Leukoderma induced by rhododendrol is different from leukoderma of vitiligo in pathogenesis: A novel comparative morphological study

Rhododendrol (rhododenol), an inhibitor of tyrosinase activity, is used as a skin‐whitening component. Many cases of leukoderma after the application have been reported, termed rhododenol‐induced leukoderma (RIL). The aim of this study was to clarify the pathogenesis of RIL morphologically through comparison with vitiligo.

[1]  K. Ezzedine,et al.  New discoveries in the pathogenesis and classification of vitiligo. , 2017, Journal of the American Academy of Dermatology.

[2]  A. Wagner Weedon’s Skin Pathology , 2017, Aktuelle Dermatologie.

[3]  T. Yamashita,et al.  Clinical and epidemiological analysis in 149 cases of rhododendrol‐induced leukoderma , 2017, The Journal of dermatology.

[4]  K. Wakamatsu,et al.  Rhododenol-induced leukoderma in a mouse model mimicking Japanese skin. , 2016, Journal of dermatological science.

[5]  Koichiro Nakamura,et al.  T-Cell Responses to Tyrosinase-Derived Self-Peptides in Patients with Leukoderma Induced by Rhododendrol: Implications for Immunotherapy Targeting Melanoma , 2015, Dermatology.

[6]  K. Wakamatsu,et al.  Tyrosinase‐catalyzed metabolism of rhododendrol (RD) in B16 melanoma cells: production of RD‐pheomelanin and covalent binding with thiol proteins , 2015, Pigment cell & melanoma research.

[7]  M. Yamakawa,et al.  An immune pathological and ultrastructural skin analysis for rhododenol-induced leukoderma patients. , 2015, Journal of dermatological science.

[8]  Y. Tokura,et al.  Melanocyte-specific cytotoxic T lymphocytes in patients with rhododendrol-induced leukoderma. , 2015, Journal of dermatological science.

[9]  M. Wataya-Kaneda,et al.  4-(4-hydroroxyphenyl)-2-butanol (rhododendrol) activates the autophagy-lysosome pathway in melanocytes: insights into the mechanisms of rhododendrol-induced leukoderma. , 2015, Journal of dermatological science.

[10]  Y. Tokura,et al.  Biochemical, cytological, and immunological mechanisms of rhododendrol-induced leukoderma. , 2015, Journal of dermatological science.

[11]  I. Katayama,et al.  Possible involvement of CCR4+ CD8+ T cells and elevated plasma CCL22 and CCL17 in patients with rhododenol-induced leukoderma. , 2015, Journal of dermatological science.

[12]  T. Yamashita,et al.  Guide for medical professionals (i.e. dermatologists) for the management of Rhododenol‐induced leukoderma , 2015, The Journal of dermatology.

[13]  K. Wakamatsu,et al.  Human tyrosinase is able to oxidize both enantiomers of rhododendrol , 2014, Pigment cell & melanoma research.

[14]  A. Hachiya,et al.  Depigmentation caused by application of the active brightening material, rhododendrol, is related to tyrosinase activity at a certain threshold. , 2014, Journal of dermatological science.

[15]  K. Wakamatsu,et al.  Tyrosinase‐catalyzed oxidation of rhododendrol produces 2‐methylchromane‐6,7‐dione, the putative ultimate toxic metabolite: implications for melanocyte toxicity , 2014, Pigment cell & melanoma research.

[16]  Tamio Suzuki,et al.  Rhododendrol, a depigmentation‐inducing phenolic compound, exerts melanocyte cytotoxicity via a tyrosinase‐dependent mechanism , 2014, Pigment cell & melanoma research.

[17]  S. Orlow,et al.  Vitiligo inducing phenols activate the unfolded protein response in melanocytes resulting in upregulation of IL6 and IL8 , 2012, The Journal of investigative dermatology.

[18]  S. Ghosh,et al.  Chemical leucoderma: a clinico‐aetiological study of 864 cases in the perspective of a developing country , 2009, The British journal of dermatology.

[19]  Eun-So Lee,et al.  Histopathologic Features in Vitiligo , 2008, The American Journal of dermatopathology.

[20]  Wei Zhou,et al.  MHC haplotypic association in Chinese Han patients with vitiligo , 2006, Journal of the European Academy of Dermatology and Venereology : JEADV.

[21]  R. Boissy,et al.  4-Tertiary butyl phenol exposure sensitizes human melanocytes to dendritic cell-mediated killing: relevance to vitiligo. , 2005, The Journal of investigative dermatology.

[22]  J. Abulafia,et al.  Value of histopathology in vitiligo , 2003, International journal of dermatology.

[23]  E Panzig,et al.  In vivo and in vitro evidence for hydrogen peroxide (H2O2) accumulation in the epidermis of patients with vitiligo and its successful removal by a UVB-activated pseudocatalase. , 1999, The journal of investigative dermatology. Symposium proceedings.

[24]  O. Yamamoto,et al.  Keratinocyte degeneration in human facial skin: Documentation of new ultrastructural markers for photodamage and their improvement during topical tretinoin therapy , 1995, Experimental dermatology.

[25]  S. Im,et al.  BIOLOGIC CHARACTERISTICS OF CULTURED HUMAN VITILIGO MELANOCYTES , 1994, International journal of dermatology.

[26]  K. Hashimoto,et al.  Ultrastructural Study of Vitiligo , 1993, International journal of dermatology.

[27]  E. Medrano,et al.  Structural aberration of the rough endoplasmic reticulum and melanosome compartmentalization in long-term cultures of melanocytes from vitiligo patients. , 1991, The Journal of investigative dermatology.

[28]  L. Mehta,et al.  Histopathology of Vitiliginous Skin , 1983, International journal of dermatology.

[29]  J. Bhawan,et al.  Keratinocyte damage in vitiligo , 1983, Journal of cutaneous pathology.

[30]  T. Fitzpatrick,et al.  Mechanism of depigmentation by hydroquinone. , 1974, The Journal of investigative dermatology.

[31]  P. A. Riley ACQUIRED HYPOMELANOSIS , 1971, The British journal of dermatology.

[32]  G. Kahn Depigmentation caused by phenolic detergent germicides. , 1970, Archives of dermatology.

[33]  I. Hara,et al.  A study of cases of leucomelanodermatosis due to phenyl-phenol compounds. , 1968, Bulletin of Pharmaceutical Research Institute.

[34]  T. Fitzpatrick,et al.  Inhibition of melanin formation by chemical agents. , 1952, The Journal of investigative dermatology.