Langan, E.A.; Nie, Z.; Rhodes, L.E.
doi: 10.1111/j.1365-2133.2010.09891.xpmid: 20545686
SummaryWhile ultraviolet radiation (UVR) is a major cause of skin ageing and carcinogenesis, public pursuit of a novel tanning strategy circumventing the need for UVR is increasingly reported in the media and scientific press. This involves the subcutaneous self‐administration of unregulated products labelled as melanotan I and/or II, synthetic analogues of α‐melanocyte stimulating hormone (α‐MSH), as obtained via the internet, tanning salons and gyms. The Medicines and Healthcare products Regulatory Authority has recently raised awareness of the public health risk of transmission of blood‐borne viruses from the needle sharing that may occur, and of the potential impurity of these products. Dermatologists should also be aware that these agents can complicate the clinical presentation of patients with pigmented lesions; their use may be suspected in unexpectedly tanned individuals with rapidly pigmenting naevi. Meanwhile, the regulated α‐MSH analogue afamelanotide (Clinuvel Pharmaceuticals Ltd, Melbourne, Australia) is showing promise for its photoprotective potential, and is undergoing phase II and III clinical trials in people with photosensitivity disorders and those prone to nonmelanoma skin cancer. The photoprotective and other biological effects of α‐MSH analogues await full determination.
doi: 10.1111/j.1365-2133.2010.09958.xpmid: N/A
SummaryThe 9th Nottingham Evidence Based Update Meeting was held in Loughborough on 13 May 2010. The theme of the 1‐day meeting was eczema and was attended by delegates from the U.K. and Europe. The broad range of topics included the systemic treatment of severe eczema, eczema educational programmes for patients and their families, the role of allergy testing, the impact of nurse practitioner‐led eczema clinics and the use of probiotics both in the treatment and prevention of eczema.
Sylvestre, J.‐P.; Bouissou, C.C.; Guy, R.H.; Delgado‐Charro, M.B.
doi: 10.1111/j.1365-2133.2010.09805.xpmid: 20394632
SummaryBackground Amino acid (AA) levels in stratum corneum (SC) are potential biomarkers of skin health while their systemic levels may be used to diagnose inherited metabolic diseases.Objectives To examine reverse iontophoresis, in human volunteers, as a minimally invasive tool to analyse AAs within the skin and subdermally.Methods In four volunteers, the amounts of iontophoretically extracted AAs were compared with those determined in the SC following repetitive tape stripping and with the plasma concentrations. Glucose levels, evaluated in the different compartments, were used as a control.Results SC concentrations of 13 essentially zwitterionic AAs were ∼100‐fold higher than the respective plasma levels. Passive and reverse iontophoretic extraction for 4 h did not deplete the SC depot of AAs, a fact reinforced by postextraction tape stripping, which revealed that AAs remained in the SC at this time. In contrast, glucose was much less abundant in the SC and was fully and relatively quickly extracted by reverse iontophoresis.Conclusions It follows that reverse iontophoresis is useful for quantifying AAs in the SC and these data are highly correlated with levels obtained by tape stripping. However, reverse iontophoresis is impractical for the routine monitoring of AA plasma concentrations (unlike the situation for glucose, the skin reservoir of which is much smaller).
Moneib, H.A.M.; Salem, S.A.M.; Darwish, M.M.
doi: 10.1111/j.1365-2133.2010.09820.xpmid: 20426777
SummaryBackground Necrolytic acral erythema (NAE) is considered a cutaneous sign of hepatitis C virus infection. Its exact pathogenesis is still not fully understood, with some reports about decreased serum zinc levels but none about its level in the skin.Objectives To assess skin (lesional and perilesional) and serum zinc levels in patients with NAE and compare them with levels in control subjects.Methods Fifteen patients with NAE and 10 healthy controls were included in this study. Assessment of zinc level, in serum by graphite furnace atomic absorption spectrophotometry and in lesional and perilesional skin biopsies by flame atomic absorption spectrometry, was done in all subjects. Re‐evaluation of serum and lesional skin zinc level was done after oral zinc treatment.Results Mean ± SD zinc levels were significantly lower in patients (serum 0·44 ± 0·13 mg L−1; lesional skin 42·6 ± 18·9 mg L−1; perilesional skin 32·5 ± 17·2 mg L−1) than controls (serum 1·17 ± 0·29 mg L−1; skin 100·1 ± 2·77 mg L−1), with a positive correlation between lesional and perilesional skin zinc (r = 0·91, P < 0·01). Oral zinc supplementation significantly increased serum and skin zinc levels (by 159% and 4%, respectively; P < 0·05).Conclusions NAE is associated with decreased serum and skin zinc levels. Oral zinc supplementation corrects decreased levels of plasma and skin zinc much earlier than the desired clinical benefits appear.
Thompson, A.R.; Clarke, S.A.; Newell, R.J.; Gawkrodger, D.J.; ,
doi: 10.1111/j.1365-2133.2010.09828.xpmid: 20426784
SummaryBackground Vitiligo is a visible condition that is more noticeable in darker‐skinned people. Beliefs about illness have been linked to psychosocial adjustment. There is some evidence that such beliefs may be influenced by cultural factors. Surprisingly little is known about beliefs in relation to vitiligo.Objectives The study sought to explore in depth the ways in which British Asian women manage and adjust psychosocially to vitiligo, and the potential role of ethnicity and culture in this process.Methods In‐depth semistructured interviews were conducted with seven British women of South Asian decent and analysed using the qualitative method of template analysis.Results Participants described feeling visibly different and all had experienced stigmatization to some extent. Avoidance and concealment were commonplace. Experiences of stigmatization were often perceived to be associated with cultural values related to appearance, status, and myths linked to the cause of the condition.Conclusions The findings of this study present a unique in‐depth analysis of British South Asians living with vitiligo and suggest there is a need for further research to explore cultural associations of disfigurement and of adjustment to chronic skin conditions. Furthermore, they suggest that in addition to individual therapeutic interventions there may be a need for community interventions aimed at dispelling myths and raising awareness of sources of support and treatment.
Showing 1 to 10 of 49 Articles
SummaryBackground Hyperkeratosis and acanthosis occur in inflamed skin. Proliferation and differentiation of keratinocytes are important processes during epidermal repair after inflammation. Neuropsin and its human homologue kallikrein‐related peptidase 8 (KLK8) have been reported to be involved in epidermal proliferation and differentiation, but the involved molecular mechanisms are obscure.Objectives To explore the molecular mechanism of KLK8/neuropsin‐induced hyperkeratosis and acanthosis in inflamed skin.Methods The molecular mechanism involved in KLK8/neuropsin‐induced hyperkeratosis and acanthosis in inflamed skin was investigated both in vivo and in vitro using neuropsin knockout mice and KLK8 knockdown human keratinocytes. Neuropsin‐related genes were identified by differential gene display. The localization and functional relationship of the molecules affected downstream of KLK8/neuropsin in normal and inflamed skin were analysed by in situ hybridization and immunohistochemistry.Results Hyperkeratosis and acanthosis in sodium lauryl sulphate‐stimulated skin were markedly inhibited in neuropsin knockout mice. Knockdown of KLK8/neuropsin increased transcription factor activator protein‐2α (AP‐2α) expression and decreased keratin 10 expression in human keratinocytes and mouse skin, respectively. AP‐2α has been reported to inhibit epidermal proliferation and keratin 10 expression. Distributional analysis showed that KLK8/neuropsin was expressed in the stratum spinosum, AP‐2α was expressed in the stratum basale and the lower part of the stratum spinosum, and keratin 10 was expressed throughout the stratum spinosum.Conclusions The above findings suggest the following mechanism of events underlying KLK8/neuropsin‐induced hyperkeratosis: (i) skin inflammation increases KLK8/neuropsin expression in the stratum spinosum; (ii) the released KLK8/neuropsin inhibits AP‐2α expression in the cells of the stratum basale and stratum spinosum; (iii) the decrease in AP‐2α results in cell proliferation in the stratum basale and cell differentiation in the stratum spinosum, with an increase in keratin 10 expression.