Literature DB >> 27882588

Clinical and epidemiological analysis in 149 cases of rhododendrol-induced leukoderma.

Momoko Yoshikawa1, Yasuyuki Sumikawa1, Tokimasa Hida1, Takafumi Kamiya1, Kimi Kase1, Yasue Ishii-Osai1, Junji Kato1, Yuji Kan1, Shiori Kamiya1, Yuki Sato1, Toshiharu Yamashita1.   

Abstract

Rhododendrol-induced leukoderma is an acquired depigmentation that develops mainly at the contact site after repeated use of skin-whitening cosmetics containing rhododendrol. In most cases, cessation of further depigmentation or occurrence of repigmentation is observed after discontinuing the use of cosmetics. However, some patients develop vitiligo vulgaris through the spread of depigmentation into the non-exposed areas. Our study aims to investigate the patient-specific factors that may affect the extent of depigmentation or repigmentation, as well as development of vitiligo vulgaris. The degree of depigmentation of the face, neck and hands where exposed to rhododendrol was scored using photographs over time. The relationships between depigmentation score at first visit/improvement rate of depigmentation score and patient demographics were evaluated and three important clinical observations were made. First, repigmentation of the face was superior compared with that of the hands and neck, suggesting a possible role for the migration and differentiation of melanocyte stem cells from hair follicles, as a mechanism of repigmentation. Second, the intensity of rhododendrol exposure did not contribute to differences in the severity of depigmentation. This suggested a possibility of underlying genetic susceptibility to melanocyte cytotoxicity or immune reaction. Third, depigmentation score at first visit and past history of atopic dermatitis were significantly high in patients who developed vitiligo vulgaris. This suggested that severe chemical damage of melanocytes by rhododendrol leads to a higher risk of developing vitiligo vulgaris through the possible involvement of an immune reaction. These clinical observations may help to further understand the pathogenesis of rhododendrol-induced leukoderma.
© 2016 Japanese Dermatological Association.

Entities:  

Keywords:  chemical leukoderma; cosmetics; melanocyte toxicity; rhododendrol; vitiligo vulgaris

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Year:  2016        PMID: 27882588     DOI: 10.1111/1346-8138.13694

Source DB:  PubMed          Journal:  J Dermatol        ISSN: 0385-2407            Impact factor:   4.005


  3 in total

1.  Action of tyrosinase on alpha and beta-arbutin: A kinetic study.

Authors:  Antonio Garcia-Jimenez; Jose Antonio Teruel-Puche; Jose Berna; José Neptuno Rodriguez-Lopez; Jose Tudela; Francisco Garcia-Canovas
Journal:  PLoS One       Date:  2017-05-11       Impact factor: 3.240

2.  Open-label pilot study to evaluate the effectiveness of topical bimatoprost on rhododendrol-induced refractory leukoderma.

Authors:  Saki Fukaya; Masahiro Kamata; Tomoko Kasanuki; Makoto Yokobori; Shintaro Takeoka; Kotaro Hayashi; Takamitsu Tanaka; Atsuko Fukuyasu; Takeko Ishikawa; Takamitsu Ohnishi; Satoshi Iimuro; Yayoi Tada; Shinichi Watanabe
Journal:  J Dermatol       Date:  2018-08-29       Impact factor: 4.005

3.  Carvedilol, an Adrenergic Blocker, Suppresses Melanin Synthesis by Inhibiting the cAMP/CREB Signaling Pathway in Human Melanocytes and Ex Vivo Human Skin Culture.

Authors:  Myoung Eun Choi; Hanju Yoo; Ha-Ri Lee; Ik Joon Moon; Woo Jin Lee; Youngsup Song; Sung Eun Chang
Journal:  Int J Mol Sci       Date:  2020-11-20       Impact factor: 5.923

  3 in total

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