जर्नल ऑफ डर्मेटोलॉजी एंड डर्मेटोलॉजिकल डिजीज

Background: Vitiligo is an acquired hypomelanotic skin disorder resulting from the loss of functional melanocytes from the cutaneous epidermis. Low catalase (CAT) activity and accumulation of hydrogen peroxide (H2O2) have been demonstrated in the epidermis of vitiligo patients. Some polymorphisms on catalase gene may have effect on the quantity and activity of catalase enzyme. The aim of this study was to investigate whether catalase (CAT) gene polymorphisms are associated with susceptibility to vitiligo in Egyptian population. Materials and methods: Thirty patients with vitiligo and twenty gender, age and ethnic matched controls were enrolled in the study. Genotyping was done by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results: The CAT gene -89A>T and 389C>T genotypes and allele frequencies of vitiligo patients did not differ significantly from those of healthy controls. Conclusions: We found no association between CAT gene -89A>T and 389C>T polymorphism and vitiligo susceptibility in Egyptian vitiligo patients. Further studies with greater sample size should be performed to verify these results.

Vitiligo is an acquired pigmentary disorder characterized by areas of depigmented skin resulting from loss of epidermal melanocytes. The cause of the destruction of epidermal melanocytes is complex and not yet fully understood. However, there are several hypotheses related to biochemical, neural and genetic aspects as well as oxidative stress and autoimmune mechanisms proposed to understand this disorder. Oxidative stress has a role in vitiligo onset, while autoimmunity contributes to disease progression. In this review, we discuss the mechanisms that link triggering factors with the disease progression. Oxidative stress causes disruption in redox potentials that extend to the Endoplasmic Reticulum (ER), causing accumulation of misfolded proteins, which activates the Unfolded Protein Response (UPR). Melanocytes at the periphery of vitiligo lesions show dilation of the ER. Following exposure to various triggers of vitiligo melanocytes produce cytokines that activate immune response. These studies expand our understanding of the possible underlying mechanisms of melanocyte loss in vitiligo pathogenesis highlighting the possible mechanisms linking ER stress to oxidative stress and autoimmunity.

Burn scars remain a serious physical and psychological problem for the affected people. Clinical studies as well as basic scientific research have shown that medical needling can significantly increase the quality of burn scars with comparatively low risk and stress for the patient with regards to skin elasticity, moisture, erythema and transepidermal water loss. However, needling has no influence on repigmentation of large hypopigmented scars. The goal is to evaluate whether both established methods – needling improvement of scar quality) and ReCell® (repigmentation) – can be combined. So far, 20 patients with mean age of 35 years (7-61 years) with deep second and third degree burn scars have been treated. The average treated tissue surface was 8% (2-18% TBSA) and was focused on areas like face, neck, chest and arm. Percutaneous collagen induction or “medical needling” is performed using a roller covered with 3mm long needles. The roller is vertically, horizontally and diagonally rolled over the scar, inducing microtrauma. Then, ReCell® is applied, according to the known protocol. The patients have been followed 12 months postoperatively. Pigmentation changes are measured objectively, as well as with patient and observer ratings. Patient satisfaction/preference is also obtained. With this article we present first results of our ongoing study. Taken together, the pigmentation ratings and objective measures indicate improvement in all study participants. Medical needling in combination with ReCell® shows promise for repigmentation of burn scars.

Eyes can be affected by a wide variety of epibulbar lesions. The incidence and prevalence of the epibulbar lesions is significantly high, with an incidence of 89.8% of the benign lesions as compared to the malignant lesions that accounted for 10.2% of the lesions. Considering the significance of the knowledge of the different types of epibulbar lesions, there is a need to perform a brief discussion of these lesions to develop the information of these lesions among the general population and the healthcare professionals. This would enable the successful diagnosis of the different types of epibulbar lesions. Epibulbar pigmented lesions include conjunctival epithelial melanosis, conjunctival freckle, primary acquired melanosis, conjunctival nevus, congenital ocular melanocytosis, and malignant melanoma.

The color of the hair is dependent on the existence and function of the melanin producing cells, the melanocytes, in the hair matrix of the bulb. In vitiligo, the loss of color of the affected skin is due to loss of epidermal melanocytes, which may also be accompanied by loss of the bulbar melanocytes with subsequent loss of the hair color. Lymphocytic immune-cytotoxic process maybe involved in the destruction of epidermal or bulbar melanocytes. Hair depigmentation is said to follow surface depigmentation in long standing disease. This delay in development of leukotrichia in vitiligo could be claimed to the difference in melanization nature of hair follicle in comparison to epidermal melanization process. In rare cases, follicular melanocytes can be primarily destroyed in vitiligo without destruction of epidermal melanocytes. Apart from mature melanocytes, the hair follicles possess also immature form of melanocytes residing in the bulge area, outer root sheath, dermal papilla and sometimes the hair matrix. These immature cells usually escape the vitiligo immune destructive process. The existence of leukotrichia used to be a sign of disease recalcitrance and expected treatment failure. In such cases several surgical procedures were introduced to help repigmenting the skin. It was found that activation of the immature melanocytic precursors in hair follicles is responsible for the repigmentation of epidermis and hair follicles due to the supply with new mature melanocytes.

The natural evolution of Spitz-Reed nevi is poorly understood, owing to the lack of studies investigating their longterm clinical evolution and the fact that most of the lesions are surgically excised. The surgical approach is indicated because of the clinical and histopathologic similarities with melanoma that may create diagnostic confusion in some cases. Hence nowadays, due to the low incidence of melanoma in children and the development of diagnostic dermoscopic criteria, a less aggressive approach to SRN may be reserved, especially in cases with typical features. We report a case of a pigmented lesion that showed gradual changes, from a Spitz Reed Nevus with typical clinical and dermoscopic features, to a common nevus.

Diagnosis of melanocytic tumors poses two big problems for a histopathologist, firstly to diagnose it as melanocytic tumor and the other important problem is the determination of whether the lesion of obvious melanocytic nature is benign or malignant. Here we wish to provide few key histopathological features of some important tumors that will guide a histopathologist in overcoming these problems Melanocytes are generally positive for melanin stains (such as the Fontana- Masson silver stain), tyrosinase, DOPA reaction, S-100 protein, NSE, Mart-1/MelanA (A103), microphthalmia transcription factor, Sox10 (a neural crest transcription factor) PAX3 (a transcription factor with an important role in the development of melanocytes during embryogenesis), and vimentin; the intensity of these reactions shows marked variability, possibly depending on the functional status of the cell. Stains for neurofilaments and glial fibrillary acidic protein are negative. Stains for HMB-45 are generally negative in normal resting melanocytes but positive in activated melanocytes, including those of malignant melanoma. Keratin is another marker that is consistently absent in normal melanocytes but sometimes expressed in their neoplastic counterpart. The fact that normal melanocytes show strong immunoreactivity for the BCL2 proto-oncogene product has been recorded. This is also expressed in benign nevi and less commonly in malignant melanomas. Though it is a challenge for a histopathologist to make a specific diagnosis of a case of melanocytic tumor but with clinical correlation and step by step approach aided with IHC, most of the tumors can be diagnosed correctly. Staging of the tumors is obviously done after proper consultation with dermatologist.

The rapid whitening of hair in a short period of time characterizes the phenomenon called "overnight graying". Diffuse alopecia areata is considered the most likely cause to explain this phenomenon, since there is predominant involvement of the dark pigmented hair and, subsequently, its fall. Thus, the patient who already has a few white hairs, when suffering the fall of dark pigmented hair, has the feeling that his/her hair became totally white "overnight". It is believed that this is an immune-mediated disease, although other factors may be involved: stress, neurological factors, infectious agents and intrinsic abnormalities of keratinocytes and melanocytes. We report a case of "overnight graying" phenomenon in a 56-year-old patient, after being diagnosed with prostate cancer.