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Photosensitivity represents an increased inflammatory reaction to sunlight, which can be observed particularly in the autoimmune disease lupus erythematosus. Cutaneous lupus erythematosus (CLE) can be provoked by ultraviolet (UV) radiation and can cause both acute, nonscarring and chronic, scarring skin changes. In systemic lupus erythematosus, on the other hand, provocation by UV radiation can lead to flare or progression of systemic involvement. The etiology of lupus erythematosus is multifactorial and includes genetic, epigenetic and immunologic mechanisms. In this review, we address the effect of UV radiation on healthy skin and photosensitive skin using the example of lupus erythematosus. We describe possible mechanisms of UV-triggered immune responses that could offer therapeutic approaches. Currently, photosensitivity can only be prevented by avoiding UV exposure itself. Therefore, it is important to better understand the underlying mechanisms in order to develop strategies to counteract the deleterious effects of photosensitivity., (© 2024. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, ein Teil von Springer Nature.)

A man in his 50s was diagnosed with solar urticaria following monochromated light testing that demonstrated exquisite photosensivity to ultraviolet (UV) A, UV B (UVB) and visible light.Treatment options for this photodermatosis are limited; UVB phototherapy is one modality that can be appropriate in some patients. This is administered at very low doses in a controlled environment to induce skin hardening. 1 To self-treat his condition, the patient used a commercial sunbed on two occasions several days apart. He noted an immediate flare of solar urticaria after first use with associated dizziness. Following the second use, he felt generally unwell and was witnessed to lose consciousness and displayed jerky movements of his limbs while a passenger in a car. Investigations including a head MRI and an EEG were normal; an anoxic seizure caused by a flare of solar urticaria was later confirmed.Solar urticaria is a rare photodermatosis that is poorly understood and difficult to treat. The condition has a significant impact on the quality of life of patients. Severe cases can be associated with systemic symptoms that could be life-threatening., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2024. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Ultraviolet radiation can aggravate facial erythema in atopic dermatitis (AD) patients., Objective: To investigate the photobiological testing results of Chinese AD patients with refractory facial erythema., Methods: We conducted a retrospective analysis of 82 AD patients with refractory facial erythema who visited our department during 2004-2021. All of them completed phototesting and photopatch testing., Results: 82 patients were enrolled in the study, and 53 (64.6%) were between 18 and 30 years old. 51.2% (42/82) had positive phototesting results and were considered photosensitive AD (PhAD) patients. One-third of them were both allergic to ultraviolet A and ultraviolet B. 65.9% (54/82) suffered from photoallergic contact dermatitis. Chlorpromazine (50.7%), potassium dichromate (13.2%), and thimerosal (11.8%) were the top three common photoallergens. Overall, 86.3% of AD patients with refractory facial erythema had direct photoallergy or photocontact allergy. PhAD patients had fewer allergic comorbidities than the other group (p = .007). More non-PhAD patients (55.0%) suffered from AD at 2-14 years old (p = .015)., Conclusions: Photosensitivity contributes a lot to the facial lesions of AD patients, especially in their 20s. 86.3% of these patients had direct photoallergy or photocontact allergy. Therefore, AD patients with facial erythema should undergo phototesting and photopatch testing routinely., (© 2022 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Overexposure to ultraviolet B (UVB) rays can cause damage to the skin. Liquiritin has a variety of pharmacological effects, such as anti-inflammatory and antioxidant. In the present study, the effect of liquiritin on UVB irradiated rat skin was investigated. Results showed that UVB irradiation caused erythema and wrinkles on the skin surface, as well as thickening and loss of elasticity of the epidermis and a significant increase in the level of ROS in the skin tissue. At the same time, western blot detected an increase in nuclear factor kappa-B (NF-κB) and matrix metalloproteinases (MMPs) and Elisa also detected an increase in pro-inflammatory factors. Therefore, we hypothesized that UVB irradiation-induced damage is associated with inflammation. Interestingly, application of liquiritin to exposed skin of rats reduced the increase in ROS, pro-inflammatory factors, and MMPs caused by UVB irradiation and increased the levels of Sirtuin3 (SIRT3) and Collagen α1. In addition, after intraperitoneal injection of the SIRT3 inhibitor 3-TYP in rats, the protective effect of liquiritin against UVB damage was found to be diminished. These results suggested that promotion of SIRT3 with liquiritin inhibits UVB-induced production of pro-inflammatory mediators, possibly acting through the SIRT3/ROS/NF-κB pathway. In conclusion, this study suggests that liquiritin is an effective drug candidate for the prevention of UVB damage., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Phytophotodermatitis is a cutaneous reaction that occurs after exposure to plant-derived furocoumarins and ultraviolet A light. Psoralen is the most common phototoxic furocoumarin and is present in varying levels within many different plant species. This article focuses on the diagnosis and management of psoralen-induced phytophotodermatitis along with other clinical applications., Competing Interests: The authors have no funding or conflicts of interest to declare., (Copyright © 2020 American Contact Dermatitis Society. All Rights Reserved.)

Solar urticaria has unique spectra, such as inhibition and augmentation. The clinical significance of these spectra, especially augmentation, is not well understood. Reported cases of solar urticaria with augmentation spectra are extremely rare in the published English-language work. The purposes of this study were to evaluate the clinical features of solar urticaria with augmentation spectra and to elucidate the mechanisms and clinical importance of the spectra. We experienced 11 cases (five females, six males; mean age, 40.1 years; range, 1-74) of solar urticaria with augmentation spectra from April 2007 to July 2019. Augmentation spectra were UV-B in three cases, UV-A in two, visible light in four, UV-A and UV-B in one, and UV-A and visible light in one. Augmentation spectra were observed before action spectra in four cases, after in six, and before and after in one. Injection of sera irradiated with action spectra and augmentation spectra in vitro induced stronger immediate reactions than those of only action spectrum-irradiated sera in four of five cases. The results of injection tests suggested that augmentation spectra enhance the production of urticaria-forming factor. Clinically, we observed severe urticarial reactions in four cases, including anaphylaxis in three and moderate urticarial reactions in three. These results suggest that augmentation spectra are not as rare as previously thought and that they are associated with the severity of solar urticaria. Therefore, phototesting for both augmentation and action spectra should be performed to provide appropriate guidance for patients with solar urticaria., (© 2020 Japanese Dermatological Association.)

UVB-induced skin damage is attributable to reactive oxygen species, which are triggered by intracellular Ca 2+ signals. However, exactly how the reactive oxygen species are triggered by intracellular Ca 2+ upon UVB irradiation remains obscure. Here, we show that UVB induces Ca 2+ signals via sequential generation of the following Ca 2+ messengers: inositol 1,4,5-trisphosphate, nicotinic acid adenine dinucleotide phosphate, and cyclic ADP-ribose. UVB induced H 2 O 2 production through NADPH oxidase 4 activation, which is downstream to inositol 1,4,5-trisphosphate and nicotinic acid adenine dinucleotide phosphate. H 2 O 2 derived from NADPH oxidase 4 activated CD38 to produce cyclic ADP-ribose. UVB first evoked the pannexin channel to release ATP, which acts on P2X7 receptor to generate inositol 1,4,5-trisphosphate. Inhibitors of these messengers, as well as antioxidants, blocked UVB-induced Ca 2+ signals and IL-1β secretion in keratinocytes. Furthermore, ablation of CD38 and NADPH oxidase 4 protected against UVB-induced inflammation and IL-1β secretion in the murine epidermis. These results show that UVB induces IL-1β secretion through cross-talk between Ca 2+ and reactive oxygen species, providing insight towards potential targets against UVB-induced inflammation., (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)

Lupus erythematosus (LE) represents a spectrum of inflammatory autoimmune disease comprising varying clinical entities ranging from primary cutaneous to systemic disease. There is a clear relationship between ultraviolet irradiation (UVR) and the clinical manifestations of LE in both adult and pediatric populations. Although it has been established that UVR exacerbates pre-existing LE, it remains unclear whether UVR induces the development of the disease. This review serves to discuss effective photoprotective measures in LE and describe the pathogenic relationship of UVR and LE.

Chemical substances that induce an allergic response in skin upon contact are called skin allergens or sensitizers, while chemical substances that elicit an allergic response only in presence of light are called photoallergens or photo sensitizers. The Direct Peptide Reactivity Assay (DPRA, OECD N⁰ 442C, 2015) and the Amino Acid Derivative Reactivity Assay (ADRA) are in chemico assays used to discriminate between allergens and non-allergens. The DPRA and the ADRA, respectively, monitor the depletion of model peptides and modified amino acids induced by crosslinking with test chemicals. In the current study we compared these two assays and analyzed their suitability to predict skin sensitization potential of several chemical substances.  In order to study the combined effect of a chemical compound and UV light, we modified DPRA (photo-DPRA) as well as ADRA (photo-ADRA) by introduction of a photo-irradiation parameter. Analysis using photo-DPRA and photo-ADRA correctly distinguished known photoallergens from non-photoallergens. Upon irradiation, photoallergens selectively showed higher depletion of model peptides or modified amino acids. Thus, photo-DPRA and/or photo-ADRA can serve as non-animal in vitro methods for the identification and assessment of photoallergens/ photosensitizers.

Excess ultraviolet (UV) radiation causes numerous forms of skin damage. The aim of the present study was to assess and compare the photoprotective effects of cyanidin-3- O-glucoside (C3G) alone and encapsulated in chitosan nanoparticles (Nano-C3G) in a UVB-induced acute photodamage mouse model. Nano-C3G was developed from chitosan and sodium tripolyphosphate (TPP) by ionic gelation. The particle size, zeta potential, entrapment efficiency, drug loading, and in vitro release in 6 days were determined. Kunming (KM) mice were treated with Nano-C3G (125, 250, 500 μM) or C3G (500 μM) after part of the dorsal skin area was dehaired and then exposed to 2 J/cm 2 of UVB. The nanocapsules were successfully produced and had a uniform and complete spherical shape without agglomeration. The size, zeta potential, entrapment efficiency, and drug loading of Nano-C3G was 288 nm, +30 mV, 44.90%, and 4.30%, respectively. C3G in the nanocapsules was released quite rapidly, and the release rate slowed down at higher pH. The animal experiment demonstrated that Nano-C3G could effectively reduce the UVB-induced lipid peroxidation, malondialdehyde, and 8-hydroxy-2'-deoxyguanosine contents; downregulate p53, Bcl-2-associated X (Bax), and caspase-3 and -9 expression; and balance the B-cell lymphoma-2/leukemia-2 ratio. Moreover, Nano-C3G (125, 250, 500 μM) improved the visual appearance, skin moisture, histologic appearance, and apoptotic index (based on TUNEL staining) under UVB exposure. In conclusion, these results suggest that Nano-C3G can reduce UVB-induced epidermal damage through the p53-mediated apoptosis signaling pathway. Moreover, Nano-C3G was more efficient than C3G at the same concentration (500 μM).

Polymorphous light eruption (PLE) is the commonest immuno-mediated photodermatosis. It occurs after solar or artificial UV-light exposure and affects only the sun-exposed areas with preference of the V-area of the chest, of arms and forearms, legs, upper part of the back, and rarely the face. The lesions are itching or burning, and vary morphologically from erythema to papules, vesico-papules and occasionally blisters, plaques, sometimes erythema multiforme-like, insect bite-like wheals and purpura. The clinical manifestations befall within a few hours to days from light exposure, last a few days, and subside in about a week without sequelae. Its diagnosis is based on history, morphology and phototests. PLE is considered as a delayed hypersensitivity response to newly UV induced, but still unidentified, antigen(s). Usually, MED is normal, but the provocative phototests with UVA or UVB reproduce the spontaneous lesions in about 50% of the patients. Broad spectrum sunscreens and antioxidants, photohardening with PUVA or narrow band UVB may be beneficial to prevent the disease. Therapy is based mainly on topical or systemic corticosteroids.

Skin colour (specifically in relation to its melanin content and composition) has a marked influence on its interaction with ultraviolet light. Eumelanin has mainly photoprotective properties while pheomelanin has the ability to cause formation of reactive oxygen species. This difference is responsible for the difference in incidence and presentation of various idiopathic photodermatoses in dark skinned patients compared to those with lighter skin types. Certain conditions are peculiar to darker skins including pin point popular variant of polymorphous light eruption. These differences are discussed in this chapter while also highlighting the challenges faced in performing phototesting in patients with dark skin.

The cytokine TNF-like weak inducer of apoptosis (TWEAK) and its receptor Fn14 are involved in cell survival and cytokine production. The TWEAK/Fn14 pathway plays a role in the pathogenesis of spontaneous cutaneous lesions in the MRL/lpr lupus strain; however, the role of TWEAK/Fn14 in disease induced by ultraviolet B (UVB) irradiation has not been explored. MRL/lpr Fn14 knockout (KO) was compared to MRL/lpr Fn14 wild-type (WT) mice following exposure to UVB. We found that irradiated MRL/lpr KO mice had significantly attenuated cutaneous disease when compared to their WT counterparts. There were also fewer infiltrating immune cells (CD3 + , IBA-1 + and NGAL + ) in the UVB-exposed skin of MRL/lpr Fn14KO mice, as compared to Fn14WT. Furthermore, we identified several macrophage-derived proinflammatory chemokines with elevated expression in MRL/lpr mice after UV exposure. Depletion of macrophages, using a CSF-1R inhibitor, was found to be protective against the development of skin lesions after UVB exposure. In combination with the phenotype of the MRL/lpr Fn14KO mice, these findings indicate a critical role for Fn14 and recruited macrophages in UVB-triggered cutaneous lupus. Our data strongly suggest that TWEAK/Fn14 signalling is important in the pathogenesis of UVB-induced cutaneous disease manifestations in the MRL/lpr model of lupus and further support this pathway as a possible target for therapeutic intervention., Competing Interests: The authors report no conflicts of interest., (© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Purpose: To report a mass presentation of photokeratitis arising from exposure to an unprotected ultraviolet-B (UV-B) light source., Results: A cluster of 22 patients presented within a 24-h period to a single eye casualty with symptoms of photokeratitis following recent intense UV-B exposure at a local nightclub. Patients were treated with a short course of chloramphenicol, steroid or lubricant eye drops. No patients re-attended., Conclusion: This report highlights the hazards of ultraviolet lamps used in public places and the need for strict guidance and enforcement of UV radiation safety protocols to avoid the potential public health risk., (Copyright © 2016 British Contact Lens Association. Published by Elsevier Ltd. All rights reserved.)

The healing properties of sunlight has been known for millennia, however the gradual deterioration of the ozone layer and the increased use of sun tanning beds in recent decades are causing an increase in skin damaging ultraviolet exposure. In this article the most common photodermatoses and the principles of their treatments are reviewed.

Nucleotide excision repair (NER) protects against sunlight-induced skin cancer. Defective NER is associated with photosensitivity and a high skin cancer incidence. Some clinical treatments that cause photosensitivity can also increase skin cancer risk. Among these, the immunosuppressant azathioprine and the fluoroquinolone antibiotics ciprofloxacin and ofloxacin interact with UVA radiation to generate reactive oxygen species that diminish NER capacity by causing protein damage. The replication protein A (RPA) DNA-binding protein has a pivotal role in DNA metabolism and is an essential component of NER. The relationship between protein oxidation and NER inhibition was investigated in cultured human cells expressing different levels of RPA. We show here that RPA is limiting for NER and that oxidative damage to RPA compromises NER capability. Our findings reveal that cellular RPA is surprisingly vulnerable to oxidation, and we identify oxidized forms of RPA that are associated with impaired NER. The vulnerability of NER to inhibition by oxidation provides a connection between cutaneous photosensitivity, protein damage, and increased skin cancer risk. Our findings emphasize that damage to DNA repair proteins, as well as to DNA itself, is likely to be an important contributor to skin cancer risk.

Pseudoporphyria refers to a rare bullous dermatosis characterized by the clinical and histological features of porfiria cutanea tarda without abnormalities in porphyrin metabolism. The pathogenesis is heterogeneous and several exogenous factors may promote the bullous lesion formation, including medications, end stage renal disease, dialysis and tanning beds. Regarding treatment of this condition, in literature different therapy have been reported, such as glutathione and his precursor N-acetylcysteine, which presents anti-oxidant properties; however even more toxic drugs, such as chloroquine, are used. Moreover, in patients with drug-induced PP discontinuation of the offending agent, if possible, is a crucial aspect of the clinical management. We report two cases of dialysis patients presenting blisters on extremities, which healed with the avoidance of UV exposure and oral Vitamin D supplementation. Interestingly Vitamin D despite the lack of antioxidant properties led to a completely resolution of PP in both our patients within 30 days. A possible explanation of this finding is that Vitamin D, playing a key role in the regulation of serum Ca2+, can modulated cadherin-cadherin interactions and led to healing of pseudoporphyria bullous lesions. Finally we highlight the prominent role of UV-exposure in PP elicitation thus a good photoprotection is essential for all patients with pseudoporphyria.

Background: Skin is exposed to various abiotic and biotic factors. Solar radiation, of which ultraviolet (UV) rays are a principle component, increases the free radical load, and the accumulation of reactive oxygen species (ROS) causes lipid peroxidation, DNA damage and apoptosis, and is also associated with inflammatory responses recruiting molecules [nuclear factor (NF)-κB, interleukin (IL)-6] that can potentially further aggravate the damaged milieu of the cells. One of the potent causes of skin cancers is exposure to UV rays. UV radiation generates a wide range of biological responses such as adaptive, inflammatory and immunological reactions in the skin., Objective: To examine the effects of pretreatment with melatonin on UVB (290-320 nm) radiation-mediated damage to the skin of a diurnal rodent Funambulus pennanti., Results: The UVB radiation (1·5 J cm(-2) for 30 min daily on the shaved abdominal area) for 4 days caused a significant increase in the lipid peroxidation products (thiobarbituric acid reactive substances, TBARS) and decreased the activity of the antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) of the skin. Pretreatment with melatonin (100 μg 100 g(-1) bodyweight subcutaneously) improved the damage induced by UVB radiation on the skin and might act via a receptor-independent mechanism. No significant effect of melatonin pretreatment was found on the expression pattern of MT1 (melatonin membrane receptor) and RORα (nuclear retinoic orphan receptor alpha), which suggests a receptor-independent action. However, NF-κB and inflammatory cytokine IL-6 levels were downregulated in the squirrels pretreated with melatonin before the UVB radiation., Conclusion: UVB radiation induced oxidative stress in the skin culminating in an inflammatory response. The action of melatonin in protecting the skin from oxidative damage occurs in a receptor-independent manner by lowering the oxidative damage and inflammatory response. On the other hand, melatonin decreased the expression of NF-κB and the circulating proinflammatory cytokine IL-6, suggesting an anti-inflammatory action in protecting the skin from UVB radiation., (© 2014 British Association of Dermatologists.)

Actinic prurigo is a chronic photodermatosis with onset in childhood or before 20 years of age. It is most prevalent in Amerindians and Latin American mestizos, although it has been reported worldwide. Patients present with photodistributed, erythematous excoriated papules, cheilitis, and conjunctivitis. There is strong association with human leukocyte antigen DR4, especially the DRB1*0407 subtype. Treatment consists of photoprotection and the use of thalidomide., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Polymorphous light eruption is an immunologically mediated photodermatosis with high prevalence, particularly among young women in temperate climates, characterized by pruritic skin lesions of variable morphology, occurring in spring or early summer on sun-exposed body sites. A resistance to ultraviolet radiation (UVR)-induced immunosuppression and a subsequent delayed-type hypersensitivity response to a photoantigen have been suggested as key factors in the disease. Molecular and immunologic disturbances associated with disease pathogenesis include a failure of skin infiltration by neutrophils and other regulatory immune cells on UVR exposure linked to a disturbed cytokine microenvironment. Standard management is based on prevention., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Photoaggravated skin disorders are diseases that occur without UV radiation but are sometimes or frequently exacerbated by UV radiation. In conditions, such as lupus erythematosus, photoaggravation occurs in a majority of patients, whereas in conditions, such as psoriasis and atopic dermatitis, only a subset of patients demonstrate photoaggravation. Polymorphous light eruption is a common photodermatosis in all skin types, making it important to differentiate photoaggravation of an underlying disorder, such as lupus erythematosus, from superimposed polymorphous light eruption. Disease-specific treatments should be instituted where possible. A key component of management of photoaggravated conditions is photoprotection with behavioral change, UV-protective clothing, and broad-spectrum sunscreen., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Solar urticaria is an uncommon condition characterized by erythema and whealing shortly after exposure to ultraviolet (UV) and/or visible light. We report a 25-year-old woman with an erythematous, edematous, pruritic reaction minutes after sun exposure while she was taking terbinafine for onychomycosis. Phototesting revealed a UVB-sensitive urticarial reaction, confirming the diagnosis of solar urticaria. This report describes the first patient with possible terbinafine-associated solar urticaria.

Background: Chronic actinic dermatitis is a photosensitivity disorder with scant epidemiologic data. Case series in Europe have previously shown that improvement or resolution of chronic actinic dermatitis occurs over time in most patients. However, the natural history of chronic actinic dermatitis in patients in the United States has not been studied., Objective: To study the natural history of chronic actinic dermatitis in patients in the United States., Methods: We performed a retrospective chart review and telephone questionnaire after a 3- to 19-year follow-up period., Results: Of 20 patients with chronic actinic dermatitis, 7 patients (35%) experienced resolution and an additional 11 patients (55%) experienced improvement of their photosensitivity to sunlight during the follow-up period. The proportion of patients experiencing improvement or resolution of their chronic actinic dermatitis increased at 5, 10, and 15 years after diagnosis., Conclusions: Our study demonstrates that abnormal photosensitivity to sunlight in chronic actinic dermatitis improves or resolves over time in most patients in New York. The rates of improvement or resolution in our patients in New York are similar to the rates in case series in Europe despite likely patient demographic differences.

Background: A preliminary investigation showed that ultraviolet radiation (UVR) emissions from compact fluorescent lamps (CFLs) can pose a risk to the skin of photosensitive individuals., Objectives: To carry out a larger-scale study, in patients with a range of photodermatoses, to assess this risk. To determine a safe alternative light source for photosensitive individuals. To investigate if CFL emissions have the potential to induce skin responses in normal individuals., Methods: Two hundred patients were directly exposed to a single-envelope CFL as part of their routine management. Irradiation was carried out on the inner forearm with lamps positioned at 5 cm. Skin assessments were made immediately and 24 h postirradiation. Eleven of these patients were further tested to a double-envelope CFL. One hundred and one patients were tested to emissions from a light-emitting diode (LED). A study involving 20 healthy individuals was carried out with exposure to the single-envelope CFL., Results: Skin erythema was induced by the single-envelope CFL in the following cases: 16 of 53 chronic actinic dermatitis, seven of 52 polymorphic light eruption, five of nine solar urticaria, one of two actinic prurigo, one of one erythropoietic protoporphyria and two of 20 healthy subjects. The double-envelope CFL eliminated or reduced the skin response in all 11 patients tested. The LED did not induce any UVR-provoked skin responses., Conclusions: UVR from CFLs can aggravate the skin of photosensitive and healthy individuals when situated in close proximity. Double-envelope lamps reduce this risk. LEDs offer a safer alternative light source that eliminates the risk of UVR-induced skin erythema., (© 2013 British Association of Dermatologists.)

Background: The principal risk factor for development of skin cancers is exposure to ultraviolet (UV) radiation. The universal solar UV index (UVI) consists of a simple measurement of UV radiation at the earth's surface, which provides an indicator of the risk of skin lesions in the absence of protective measures and taking into account individual phototype. The UVI is recommended by the WHO and is used to educate populations about the need to take protective measures in the event of exposure to UV radiation. There have been very few studies to assess understanding of this index, and these have been conducted primarily among the general population. Our study assesses understanding and use of the UVI among dermatologists in metropolitan France., Materials and Methods: This survey was conducted in December 2011 among 400 randomly selected French dermatologists. The questions asked concerned their personal and professional knowledge and their use of the UVI., Results: We analysed 165 (41.5%) of the answers. The UVI was known to 79% of the dermatologists questioned. Less than one third of dermatologists knew the key values in the UVI. Less than half of the dermatologists aware of the UVI reported acting upon the values in question. Only 12.1% of the dermatologists said that they used the index in their communication concerning prevention of sunburn., Discussion: The results of our study show that the UVI is poorly known and not very widely used among dermatologists in France. This index, readily understood by anyone, could be incorporated by dermatologists in their prevention messages concerning solar radiation and it could be used throughout the year, particularly in target populations such as schoolchildren and children taking part in outdoor sports., (Copyright © 2012 Elsevier Masson SAS. All rights reserved.)

Excessive exposure to solar or artificial sources of UV radiation is deleterious to the skin and can cause or worsen several diseases. Detrimental effects of UV radiation exert an important role in the development of skin cancers, cause alterations on the immune response, and act as a trigger or aggravating factor for pigmentary disorders. A group of measures, including education, change of habits, use of physical barriers and sunscreens constitutes a significant part of the treatment of many skin disorders and are valuable preventive tools. This article summarizes the relevant studies addressing these issues, emphasizing the many aspects of photoprotection., (Copyright © 2012 Elsevier Masson SAS. All rights reserved.)

Erythropoietic protoporphyria arises from an inherited disorder of porphyrin metabolism which leads to an accumulation of protoporphyrin IX in the erythropoietic system and other tissues. It is characterized by cutaneous photosensitivity, usually difficult to keep under control. Among the scant therapeutic options proposed to reduce photosensitivity in erythropoietic protoporphyria, narrow-band UVB phototherapy has occasionally been used to induce sunlight tolerance. We report an adult case of erythropoietic protoporphyria with a severe photosensitivity treated with narrow-band UVB that developed an appropriate sunlight phototolerance, without adverse events during phototherapy., (© 2012 John Wiley & Sons A/S.)

Solar ultraviolet (UV) radiation reaching the earth is a combination of UVB (290-320 nm) and UVA (320-400 nm) wavelengths. Since UVA is less energetic than UVB, UVB has long been thought to be the factor responsible for the damaging effects of solar radiation. But with modern tools such as in vitro models, it has been proven that UVA plays a major role. The objective of this review is to show how skin may be exposed to UV light and to highlight the clinical aspects of UV-induced skin damages with the respective contribution of UVB or UVA. Even if UVA is less energetic than UVB, it is more abundant and penetrates deeper into the skin, reaching as far as the dermis. Various factors also influence skin exposure to UV light: the latitude, season, and time of the day. Acute as well as chronic sun exposure induces short- and long-term clinical damages. Erythema and pigmentation are immediate responses of normal human skin exposed to UV radiation. The long-term effects are photoaging and photocarcinogenesis. In particular, UVA appears to play a major role in the deterioration of dermal structure leading to the photoaged appearance of the skin.

A number of skin conditions are characterised by photosensitivity to UVA. Some of these are exclusively UVA-mediated conditions, while others include UVA in the action spectrum which also include UVB and/or visible light. This review aims to describe this diverse range of conditions for non-dermatologist scientists with an interest in this topic. As such, clinical details, including treatments, are brief and succinct. Recent advances in understanding the pathogenesis of these conditions is highlighted., (This journal is © The Royal Society of Chemistry and Owner Societies 2012)

Interactions with ultraviolet radiation (UVR) and chromophores in the skin happen on a daily basis. Photodermatoses, which are abnormal responses to UV exposure, can be classified into subgroups based on pathogenesis. This review will discuss the clinical features, pathogenesis, photobiologic evaluation, prognosis and therapies of the most common photodermatoses., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Systemic photosensitivity due to the intake of plants or herbal compounds is a rare phenomenon. Goji berries are widely used as a well-being and anti-aging remedy. In spite of this, only a few adverse reactions and no cases of photosensitivity have been reported to date. A 53-year-old male consulted due to a pruriginous eruption located on sun-exposed areas of 2 weeks of duration. He had been taking Goji berries and infusions of cat's claw herb for 5 and 3 months, respectively. Minimal erythema dose for UVB (MED-UVB) was diminished when the patient was taking these products, and became normal when they were withdrawn. Photoprovocation tests with Goji berries and cat's claw were performed. MED-UVB decreased after the intake of Goji berries, and was normal with cat's claw. We report the first case of systemic photosensitivity due to Goji berries., (© 2011 John Wiley & Sons A/S.)

Aim: Idiopathic photodermatoses (IP) are a recurrent, acquired sunlight-induced rash of delayed onset, appearing after exposure to ultraviolet radiation in susceptible individuals. The aim of this study was to assess the photoprotective activity of polypodium leucotomos (PL) in IP., Methods: Fifty-seven patients affected by IP were recruited for the study (53 with polymorphic light eruption and 4 with solar urticaria). The use of UV protection filters or other drugs that could in some way interfere with exposure to light were excluded. All patients exposed themselves to sunlight while consuming 480 mg/day of PL extract orally. A statistical evaluation of the basal clinical conditions compared to those after sunlight exposure with PL was performed., Results: About 73.68% of the patients had a benefit from the administered PL, with a significant reduction of skin reaction and subjective symptoms. No side effects were observed. Results were statistically significant (P<0.05)., Conclusion: PL complete absence of toxicity combined with its multifactorial protection, makes it an effective and safe treatment for photoprotection in IP.

Hyperpigmented fixed eruption is a phenomenon usually related with drug antigens, and known as fixed drug eruption. A woman had a skin condition with clinical and histopathologic indications of fixed drug eruption. The disease first appeared when she went to a swimming pool and left with hyperpigmented macules. Previously affected skin reactivated on three other occasions when she again visited swimming pools. Sunlight involvement (UVA-UVB) was demonstrated through phototests. Sunlight should be considered as a cause of fixed drug-like eruption and a possible cause of some cases of FDE without any apparent etiological factor., (© 2010 The International Society of Dermatology.)

Genotoxic stress triggers the p53 tumor suppressor network to activate cellular responses that lead to cell cycle arrest, DNA repair, apoptosis or senescence. This network functions mainly through transactivation of different downstream targets, including cell cycle inhibitor p21, which is required for short-term cell cycle arrest or long-term cellular senescence, or proapoptotic genes such as p53 upregulated modulator of apoptosis (PUMA) and Noxa. However, the mechanism that switches from cell cycle arrest to apoptosis is still unknown. In this study, we found that mice harboring a hypomorphic mutant p53, R172P, a mutation that abrogates p53-mediated apoptosis while keeping cell cycle control mostly intact, are more susceptible to ultraviolet-B (UVB)-induced skin damage, inflammation and immunosuppression than wild-type mice. p53(R172P) embryonic fibroblasts (MEFs) are hypersensitive to UVB and prematurely senesce after UVB exposure, in stark contrast to wild-type MEFs, which undergo apoptosis. However, these mutant cells are able to repair UV-induced DNA lesions, indicating that the UV hypersensitive phenotype results from the subsequent damage response. Mutant MEFs show an induction of p53 and p21 after UVR, while wild-type MEFs additionally induce PUMA and Noxa. Importantly, p53(R172P) MEFs failed to downregulate anti-apoptotic protein Bcl-2, which has been shown to play an important role in p53-dependent apoptosis. Taken together, these data demonstrate that in the absence of p53-mediated apoptosis, cells undergo cellular senescence to prevent genomic instability. Our results also indicate that p53-dependent apoptosis may play an active role in balancing cellular growth.

Cutaneous lupus erythematosus (CLE) is a heterogeneous autoimmune disease involving well-defined skin lesions that can be categorized as acute CLE (ACLE), subacute CLE (SCLE), chronic CLE (CCLE), or intermittent CLE (ICLE). It is commonly accepted that ultraviolet (UV) exposure can induce and exacerbate skin lesions in patients with certain subtypes of CLE. Phototesting with UVA and UVB irradiation using a standardized protocol has proven to be a reliable model to study photosensitivity in CLE and to analyse the underlying pathomechanisms of the disease. In addition to UV-mediated induction of apoptosis, the molecular and cellular factors that may underlie the abnormal long-lasting photoreactivity in CLE include mediators of inflammation such as cytokines and chemokines, inducible nitric oxide (NO) synthase (iNOS), and cellular adhesion molecules. The photosensitivity associated with CLE requires education of the patient about avoidance of excessive sun exposure, continuous photoprotection through physical measures such as protective clothing, and daily application of broad-spectrum sunscreens. Novel approaches to UV-protection, such as alpha-MSH or thymidine dinucleotides, might also have an impact on photosensitivity in patients with CLE. In this review, we summarize the current knowledge about photosensitivity in patients with CLE, including an overview of standardized phototesting procedures, possible molecular pathomechanisms, and photoprotection.

(+) and (-) alpha-methylene-hexahydrobenzofuranone derivatives with a stereochemically pure cis ring junction were used as models of sesquiterpene lactones to study their photoreactivity toward thymidine. After 313 nm irradiation of a deoxygenated acetone solution of lactone models and thymidine, six [2+2] photoadducts were isolated for each enantiomer and fully characterized by a combination of NMR experiments. A common syn regioselectivity and exo stereoselectivity were observed for photoadducts. This high photoreactivity of alpha-methylene-gamma-butyrolactone ring toward thymidine could be an explanation of the progressive evolution of allergic contact dermatitis toward chronic actinic dermatitis.

Patients with photosensitive dermatologic and systemic diseases often question the ultraviolet light (UVL) output of household lighting sources. Such individuals have increasing concern about potential UVL exposure from energy-efficient compact fluorescent lamps (CFL), as little data have been presented concerning their UVL output. The objective was to compare, via pilot study, the levels of ultraviolet A (UVA) and ultraviolet B (UVB) leak between residential lighting sources. Equivalent wattage CFL, incandescent and halogen bulbs were purchased from local retailers in Oklahoma City, Oklahoma, USA. The UVA and UVB outputs of these sources were measured under controlled conditions at 10, 25, 50, 100 and 150 cm away from the light source using an IL-1700 research radiometer equipped with UVA and UVB detectors. Negligible UVB and UVA was detected at 100 and 150 cm. Therefore, data were analysed from measurements at 10, 25 and 50 cm only. The results demonstrated UVA leak highest from incandescent and halogen bulbs, and UVB leak highest from CFL. The overall UVA/UVB leak was lowest from CFL shielded during the manufacturing process. In conclusion, patients with photosensitivity have choices depending on their relative risk from different UVL wavelength spectra. UVB exposure risk may be reduced the greatest by utilising CFL with manufacturer-provided shields.

An abnormal immune response has long been thought responsible for the patho-aetiology of polymorphic light eruption, the most common photodermatosis. Recent evidence indicates that polymorphic light eruption patients are resistant to the immune suppressive effects of sunlight, a phenomenon that leads to the formation of skin lesions upon seasonal sun exposure. This immunological abnormality in polymorphic light eruption supports the concept of the biological significance and evolutionary logic of sunlight-induced immune suppression, i.e. the prevention of immune responses to photo-induced neo-antigens in the skin, thereby preventing autoimmunity and skin rashes. This article focuses on the immunological alterations in polymorphic light eruption and the pathogenic significance to the disease state and skin carcinogenesis.

Polymorphous light eruption is the most common photodermatosis, with a prevalence of as high as 10-20% in Western Europe and in the USA. It starts during the second and third decades of life. Although not life-threatening it can severely impair the quality of life, in particular during leisure activities and in outdoors workers. Polymorphous light eruption belongs to the group of so-called idiopathic photodermatoses. This term denotes dermatoses that occur in otherwise healthy individuals from exposure to sunlight or artificial light without the intervention of an exogenous photosensitizing agent. These diseases have two factors in common: they are precipitated by ultraviolet or visible radiation; and their exact pathomechanism remains obscure but is presumably immunologic in nature.