Solar urticaria in 145 patients: Assessment of action spectra and impact on quality of life in adults and children.

BACKGROUND: Solar urticaria (SU) is a rare chronic inducible urticaria triggered via uncharacterized chromophores. We detail responses of a large patient series to monochromator phototesting and broadband ultraviolet radiation (UVR); relationship to life quality is explored. METHODS: Retrospective review of all SU patients undergoing standardized diagnostic photoinvestigation at a specialist centre during 2000-2016. From 2011, patients completed dermatology life quality index (DLQI) questionnaires for the past week and year. RESULTS: In 145 patients (mean: 35.8, range: 3-69 years; 18 aged <18 years; 100 female), combined phototesting with broadband UVR and monochromator sources successfully provoked 74.5% patients, with 65.6% provoked by broadband UVR alone and 57.9% by monochromated radiation alone. The narrow wavebands most frequently eliciting wheal and flare response were between 370 and 400 nm, with 25% patients at 300 ± 5 nm, 53.6% at 320 ± 10 nm, 66.7% at 330 ± 10 nm, 77.4% at 350 ± 20 nm, 83.3% at 370 ± 20 nm, 86.9% at 400 ± 20 nm, 44% at 500 ± 20 nm and 17.8% at 600 ± 20 nm. In 62 patients, the DLQI revealed 56.1% had very to extremely large impact in the past week (all patients: mean score: 11.1, range: 0-29) rising to 69.8% for the past year (12.5, 0-30); adults and children were similarly affected. Patients with positive photoprovocation had higher DLQI score than those who were negative (DLQI for past week: mean: 12.6 ± SEM 1.1 vs 4.6 ± 1.4, P < .01). CONCLUSION: SU is predominantly provoked by longer UVA-shorter visible radiation, which penetrates window-glass and where sunscreens are less effective; impact on life quality is considerable. Photoprotective agents effective against this spectrum are needed.

Impact of photosensitivity disorders on the life quality of children.

BACKGROUND/PURPOSE: Abnormal cutaneous sensitivity to the ultraviolet and/or visible radiation in sunlight characterizes photosensitivity disorders. Little is known regarding their impact in childhood. Our objective was to characterize childhood photosensitivity disorders presenting to a photoinvestigation unit, evaluating their impact on quality of life (QoL). METHODS: Photoinvestigation records of children attending from 2000 to 2007 were evaluated for diagnosis, clinical, demographic and phototest parameters. These children were subsequently contacted during summertime to evaluate the impact of photosensitivity on QoL, utilizing the children's dermatology life quality index (CDLQI). RESULTS: 83 children underwent photoinvestigation; 62 (74.7%) were diagnosed photosensitive (mean age 8.6 years, range 2-16; 33 female), with abnormal phototest findings in 35 children. 38/55 questionnaires (69.1%) were returned. Mean (± standard deviation) CDLQI score (all diagnoses) was 10.2 ± 7.3 with very high scores in xeroderma pigmentosum (20.7 ± 5.7; n = 3) and actinic prurigo (18.2 ± 7.1; n = 6) and moderate scores in photoaggravated eczema (7.9 ± 4.2; n = 8) and polymorphic light eruption (6.2 ± 4.4 n = 18). CDLQI correlated with number of months affected per year (r = 0.595, P = 0.001). CONCLUSION: Photosensitivity disorders have a substantial impact, ranging from moderate to extremely large, on QoL in childhood, and the psychological consequences should be considered in their management.

The sunburn response in human skin is characterized by sequential eicosanoid profiles that may mediate its early and late phases.

Sunburn is a commonly occurring acute inflammatory process, with dermal vasodilatation and leukocyte infiltration as central features. Ultraviolet (UV) B-induced hydrolysis of membrane phospholipids releases polyunsaturated fatty acids, and their subsequent metabolism by cyclooxygenases (COXs) and lipoxygenases (LOXs) may produce potent eicosanoid mediators modulating different stages of the inflammation. Our objective was to identify candidate eicosanoids formed during the sunburn reaction in relation to its clinical and histological course. We exposed skin of healthy humans (n=32) to UVB and, for 72 h, examined expression of proinflammatory and anti-inflammatory eicosanoids using LC/ESI-MS/MS, and examined immunohistochemical expression of COX-2, 12-LOX, 15-LOX, and leukocyte markers, while quantifying clinical erythema. We show that vasodilatory prostaglandins (PGs) PGE(2), PGF(2alpha), and PGE(3) accompany the erythema in the first 24-48 h, associated with increased COX-2 expression at 24 h. Novel, potent leukocyte chemoattractants 11-, 12-, and 8-monohydroxy-eicosatetraenoic acid (HETE) are elevated from 4 to 72 h, in association with peak dermal neutrophil influx at 24 h, and increased dermal CD3(+) lymphocytes and 12- and 15-LOX expression from 24 to 72 h. Anti-inflammatory metabolite 15-HETE shows later expression, peaking at 72 h. Sunburn is characterized by overlapping sequential profiles of increases in COX products followed by LOX products that may regulate subsequent events and ultimately its resolution.

Comparison of Demographic and Photobiological Features of Chronic Actinic Dermatitis in Patients With Lighter vs Darker Skin Types.

Importance: Chronic actinic dermatitis (CAD) is classically described in older, white men, although increasing reports describe younger patients with darker skin types, particularly South Asians. Photocontact allergy occurs in CAD but is less studied than contact allergy in this exquisitely photosensitive condition. Objective: To evaluate for differences in demographic and photobiological features between persons with darker and lighter skin types who have CAD. Design, Setting, and Participants: This retrospective review included 70 consecutive adult patients (≥18 years) undergoing investigation for photosensitivity who were diagnosed with CAD from November 1, 2000, through August 31, 2015, at the specialist Photobiology Unit of a tertiary academic referral center. Main Outcomes and Measures: Patient age, sex, ethnicity, clinical features, and phototesting outcomes. Results: A total of 70 patients (37 men [53%] and 33 women [47%]; mean [SD] age, 50.9 [2.3] years) were diagnosed with CAD. Of these, 36 were non-Hispanic and non-Latino white, 31 were Asian (including 24 South Asian, 4 East Asian, and 3 Middle Eastern), and 3 were black. Patients were aged 9 to 83 years at diagnosis, with a mean (SD) age at onset of 42.6 (2.4) years and duration of disease of 8.8 (1.3) years. Forty-one had lighter skin types (Fitzpatrick skin types I-IV), and 29 had darker skin types (Fitzpatrick skin types V and VI). Patients with darker skin types and CAD were younger at diagnosis (mean [SD] age, 40.7 [3.5] vs 58.1 [2.5] years; P < . 001) and had earlier onset of photosensitivity (mean [SD] age, 35.5 [3.9] vs 47.5 [2.9] years; P = .01) compared with patients with lighter skin types. Of note, the male to female ratio in the lighter skin group was 2:1 compared with 1:2 in the darker skin group. Phototest reactions were equally severe in Fitzpatrick skin types V to VI and I to IV, with minimal erythemal doses to monochromatic UV-B, UV-A, and visible radiation and broadband provocation testing showing similar results. Photoallergic contact reactions to UV filters, personal sunscreen products, and nonsteroidal anti-inflammatory drugs were seen in both groups; 14 of 61 patients (23%) undergoing photopatch testing showed positive photopatch reactions. Conclusions and Relevance: Chronic actinic dermatitis presents with an earlier age at onset and an inverted male to female ratio in patients with darker compared with lighter skin types. Clinicians should thus be cognizant of CAD in younger women with darker skin types. Photopatch testing should be considered in patients with CAD, with coexistent photocontact allergy occurring in a substantial proportion.

Prostaglandin-E2 is produced by adult human epidermal melanocytes in response to UVB in a melanogenesis-independent manner.

Excessive ultraviolet radiation (UVR) exposure induces erythema, mediated in part by prostaglandin-E(2) (PGE(2)). While keratinocytes are a major PGE(2) source, epidermal melanocytes (EM) also express PGE(2)-production machinery. It is unclear whether EM-produced PGE(2) contributes to UVR-induced skin inflammation, and whether this is correlated with melanogenesis. Epidermal melanocytes were cultured from skin phototype-1 and -4 donors, followed by assessment of PGE(2) production and melanogenesis. Epidermal melanocytes expressed cytoplasmic phospholipase-A(2), cyclooxygenase-1, cytoplasmic prostaglandin-E synthase and microsomal prostaglandin-E synthase-1, -2. Epidermal melanocytes produced PGE(2) under basal conditions, which increased further after arachidonic acid stimulation. Epidermal melanocytes expressed cyclooxygenase-2 (COX-2) mRNA and a selective COX-2 inhibitor (NS-398) reduced PGE(2) production. Ultraviolet B-induced PGE(2) production was positively correlated with skin phototype-1, despite variability between individual EM donors. By contrast, there was no correlation between PGE(2) production by EM and their melanogenic status. Thus, EM may contribute to UVR-induced erythema, with role of donor skin phototype more important than their melanogenic status.

Collagen secretion after photodynamic therapy versus scar-inducing anti-cancer modalities: an in vitro study.

Photodynamic therapy (PDT) has been associated anecdotally with good quality healing and an absence of scar formation. Our previous studies, examining the levels of the collagen specific molecular chaperone Hsp47, have noted differences in the response after photodynamic therapy and hyperthermia at both the transcriptional and translational levels. In the present study the levels of Hsp47 after exposure to two chemotherapeutic agents (bleomycin and mitomycin). ionising radiation, hyperthermia and haematoporphyrin ester (HpE) mediated PDT were compared in both mouse and human fibroblast cell lines. A rapid assay for soluble collagen has also been used to quantify soluble collagen levels at early time points after treatment. Peak Hsp47 levels were found to correlate well with peak collagen levels. The results show that the levels of collagen measured in vitro are elevated in modalities associated with scarring in vivo but not after HpE-PDT.