Malassezia‐derived aryl hydrocarbon receptor ligands enhance the CCL20/Th17/soluble CD163 pathogenic axis in extra‐mammary Paget's disease

Malassezia yeast play a role in the pathogenesis of chronic dermatitis, especially in apocrine areas, by polarizing the local immunologic background to a Th2/Th17 state through aryl hydrocarbon receptor (AhR)‐dependent pathways. Extra‐mammary Paget's disease (EMPD) is an adenocarcinoma of apocrine origin, and except for cases associated with Malassezia yeast and their metabolites, the lesions typically develop in areas not exposed to environmental material. The purpose of this study was to investigate (a) the immunomodulatory effects of Malassezia metabolites on normal human keratinocytes (NHKCs), focusing on interleukin (IL)‐17 and related cytokines/chemokines (IL‐23, IL‐36γ, CCL20), (b) the expression of these factors in lesion‐affected skin in EMPD and (c) the activation of tumor‐associated macrophages (TAMs) by these factors. Malassezia metabolites augmented the expression of cytochrome P450, family 1, subfamily A, polypeptide 1 (CYP1A1), CCL20 and IL‐36γ mRNA in NHKCs in vitro. In lesion‐affected skin of patients with EMPD, epidermal keratinocytes expressed CYP1A1 and CCL20. In addition, Paget cells expressed CCL20 and IL‐23. IL‐17–producing cells were distributed adjacent to Paget cells. Compared to healthy donors, patients with EMPD exhibited significantly increased serum levels of soluble (s)CD163, CXCL5, CXCL10 and CCL20. In addition, serum levels of sCD163 decreased significantly following tumor resection. Our study demonstrates a possible mechanism for the development of EMPD involving AhR‐mediated signalling by epidermal keratinocytes and RANKL‐induced recruitment of Th17 cells and TAMs.     

Malassezia yeasts activate the NLRP3 inflammasome in antigen‐presenting cells via Syk‐kinase signalling

Although being a normal part of the skin flora, yeasts of the genus Malassezia are associated with several common dermatologic conditions including pityriasis versicolour, seborrhoeic dermatitis (SD), folliculitis, atopic eczema/dermatitis (AE/AD) and dandruff. While Malassezia spp. are aetiological agents of pityriasis versicolour, a causal role of Malassezia spp. in AE/AD and SD remains to be established. Previous reports have shown that fungi such as Candida albicans and Aspergillus fumigatus are able to efficiently activate the NLRP3 inflammasome leading to robust secretion of the pro‐inflammatory cytokine IL‐1β. To date, innate immune responses to Malassezia spp. are not well characterized. Here, we show that different Malassezia species could induce NLRP3 inflammasome activation and subsequent IL‐1β secretion in human antigen‐presenting cells. In contrast, keratinocytes were not able to secrete IL‐1β when exposed to Malassezia spp. Moreover, we demonstrate that IL‐1β secretion in antigen‐presenting cells was dependent on Syk‐kinase signalling. Our results identify Malassezia spp. as potential strong inducers of pro‐inflammatory responses when taken up by antigen‐presenting cells and identify C‐type lectin receptors and the NLRP3 inflammasome as crucial actors in this process.     

Utilization of matrix‐assisted laser desorption and ionization time‐of‐flight mass spectrometry for identification of infantile seborrheic dermatitis‐causing Malassezia and incidence of culture‐based cutaneous Malassezia microbiota of 1‐month‐old infants

Matrix‐assisted laser desorption and ionization time‐of‐flight mass spectrometry (MALDI‐TOF‐MS) has been utilized for identification of various microorganisms. Malassezia species, including Malassezia restricta, which is associated with seborrheic dermatitis, has been difficult to identify by traditional means. This study was performed to develop a system for identification of Malassezia species with MALDI‐TOF‐MS and to investigate the incidence and variety of cutaneous Malassezia microbiota of 1‐month‐old infants using this technique. A Malassezia species‐specific MALDI‐TOF‐MS database was developed from eight standard strains, and the availability of this system was assessed using 54 clinical strains isolated from the skin of 1‐month‐old infants. Clinical isolates were cultured initially on CHROMagar Malassezia growth medium, and the 28S ribosomal DNA (D1/D2) sequence was analyzed for confirmatory identification. Using this database, we detected and analyzed Malassezia species in 68% and 44% of infants with and without infantile seborrheic dermatitis, respectively. The results of MALDI‐TOF‐MS analysis were consistent with those of rDNA sequencing identification (100% accuracy rate). To our knowledge, this is the first report of a MALDI‐TOF‐MS database for major skin pathogenic Malassezia species. This system is an easy, rapid and reliable method for identification of Malassezia.     

Is topical antimycotic treatment useful as adjuvant therapy for flexural atopic dermatitis: randomized, double-blind, controlled trial using one side of the elbow or knee as a control

Background Certain factors are known to cause exacerbation of atopic dermatitis (AD), e.g. soap, detergent, dry skin, staphylococcal colonization, and herpes infection. Other factors are suspected, but not yet proven, e.g. yeasts belonging to the Malassezia genus. It is known that antimycotics may be beneficial in a small subset of adult patients with dermatitis affecting the head and neck region; however, it is not known whether AD patients, many of whom also have head and neck involvement, may also find antimycotics useful. A previous study has demonstrated no treatment difference in adult AD patients; however, the measurement method was criticized and 1% hydrocortisone cream may have too weak an effect in adult patients. Therefore, we designed this randomized, double‐blind, controlled trial to examine this question. Younger AD patients were recruited and different methods of measuring outcomes were used. Objective To evaluate the usefulness of topical antimycotic treatment as adjuvant therapy for flexural AD. Methods This was a randomized, double‐blind, controlled trial in AD patients using one side of the elbow or knee as a control. There were three independent outcomes: (i) to compare the ability to relieve symptoms; (ii) to compare the ability to improve clinical signs; and (iii) to compare the ability to provide lasting clinical effects. Results All three outcomes showed unequivocally that the addition of antimycotic did not provide extra benefit to the standard treatment. Conclusion The addition of antimycotic does not seem to provide extra benefit to AD patients, and the beneficial effect of this medication seems to be restricted to a small subset of adult patients with dermatitis affecting the head and neck region.     

Malassezia species in healthy skin and in dermatological conditions

The genus Malassezia comprises lipophilic species, the natural habitat of which is the skin of humans and other warm‐blooded animals. However, these species have been associated with a diversity of dermatological disorders and even systemic infections. Pityriasis versicolor is the only cutaneous disease etiologically connected to Malassezia yeasts. In the other dermatoses, such as Malassezia folliculitis, seborrheic dermatitis, atopic dermatitis, and psoriasis, these yeasts have been suggested to play pathogenic roles either as direct agents of infection or as trigger factors because there is no evidence that the organisms invade the skin. Malassezia yeasts have been classified into at least 14 species, of which eight have been isolated from human skin, including Malassezia furfur, Malassezia pachydermatis, Malassezia sympodialis, Malassezia slooffiae, Malassezia globosa, Malassezia obtusa, Malassezia restricta, Malassezia dermatis, Malassezia japonica, and Malassezia yamatoensis. Distributions of Malassezia species in the healthy body and in skin diseases have been investigated using culture‐based and molecular techniques, and variable results have been reported from different geographical regions. This article reviews and discusses the latest available data on the pathogenicity of Malassezia spp., their distributions in dermatological conditions and in healthy skin, discrepancies in the two methods of identification, and the susceptibility of Malassezia spp. to antifungals.     

Analysis of the response of human keratinocytes to Malassezia globosa and restricta strains

Malassezia spp. are saprophyte yeasts involved in skin diseases with different degrees of severity. The aim of our study was to analyze the response of human epidermal keratinocytes to Malassezia globosa and restricta strains evaluating the host defence mechanisms induced by Malassezia spp. colonization. Our results showed a different modulation of the inflammatory and immunomodulatory cytokine pathways obtained with the different strains of Malassezia tested. In addition, this expression is altered by blocking the TLR2 receptor. In comparison with M. furfur, M. globosa and restricta displayed an unexpected and striking cytotoxicity on keratinocytes. The differences observed could be related to the different modalities of interaction between keratinocytes and Malassezia strains, but also to their growth condition. Taken together, these results indicate that M. globosa or M. restricta colonization exert a different control on the cytokine inflammatory response activated in the human keratinocyte in which TLR2 might be involved. M. globosa and M. restricta may play a synergistic role in the exacerbation of skin diseases in which both are found.     

Distribution of Malassezia Species on the Scalp in Korean Seborrheic Dermatitis Patients

Background

Malassezia species play an important role in the pathogenesis of seborrheic dermatitis. In particular, M. restricta and M. globosa are considered to be the predominant organisms in seborrheic dermatitis of Western countries. However, species distribution of Malassezia in seborrheic dermatitis has not been clearly determined yet in Asia.

Objective

To identify the distribution of Malassezia species on the scalp of seborrheic dermatitis patients in Korea using 26S rDNA PCR-RFLP analysis.

Methods

A total of 40 seborrheic dermatitis patients and 100 normal healthy volunteers were included in this study. For the identification of Malassezia species, the scalp scales of the subjects were analyzed by 26S rDNA PCR-RFLP analysis.

Results

The most commonly identified Malassezia species were M. restricta in the seborrheic dermatitis patients, and M. globosa in the normal controls. In the seborrheic dermatitis group, M. restricta was identified in 47.5%, M. globosa in 27.5%, M. furfur in 7.5%, and M. sympodialis in 2.5% of patients. In the healthy control group, M. globosa was identified in 32.0%, M. restricta in 25.0%, M. furfur in 8.0%, M. obtusa in 6.0%, M. slooffiae in 6.0%, and M. sympodialis in 4.0% of subjects.

Conclusion

M. restricta is considered to be the most important Malassezia species in Korean seborrheic dermatitis patients.     

Evaluation of Expression of Lipases and Phospholipases of Malassezia restricta in Patients with Seborrheic Dermatitis

Background

Malassezia species (spp.) are cutaneous opportunistic pathogens and associated with various dermatological diseases including seborrheic dermatitis, dandruff and atopic dermatitis. Almost all Malassezia spp. are obligatorily lipid-dependent, which might be caused by lack of the myristic acid synthesis. Recent genome analysis of M. restricta and M. globosa suggested that the absence of a gene encoding fatty acid synthesis might be compensated by abundant genes encoding hydrolases, which produce fatty acids, and that lipases and phospholipases may play a role in virulence of the fungus.

Objective

The current study aimed to investigate the contribution of lipases and phospholipases in virulence of the M. restricta as being the most frequently isolated Malassezia spp. from the human skin.

Methods

Swap samples of two different body sites of at least 18 patients with seborrheic dermatitis were obtained and in vivo expression of lipases and phospholipases of M. restricta was analyzed by the gene specific two-step nested RT-PCR.

Results

The results of the current study suggest that majority of the patients display expression of lipase RES_0242.

Conclusion

These data imply a possible role of lipase in the host environment to produce free fatty acids for the fungus.     

Enzymes involved in the conversion of arachidonic acid to eicosanoids in the skin of atopic dogs

Please cite this paper as: Enzymes involved in the conversion of arachidonic acid to eicosanoids in the skin of atopic dogs. Experimental Dermatology 2010; 19 : e317–e319. Abstract: Canine atopic dermatitis (AD), a chronic inflammatory skin disease, shares characteristics with its human counterpart. To get insight into the role of enzymes involved in production of prostaglandin E₂ (PGE2) and leukotriene B₄ (LTB₄), potent inflammatory mediators originating from membrane‐derived arachidonic acid (AA), expression of genes encoding these enzymes and receptors was quantified by qPCR in non‐lesional and lesional skin from atopic dogs and in healthy skin. Significantly higher mRNA expression of the key enzymes 5‐lipoxygenase (5‐LO), 5‐LO activating protein (FLAP), leukotriene A₄ hydrolase (LTA₄H) and prostaglandin E synthase 1 (mPGES‐1) and their receptors (PGE receptors 2 and 3) were observed. Being responsible for elevated levels of metabolites of the 3‐series prostaglandins and the 5‐series leukotrienes these enzymes may be interesting targets for therapy that should result in amelioration of clinical signs in canine atopic dermatitis.     

Case of Fusarium paronychia successfully treated with occlusive dressing of antifungal cream

We report a case of refractory Fusarium paronychia in a 42‐year‐old man with Behçet's disease receiving oral cyclosporin and corticosteroid. Symptoms resembling candidal paronychia of his little finger could not be cured by topical ketoconazole and oral terbinafine. The pathogen was identified as Fusarium solani species complex by gene analysis, and was multiple drug resistant. The case eventually resolved by occlusive dressing therapy with 0.5% amorolfine cream for 3 months.     

Osthole attenuates mouse atopic dermatitis by inhibiting thymic stromal lymphopoietin production from keratinocytes

Atopic dermatitis is one of the most common skin diseases. Dysregulation of immune system and chronic inflammation were believed to be associated with atopic dermatitis. Osthole was reported to play important roles in antitumor and anti‐inflammation. However, whether osthole has effects on atopic dermatitis remains unclear. In this present study, we explored the biological role of osthole in atopic dermatitis and the molecular mechanism. Atopic dermatitis was induced by 2,4‐dinitrochlorobenzene. Pathological damage of ear was detected by H&E staining. IgE level in serum or thymic stromal lymphopoietin (TSLP) level in supernatant was detected by ELISA. Interleukin (IL)‐4 expression and IL‐13 expression in CD4⁺ T cells were detected using flow cytometry. The expression levels of mRNA or protein levels were detected by RT‐PCR or Western blot. Osthole attenuated atopic dermatitis development in mouse model. Osthole inhibits Th2 cell response, but have on influence on Th1 or Th17 cell response in the skin. In mouse model, osthole treatment significantly inhibited atopic dermatitis via directly inhibiting TLSP expression levels in keratinocytes. Osthole treatment alleviates atopic dermatitis through directly down‐regulating TSLP production from keratinocytes. Osthole may serve as a potential choice for atopic dermatitis treatment in clinic.     

Revival of favus in Japan caused by Trichophyton schoenleinii

Favus is a type of dermatophytosis known to produce yellow scutula around hair follicles. Most cases of this disease worldwide are infections of Trichophyton schoenleinii. Favus has rarely been reported in Japan throughout the last four decades, and T. schoenleinii has not been clinically isolated in any case during the period. Here, we report a case of favus of vellus hair observed in a 63‐year‐old Japanese woman. Fungal culture showed negative; however, we detected fungal elements in the crust and hair bulbs by Grocott staining. Pathogenic fungi were identified as T. schoenleinii by polymerase chain reaction‐based DNA sequencing, targeting the internal transcribed spacer regions of the rRNA gene using the formalin‐fixed, paraffin‐embedded tissue sample. She was successfully treated with p.o. administration of terbinafine and topical application of luliconazole cream.     

Epidemiologic Study of Malassezia Yeasts in Seborrheic Dermatitis Patients by the Analysis of 26S rDNA PCR-RFLP

Background

This case-control study concerns a molecular biological method based on the data gathered from a group of Korean subjects to examine the distribution of Malassezia yeasts in seborrheic dermatitis (SD) patients. Cultures for Malassezia yeasts were taken from the foreheads, cheeks and chests of 60 patients with SD and in 60 healthy controls of equivalent age.

Objective

The purpose of this study is to identify the relationship between certain species of Malassezia and SD. This was done by analyzing the differences in the distribution of Malassezia species in terms of age and body parts of the host with healthy controls.

Methods

26S rDNA PCR-RFLP, a fast and accurate molecular biological method, was used to overcome the limits of morphological and biochemical methods.

Results

The positive Malassezia culture rate was 51.7% in patients with SD, which was lower than that of healthy adults (63.9%). M. restricta was dominant in patients with SD (19.5%). Likewise, M. restricta was identified as a common species (20.5%) in healthy controls. In the ages 31~40, M. restricta was found to be the most common species (31.6%) among SD patients.

Conclusion

According to the results of the study, the most frequently isolated species was M. restricta (19.5%) in patients with SD. There was no statistically significant difference in the distribution of Malassezia species between the SD patients and healthy control groups.     

Dietary habits in adult Japanese patients with atopic dermatitis

Dietary habits can modulate the pathogenesis of atopic dermatitis. We evaluated these habits in adult Japanese patients with atopic dermatitis using a validated, brief‐type self‐administered diet history questionnaire and compared the results to those of age‐ and sex‐matched healthy controls. Patients with atopic dermatitis showed higher intakes of carbohydrate and potatoes and lower intakes of alcohol, niacin, meat and oils/fats compared with those of the healthy controls. The results of logistic regression analysis showed that the intake of alcohol was negatively associated with atopic dermatitis (odds ratio, 0.905; 95% confidence interval, 0.832–0.983; P = 0.0181). The intakes of vitamin B₆ and fruit were positively correlated with the severity scoring of atopic dermatitis. Multiple regression analysis revealed that vitamin B₆ intake was a predictor of the severity scoring of atopic dermatitis (β = 26.98508709, t = 2.3995292, P = 0.01933781). The intakes of vegetable fat, n‐6 polyunsaturated fatty acid, and confections were lower in the severe atopic dermatitis group (severity scoring of atopic dermatitis, ≥33) than those in the mild group. Atopic dermatitis is negatively associated with alcohol intake, and intake of vitamin B₆ is a predictor of severity scoring of atopic dermatitis. The intake of n‐6 polyunsaturated fatty acid is lower in the severe atopic dermatitis group than that in the mild group. Further study is warranted on the relationships of these results with abnormal immune responses, impaired skin barrier or pruritus in atopic dermatitis.     

Mechanism of action of antifungals and combination therapy

Biochemical studies have identified a number of potential targets for antifungal chemotherapy, including cell wall synthesis, membrane sterol biosynthesis, nucleic acid synthesis, metabolic inhibition and macromolecular biosynthesis. The inhibition of cell wall synthesis would be in theory highly specific since only fungal cells build their cell wall with chitin and glucan. Despite this defined specificity, none of the clinically available drugs act there. Most antifungals interfere with enzymatic steps involved in the complicated synthesis of ergosterol. Allylamines interfere with the squalene epoxidation leading to an intracellular accumulation of squalene. The imidazole and triazole derivatives interact with the cytochrom P-450-dependent C₁₄-demethylase system. C₁₄-methyl-sterols like lanosterol are accumulated within the fungal cell. Under treatment of morpholine derivatives like amorolfine, ignosterol a sterol containing a Δ₁₄ double bond is accumulated. Amorolfine inhibits two steps in the pathway of ergosterol biosynthesis namely the Δ₁₄ reductase and the Δ_7,8 isomerase.Amorolfine possesses a broad antimycotic spectrum against fungi pathogenic to plants and humans. The drug not only inhibits the fungal growth, it also shows a strong fungicidal activity which is both concentration- and time-dependent. The fungicidal activity against dermatophytes is in the same order as the one of terbinafine. Amorolfine also shows good fungicidal activity against yeasts, dimorphic and dematiaceous fungi.Amorolfine exerts synergistic activity in combination with several other antifungals such as ketoconazole, terbinafine, itraconazole and griseofulvin. The fungistatic activity of all these antifungals against dermatophytes is slightly increased by addition of amorolfine. The synergistic effect seen in vitro is, however, more pronounced in an animal model. Combination therapy of amorolfine with terbinafine, itraconazole and griseofulvin was studied in a murine trichophytosis model. Murine trichophytosis is self-healing, the course of infection reaches a plateau on day 7 and declines thereafter throughout the second week. Mice infected with trichophyton and treated with various antifungal drugs generally responded to the treatment in a dose-dependent manner, showing a significant reduction in the appearance of mycotic foci in comparison to untreated animals. The combinations of amorolfine with griseofulvin, terbinafine, itraconazole and fluconazole were always more efficient than the individual drug treatment alone, provided that the single therapy is not overwhelmingly efficacious per se. Antagonism was never observed.     

Baicalein increases keratin 1 and 10 expression in HaCaT keratinocytes via TRPV4 receptor activation

In this study, we characterized the effect of baicalein on the regulation of keratinocyte differentiation and proliferation, which are abnormal in atopic dermatitis or psoriasis. Treatment of HaCaT keratinocytes with 10 μm baicalein slightly inhibited cell growth, caused morphological differentiation and increased expression of keratins 1 and 10 (K1/K10) without affecting ROS generation, cytochrome c release or apoptosis. Baicalein treatment caused growth arrest in G₀/G₁ phase and also induced Ca²⁺ influx via TRPV4 receptor activation. Phosphorylation of ERK, Akt and p38 MAPK, but not JNK, was increased by baicalein, and inhibition of phosphorylation of ERK, but not that of Akt or p38 MAPK, blocked the baicalein‐induced increase in K1/K10 expression, suggesting that ERK activation is involved in this increase. Removal of extracellular Ca²⁺ or blockade of Ca²⁺ influx by pharmacological inhibition or silencing of the TRPV4 receptor did not affect growth arrest, ROS generation or apoptosis, but inhibited baicalein‐induced ERK phosphorylation and K1/K10 expression. Thus, baicalein treatment increases differentiation, and decreases proliferation, of keratinocytes. The mechanism of differentiation of keratinocytes is distinct from that of proliferation, the former being Ca²⁺ dependent and the latter Ca²⁺ independent.     

DAMP molecules S100A9 and S100A8 activated by IL‐17A and house‐dust mites are increased in atopic dermatitis

S100A9 and S100A8 are called damage‐associated molecular pattern (DAMP) molecules because of their pro‐inflammatory properties. Few studies have evaluated S100A9 and S100A8 function as DAMP molecules in atopic dermatitis (AD). We investigated how house‐dust mites affect S100A9 and S100A8 expression in Th2 cytokine‐ and Th17 cytokine‐treated keratinocytes, and how secretion of these molecules affects keratinocyte‐derived cytokines. Finally, we evaluated expression of these DAMP molecules in AD patients. S100A9 expression and S100A8 expression were strongly induced in IL‐17A‐ and Dermatophagoides (D.) farinae‐treated keratinocytes, respectively. Furthermore, co‐treatment with D. farinae and IL‐17A strongly increased expression of S100A9 and S100A8 compared with D. farinae‐Th2 cytokine co‐treatment. The IL‐33 mRNA level increased in a dose‐dependent manner in S100A9‐treated keratinocytes, but TSLP expression did not change. S100A8/A9 levels were also higher in the lesional skin and serum of AD patients, and correlated with disease severity. Taken together, S100A9 and S100A8 may be involved in inducing DAMP‐mediated inflammation in AD triggered by IL‐17A and house‐dust mites.     

Aldo‐keto reductase 1C3 is overexpressed in skin squamous cell carcinoma (SCC) and affects SCC growth via prostaglandin metabolism

Aldo‐keto reductase 1C3 (AKR1C3) is an enzyme involved in metabolizing prostaglandins (PGs) and sex hormones. It metabolizes PGD₂ to 9α11β‐PGF₂, diverting the spontaneous conversion of PGD₂ to the PPARγ agonist, 15‐Deoxy‐Delta‐12, 14‐prostaglandin J2 (15d‐PGJ₂). AKR1C3 is overexpressed in various malignancies, suggesting a tumor promoting function. This work investigates AKR1C3 expression in human non‐melanoma skin cancers, revealing overexpression in squamous cell carcinoma (SCC). Effects of AKR1C3 overexpression were then evaluated using three SCC cell lines. AKR1C3 was detected in all SCC cell lines and its expression was upregulated in response to its substrate, PGD₂. Although attenuating AKR1C3 expression in SCC cells by siRNA did not affect growth, treatment with PGD₂ and its dehydration metabolite, 15d‐PGJ₂, decreased SCC proliferation in a PPARγ‐dependent manner. In addition, treatment with the PPARγ agonist pioglitazone profoundly inhibited SCC proliferation. Finally, we generated an SCC cell line that stably overexpressed AKR1C3 (SCC‐AKR1C3). SCC‐AKR1C3 metabolized PGD₂ to 9α11β‐PGF₂ 12‐fold faster than the parent cell line and was protected from the antiproliferative effect mediated by PGD₂. This work suggests that PGD₂ and its metabolite 15d‐PGJ₂ attenuate SCC proliferation in a PPARγ‐dependent manner, therefore activation of PPARγ by agonists such as pioglitazone may benefit those at high risk of SCC.     

Molecular Analysis of Malassezia Microflora on the Skin of the Patients with Atopic Dermatitis

Background

The yeasts of the genus Malassezia are members of the normal flora on human skin and they are found in 75~80% of healthy adults. Since its association with various skin disorders have been known, there have been a growing number of reports that have implicated Malassezia yeast in atopic dermatitis (AD).

Objective

The aim of the present study is to isolate the various Malassezia species from AD patients by using 26S rDNA (ribosomal Deoxyribonucleic acid) PCR-RFLP and to investigate the relationship between a positive Malassezia culture and the severity of AD.

Methods

Cultures for Malassezia yeasts were taken from the scalp, cheek, chest, arm and thigh of 60 patients with atopic dermatitis. We used a rapid and accurate molecular biological method 26S rDNA PCR-RFLP, and this method can overcome the limits of the morphological and biochemical methods.

Results

Positive Malassezia growth was noted on 51.7% of the patients with atopic dermatitis by 26S rDNA PCR-RFLP analysis. The overall dominant species was M. sympodialis (16.3%). M. restricta was the most common species on the scalp (30.0%) and cheek (16.7%). M. sympodialis (28.3%) was the most common species on the chest. The positive culture rate was the highest for the 11~20 age group (59.0%) and the scalp showed the highest rate at 66.7%. There was no significant relationship between the Malassezia species and SCORing for Atopic Dermatitis (SCORAD).

Conclusion

The fact that the cultured species was different for the atopic dermatitis lesion skin from that of the normal skin may be due to the disrupted skin barrier function and sensitization of the organism induced by scratching in the AD lesion-skin. But there was no relationship between the Malassezia type and the severity score. The severity score is thought to depend not on the type, but also on the quantity of the yeast.     

Comparative Assessment of the Efficacy and Safety of Sertaconazole (2%) Cream Versus Terbinafine Cream (1%) Versus Luliconazole (1%) Cream In Patients with Dermatophytoses: A Pilot Study

Background:

Sertaconazole is a new, broad spectrum, fungicidal and fungistatic imidazole with added antipruritic and anti-inflammatory activity that would provide greater symptomatic relief and hence would be beneficial in improving the quality of life for the patient with dermatophytoses.

Aims and Objectives:

To compare efficacy and safety of sertaconazole, terbinafine and luliconazole in patients with dermatophytoses.

Materials and Methods:

83 patients with tinea corporis and tinea cruris infections were enrolled in this multicentre, randomized, open label parallel study. The initial ‘Treatment Phase’ involved three groups receiving either sertaconazole 2% cream applied topically twice daily for four weeks, terbinafine 1% cream once daily for two weeks, luliconazole 1% cream once daily for two weeks. At the end of treatment phase, there was a ‘Follow-up Phase’ at end of 2 weeks, where the patients were assessed clinically and mycologically for relapse.

Results:

Of the 83 patients, 62 completed the study, sertaconazole (n = 20), terbinafine (n = 22) and luliconazole (n = 20). The primary efficacy variables including change in pruritus, erythema, vesicle, desquamation and mycological cure were significantly improved in all the three groups, as compared to baseline, in the Treatment and Follow-up phase. Greater proportion of patients in sertaconazole group (85%) showed resolution of pruritus as compared to terbinafine (54.6%); and luliconazole (70%), (P < 0.05 sertaconazole vs terbinafine). There was a greater reduction in mean total composite score (pruritus, erythema, vesicle and desquamation) in sertaconazole group (97.1%) as compared to terbinafine (91.2%) and luliconazole (92.9%). All groups showed equal negative mycological assessment without any relapses. All three study drugs were well tolerated. Only one patient in sertaconazole group withdrew from the study due to suspected allergic contact dermatitis.

Conclusion:

Sertaconazole was better than terbinafine and luliconazole in relieving signs and symptoms during study and follow up period. At the end of ‘Treatment Phase’ and ‘Follow-up’ Phase, all patients showed negative mycological assessment in all three treatment groups suggesting no recurrence of the disease.