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PubMed1978

Tinea faciei.

A 62-year-old man had a long-standing fungal infection of the face. The eruption had been treated as a photosensitivity disorder for 22 years. A literature review revealed only 35 reported cases classified as tinea faciei, most of which also were misdiagnosed originally. Pertinent clinical findings include facila erythema, pruritus, and scaling patches with arcuate or annular borders. The most common organisms isolated with Trichophyton rubrum or T mentagrophytes. To our knowledge, this unique case represents the longest duration of Tinea faciei.

Chronic Disease↗
PubMed1999

Carotenoids and human health.

After the discovery of vitamin A in 1913, the yellow pigments of fruits and vegetables were soon implicated as compounds with similar nutritional effects. beta-Carotene was shown to be converted into vitamin A by Moore in 1929, and the chemical structures of both vitamin A and beta-carotene were determined two years later. Thus, the sole function of beta-carotene in human health was considered to be its conversion into vitamin A. On the basis of observational epidemiologic studies, conducted in the mid-1970s, however, carotenoids were implicated as protective agents, first against lung cancer and then against a variety of other chronic diseases. Intervention trials employing beta-carotene, however, either have shown no preventive effect or indeed, in two cases, have enhanced the incidence of lung cancer in middle-aged male smokers and asbestos workers. The possible protective action of carotenoids can be attributed to their properties as singlet oxygen quenchers and as antioxidants, whereas their cancer-enhancing actions in lung can be ascribed to the prooxidant action of carotenoid free radicals in damaged cells. Apart from chronic diseases, beta-carotene has shown significant therapeutic value in individuals suffering from photosensitivity disorders and provides temporary relief to persons afflicted with leukoplakia. A part from a medical context, the colored carotenoids found in many living organisms and in many foods delight both the eye and the palate. Thus, human health and the enjoyment of life are greatly benefited by the presence of these interesting pigments in nature, whether or not they ultimately prove to have more specific protective effects against chronic diseases.

Antioxidants↗
PubMed1989

Adverse effects of sunscreens in photosensitive patients.

Experimental and epidemiological evidence shows that the common photosensitive disorder of polymorphic light eruption is caused by the ultraviolet A component of sunlight. Sunscreens protect mainly against ultraviolet B; consequently they reduce sunburn and allow longer periods of exposure to the sun and to greater doses of ultraviolet A than would otherwise be possible. Patients with polymorphic light eruption who intend to obtain a tan by sunbathing should not, therefore, be treated with sunscreens which may worsen their rash, but should be advised to sunbathe without sunscreens for a shorter time.

Disease Susceptibility↗
PubMed1980

Erythropoietic protoporphyria.

Erythropoietic protoporphyria (EPP) is an inherited photosensitivity disorder producing mild to severe symptoms and attributable to an excessive amount of endogenous protoporphyrin accumulating in body tissues. Following sun exposure, the symptoms are burning pain, edema, erythema, vesicles, and bullare, which at times are hemorrhagic. This condition was first described in 1961. However, some patients previously diagnosed as having solar urticaria, lipoid proteinosis, or hydroa aestivale because of their clinical features ae now known to have EPP. Porphyrins are biochemical intemediates in the synthesis of heme, a moiety that occurs in all living cells and is a basic requirement for aerobic and anaerobic metabolism.

Child↗
PubMed2002

Evaluation of the role of contact sensitization and photosensitivity in the pathogenesis of poikiloderma of Civatte.

BACKGROUND: Poikiloderma of the face and neck (Civatte) is a rather common, indolent, chronic dermatosis, most often affecting menopausal females. Cumulative excessive sun exposure, a phototoxic or a photoallergic reaction, hormonal changes of menopause and genetic factors have all been incriminated in its obscure aetiopathogenesis. OBJECTIVE: To evaluate the role of contact sensitization and photosensitivity in the pathogenesis of poikiloderma of Civatte (PC). METHODS: Thirty-two patients (24 females and eight males, age range 38-74 years) with PC were patch tested with the European standard series and the fragrance series, and were photopatch tested with the photoallergens series. Additionally, photo-testing with a monochromator was performed. RESULTS: Thirteen of 32 patients (40.62%) had one or more positive reactions to allergens of the standard series. Eight patients (25%) had positive reactions to fragrance mix and/or Balsam of Peru, which are included in the standard series, or to allergens of the fragrance series. Nickel sulphate was the single most common cause of contact sensitization (18.75%) among our patients. Ninety-seven subjects, who were patch tested with the standard series for suspected allergic contact dermatitis of the face and/or neck, served as age, sex and site controls. Of these, nine (9.27%) had one or more positive reactions to fragrance compounds. Statistical analysis showed a statistically significant difference in the frequency of positive reactions to fragrances between the PC group and the control group (chi2 value = 3.91, P < 0.05). In contrast, none of the PC patients had a positive photopatch test for the allergens included in the photoallergens series. The estimated minimal erythemal dose for the PC group was in all cases within normal limits for all wavelengths of ultraviolet (UV) radiation examined. CONCLUSIONS: Contact sensitization, mostly to perfume ingredients, may develop in PC, possibly playing a pathogenetic part, at least in a subset of patients. Despite negative results of photopatch testing, an allergic photo-contact reaction cannot be definitely excluded. PC seems not to be a photosensitivity disorder of the type of chronic actinic dermatitis. UV radiation-induced dermal connective tissue changes are the predominant histological feature of PC, leading to telangiectasia due to loss of vascular support. Reticular pigmentation may result from a delayed hypersensitivity reaction to perfume and/or cosmetic ingredients. Patch testing with the standard series and avoidance of documented allergens may be of value in patients with PC.

Adult↗
PubMed2003

Treatment of polymorphic light eruption.

Polymorphic light eruption (PLE) is a highly prevalent photosensitivity disorder, estimated to affect 11-21% people in temperate countries. Typically, PLE appears as a recurrent pruritic eruption comprising papules and/or vesicles and/or plaques, which occurs on photo-exposed skin sites following sun exposure, and which heals without scarring. Commoner in females, the aetiology is uncertain, although there is evidence of an immune basis. We perform a review of the prophylaxis and treatment of this condition. While sun protection, corticosteroids and desensitization phototherapy are the mainstays of management, a range of anti-inflammatory and immunomodulatory agents are reported.

Adrenal Cortex Hormones↗
PubMed2001

Xeroderma pigmentosum--bridging a gap between clinic and laboratory.

Xeroderma pigmentosum (XP) is an autosomal recessive photosensitive disorder with an extremely high incidence of UV-related skin cancers associated with impaired ability to repair UV-induced DNA damage. There are seven nucleotide excision repair (NER) complementation groups (A through G) and an NER proficient form (XP variant). XPA, B, D and G patients may also develop XP neurological disease. The laboratory diagnosis of XP can be performed by autoradiography. Recently, the isolation and characterization of the genes responsible for XP have made it possible to use molecular biological techniques to diagnose XP patients, for carrier detection and for prenatal diagnosis, especially in Japanese XPA patients. These techniques include polymerase chain reaction (PCR) and plasmid host cell reactivation assays with cloned XP genes. DNA damage is not repaired by the NER system equally throughout the genome. There are two DNA repair pathways: 1) transcription-coupled repair, and 2) global genome repair. Many factors involved in these pathways are related to the pathogenesis of XP and a related photosensitive disease, Cockayne syndrome. Clinical management consists of early diagnosis followed by a rigorous program of sun protection including avoidance of unnecessary UV exposure, wearing UV blocking clothing, and use of sunblocks on the skin. Although there is no cure for XP, the efficacy of oral retinoids for the prevention of new skin cancers, local injection of interferon, and the external use of a prokaryotic DNA repair enzyme have been reported.

Cockayne Syndrome↗
PubMed1993

Determination of threshold UV-A elicitation dose in photopatch testing.

Photopatch testing, although widely used in the diagnosis of photosensitivity disorders, is not standardized. We performed this study to determine the threshold ultraviolet light A (UV-A) dose required to elicit photopatch test responses. 4 patients with previously positive tests were reexposed to the offending allergen, using an incremental dosage regime. Isopropyl dibenzoylmethane (Eusolex 8020), mexenone (benzophenone-10) and oxybenzone (benzophenone-3) produced positive responses at 1.0, 1.0 and 0.7 J/cm2, respectively. Responses to phenothiazines were deemed phototoxic. These results demonstrate that high doses of UV-A (e.g., 10-15 J/cm2) are unnecessary, and that 5 J/cm2 should become the current standard.

Adult↗
PubMed2002

Decreased photodamage and low incidence of non-melanoma skin cancer in 136 sun-exposed caucasian patients with vitiligo.

BACKGROUND: It is well established that ultraviolet radiation is related to non-melanoma skin cancer (NMSC) in Caucasians. Considering that patients with vitiligo have often no protective pigment in sun-exposed depigmented/white skin together with severe oxidative stress due to accumulation of millimolar epidermal hydrogen peroxide (H(2)O(2)), it would be expected that these patients develop a higher risk for early photodamage and NMSC. However, scattered reports on low patient numbers documented no increased risk for sun-induced skin cancers in this disease. OBJECTIVE: The aim of this study was to validate the possible photodamage and the development of epidermal neoplasia in a randomly selected larger patient group with emphasis on each patient's sun sensitivity and the history of solar habits. Furthermore we wished to compare histological signs for epidermal photodamage in a random representative patient group (mean age >30 years) and age-matched healthy controls. METHODS: One hundred and thirty-six randomly selected patients (females n = 93; males n = 43; mean age 42.4 years, range 14-70 years) were included in this study. To assess signs of photodamage and skin cancer, all patients underwent a thorough full-body examination by Wood's light and dermatoscopy. In order to learn about each patient's individual sun sensitivity and solar habits, a direct questionnaire was used. In addition full skin punch biopsies of sun-exposed depigmented/pigmented skin were taken under local anaesthesia and evaluated by light microscopy. RESULTS: There was no evidence for sun-related damage in the entire patient group, despite a significant number of positive cases with a history of sunburns in early childhood and continuous accumulation of epidermal H(2)O(2). Histological examination of the epidermis showed no signs of increased photo-ageing and confirmed the absence of apoptosis in these patients. Furthermore surprisingly there was no increased risk for photosensitivity disorders, i.e. polymorphous light reaction, solar urticaria and acute actinic dermatitis. CONCLUSION: The results of this study confirm in a large group of patients with vitiligo the absence of an expected high risk for sun-induced damage and skin cancer. Based on these results together with a recent report on increased functional wild-type p53 expression in these patients we would like to propose that in vitiligo there may be a direct association between this important tumour suppressor and the absence of photodamage and NMSC.

Adolescent↗
PubMed1995

The action spectrum for induction of chronic actinic dermatitis is similar to that for sunburn inflammation.

The action spectrum for induction of the abnormal cutaneous response at 24 h in the photosensitivity disorder chronic actinic dermatitis (CAD) was determined in 15 patients and found to be the same in shape as that for normal sunburn in fair-skinned individuals at 24 h, as determined for 47 control volunteers, although displaced in magnitude. This suggests that an endogenous chromophore(s), the same as or similar to that/those responsible for human sunburn, may be responsible for initiation of the abnormal reaction to irradiation in CAD, and that the putative antigen associated with the CAD reaction may be derived from that/those or associated molecules.

Aged↗
PubMed1992

Investigation of the photosensitive child.

Photosensitivity disorders in childhood frequently can be diagnosed and managed in the general dermatology clinic. Occasionally, when diagnostic doubt exists, referral to a specialist unit is required for diagnostic phototesting. Light testing equipment is fickle by nature, making such units uncommon. Phototesting using monochromator or provocation systems takes approximately 45 minutes. Immediate and delayed readings over the following 48 hours as appropriate are required to cover the diagnostic possibilities. Individual diseases are characterized by particular patterns of wavelength dependency and evolution of the abnormal response. Other investigations that may be required are autoantibodies to exclude lupus erythematosus, a porphyrin scan leading to full studies and, on occasion, cell mutation or survival, and chromosome studies for the rarer genophotodermatoses. Good investigative data frequently help clarify the common clinical variants.

Child↗
PubMed1995

Ambulatory monitoring of ultraviolet erythema in photosensitive subjects.

Little is known about whether patients with photosensitive disorders exhibit a different ultraviolet erythema time course from subjects with a normal response to sunlight. We have described the application of an instrument for ambulatory monitoring of the development of ultraviolet erythema by a reflectance method in a group of patients with chronic actinic dermatitis (CAD) and in a group of normal subjects. Investigations of the time course have been reported previously but the techniques used relied upon manual measurement. Consequently sampling frequencies have been considerably lower than the one-minute sample rate used here. We have not demonstrated any difference in the rate at which erythema develops and peaks between patients with CAD and subjects with a normal response to sunlight.

Adult↗
PubMed2003

The successful use of topical tacrolimus treatment for a chronic actinic dermatitis patient with complications of idiopathic leukopenia.

Chronic actinic dermatitis (CAD) is a photosensitivity disorder marked by severe eczematous lesions on exposed areas. Although associations with contact dermatitis, atopic dermatitis, and human immunodeficiency virus (HIV) have been suggested, its pathogenesis remains unknown. CAD is often refractory, and systemic administration of cyclosporin A has been the treatment of choice. Recently, topical tacrolimus therapy has been reported to be effective. We report the efficacy of topical tacrolimus treatment in a CAD patient who also had the complication of idiopathic leukopenia. A phototest showed marked suppression of erythema formation in the skin pre-treated with tacrolimus before UVB radiation but not in the skin treated after the irradiation. Therefore, it is suggested that tacrolimus may prevent UV-B induced erythema by suppressing a very early phase of the inflammatory process in CAD.

Administration, Cutaneous↗
PubMed2001

Polymorphic light eruption and the HLA DRB1*0301 extended haplotype are independent risk factors for cutaneous lupus erythematosus.

Recent evidence suggests that polymorphic light eruption (PLE) is an inherited photosensitivity disorder which may predispose to cutaneous lupus erythematosus (LE). In this study we examine the relative risk (RR) attributable to the presence of PLE, together with the effect of the major histocompatibility complex (MHC) in the development of cutaneous LE. Eighty-five Caucasian patients with annular subacute cutaneous LE (SCLE) and discoid LE (DLE) were recruited, together with 102 first degree relatives and 200 healthy local Caucasian controls. Symptoms suggestive of PLE were elicited in patients and relatives, and human leukocyte antigen (HLA) typing determined by PCR-SSP. Standard association analysis and family transmission disequilibrium testing (TDT) were then used to compare the HLA frequencies between groups. We found a significant (P < 0.05) association of the HL4 A*01, B*08, DRB1*0301 extended haplotype with both SCLE and DLE and also significant association of DLE with the HLA A*03, B*07, DRB1*15 haplotype, with a possible protective effect in SCLE for HLA B*44 and DRB1*04 (P=0.002 and 0.001 respectively). Association was observed between PLE and cutaneous LE (P < 0.001), but not between PLE and any HLA allele. From these figures we estimate, for the general population, that the RR of developing SCLE given the presence of (a) PLE, (b) DRB1*0301 and (c) both PLE and DRB1*0301 is 3.37, 5.45 and 12.03, respectively. For DLE, equivalent RRs are 3.11, 2.15 and 6.94. In conclusion, these data imply the involvement of both PLE and HLA DRB1*0301 in the development of SCLE and DLE. They form a basis for examining the genetic architecture of photosensitivity, some aspects of which may be common to both cutaneous LE and PLE.

Alleles↗
PubMed1986

Photosensitivity and photodermatitis in childhood.

Photosensitivity disorders of children are uncommon, except for banal overexposure reactions to sunlight. Although the long-term sequelae of chronic or intense sun exposure are not often seen in children, physicians should advise patients of the harmful effects and irreversible skin damage that results from unduly prolonged sun exposure. Damage accumulates over the years to cause premature aging, senile elastosis, actinic keratoses, and squamous- and basal-cell carcinomas. Besides the pigmentary changes, wrinkles, and skin cancers--genuine sources of altered appearance and morbidity--we now know that sunburned children develop a higher incidence of melanoma, which is not a rare cause of death in young adults. In Australia, where the incidence of melanoma is highest, a strong correlation exists for melanoma in children who get sunburn before the age of 10. Also, the incidence of melanoma is 50 times as great in bikini wearers who get sunburn as in girls who wear one-piece bathing suits.

Adolescent↗
PubMed1991

The prevalence of antinuclear antibodies in patients with apparent polymorphic light eruption.

Polymorphic light eruption (PLE) is a very common photosensitive disorder, the most important differential diagnosis of which is lupus erythematosus (LE). One-hundred and forty-two patients with PLE were screened for circulating antinuclear (ANA), Ro and La antibodies over a 2-year period. Results were negative in 66 patients. Sixty-two patients had low-titre ANA of various patterns, ranging from trace to 1/80 without evidence of LE although one later developed subacute cutaneous LE. Fourteen had more significant findings, six with ANA ranging from 1/160 to 1/1280 but no anti-Ro antibodies, four with ANA ranging from 1/160 to 1/1280 and also with anti-Ro antibodies and four patients with anti-Ro antibodies but low-titre ANA, one of whom later developed discoid LE. Three of these 14 patients fulfilled the American Rheumatism Association criteria for the diagnosis of systemic LE, but it was not certain in any of the patients whether the PLE-like rash represented cutaneous LE or coincidental PLE. However the overall 10% incidence of definite or possible LE in patients with suspected PLE suggests that all PLE patients should be screened for LE.

Adult↗
PubMed2002

Polymorphous light eruption.

Polymorphous light eruption (PLE) is a common idiopathic photosensitivity disorder with an estimated prevalence of 10-20%. It is characterized by an intermittent skin reaction to ultraviolet (UV) radiation exposure, consisting of non-scarring pruritic erythematous papules, vesicles or plaques that develop on light-exposed skin. Despite the different morphology in different individuals, the eruption tends to have a monomorphous presentation in any single subject. The histopathological features of PLE are distinct and comprise a perivascular lymphocytic infiltrate in the dermis, subepidermal oedema and variable epidermal changes. The pathogenesis of PLE is not well known, but findings suggest that it is a delayed-type hypersensitivity reaction to one or more UV-modified cutaneous antigens. The principal action of PLE is mainly in the UVA region, although some subjects exhibit sensitivity to UVB alone or to both UVA and UVB radiation at the same time. Preventive measures in PLE include the regular use of photoprotective methods combined with graduated exposures to natural sunlight. The induction of immune tolerance by phototherapy and photochemotherapy are useful prophylactic methods in moderate to severe cases. The role of systemic agents in the management of PLE is under investigation. This article reviews the epidemiological, pathogenetic and clinical aspects of PLE and discusses recent advances in the diagnostic approach and management of this condition.

Diagnosis, Differential↗
PubMed2000

UVs syndrome: establishment and characterization of fibroblastic cell lines transformed with simian virus 40 DNA.

Ultraviolet-sensitive syndrome (UVsS) is a newly established photosensitive disorder. Patients with UVsS showed mild clinical manifestations similar to classical types of xeroderma pigmentosum, and had biochemical phenotypes of Cockayne syndrome but not those of xeroderma pigmentosum. Fibroblasts from a UVsS patient were treated with simian virus 40 DNA containing the large T antigen with a defective origin of DNA replication to establish a transformed cell line. We obtained two independent transformed cell lines (Kps3SVY and Kps3SVI3) and report their initial characterization. These cells showed the same pattern in variable number of tandem repeat analyses as a primary fibroblast cell strain, Kps3, and retain the UVsS phenotype as demonstrated by increased UV sensitivity (three to four times more sensitive to UV than normal cells) and by reduced recovery of RNA synthesis after UV irradiation (20% - 30% of that of normal cells). These cells, however, showed different phenotypes as regards plating efficiency, doubling time, and transfection efficiency in spite of the fact that the same method was used to transform the cells. Kps3SVY cells were closer in phenotype to Kps3 cells than Kps3SVI3 cells. As a variable number of tandem repeat analyses also showed that Kps3SVI3 cells have lost one of the two alleles in some chromosomes, this may explain the different phenotypes between Kps3SVY and Kps3SVI3 cells. Moreover, these cells were distinct from cells with Cockayne syndrome group A or B. Thus, these cell lines provide the opportunity to conduct transfection studies on cells with the UVsS defect in DNA repair and transcription.

Cell Line, Transformed↗