Angela Panske

Rapid initiation of repigmentation in vitiligo with Dead Sea climatotherapy in combination with pseudocatalase (PC-KUS).

Background Low catalase levels and cellular vacuolation in the epidermis of patients with vitiligo support major oxidative stress in this compartment. There is now in vivo evidence for increased epidermal hydrogen peroxide (H2O2) accumulation in this patient group by utilizing noninvasive Fourier Transform Raman spectroscopy (FT Raman). Epidermal H2O2 can be removed with a topical application of narrow band UVB activated pseudocatalase cream (PC‐KUS). (Mn/EDTA‐bicarbonate complex, patent No. EPO 58471 1 A), yielding initiation of repigmentation. Dead Sea climatotherapy is another successful treatment modality for vitiligo, but the mode of action has escaped definition so far.

Decreased Photodamage and Low Incidence of Non-Melanoma Skin Cancer in 136 Sun-Exposed Caucasian Patients with Vitiligo

Background: It is well established that ultraviolet radiation is related to non-melanoma skin cancer (NMSC) in Caucasians. Considering that patients with vitiligo have often no protective pigment in sun-exposed depigmented/white skin together with severe oxidative stress due to accumulation of millimolar epidermal hydrogen peroxide (H2O2), it would be expected that these patients develop a higher risk for early photodamage and NMSC. However, scattered reports on low patient numbers documented no increased risk for sun-induced skin cancers in this disease. Objective: The aim of this study was to validate the possible photodamage and the development of epidermal neoplasia in a randomly selected larger patient group with emphasis on each patient’s sun sensitivity and the history of solar habits. Furthermore we wished to compare histological signs for epidermal photodamage in a random representative patient group (mean age >30 years) and age-matched healthy controls. Methods: One hundred and thirty-six randomly selected patients (females n = 93; males n = 43; mean age 42.4 years, range 14–70 years) were included in this study. To assess signs of photodamage and skin cancer, all patients underwent a thorough full-body examination by Wood’s light and dermatoscopy. In order to learn about each patient’s individual sun sensitivity and solar habits, a direct questionnaire was used. In addition full skin punch biopsies of sun-exposed depigmented/pigmented skin were taken under local anaesthesia and evaluated by light microscopy. Results: There was no evidence for sun-related damage in the entire patient group, despite a significant number of positive cases with a history of sunburns in early childhood and continuous accumulation of epidermal H2O2. Histological examination of the epidermis showed no signs of increased photo-ageing and confirmed the absence of apoptosis in these patients. Furthermore surprisingly there was no increased risk for photosensitivity disorders, i.e. polymorphous light reaction, solar urticaria and acute actinic dermatitis. Conclusion: The results of this study confirm in a large group of patients with vitiligo the absence of an expected high risk for sun-induced damage and skin cancer. Based on these results together with a recent report on increased functional wild-type p53 expression in these patients we would like to propose that in vitiligo there may be a direct association between this important tumour suppressor and the absence of photodamage and NMSC.

Molecular evidence that halo in Sutton's naevus is not vitiligo.

Both halo naevus and vitiligo are acquired leucodermas of unknown aetiology. To date a significant contribution of oxidative stress through accumulation of hydrogen peroxide (H2O2) has been documented in the pathomechanism of vitiligo but not in halo naevus. Both epidermal pterin-4a-carbinolamine dehydratase (PCD) and catalase are sensitive markers to follow H2O2 concentration-dependent deactivation of these proteins. In situ protein expression of PCD and catalase was examined in full-skin biopsies from skin phototype-matched controls (n=5), untreated and treated vitiligo patients (n=5) and patients with untreated halo naevus in association with vitiligo (n=3). Vitiligo was treated with pseudocatalase (PC-KUS) only. Catalase levels were determined in epidermal suction blister extracts using fast protein liquid chromatography (FPLC). In addition, epidermal H2O2 levels were followed in vivo by Fourier-transform Raman spectroscopy. The results of this study ruled out a contribution of H2O2 in the millimolar range in the depigmentation process of halo naevus as previously documented in vitiligo. Therefore, it can be concluded that both leucodermas exercise distinct concentration-dependent H2O2 signalling in their pathomechanisms.

Disease-related behavioral patterns and experiences affect quality of life in children and adolescents with vitiligo.

Background  Vitiligo is an acquired, non‐contagious depigmentation disorder involving a patchy loss of skin color. It often leads to stigmatization, embarrassment, and reduced quality of life (QoL) in adult patients. Little is known about children’s reactions.

Ineffective topical treatment of vitiligo with Cucumis melo extracts

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