Clinical and ultrastructural study of nevus depigmentosus
Author(s) -
ArwaM Hassan,
El-SayedS Hewedy,
EhsanF Salah,
FersanA Sallam,
NaeemM Dawood,
RedaH Al-Bakary,
HagarA Al-Sharnoby
Publication year - 2013
Publication title -
journal of microscopy and ultrastructure
Language(s) - English
Resource type - Journals
eISSN - 2213-8803
pISSN - 2213-879X
DOI - 10.1016/j.jmau.2013.06.006
Subject(s) - melanosome , ultrastructure , nevus , pathology , lesion , medicine , melanocytic nevus , dermatology , pathogenesis , hyperpigmentation , melanin , histology , melanoma , biology , genetics , cancer research
BackgroundNevus depigmentosus is a congenital, non-progressive, hypopigmented macule or patch that is stable in its relative size and distribution throughout life. The lesions are often single but may be multiple, circumscribed and either isolated, dermatomal or in whorls. The lesions are uniformly hypomelanoic but not amelanotic. The aetiopathogenesis of nevus depigmentosus is not yet fully understood. A defect in the transfer of melanosomes from melanocytes to keratinocytes has been reported.ObjectiveThis work aimed at evaluation of the clinical and ultrastructural characteristics of nevus depigmentosus in a trial to understand its pathogenesis.Patients and methodsThis study included 15 patients having nevus depigmentosus. Ultrastructural study was performed for 5 patients. 2 punch biopsies were taken from each patient, one from the center of the lesion and another from the nearby apparently normal skin as a control.ResultsThe lesions were mostly present before 3 years of age, mostly on the trunk. Six patients (40%) had the isolated type and 9 (60%) had the segmental type. Under Wood's lamp, the lesions exhibited an off-white accentuation without fluorescence. Ultrastructural study showed apparent reduction in melanosomal content of lesional melanocytes and keratinocytes. Immature and aggregated melanosomes were more present in lesional keratinocytes. Electron microscopic DOPA oxidase reaction was decreased in lesional skin compared to control indicating a reduced tyrosinase activity.ConclusionThe results of this study support the hypothesis that nevus depigmentosus is caused by functional defect of melanocytes and morphologic abnormalities of melanosomes
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom