[Tinea in the genital area : A diagnostic and therapeutic challenge]. / Tinea im Genitalbereich : Eine diagnostische und therapeutische Herausforderung.

Pubogenital tinea or tinea genitalis represents a rare type of dermatophytosis which, however, is increasingly being diagnosed. The mons pubis is affected, but also the outer regions to the penis shaft and the labia together with the groins. Pubogenital tinea is a more superficial erythrosquamous type, but strong inflammatory dermatomycoses of the genital area as tinea genitalis profunda ranging to kerion celsi are observed. A total of 30 patients (14-63 years of age, 11 men and 19 women) with pubogenital tinea are described. Most patients originated from Graz, Austria, while 2 patients were from Germany (Saxony and Isle of Sylt). Causative agents were mainly zoophilic dermatophytes: Microsporum (M.) canis (11), Trichophyton (T.) interdigitale (9), T. anamorph of Arthroderma benhamiae (2), and T. verrucosum (1). Anthropophilic fungi were T. rubrum (6) and T. tonsurans (1). Anamnestic questions should include contact with pets, physical activities, and travel. Genital shaving and concurrent tinea pedis and onychomycosis are disposing factors. Treatment consisted of oral antifungals except in the three women who were pregnant. Preferably, itraconazole or terbinafine was used, while in a single case, fluconazole was administered. Griseofulvin was not used, because this classic systemic antifungal agent is not allowed any more in Austria. In one patient, oral antifungal therapy was changed from itraconazole to terbinafine due to inefficacy.

Characterisation of psoriasis susceptibility locus 6 (PSORS6) in patients with early onset psoriasis and evidence for interaction with PSORS1.

BACKGROUND: Psoriasis is a genetically complex, chronic inflammatory skin disease. The authors have previously identified a susceptibility locus on chromosome 19p13 (PSORS6). METHODS AND RESULTS: In a follow-up linkage disequilibrium (LD) study in an independent family based cohort, the authors found evidence for association to a newly discovered microsatellite at this locus (D19SPS21, p<5.3x10(-5)). An LD based association scan in 300 trios revealed association to several single, single nucleotide polymorphisms (SNPs) in one LD block. When the authors stratified this cohort for carrying the PSORS1 risk allele at the HLA-C locus, evidence for association became much stronger at single SNP and haplotype levels (p values between 1.0x10(-4) and 8.0x10(-4)). In a replication study of 1114 patients and 937 control individuals, evidence for association was also observed after stratification to the PSORS1 risk allele. In both study groups, logistic regression showed evidence for interaction between the risk alleles at PSORS1 and PSORS6. Best p values for rs12459358 in both study groups remained significant after correction for multiple testing. The associated LD block did not comprise any known genes. Interestingly, an adjacent gene, MUC16, coding for a large glycosylated protein expressed in epithelia and of unknown function, could be shown to be also expressed in tissues relevant for pathogenesis of psoriasis such as skin and thymus. Immunohistochemical analyses of skin revealed focal staining for MUC16 in suprabasal epidermal cells. Further functional studies are required to clarify its potential role in psoriasis and identify the causal variant(s) at this locus. CONCLUSION: The data establish PSORS6 as a confirmed psoriasis susceptibility locus showing interaction with PSORS1.

Serum mast cell tryptase is not a useful marker for disease severity in psoriasis or atopic dermatitis.

BACKGROUND: Severity in psoriasis and atopic dermatitis (AD) is commonly assessed with the Psoriasis Area and Severity Index (PASI) and the SCORing Atopic Dermatitis (SCORAD), respectively. Until today no serum marker is available to reflect the clinical scoring in both diseases. As mast cells play an important role in the pathogenesis of early psoriasis and AD, tryptase, a major compound of mast cell granules that is released upon activation, could in principle serve as such a marker. OBJECTIVES: To assess the correlation between serum tryptase and severity of psoriasis and AD as well as the correlation between total IgE levels and severity of AD. METHODS: Serum samples from patients hospitalized for psoriasis and AD were collected at time of admission and time of discharge from hospital. PASI and SCORAD assessments were performed at the same time points. Outpatients presenting with naevi and other benign noninflammatory skin lesions served as control group. Serum tryptase values and total IgE levels of patients with AD were measured using a fluoroenzyme immunoassay technique. RESULTS: No correlation of serum tryptase level with either the severity of psoriasis or the severity of AD was seen. Total IgE levels in patients with AD at time of admission and discharge from hospital remained the same. CONCLUSIONS: Serum total tryptase did not prove to be a useful tool in assessing severity of psoriasis or AD. Total IgE levels did not correlate with severity of AD.