Urocanic acid (UCA) is present at millimolar concentrations in mammalian epidermis and undergoes photoisomerization from the naturally occurring trans-isomer to the cis-isomer on exposure to ultraviolet radiation (UVR). Cis-UCA causes downregulation of various immune responses in mouse and human experimental models and has been proposed as both a chromophore and a mediator of UV-induced immune suppression. In this study, the wavelength dependence from 260-340 nm for trans to cis-UCA photoisomerization in human skin was analyzed in five healthy volunteers. The resulting action spectrum demonstrated maximal cis-UCA production in the UVB spectral region of 280-310 nm. This spectral peak is red-shifted to longer wavelengths compared with the erythemal action spectrum. The cis-UCA action spectrum can be used to predict the ability of sunscreens to protect against UVR-induced cis-UCA formation and may assist in explaining discrepancies between sunscreens' abilities to protect against erythema and photoimmunosuppression.

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According to the literature, IFN-gamma has a pathogenic role in the development of SLE. We observed a decreased proportion of IFN-gamma-secreting cells, which we think is presumably one of the beneficial effects of UVA1 therapy. On the basis of our study, UVA1 phototherapy does seem to be an effective adjuvant in the treatment of SLE patients.

SummaryPhotosensitivity in childhood is caused by a diverse group of diseases. It usually indicates idiopathic photodermatoses, first of all polymorphic light eruption. It may be an early symptom of genetic disorders such as porphyria or very rare genophotodermatoses. Photosensitivity secondary to topical or systemic external agents as well as photoexacerbated dermatoses is not so frequent in childhood. Here we present our experience with childhood photosensitivity skin diseases collected over a 40-year period. L ight-induced skin eruptions are not a common problem in pediatric dermatology. However, the condition often causes trouble and discomfort to the affected child and the parents.The literature on childhood photodermatoses (PDs) is relatively scanty. The incidence of PDs in childhood is much lower than in adults (1). According to the paper published by Jansén (2), photosensitivity started at the age of 15 years or earlier in 26% of the cases out of a total of 370 PD patients. There is also a shortage of primary data on the prevalence of PDs classified recently by Yashar and Lim (3) such as (i) idiopathic PD: polymorphic light eruption (PLE), juvenile spring eruption of the ears (JSE), solar urticaria (SU), hydroa vacciniforme (HV), (ii) photosensitivity secondary to exogenous agents, (iii) cutaneous porphyrias, (iv) genophotodermatoses and (v) photoexacerbated/aggravated disorders. The paper presents experience with PDs in childhood (83 cases) collected at the Department of Dermatology, Debrecen, between 1967 and 2006.The diagnosis in the vast majority of PD cases in children is PLE, whereas the order of other diseases is quite variable depending on geographic and genetic conditions. In the Finnish report (2) mentioned before, PLE was followed by xeroderma pigmentosum (XP) and then erythropoietic protoporphyria (EPP), while no cases were recorded from external photosensitizers. According to other literary data, phototoxic dermatitis occurs relatively often besides idiopathic PDs during childhood (4). Similar to these findings the most frequent diagnosis at our Department of Dermatology was also PLE. However, we recorded a rather high number of EPP cases and some porphyria cutanea tarda (PCT) as well, but only a few cases of XP (Table 1).Diagnosis of PD in childhood is not as easy as in adulthood (5). In the history occasionally (mostly in EPP) a family history is noted, such as in our patient material (6). The clinical picture is featured by various kinds of eruptions localized typically on the sun-exposed skin. The diagnosis in childhood can also be confirmed by phototests. Most informative is the provocation test used to reproduce lesions of idiopathic PDs (5). We perform it with ultraviolet (UV)B and UVA separately (Multitester SBB LT 400; Saalmann, Herford, Germany) (7) according to the protocol of Lehmann et al. (8). Photopatch testing for identifying external photosensitizer(s) is not performed commonly in children. We have not used it in our practice. Concerning laboratory tests, in porphyrias spect...

We report the case of a 39-year-old Hungarian woman who cyclically experienced painful, erythematous, patchy skin lesions on her face and chest. Because of her irregular menses and hysterectomy performed later on to manage endometriosis, it was difficult to link her symptoms to the menstrual cycle. But on the basis of the cyclic nature of the rash and the previous negative results - acne vulgaris, psoriasis, atopic dermatitis, lichen planus, systemic lupus erythematosus and infections were ruled out - autoimmune progesterone dermatitis was suspected. As progesterone is not available in aqueous solution for intradermal allergen test in Hungary, we performed progesterone provocation vaginally. The patient developed the usual skin lesions to vaginal progesterone exposure, which confirmed the diagnosis. The patient became symptom free to gonadotropine-analogue treatment and remained so even after the cessation of the therapy after 6 months. To our knowledge, this is the first case in the medical literature, in which autoimmune progesterone dermatitis was proved by vaginal progesterone provocation.

Melanocortin-1 receptor (MC1R) and agouti signaling protein (ASIP) play pivotal roles in the regulation of human pigmentation. We aimed to study whether single nucleotide polymorphisms (SNPs) of the MC1R and ASIP genes contribute to the pathogenesis of the polygenic pigment skin disorder, vitiligo. The PCR-amplified, full-length MC1R gene was studied with sequence analysis, and the 3' untranslated region (3' UTR) SNP of ASIP was detected using restriction fragment length polymorphism. The allele frequency of the ASIP SNP did not show any difference between the skin type, hair color and eye color-matched 97 vitiligo patients and the 59 healthy control individuals. As one of the MC1R polymorphisms showed significantly higher incidence among fair-skinned individuals (Fitzpatrick I+II, n=140) than among dark-skinned individuals (Fitzpatrick III+IV, n=90), both vitiligo patients and controls were divided into two groups and the frequency of the MC1R alleles was studied separately in fair-skinned and dark-skinned subgroups of diseased and healthy groups. C478T, one of the MC1R SNPs studied in 108 fair-skinned vitiligo patients and in 70 fair-skinned healthy control individuals, showed a significant difference (P=0.0262, odds ratio [95% confidence interval]=3.6 [0.0046-0.1003]) in allele frequency between the two groups: the allele frequency was higher in the control group, suggesting protection against vitiligo. Computer prediction of antigenicity has revealed that the Arg160Trp amino acid change caused by this SNP results in a decrease in antigenicity of the affected peptide epitope.

Pentoxifylline reduced SBC formation in our supravital human skin model. It presumably acts as an antioxidant agent.