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01-09-2011 | Dermatology | Article

Acral vitiligo lesions respond to PUVA without repigmentation


Free abstract

MedWire News: Acral vitiligo lesions respond to PUVA therapy in the same way that lesions on the trunk and proximal limbs do, but these changes fail to induce repigmentation, show study findings investigating factors associated with mechanisms of repigmentation following phototherapy.

"Factors such as inherent lower melanocyte density, lower melanocyte stem cell reservoirs and/or lower baseline epidermal stem cell factor may be considered as possible play makers in this respect," say OA Zeid (Cairo University, Egypt) and co-authors.

In total, 20 patients aged 18-53 years with active vitiligo for a minimum of 1.5 years took part in the study. Skin biopsies were taken before and after PUVA therapy from lesional and perilesional skin of areas expected to respond to treatment (trunk and proximal limb; Type A), as well as skin from acral areas highly unlikely to repigment (Type B).

Sections were stained with haematoxylin and eosin, melan-A, major histocompatibiltiy complex (MHC) II, the transmembrane glycoprotein CD1a , and stem cell factor (SCF) and its receptor, c-kit.

B-microscopic examination of H&E sections showed a perivascular lymphocytic infiltrate of variable densities in the upper dermis that was significantly higher in lesional compared with perilesional areas in both type A and B skin.

C-immunohistochemical staining revealed that melanocytes were absent from all lesional skin before treatment and appeared only in responding lesional skin after treatment. Perilesional melanocytes were significantly higher in type A than in type B skin both before and after PUVA (0.099 vs 0.0565 and 0.1055 vs 0.0645 perilesional melanocytes per 100 basal keratinocytes, respectively).

Before treatment, both type A and B skin lesions showed higher CD1a+ Langerhans cells compared with perilesional skin. Type B lesions showed significantly lower density than type A lesional skin. Following treatment, both types showed significant reduction of Langerhan cell density in lesional skin, at 7.09 vs 2.35 for type A and 2.56 versus 1.51 for type B.

"This shows that type B lesions responded to PUVA the same way as type A lesions by reducing Langerhan cell density, which is one of the mechanisms suggested for PUVA-induced repigmentation," say the authors.

Overall, MHC II was significantly higher in lesional skin than in perilesional skin, with significant reductions occurring after treatment in both lesional and perilesional skin.

Before treatment, lesional skin for type A showed significantly higher expression of SCF compared with perilesional skin, with lesional type B showing significantly lower expression of SCF than type A. Significant reductions in SCF expression were noted in both groups, with all type B lesional skin cases showing weak staining after treatment compared with 14 of the 20 type A lesional skin cases.

Complete absence of c-kit was seen in lesional areas in both groups, which was associated with significantly higher expression of SCF by keratinocytes in vitiligous lesions in both types A and B. Following PUVA treatment, c-kit receptor was expressed in the lesional skin in responding areas in type A but not type B, most likely to due to failure of appearance of melanocytes in acral lesions after therapy.

"The cytotoxic potential of acral skin as well as melanocyte motility and other melanocyte mitogens need to be studied," conclude the authors in the Journal of the European Academy of Dermatology and Venereology.

MedWire ( is an independent clinical news service provided by Springer Healthcare Limited. © Springer Healthcare Ltd; 2011

By Ingrid Grasmo