Hydrofluoric acid (HFA) burns have been occurring with ever-increasing frequency due to the wide use of HFA in industrial fields, such as electronics and semiconductor industries. HFA is one of the strongest inorganic acids and is capable of producing extremely serious and progressively destructive skin burns, with potential serious systemic effects and even death. It is therefore of great importance that clinicians understand the unique characteristics of such burns and the fundamentals of their treatment. Herein we aim to present the clinical features of HFA burns, histopathological studies using guinea pigs and several therapeutic methodologies along with 4 cases of HFA burns we experienced, showing the importance of early initial treatment.
UV light exposure has been incriminated for the steady rise in skin cancer incidence observed during the last years. However, individual responses to the oncogenic effects of UV light are greatly variable. Among the many factors modulating the response to UV light, genetic variations play a pivotal role. This review examines major progress in our understanding of major hereditary and nonhereditary genetic modifiers involved in the pathogenesis of UV-induced skin cancer.
Fifteen grapevine workers developed skin reactions resembling erythema multiforme (EM) and Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) following exposure to Dormex, a plant growth regulator, the active ingredient of which is hydrogen cyanamide. Five patients needed hospitalization, and all recovered following treatment. Whether these were contact EM-like reactions due to hydrogen cyanamide or classical EM, SJS-TEN induced by this chemical remains elusive. An awareness regarding the safe use of agricultural chemicals is needed among the general population.
In order to clarify the mechanisms underlying the surfactant-induced dehydration of the stratum corneum (SC), we first examined the constitutive water-holding function of the SC by removing intercellular lipids as well as hygroscopic materials from intact human SC. The dehydration of the SC can be easily induced by depletion of intercellular lipids, but was not affected by an additional water treatment, which releases a large amount of hygroscopic materials including amino acids. Consistent with this, the application of isolated intercellular lipids or their subfractions to the lipid-depleted and dehydrated SC rescues the decreased water content as well as marked scaling, although glycerine did not have such an effect. Parallel differential scanning calorimetry analysis revealed that lipid depletion causes the SC to reduce the nonfreezable bound water content and that application of isolated intercellular lipids recovered the bound water content up to the control level. On the other hand, the additional release of hygroscopic materials from lipid-depleted SC did not affect the bound water content. Based upon the above constitutive water-holding mechanism in the SC, we assessed the physicochemical mechanisms involved in surfactant-induced dehydration of the SC, leading to tight sensation and skin roughness. Similar to treatment with acetone/ether, treatment with surfactant releases a significant amount of intercellular lipids, the intensity of which varies among various surfactants but correlates well with the intensity of the induced dehydration of the SC leading to the tight skin sensation and skin roughness. Recovery or inhibition experiments revealed that the dehydration of the SC induced by surfactant treatment is significantly attenuated by the application of isolated intercellular lipids or by the addition of monoglyceride (MG) during the washing process, which results in a significant reduction in skin roughness. The latter study showed that whereas the release of sebum components and amino acids during surfactant treatment is not affected by the addition of MG, the removal of ceramides is significantly attenuated by the addition of MG, which suggests an essential role for ceramide depletion in the induction of the surfactant-induced dehydration of the SC. In conclusion, the above findings collectively suggest that the ceramide content in the SC is strongly associated with the regulation of SC hydration and that its deficiency due to surfactant treatment is essentially responsible for the surfactant-induced dehydration of the SC. This hypothesis is further strengthened by the fact that synthetic pseudoceramides are remarkably effective in preventing or abolishing the dehydration of the SC which is an intrinsic factor for inducing the tight sensation and roughness of the skin and which provides a pathological basis for atopic dry skin.
Itch is a common sensation and a component of numerous disease states. Itch can be classified according to its origin and may be modulated by both endogenous and exogenous factors. Recent research has led to a better understanding of the mechanisms of itch, but there are still many areas to be explored. The purpose of this article is to classify the common causes of exogenous itch in humans. To facilitate this, a Medline literature review was conducted using the MeSH search term ‘pruritus’ along with relevant associated subheadings to identify articles dealing with exogenous factors related to itch. Factors relevant to exogenous itch were classified into mechanical, chemical, and environmental components. A better understanding of the various mechanisms of pruritus is critical to effective research into the treatment of itch.
The fragrance material amylcinnamic aldehyde (ACA) has been cited as a frequent cause of allergic contact dermatitis (ACD). A review of the literature shows that when the underlying clinical and experimental data are analyzed, a clear cause-effect relationship has infrequently or rarely been established. On the basis of the generally weak sensitizing potential of this substance coupled with its generally low exposure conditions, the prevalence of clinical cases would not be expected to be particularly high. This is not to say that ACA is a frequent inducer of low-intensity but subclinical, type IV allergy in members of the public. It remains to be seen however, how often such allergy, once established, is responsible for any of the cases of ACD commonly ascribed in the literature. Indeed, in some cases, patch test conditions may not be optimal for differentiating between clinically relevant and irrelevant allergy to ACA.
The health and beauty of human hair have immeasurable psychological importance. Hair structure and its cycle are influenced by intentionally or nonintentionally delivered factors such as grooming, heat styling, chemical agents and climatic exposure. All of these factors are capable of causing loss of hair color and luster, harshness, stiffness, weakness, brittleness and flyaway, transient loss of hair or scarring alopecia. In this review we describe the effects of various exogenous agents on hair, including hair cosmetics, traction, heat, water, solar radiation and X-irradiation.
Background: Although it is well known that chemical oxidation with alkaline hydrogen peroxide damages human hair, little is known about the effects of bleaching during daily life activities which may alter hair components. Objective: To determine the effects of bleaching combined with daily weathering on lipids and amino acids in hair. Methods: Levels of lipids and amino acids were analyzed by chromatography in scalp hair fibers collected from three different females and in experimentally treated hair. Results: Bleaching combined with daily weathering induced the loss of 18-methyleicosanoic acid (18-MEA) and the conversion of half-cystine (H-CYS) to cysteic acid (CYS-A), which were the most remarkable changes among all lipids and amino acids tested. Although a single bleaching had no effect, repeated bleaching combined with daily weathering elicited significant decreases in other intrinsic endogenous lipids and alterations in amino acids that are characteristic for the cuticle. Conclusion: Hair damage, eventually leading to the worst damage such as splitting, is caused by bleaching during daily life activities and is mainly attributable to the loss of 18-MEA as well as the conversion of H-CYS to CYS-A.
Mosquito bites in humans are characterized by an immediate wheal-and-flare type I hypersensitivity response, followed by a delayed type IV papular reaction approximately 24 h later. An intense pruritic reaction may accompany all phases of the bite. Prophylactically administered oral second-generation antihistamines inhibit the immediate histamine induced wheal-and-flare in skin, and some studies show that they are also useful in alleviating delayed bite symptoms. Topical antihistamines have not been documented to be useful in treatment; however, topical ammonium solution and other common allergic reaction remedies are promising as after-bite treatments. This review assesses the current evidence analyzing the efficacy of prophylactic, oral, second-generation antihistamines as well as topical therapies for mosquito bites.
Certain ingredients in moisturizing creams may influence the skin susceptibility to irritants. One agent of particular interest is the well-known humectant urea. The present placebo-controlled study on 28 subjects was designed to evaluate the effects of urea treatment on three types of sodium lauryl sulphate (SLS) exposures: (1) repeated exposure to SLS for 15 days with concurrent cream treatment, (2) the skin susceptibility to SLS following prophylactic treatment with urea and (3) SLS exposure after recovery of the surfactant-damaged skin by urea treatment. Parameters measured were transepidermal water loss (TEWL) and skin blood flow. Repeated exposure to SLS induced a slight but significant barrier damage, measured as TEWL, and the difference between the treatments was almost significant (p = 0.06). Treatment of normal skin reduced TEWL in the urea-treated area, and the irritant reaction to SLS was significantly decreased. Treatment of surfactant-damaged skin promoted barrier recovery, and the second exposure to SLS induced a less pronounced reaction in the urea-treated area compared to the placebo-treated site. In conclusion, urea promotes barrier recovery in SLS-damaged skin and makes both normal and irritated skin less susceptible to irritation. The findings may be of clinical relevance in attempts to reduce contact dermatitis due to irritant stimuli.
Background: Atopic dermatitis (AD) can be considered a barrier disease in which antigens and irritants that can easily penetrate clinically normal, nonlesional skin due to its defective barrier function trigger and worsen the dermatitis. Thus, replenishing the barrier function in clinically normal, nonlesional skin of patients with AD seems to be a key for preventing the refractory nature of the dermatitis. Objective: To determine whether the disrupted barrier function of AD nonlesional skin can be repaired by topical application of a synthetic ceramide known to induce barrier recovery and to subsequently evaluate the relationship between enhanced barrier function and improved dry skin conditions. Methods: We applied topically a synthetic ceramide (CER) or hirudoid (HIRU)-containing cream to the nonlesional skin of AD patients for 4 weeks and evaluated their efficacy by measuring transepidermal water loss (TEWL) and capacitance values as well as clinical scoring for scaling/dryness/itchiness. Results: Treatment for 4 weeks with the CER cream significantly reduced dryness/scaling/itchiness which was accompanied by significant decreases in TEWL and increases in capacitance values at 2 and 4 weeks. In contrast, treatment for 4 weeks with the HIRU cream elicited a similar but lesser reduction in dryness/scaling/itchiness which was accompanied by significant but lesser decreases and increases in TEWL and capacitance values, respectively, at 2 and 4 weeks. Comparison of TEWL and capacitance values during the 4 weeks of treatment with CER or HIRU creams revealed that while the two parameters of CER cream-treated skin were generally similar to healthy control skin, those of the HIRU cream-treated skin remained similar to mild or moderate AD skin. Conclusion: It is likely that the recovery of barrier function reflects the improvement in clinically evaluated dry skin conditions of the nonlesional skin to a greater extent than that in water deficiency, which suggests that the barrier-replenishing effect is a more important factor for treatment of AD nonlesional skin than is the improvement of water deficiency.
Psoriasis is a chronic relapsing disease characterized by variable clinical features. Several factors may exacerbate its manifestations, or even trigger the disease, such as traumatic injury to the skin, physical and psychological stress, cold weather, excessive alcohol intake, and drugs such as lithium and beta-blockers. We describe the most common features of psoriasis and the exogenous factors that may induce, trigger or exacerbate the disease.
Background: The etiology of the nonlesional dry and barrier-disrupted skin of patients with atopic dermatitis (AD) is still unclear. Objective: To determine whether disrupted barrier function in the nonlesional skin is associated with inflammatory or postinflammatory events, which are relevant to the severity of AD or local dry skin properties, respectively. Methods: We evaluated the barrier function and the water content of nonlesional forearm skin and compared these with the severity of AD and the intensity of dryness/scaling/itchiness at the same skin sites. Results: The transepidermal water loss (TEWL) significantly increased in proportion to the severity of AD with a markedly high correlation coefficient (r = 0.834, p < 0.0001, n = 106), while the capacitance decreased in proportion to the severity of AD with a relatively lower correlation coefficient (r = –0.720, p < 0.0001, n = 106) compared with TEWL. Relationship between TEWL and capacitance values in association with the AD severity revealed that the two parameters are well distributed, corresponding to the severity of AD, and that the elevated TEWL more adequately reflects the difference between healthy control and the mild group of AD compared with the reduced capacitance. Comparison with dry skin properties revealed that while the capacitance values were highly correlated with dryness (r = –0.752, p < 0.0001, n = 106) and with scaling (r = –0.697, p < 0.0001, n = 106), the TEWL was also related to dryness (r = 0.788, p < 0.0001, n = 106) with a higher correlation coefficient compared with capacitance and to scaling (r = 0.697, p < 0.0001, n = 106). Conclusion: Our results indicate that the barrier disruption in the nonlesional skin is well suited to reflect the severity of AD as well as the dry skin properties, providing a useful insight into understandings of diagnosis and clinical improvement during therapy.
The ability of topically applied dosage forms to penetrate the skin depends on the interactions of the formulation ingredients with the intrinsic components of the skin. These interactions define the penetration route as well as the distribution of the drug in the skin tissue. The present study focused on monitoring components of externally applied formulations through the skin (ex vivo) via mid-infrared microspectroscopic techniques. Infrared microspectroscopy represents a new bioanalytical method, combining the powerfulness of chemical component analysis by means of infrared spectroscopy and using the high lateral resolution (∼20 µm) as obtained from microscopy. Two methods are applied for analysing tissues: the mapping and the imaging approach. A major breakthrough using infrared microspectroscopy in tissue diagnostics was the development and implementation of so-called focal plane array detectors. Using these detectors, sample areas of about 0.25–16 mm2 can be analyzed. The highest lateral resolution obtained by the transmission techniques approaches the mid-infrared diffraction limit of approximately 6 µm. Using mid-infrared microspectroscopic imaging, a large amount of biochemical information, at high lateral resolution, is generated, not yet available by other methods. Additional advantages are: it is a non-invasive, non-destructive approach, requiring no complex and time-consuming tissue staining procedures. In the present study, mid-infrared microspectroscopic mapping and imaging techniques in transmission are used for the biochemical characterisation of skin samples (e.g. lipid/protein distribution). This information provides new insight into the morphology of the tissue constitution. Additionally, examples are presented concerning the analysis of the distribution of topically applied drugs (e.g. UV B blocker or liposomes) through the skin. The potential as well as the limits of the methods for dermatological research are discussed.
Department of Dermatology, Showa University School of Medicine, Tokyo , Japan pigmentation, teleangiectasia and mild atrophy on the extensor aspect of her right forearm and the dorsal aspect of the right hand ( fi g. 1 ). Whitish streaks were seen on the proximal side of the lesion. We diagnosed depigmentation due to triamcinolone acetonide on the basis of history and morphology. Many cases of depigmentation and atrophy due to corticosteroid injection have been reported [1–6] . The lesions appeared after a single injection to after approximately 40 injections, and perilesional linear streaks were seen in most cases [1–6] . Although their mechanism remains unclear, the suggested cause of whitish streaks is the lymphatic spread of the corticosteroid suspension resulting in dermal and epidermal atrophy [6] . Triamcinolone is a minimally soluble corticosteroid, and the formation of acetonide leads to enhanced percutaneous absorption and subsequently a strong anti-infl ammatory effect [7, 8] . Although the incidence of depigmentation and atrophy seems to be low, we must consider the cosmetic risk of those reactions [9] . Also, the anatomical sites to which such a medicament is administered should be considered [8] . Since most of the atrophic complications were described with the dose of 40 mg of triamcinolone [1–6] , a lower dosage may be more adequate for exposed sites, e.g. the face, wrists or hands.
Vitiligo is an acquired depigmentary disorder of the skin that results from the selective destruction of melanocytes. The etiology of vitiligo is poorly understood. There appears to be a genetic predisposition, but additional factors are probably involved. The purpose of this article is to outline the factors that might play a role in the development of vitiligo. These include trauma such as vaccination, radiotherapy, and sun exposure, malignancies and treatment of malignancies like lymphoma or melanoma, bone marrow transplantation, interferon, interleukin, and other drugs, psychological factors, endocrine disease and cytotoxic compounds that cause contact vitiligo. We hope future research will shed more light on the subject and identify the precipitating factors, since in the majority of vitiligo cases the contributing factors are as yet unidentified.
Copper and its alloys are subject to chemical reactions on exposure to environmental or physiological factors, whereby products are potentially generated which become diffusible through mammalian skin. The chemistry of oxidation is reviewed as well as the factors contributing to corrosion. Skin exudates (sweat and sebum) can react with metal surfaces they come in contact with, but even in the healthy organism their composition is variable, as a function of physical, pharmacological and environmental conditions, gender, age, sweat rate or body site. This overview addresses sweat and sebum composition, and discusses components which determine the skin’s corrosive action: chloride ion, low-molecular-weight acids and amino acids in sweat, and fatty acids in sebum, which hold the potential to solubilize copper-containing metal objects. These components can form copper salts and soaps whose molecular characteristics (size and polarity) will determine the rate and route of cutaneous penetration.
Nitric oxide (NO) is a potent biological mediator that can be produced in wounds by activation of inducible nitric oxide synthase (iNOS). Its presence appears to be beneficial to the healing process by promoting vasodilation and boosting both migration and synthetic activity of fibroblasts. Chronic leg ulcers differ from acute experimental wounds because the connective tissue and microvascularization of the ulcer bed are strikingly remod elled in chronic wounds. In addition, a critical bacterial colonization from the environment is also often present, and with deleterious effects. As such, NO release in leg ulcers may prove to be beneficial by improving the microvasculature and fibroblast functions, and by its antimicrobial effect. However, any excess in NO could become cytotoxic for keratinocytes, thus impeding re- epithelialization. Furthermore, chronic NO release could be involved in the cancerogenesis process leading to Marjolin ulcer. In conclusion, NO induced by environment factors mediates contrasted effects in wound healing that may be beneficial or detrimental for the patient.
