Journal of Dermatology and Dermatologic Diseases

The pathogenesis of vitiligo based on the model of depigmentation produced by topical application of phenolic compounds that are substrates for tyrosinase is outlined. The main steps in the pathway consist of the haptenation of melanosomal proteins by the quinone products of the analogue phenols with the generation of neo-antigens which are able to elicit a cell-mediated immune response that results in loss of melanocytes and consequent epidermal depigmentation. The source and nature of the haptogenic compounds is unknown but may be of dietary origin. It is suggested that the pattern of depigmentation in vitiligo is determined by regional variations in tyrosinase activity. The possibility of utilizingquinone-mediated haptenation as a means of targeting anti-melanoma immunotherapy is briefly discussed.

Background: There are many causes of facial melanosis like melasma, frictional melanosis, acanthosis nigricanis, lichen planus actinicus, and others. But Gazelle eye like facial melanosis was not recognized as a special disease with characteristic features. Objective: To report a new recognized facial pigmentation that is not uncommonly seen among adults especially females which is locally known as a Gazelle eye like facial melanosis. Patients and methods: This case series descriptive study with histopathological examination was conducted in the Department of Dermatology, Baghdad Teaching Hospital; Baghdad, Iraq during the period from January 2009- December 2013.One hundred patients with gazelle eye like facial pigmentation were collected and evaluated by clinical and histopathological examinations. History was obtained from each patient regarding all socio- demographic aspects related to the disease. Also, clinical assessment was done including Wood’s light examination. Incisional or punch biopsy was performed from 10 patients for histopathological examination. Results: One hundred patients were recorded and examined: 88(88%) females and 12(12%) males with a female to male ratio: 6.5:1 .Their ages ranged from 16-48 (28.7 ± 5) years. The duration of the disease ranged from 5-15(8 ± 3.2) years. All patients had characteristic pigmentation that started around the eyes in a symmetrical fashion and descended down to the cheeks which ended with a tail like and there was a well demarcated white band across the cheek’s pigmentation. The pigmentation was dark brown in color that is not delineated from surrounding normal face skin with negative Wood’s light examination. Histopathological study revealed mainly dermal melanosis as many melanophages were seen in the superficial dermis with basal melanosis of the epidermis. On systemic review all patients were apparently healthy apart from facial melanosis as the main complaint. Conclusions: We think this is a new entity that commonly seen in the clinical practice as a cause of facial melanosis but it’s not well recognized. It has a characteristic location, distribution and configuration that deserve the name “Gazelle eye like facial melanosis”.

Background: Melanomas arise from multipotent neural crest derivative, the melanocytes. At the tumor-stroma interphase, melanoma cells show organized neural differentiation forming tumor-vascular complexes. The present study explores the sequence of neurogenesis from aurophilic radial glial like cells in relation to angiogenesis, utilizing the tumor-vascular-complex (TVC) as a 3D model. Methods: Serial frozen and paraffin sections stained with HE, reticulin-gold impregnation for aurophilia; dopa oxidase; immunopositivity for: neural differentiation (nestin, Glial Fibrillary Acidic Protein (GFAP), Neural Fibrillary Protein (NFP), synaptophysin); indoleamines: (serotonin and melatonin), catecholamines (dopamine (DA), Noradrenalin (NA), pigment; Dopa Oxidase (DO)); hormones: ((PRL), Prolactin; (HGH), Human Growth Hormone;) and mitosis. The pattern of neural differentiation in tumor-vascular-complexes (TVC) is assessed by positivity in layer1- layer 5 and cell counts in each layer of the perimantle zone (PMZ). Statistical Analysis: ANOVA: Kruskal-Wallis One Way Analysis of Variance; All Pairwise Multiple Comparison Procedures [Tukey Test]. [t-test or Mann-Whitney U- test]. Results: A TVC is formed during angiogenic tumor-vascular interaction. Nes +ve angiogenic tubes enter the tumor margins. Periluminar cells show aurophilia, and extend dendritic arbors into the outer layers of the mantle zone. Cells and dendritic processes in layer 1/ layer 2 show Nes, Auro and GFAP positivity. NFP and Syn positivity is seen in layer 4/ layer 5 with a transition zone between layer 2/ layer 3. As two layers accrue, a wave of mitotic activity is seen and cells acquire PRL and HGH and indoleamine positivity. Catecholamine positivity is in layer 4/ layer 5 thus establishing a polarity. Dopamine is positive in layer 3/ layer 4 coinciding with dopa-oxidase which peaks in layer 4 with NA, ACTH positivity in the outer layers is in association with pigmentation in layer 4/ layer 5. Discussion: Thus during tumor-vascular interaction, melanoma cells differentiate into aurophilic radial glial like cells, as during embryonic neurogenesis, Nes, a marker of multi-lineage progenitor cells, identifies them as MASC, which differentiate into neuronal cells. The angiogenic vessel confers polarity and an embryonal microenvironment in the perivascular mantle zone of the TVC, inducing aggressive melanoma cells to function as neuronal stem cells recapitulating neurogenesis of bio-aminergic cells. The cell cycle is orchestrated by the three pituitary hormones, PRL, HGH and ACTH. The expression of PRL and HGH is related to mitotic activity while ACTH and pigment indicate differentiated function.

Tanning refers to the practice of darkening the pigment of one's skin through exposure to natural sunlight or artificial Ultraviolet (UV) radiation. Studies have explored the molecular mechanism of tanning induced by UV radiation exposure. UV radiation triggers DNA damage in the nucleus of keratinocytes, which induces production of melanin by melanocytes. The melanin is then transported to keratinocytes and manifests as darker pigmentation. An increasing amount of data accumulate to support a role for UV exposure in the development of both melanoma and non-melanoma skin cancers. This article reviews the body of literature reporting the effects of UV exposure on melanocyte biology, skin pigmentation, and melanoma

Recently, mixed vitiligo (MV) was defined by Mulekar as the association of segmental vitiligo (SV) and nonsegmental vitiligo (NSV) in the same patient. Until now, SV and generalized NSV were considered to be separate entities with a different distribution (unilateral or bilateral). Generalized vitiligo seemed to be more frequently associated with other autoimmune diseases than SV. From the pathophysiological standpoint, it was hypothesized that NSV was an autoimmune disease, while SV may result of a sympathetic dysfunction. The first pediatric case of SV associated with NSV was reported in 2003 and 36 other observations were subsequently reported. In all these cases, segmental involvement associated usually in a second step with the onset of bilateral vitiligo patches. In this article, we describe, for the first time, two atypical cases of mixed vitiligo in which NSV involvement preceded the onset of SV. In the light of these remarkable cases, different possible aetiopathogenetic mechanisms of MV are discussed which may provide new insights into the pathogenesis of vitiligo.

Known as the “pregnancy mask,” over six million Americans are impacted by hormonally induced melasma every year, making it one of the most common skin concerns in the United States. Affecting female patients in 90% of cases, melasma appears in large, dense patches of pigmentation, usually on the malar, mandibular and centrofacial areas of the face. Although melasma can affect anyone, it tends to affect women with a Fitzpatrick skin type of III-VI living in areas of intense Ultraviolet (UV) light exposure. By understanding the melanogenesis pathway, and utilizing diagnostic tools like the MASI scale and the Wood’s Lamp, clinicians can identify this frustrating condition and proceed with a progressive treatment approach. Addressing melasma using a variety of pigment-inhibiting and correcting ingredients, as well as gentle exfoliation methods, in both daily care regimens and professional treatments will ultimately lead to the desired results the clinician and patient intend to achieve.

Malignant blue nevus is a term related to melanoma arising in association with or that resembles blue nevus. Such lesions are extremely rare with occasional reports and a few small series of cases described in the literature; therefore, the biology and prognosis of such tumors is not well clarified. Due to lack of strictly defined histopathological criteria, such lesions may present a significant diagnostic challenge. We are presenting a case of a malignant blue nevus arising in a congenital cellular blue nevus, presenting as a slowly progressing and asymptomatic pigmented lesion on the buttock of a 21-year-old woman. Histopathological analysis showed presence of a cellular blue nevus as well as features characteristic for malignant blue nevus. The definitive diagnosis was reached only at the histopathological and immunohistochemical examination. The histological features and clinical course in our patient are also discussed in context and the review of the previous related literature.