tretinoin and Sunburn

As well as for topically used dermatological agents, studies performed according to the rules of evidence-based medicine (EBM) are also needed for cosmetics. Although the concept of evidence-based cosmetics has been only partly developed so far, there are some agents and preparations available that can be considered as evidence-based. In this paper we present data from several studies that claim to have examined and demonstrated the efficacy of cosmetic preparations for the management of solar damage and aging skin as well as lentigo and melanosis according to EBM criteria. Certainly, further controlled studies are needed to cover the main application areas of dermocosmetics. Retinol and antioxidant agents such as vitamin C and coenzymes that positively act via several mechanisms on collagen biosynthesis can be considered evidence-based substances for the management of aging skin. According to the same criteria, the preventive effect of regularly applied dermocosmetic sun screens on the development of actinic keratosis could also be shown. Dermocosmetic sun screens should offer adequate protection against UV-B and UV-A light by combining compatible organic and/or non-organic UV-filters and at the same time be well tolerated. Furthermore, they may contain some additional agents such as antioxidants, DNA repair enzymes, dexpanthenol, glycerin or hamamelis distillate. In the treatment of melanosis, a substantial bleaching effect corresponding to that of 0.1% topical tretinoin can be achieved with 10% all-trans-retinol gel. Preparations containing urea, ammonium lactate or glycerol in different concentrations are considered the best characterized and most effective substances for the care of dry skin. However, the lack of controlled studies confirming the efficacy of dermocosmetic products as well as the superiority of the preparation incorporating the active agent over the corresponding base is a problem yet to be solved. Undoubtedly, the efficacy and the sustainability of the achieved effects have to be examined and proven accordingly to EBM criteria in further active cosmetic agents. Moreover, generally accepted guidelines for the examination of efficacy and tolerability of dermocosmetics have to be developed.

Topics: Antioxidants; Cosmetics; Evidence-Based Medicine; Humans; Keratolytic Agents; Keratosis, Actinic; Lentigo; Melanosis; Randomized Controlled Trials as Topic; Skin Aging; Sunburn; Sunscreening Agents; Tretinoin; Vitamin A

Overexposure to ultraviolet and visible radiation causes sunburn. Aspirin and other nonsteroidal anti-inflammatory drugs, cool baths and topical steroids offer only mild relief. Long-term sun exposure causes chronic inflammatory skin changes. Photodamage, rather than the normal aging process, may account for 90 percent of age-associated cosmetic skin problems. Physicians should stress to their patients that all ultraviolet exposure (including sun beds and tanning salons) causes skin damage. Regular sunscreen use during childhood and adolescence may result in an 80 percent reduction in the lifetime incidence of ultraviolet-induced skin damage, including nonmelanoma skin cancers.

Topics: Carcinoma, Squamous Cell; Hemoglobins; Humans; Light; Melanins; Skin; Skin Aging; Skin Neoplasms; Skin Pigmentation; Sunburn; Sunscreening Agents; Tretinoin; Ultraviolet Rays

Invasive squamous cell carcinoma (SCC) of the skin is one of the most common cancers in the United States, with no proven means for prevention other than systemic retinoids, which have significant toxicity, and sunscreen. We sought to determine the risk factors for invasive SCC on the face or ears in a high-risk population comprising 1,131 veterans in the Veterans Affairs Topical Tretinoin Chemoprevention (VATTC) Trial. Participants were required to have been diagnosed with at least two keratinocyte carcinomas (KCs) in the 5 years prior to enrollment. The median duration of follow-up was 3.7 years. Twenty-three percent of the participants developed a new invasive SCC, and the cumulative risk of invasive SCC was 30% at 5 years. The following factors independently predicted for new invasive SCCs: number of invasive SCCs and number of in situ SCCs in the 5 years prior to enrollment, actinic keratoses count at enrollment, a history of ever use of topical 5-fluorouracil, and total occupational time spent outdoors. In contrast, the use of angiotensin-convering enzyme inhibitors or angiotensin receptor blockers during the study and a history of warts anywhere on the body were found to protect against new invasive SCCs. These independent predictors remained the same for all SCCs (invasive and in situ combined). The number of basal cell carcinomas in the 5 years prior to enrollment, sunburns, sun sensitivity, and recreational sun exposure were not associated with new SCCs. These findings identify key risk factors for additional SCCs in patients with multiple prior KCs, and suggest that a history of warts may be associated with reduced SCC risk.

Topics: Aged; Aged, 80 and over; Antineoplastic Agents; Carcinoma, Basal Cell; Carcinoma, Squamous Cell; Female; Follow-Up Studies; Humans; Male; Middle Aged; Multivariate Analysis; Predictive Value of Tests; Risk Factors; Skin Neoplasms; Sunburn; Sunscreening Agents; Tretinoin; Veterans; Warts

We examined epidermal impairment in photodamaged Caucasian skin by light and electron microscopy and observed two types of degeneration of the basal and suprabasal keratinocytes. The first was an electron-lucent degeneration predominantly seen in the periphery of the cells. The marked lucent degeneration occurred in 14% of the basal and suprabasal keratinocytes, predominantly in cells immediately adjacent to melanocytes. In skin specimens with a large number of such damaged keratinocytes, bleb-like keratinocytic protrusions or electron-lucent intercellular structures were also seen. Many vacuolar structures were observed just under the dermoepidermal junction, occupying 9% of the junction length. These structures were produced by herniation of the degenerative portion of the basal and suprabasal keratinocytes, and appeared to be phagocytized by dermal macrophages. The vacuolar alterations in the basal layer and dermoepidermal junction previously reported at the light microscopic level probably represent these intercellular lucent structures, bleb-like protrusions and vacuole-like structures at the electron microscopic level. The second type, dark-staining keratinocytes, probably representing an extensive degenerative process, constituted 4% of the basal and suprabasal keratinocytes. After 12 months of topical tretinoin treatment, dramatic improvement of both degenerative processes of the keratinocytes was noted.

Topics: Administration, Cutaneous; Adult; Double-Blind Method; Facial Dermatoses; Female; Humans; Keratinocytes; Male; Microscopy, Electron; Middle Aged; Sunburn; Tretinoin; White People

Mild exposure to ultraviolet (UV) radiation is also harmful and hazardous to the skin and often causes a photosensitivity disorder accompanied by sunburn. To understand the action of UV on the skin we performed a microarray analysis to isolate UV-sensitive genes. We show here that UV irradiation promoted sunburn and downregulated filaggrin (Flg); fucoxanthin (FX) exerted a protective effect. In vitro analysis showed that UV irradiation of human dermal fibroblasts caused production of intracellular reactive oxygen species (ROS) without cellular toxicity. ROS production was diminished by N-acetylcysteine (NAC) or FX, but not by retinoic acid (RA). In vivo analysis showed that UV irradiation caused sunburn and Flg downregulation, and that FX, but not NAC, RA or clobetasol, exerted a protective effect. FX stimulated Flg promoter activity in a concentration-dependent manner. Flg promoter deletion and chromatin immunoprecipitation analysis showed that caudal type homeo box transcription factor 1 (Cdx1) was a key factor for Flg induction. Cdx1 was also downregulated in UV-exposed skin. Therefore, our data suggested that the protective effects of FX against UV-induced sunburn might be exerted by promotion of skin barrier formation through induction of Flg, unrelated to quenching of ROS or an RA-like action.

Topics: Acetylcysteine; Animals; Cell Line; Down-Regulation; Female; Fibroblasts; Filaggrin Proteins; Humans; Intermediate Filament Proteins; Mice; Radiation-Protective Agents; Reactive Oxygen Species; Skin; Sunburn; Tretinoin; Ultraviolet Rays; Xanthophylls

Skin is an important target organ for estrogens. The major reported effects of estrogens are as regulators of connective tissue molecules, namely collagen and hyaluronic acid. We investigated the regulation of connective tissue synthesis by topical estrogens in a hairless mouse model of photodamaged skin, which has been previously shown to respond to topical retinoids. The naturally occurring estrogen, 17beta-estradiol (17beta-E) and a close stereoisomer, 17alpha-estradiol (17alpha-E), were found to be as effective as all- trans-retinoic acid in stimulating the development of new connective repair zones in photodamaged skin. Furthermore, 17beta-E and 17alpha-E caused a skin thickening response in normal hairless mouse skin after three daily treatments. Skin thickening is due to water accumulation as a result of estrogen-induced hyaluronan synthesis. Our results show that topical estrogens are important regulators of connective tissue synthesis in photodamaged skin as well as normal skin. These findings are consistent with reports from human studies in which estrogen has been found to stimulate collagen production. We also demonstrated that 17alpha-E, previously thought to be a weak or inactive estrogen, is less potent than 17beta-E, but nonetheless topically effective in stimulating connective tissue synthesis.

Topics: Administration, Cutaneous; Animals; Collagen; Connective Tissue; Estradiol; Female; Hyaluronic Acid; Mice; Mice, Hairless; Receptors, Estrogen; Skin; Stereoisomerism; Sunburn; Tretinoin