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Notes: Background Tinea capitis is the most common dermatophytosis of childhood with increasing incidence. Whereas griseofulvin is considered by many as the mainstay of treatment, newer oral antifungal agents, including fluconazole, itraconazole and terbinafine have demonstrated higher efficacy, resulting in shorter treatment durations. Objectives We aimed to determine the optimum regimen for the treatment of childhood tinea capitis with itraconazole. Methods A mycological culture outcome-dependent combination of a 28-day continuous and facultative additional 14-day courses with itraconazole was used in 42 children (20 girls; 22 boys) aged 12–140 months (mean 66) with tinea capitis due to Microsporum canis (n = 26) and Trichophyton violaceum (n = 16). The drug was given orally according to the patients’ body weight (50 mg daily for 〈 20 kg; 100 mg daily for ≥ 20 kg) over 4 weeks. Direct microscopy and fungal culture as a parameter for efficacy were repeated 2 weeks after termination of treatment. Assessment of efficacy was based on the evaluation of results from light microscopy and culture at 8 weeks after initiation of treatment, and in the case of a further positive mycological culture at 14 and 20 weeks, respectively. A positive fungal culture at these times resulted in an additional course for 2 weeks with the initially chosen itraconazole dosage. Results In 34 of 42 patients a single 4-week course of itraconazole resulted in a complete mycological cure of lesions as demonstrated by light microscopy and mycological culture. Four of 42 patients had to be treated by a second itraconazole course for 2 weeks, and four children received a third course of itraconazole for 2 weeks until all lesions showed negative direct microscopy and mycological culture. No abnormal haematological or biochemical results occurred. Apart from transient, completely reversible indigestion in two children, no side-effects were observed. Conclusions A culture-based 28-day continuous therapeutic regimen plus facultative cultural outcome-dependent additional 14-day courses of a body weight-adapted dosage of itraconazole in tinea capitis due to M. canis and T. violaceum is discussed; this offers the advantage of an effective therapy with complete negative direct microscopy as well as negative cultural results, within a shorter active treatment period (cf. previous studies with continuous administration of itraconazole).

Notes: Background Prevalence data for atopic eczema based on a dermatological examination have not so far been available for East and West Germany. Possible differences in the proportions of extrinsic and intrinsic types of eczema, and how far these could explain differences in the prevalence of eczema, need to be clarified. Objectives To compare the prevalence of atopic eczema in pre-school children between different locations in East and West Germany, and over a period of 7 years, at three time points. Additionally, to determine the proportions of intrinsic and extrinsic types of eczema by taking skin prick test reactivity into account. Methods Repeated cross-sectional studies in 1991, 1994 and 1997 in 5–6-year-old pre-school children at five different locations in West Germany (n = 2075) and six in East Germany (n = 1926) were carried out. Individuals with eczema were identified by an examination performed by physicians of the Department of Dermatology. In addition, a skin prick test and a standardized questionnaire were used. Results The overall prevalence of atopic eczema in these children was 10·4%. At all three times of investigation (1991, 17·5% vs. 11·2%; 1994, 12·6% vs. 8·7%; 1997, 11·2% vs. 4·5%) and in the total group (12·9% vs. 8·2%), the prevalence was significantly higher in East than in West Germany. After controlling for influences of sex, parental history of atopic diseases, observer and socio-economic status in multiple logistic regression analyses, these differences remained significant for 1991, 1994 and for the overall group (odds ratio, OR 1·78, 95% confidence interval, CI 1·43–2·21). Girls (OR 1·56, 95% CI 1·27–1·92) and children whose parents had a higher level of school education (OR 1·17, 95% CI 1·00–1·37) were affected more frequently. Of all children, 26·6%, and of those with eczema, 41·9% exhibited at least one reaction in the prick test (OR 2·21, 95% CI 1·75–2·80; sensitization in eczema vs. no eczema). Whereas 50·4% of the children with eczema in West Germany were sensitized, only 36·5% of the diseased children in East Germany reacted positively in the prick test (OR 1·77, 95% CI 1·12–2·79). Conclusions These results are in accordance with findings regarding allergic sensitization and hay fever and might indicate that factors other than allergy are responsible for the higher prevalence of atopic eczema in East Germany.

Notes: Fourteen patients suffering from acute, exacerbated atopic eczema were screened for changes in collagen I and collagen III metabolism in serum (n = 11), urine (n = 11) and skin biopsies (n = 9) before and after medium-dose ultraviolet (UV) A1 phototherapy (15 exposures of 50 J/cm2 over a 3-week period, total dose 750 J/cm2). Mature collagen I and, to a lesser extent, mature collagen III were found to be decreased after the therapy in skin samples from the irradiated patients. As markers of collagen I degradation, the cross-links pyridoline and deoxypyridoline were analysed in urine using high-performance liquid chromatography. Both cross-links were found to be mildly increased after UVA1 phototherapy, without reaching statistical significance. As markers of de novo collagen synthesis we screened for the procollagen I-carboxyterminal peptide (PICP) and procollagen III-aminoterminal peptide (PIIINP) levels in serum and skin. The ratio of PICP to PIIINP in serum dropped significantly after the UVA1 phototherapy, suggesting a different impact of UVA1 on the two collagens. These findings were paralleled by a diminished ratio of PICP to PIIINP in tissue samples. Staining for matrix metalloproteinase 1 (MMP-1) and its specific counterpart, tissue inhibitor of MMP-1 (TIMP-1), showed slight increases for both proteins by therapeutic UVA1; this was also seen in serum for TIMP-1 but not MMP-1. In our study, high-energy UVA1 doses induced changes of the skin collagens in patients with atopic eczema which are measurable by their metabolites in serum and urine.

Notes: We report a case of persistent annular erythema of infancy in a 4-month-old boy. Physical and laboratory parameters showed no sign of internal disease or specific infection except a massive Candida albicans colonization (〉 103 organisms/mm3) of the lower gastrointestinal tract. Oral treatment with amphotericin B for 2 weeks resulted in a complete remission of the skin lesions indicating Candida colonization as a trigger.

Notes: Background  Transfersome® is a drug delivery technology based on highly deformable, ultraflexible lipid vesicles which penetrate the skin when applied non-occlusively.Objectives  To assess the advantages of this carrier-based formulation in humans, the efficacy and the atrophogenic potential of triamcinolone acetonide (TAC) in Transfersome® was compared with commercially available TAC-containing cream and ointment.Methods  Healthy volunteers were enrolled in double-blind, placebo-controlled clinical trials with random study medication assignment to the test areas.Results  A 10-fold lower dose of TAC in Transfersome® (2·5 µg cm−2) was bioequivalent to 25 µg cm−2 TAC in conventional formulations as measured by erythema suppression (cream: P = 0·01, ointment: P 〈 0·001). A skin blanching assay revealed different kinetics of the formulations, with a delayed onset of action of the Transfersome® and ointment preparations. Ultrasonic measurements revealed a significantly reduced atrophogenic potential. There was a 12·1% reduction in skin thickness given by TAC in Transfersome® compared with a 21·1% reduction given by a bioequivalent dose in TAC cream after a 6-week treatment period (P = 0·007).Conclusions  Transfersome® may significantly improve the risk–benefit ratio of topically applied glucocorticosteroids.

Notes: Summary Background Colonization of human skin by Staphylococcus aureus is a characteristic feature of several inflammatory skin diseases, which is often followed by tissue invasion and severe cell damage. A crucial role has been attributed to staphylococcal haemolysins in the cytotoxicity to epidermal structures. Objectives To investigate haemolysin-independent virulence to human keratinocytes. Methods The stable α-haemolysin, β-haemolysin double-negative S. aureus mutant DU 5720 was compared with the fully virulent parent strain 8325-4 and with its isogenic fibronectin-binding protein A/B-negative variant DU 5883 in an invasion model. Results This assay showed dose-dependent internalization of all the strains investigated by human HaCaT keratinocytes, with reduced internalization of DU 5883. Transmission electron microscopy revealed adhesion of staphylococci to cellular pilus-like extrusions, followed by the embedding of the bacteria in cellular grooves. Following attachment to the keratinocytes the staphylococci were engulfed into vesicles within the cytoplasm where some bacteria persisted for 24–48 h. Addition of cytochalasin D strongly reduced the bacterial uptake, suggesting an active keratinocyte process. Bacterial invasion was followed by severe keratinocyte cell damage showing the morphological changes of cytotoxic and, to a lesser extent, apoptotic cell death as determined by the trypan blue exclusion test and the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labelling assay. The highest levels of lethal cytotoxicity were observed in haemolysin-producing strains, whereas the induction of apoptosis seemed to depend on internalization. Conclusions Staphylococcal invasion of human keratinocytes represents a potent staphylococcal virulence factor, which, independently of α- and β-haemolysins, leads to necrotic and apoptotic cell damage.