pills. In 1984 she became pregnant, but this event did not seem to worsen the lesions. Pigmentation was more prominent after the summer months, and, occasionally, pruritic erythematous macules appeared on the face and extended to both sides of the neck. She had been treated by her dermatologist for the past 5 years with 2% hydroquinone creams and sun protection; no significant improvement had resulted. On physical examination there were patchy brownish macules over both cheeks and forehead that were surrounded by ill-defined erythematous patches (Fig. 1), Results of laboratory tests for antinuelear antibody, antiDNA, and levels of serum iron, serum copper, and urinary porphyrins were within normal limits. Histopathologie findings. Histopathologic evaluation of biopsyspecimens taken from the forehead and the right cheek revealed epidermal atrophy, liquefactive basal cell degeneration, incontinentia pigmenti, and a dermal tymphohistiocytic infiltrate. Spongiosis was absent (Fig. 2), Staining with periodic acid-Schiff showed a thickened basal layer (Fig. 3). Staining with Fontana-Masson revealed that the amount of melanin was increased in the basal layer but was decreased in the spinous and granulous layers. This was assessed by comparing the specimen with contiguous normal skin from the same area on the face. A large number of melanophages were observed in the dermis. Direct immunofluorescence studies, effected to rule out a hyperpigmented lupus erythematosus, were negative. Patch tests, Standard patch tests were done in duplicate with the use of the International Contact Dermatitis Research Group battery. Special patch tests also were performed with the cosmetics and the 2% hydroquinone 1057

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Fig. 1. Patchy brownish macules on cheek and forehead within erythematous background. Fig. 2. Photomicrograph showing epidermal atrophy, dermal melanophages, and lymphohistiocytic infiltrate. (Hematoxylin-eosin stain; ×40.) Fig. 3. Photomicrograph showing thickened basal layer. (Periodic acid-Schiff stain; X40.) Fig. 4. Complete clearing of pigmented lesions after face powder application was stopped.

cream used by the patient, along with a series of fragrances. A set of all these allergens was irradiated with a PUVA-500 unit (Herbert Waldmann, Schwenningen, West Germany). The UVA dose was 5 joules cm , Patch test findings were positive to a 2% fragrance mix,

1% hydroxycitronellal, 2% geraniol, and 10% lemon oil in petrolatum. No difference in reaction was seen between irradiated and nonirradiated patches. One week later the positive patches had not become pigmented. A small amount of the compact fact powder that showed negative results on ordinary patch tests was applied twice a day

Volume 21 Number 5, Part 2 November 1989

over the right cubital fold for 2 weeks. This produced a pruritic erythematous reaction starting 4 days after the application and ending 1 week later in a light hyperpigmentation. Course. After the manufacturer of the face powder confirmed the presence of allergens in the face powder, the patient was instructed to stop the application of hydroquinone creams and to avoid the use of cosmetics on her face. Great improvement was seen 2 months later, and a complete clearing of the pigmentary lesions was seen 6 months afterward (Fig. 4). DISCUSSION The case presented resembles what is usually called Riehl's melanosis, a condition known for its causal relationship with cosmetics. The hyperpigmented lesions in our patient may be attributed to a contact hypersensitivity reaction to the fragrances contained in a compact face powder. That these fragrances were responsible for the long-lasting face pigmented lesions is based on the following factors: 1. Occasional presence of mild erythematous or eczematous lesions 2. Positive patch tests to geraniol and other related compounds 3. Delayed itching erythematous reaction produced when the face powder was applied to the cubital fold 4. Presence of the offending fragrances in the makeup used by the patient 5. Complete clearing of the pigmented lesions a few months after the application of face powder was discontinued According to the manufacturer, the concentration of the allergens--lemon oil in particular--in the compact face powder was very low. Geraniol crossreacts with hydroxycitronellal, and the aldehyde citral is the main constituent of lemon oil. The latter chemical may be obtained artificially through oxidation of geraniol and linalol. Geraniol, a wellknown sensitizer, is perhaps the best candidate to which to attribute the contact hypersensitivity reaction that we postulate in our patient. This hypothesis is based on the sporadic eczematous lesions observed, positive patch tests, and lichenoid histologic features. According to Nakayama et al., 2 the low concentration at which fragrances are used explains why they do not provoke spongiosis in the middle of the spinous cell layer but instead require its accumulation to produce type IV allergic cytolytic reactions at

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the epidermal basal layer. When the basement membranes are destroyed by the allergic reaction, melanin from the destroyed cells is sprayed into the papillary dermis to be ingested by macrophages. 2 Histopathologically, this is manifested in the aforementioned pathologic findings, which are suggestive of a lichenoid allergic reaction rather than a toxic reaction. 6 On the other hand, the pigmentation in our patient also might be interpreted as a consequence of a phototoxic reaction to lemon oil. Lemon oil contains oxypeucedanin and bergapten, two furocoumarin derivatives with well-known phototoxic activity. Although psoralens have been removed from fragrances used in the United States, they are still used in some cosmetics sold in Europe. Naganuma et al. 7 have found that none of the lemon oils from various areas in the world is phototoxic at a concentration of 20%, which explains why the International Fragrance Association recommends a lemon oil maximum content of 10% in fragrance compounds. However, oxypeucedanin has been found to elicit photopigmentation on colored guinea pig skin without preceding visible erythema. Therefore the possibility that a concentration less than that permitted by the International Fragrance Association might be sufficient to produce photopigmentation must be considered. The main differential diagnosis in the case we present was chloasma-like hyperpigmentation, modified by the use of hydroquinone. Chloasma-like hyperpigmentation is characterized by a brownish pigmentation that has a spectacle-shaped configuration; it is frequently associated with pregnancy, ingestion of oral contraceptives, and endocrine dysfunctions. Hyperpigmentation is not a common feature of ordinary contact dermatitis. The term pigmented contact dermatitis was used by Osmundsen 8 and Pifiol Aguad6 et al. 9 in the 1970s after reporting several cases of contact dermatitis to an optical whitener in washing powders, and some of their patients presented with pigmentation without preceding eczematous lesions. Formaldehyde in packing adhesive tapes 1° and some azo dyes also have been implicated in the development of occupationally related pigmented contact dermatitis. 5,11 What is clear from these studies is that melanosis may be a feature of contact dermatitis, and this fact also may apply to the many cases observed in Japan of

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pigmented face lesions resulting from contact allergy to cosmetics. Important information on the cause of Riehl's melanosis has been provided by Pierini 12 in Argentina and by Nakayama et al., 3 Sugai et al.,4 and others in Japan. Pierini described 20 cases, all involving women, in which the melanosis was caused by an aniline dye (orange II) in face powders. In Japan a clinical picture resembling Riehl's melanosis was observed increasingly between 1960 and 1970; it was found to be due to an allergic contact dermatitis from cosmetics. The causative allergens were coal tar dyes--particularly CI 15800 Brilliant Lake Red (an azo dye)--and other 1-phenylazo-2naphthol derivatives, a, 4, 5 In a recent study5 Brilliant Lake Red was found to contain Sudan I as a major impurity and potent sensitizer. Based on these observations, the Japanese authors have proposed the name pigmented cosmetic dermatitis for this pigmentary disorder. There are similarities between pigmented contact dermatitis and pigmented cosmetic dermatitis. Both diseases result from repeated exposure to small amounts of contact allergens, and in both usually no eczematous lesions are seen. The differences between these two conditions seem to be in the affected sites, causative products, and sex and race. 2 Although in the Japanese studies fragrance materials were implicated to a lesser degree, 5 these chemicals seem to play an important role, at least in the cases of pigmented contact dermatitis reported lately. A peculiar type of airborne pigmented contact dermatitis resulting from musk ambrette in incense was reported recently by Hayakawa et al. 13 In addition, Parodi et al. 6 reported a case of photocontact pigmented dermatitis to musk ambrette in a 45-year-old m a n in whom no clinical lesions of eczema were seen and whose patches containing this fragrance showed a delayed pigmented reaction. It is believed that sunlight does not have a significant role in the development of pigmented contact dermatitis and Riehl's melanosis; but the fact that some of the implicated chemicals, such as musk ambrette, lemon oil, and some bactericide compounds (carbanilides), are well-known photosensitizers may be of significance in future research. Support of all this clinical evidence showing that

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allergic contact dermatitis can stimulate the epidermal pigment cell function in a very specific manner has been provided recently by Imokawa et al)4; they also found differences between the melanogenic potential of a limited number of allergens. According to these authors, a specific factor, perhaps different from prostaglandins, is required for the induction of the allergic hyperpigmentation. In conclusion, we want to emphasize that Riehl's melanosis may be associated with a contact sensitivity to cosmetics or to a photocontact dermatitis resulting from fragrances in cosmetics. This is an important consideration, because in this event the disease can be treated by avoidance of these allergens. REFERENCES 1. Rorsman H. Riehl's melanosis. Int J Dermatol 1982;21:75-80. 2. Nakayama H, Matsuo S, Hayakawa K, Takhashi K, Shigematsu T. Pigmented cosmetic dermatitis. Int J Dermatol 1984;23:299-305. 3. Nakayama H, Harada R, Toda M. Pigmented cosmetic dermatitis. Int J Dermatol !976;15:673, 4. Sugai T, Takahashi Y, Takagi T. Pigmented cosmetic dermatitis and coal tar dyes. Contact Dermatitis 1977;3:24956. 5. Kozuka T, Tashiro M, Sano S, et al. Brilliant Lake Red R as a cause of pigmented contact dermatitis. Contact Dermatitis 1979;5:297. 6. Parodi G, Guarrera M, Rebora A. Lichenoid photocontact dermatitis to musk ambrette. Contact Dermatitis 1987;16:136-8. 7. Naganuma M, Hirose S, Nakayama Y, Nakajima K, Someya T. A study of the phototoxicity of lemon oil. Arch Dermatol Res 1985;278:31-6. 8. Osmundsen PE. Pigmented contact dermatitis. Br J Dermatol 1970;83:296. 9. Pifiol Aguad~ J, Grimalt F, Romaguera C. Dermatitis por blanqueadores 6pticos. Med Cutan Ibero Lat Am 1971 ;5:249-66. 10. Ukei C, Oiwa K, Matsunaga K, Hayakawa R. Occupational contact dermatitis. Sldn Res 1983;23:368-76. 11. Fujimoto K, Hashimoto S, Kozuka T, Tashiro M, Sano S. Occupational pigmented contact dermatitis from azo dyes. Contact Dermatitis 1985;12:15-17. 12. Pierini LE. Melanosis de Richl. Arch Argent Dermatol 1952;2:315. 13. Hayakawa R, Matsunaga K, Arima Y. Airborne pigmented contact dermatitis due to musk ambrette in incense. Contact Dermatitis 1987;16:96-8. 14. Imokawa G, Kawai M. Differential hypermelanosis induced by allergic contact dermatitis. J Invest Dermatol 1987;89:540-46.