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Little is known about the anti-pigmenting effects of whitening agents on solar lentigos (SLs), which comprise ~ 60% of hyperpigmented facial lesions of Asian subjects. Lotions with or without 6% l-ascorbate-2-phosphate trisodium salt (APS) [test lotion (TL) and placebo lotion (PL), respectively] were applied twice daily for 24 weeks in a double-blind half-face study of 27 Japanese females with SLs on both sides of their faces. Pigmentation scores were evaluated using a photo-scale and the skin colors were assessed using a color difference meter and a mexameter for SLs and the non-lesional surrounding skin (NLS). Although the pigmentation scores were not significantly different between the TL and PL-treated SLs after 24 weeks, the L values of TL-treated SLs and NLS increased significantly with a significantly higher △L value in SLs than in NLS. In contrast, the L values of PL-treated SLs and NLS remained unchanged after the treatment. The number of subjects with > 2.0 △L was 7 of 27 (TL) and 0 of 27 (PL) in SLs and 3 of 27 (TL) and 0 of 27 (PS) in NLS. In contrast, the melanin index in TL-treated SLs and NLS significantly decreased with a significantly higher △melanin index in SLs than in NLS. Similarly, the melanin index of PL-treated SLs and NLS were significantly decreased with a significantly higher △melanin index in SLs than in NLS. These findings strongly indicate that APS has a weak but significant anti-pigmenting effect on SLs and a significant whitening effect even on normally pigmented healthy skin.

To characterize the pathobiology of solar lentigos (SLs), analyses by semiquantitative RT-PCR, Western blotting, and immunohistochemistry revealed the upregulated expression of endothelin (EDN)-1/endothelin B receptors (EDNBRs), stem cell factor (SCF)/c-KIT, and tumor necrosis factor (TNF)α in the lesional epidermis, which contrasted with the downregulated expression of interleukin (IL) 1α. These findings strongly support the hypothesis that previous repeated UVB exposure triggers keratinocytes to continuously produce TNFα. TNFα then stimulates the secretion of EDNs and the production of SCF in an autocrine fashion, leading to the continuous melanogenic activation of neighboring melanocytes, which causes SLs. A clinical study of 36 patients with SLs for six months treated with an M. Chamomilla extract with a potent ability to abrogate the EDN1-induced increase in DNA synthesis and melanization of human melanocytes in culture revealed a significant improvement in pigment scores and color differences expressed as L values. Another clinical study using a tyrosinase inhibitor L-ascorbate-2-phosphate 3 Na (ASP) demonstrated that L values of test lotion (6% APS)-treated skin significantly increased in SLs and in non-lesional skin with a significantly higher ΔL value in SLs when compared with non-lesional skin. The sum of these findings strongly suggests that combined topical treatment with EDN signaling blockers and tyrosinase inhibitors is a desirable therapeutic choice for SLs.

[...]only 54%–56% of family practitioners and internists reported skill and comfort in performing total body skin exams and fewer than 50% of referrals to dermatologists include the correct diagnosis.1 2 The asymmetry, border, colour, diameter and evolution (ABCDE) system is traditionally taught for detecting melanoma but uses exclusively rule-based criteria, whereas melanoma and its mimickers belong to ‘fuzzy’ categories in which visual features overlap on a spectrum.3 Perceptual expertise, the ability to identify objects rapidly and accurately at specific levels of categorisation, contributes to discriminating between fuzzy categories.4 Novices may develop perceptual expertise through experience or through targeted visual perception training (VPT). Previous work demonstrated that VPT successfully improved the ability of undergraduates to diagnose melanoma, although follow-up was limited to 1 week.5 This prospective cohort trial of preclinical medical students was performed to evaluate the effectiveness of a novel, technology-based VPT system for melanoma detection with retention assessed at 4 weeks. All 10 participants indicated reasons in favour of recommending the programme to a friend; all participants chose the reasons ‘(The system) increases knowledge of how to identify malignant lesions’ and ‘It is easier to learn from (the system) compared with reading a textbook’.

Cutaneous examination showed multiple round-to-oval discrete, 0.1–0.5-cm sized, dark brown-colored macules distributed in the ophthalmic and maxillary divisions of the trigeminal nerve on the right-side of the face with a sharp midline demarcation [Figure 1]a. There was no background pigmentation suggestive of a café-au-lait- macule. Eye examination revealed brown-colored macules on the bulbar conjunctiva of the right eye [Figure 1]b. Conjunctiva on the left side, oral, and nasal mucosa were not affected. {Table 1} Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms.

Cutaneous examination showed a well defined, pale brown or tan patch of size 8 cm × 12 cm, speckled with numerous small darkly pigmented macules of size 1 mm-3 mm. One vitiligo patch affected the skin of inner canthus, medial side of upper eyelid and infra-orbital region, showing ill-defined borders and some hypopigmented area in contact with normal skin suggestive of the three colors of trichrome vitiligo [Figure 1]. {Figure 2}{Figure 3} Based on typical history of evolution, characteristic clinical appearance and the histopathological findings, it was concluded as a case of \"Congenital segmental speckled lentiginous nevus,\" which was co-localized with trichrome vitiligo. Because of the very young age of patient, no aggressive treatment was offered except topical application of tacrolimus and basic fibroblast growth factor solution (bFGF) for vitiligo but patient did not turn up further. According to the current concept of ICD, a complex and altered interplay between immune cells, nerve fibres and neuromediators occurs within the primary lesion, resulting in localized immune dysregulation which may lead to the development of secondary lesion manifesting as opportunistic infections, tumors, or immune reactions/disorders.

Atypical lentiginous melanocytic proliferations in elderly patients continue to pose a diagnostic dilemma with lesions variably categorized as dysplastic nevus, atypical junctional nevus, melanoma in situ (early or evolving) and premalignant melanosis. We present pigmented lesions from 16 patients (seven male and nine female) and with the exception of one case, all were older than 50 years of age. The anatomical sites included trunk (7), head and neck (6) and upper extremity (3). The clinical diagnosis was variable and included lentigo maligna, atypical nevus, pigmented basal cell carcinoma, seborrheic keratosis and lentigo. The initial biopsies mimicked lentiginous nevus or dysplastic nevus and were characterized by a lentiginous proliferation of melanocytes at the dermoepidermal junction both as single cells and as small nests with areas of confluent growth, extending to the edges of the biopsy. The retiform epidermis was maintained and pagetoid spread of melanocytes was not prominent in hematoxylin- and eosin- stained sections. Dermal fibrosis was variably present and the melanocytic proliferation demonstrated cytological atypia. The subsequent re-excisions demonstrated similar atypical melanocytic proliferation occurring over a broad area flanking the prior biopsy sites. The diagnosis of melanoma was more easily recognized in the complete excision specimens. Immunohistochemical stains for Mitf and Mart-1 highlighted the extent of the basalar melanocytic proliferation as well as foci of pagetoid spread by melanocytes. Familiarity with this pattern of early melanoma should facilitate proper classification of lentiginous melanocytic proliferations in biopsies from older adults.

Cutaneous markers of systemic disease are vital for clinicians to recognize. This chapter outlines familial lentiginosis syndromes that include Peutz-Jeghers syndrome, Carney Complex, the PTEN hamartomatous syndromes, and LEOPARD/Noonan syndrome. The inheritance of these syndromes is autosomal dominant; they also share characteristic skin findings that offer a clue to their recognition and treatment. We will discuss the clinical presentation of these disorders, with a focus on the dermatological manifestations, and will provide an update on the molecular mechanisms involved. Recognition of cutaneous markers associated with these rare familial cancer syndromes provides the opportunity to pursue early surveillance for malignancies, as well as genetic counseling.

The non-healing character of the lesion with irregular patches of dark brown and black pigmentation (figure 1), together with the fact that the patient reported a recent left toe amputation due to malignant melanoma in his brother prompted an immediate referral to dermatology with a suspicion of malignant melanoma. Punch biopsy confirmed a primary invasive cutaneous malignant melanoma with estimated Breslow index of 2–3 mm, mitotic index of 2/mm3 and Clark level 4 (figure 2). Irregular patches of brown and black discolouration/pigmentation in any skin lesion should raise a suspicion of malignant melanoma The authors are thankful to Ali Al-Omari and Nick J Tiffin from Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK for provision of the histopathological image.