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Featured researches published by Akiyo Sano.


Medical Mycology | 2009

Malassezia folliculitis is caused by cutaneous resident Malassezia species

Narifumi Akaza; Hirohiko Akamatsu; Yasuyuki Sasaki; Masataka Kishi; Hiroshi Mizutani; Akiyo Sano; Keiko Hirokawa; Satoru Nakata; Setsuko Nishijima; Kayoko Matsunaga

Malassezia folliculitis [MF] is caused by the invasion of hair follicles by large numbers of Malassezia cells, but it remains unclear which Malassezia species are involved in the disease. To clarify this situation, Malassezia species isolated from lesions of MF patients were analyzed by both culture and non-culture methods. In addition, Malassezia species recovered from the non-lesion areas of the skin of MF patients and skin samples of healthy subjects were included in this study. The test population consisted of 32 MF patients and 40 healthy individuals. The lesions were obtained using a comedone extractor, while swabs were employed to obtain skin samples from non-lesion areas of the patients and healthy subjects. Malassezia DNA was analyzed using a real-time PCR technique. The detection limit of the culture method was 5 CFU/cm(2) as opposes 50 cells/cm(2) with non-culture procedures. The predominant species recovered from MF lesions were M. globosa and M. sympodialis by culture method analysis, and M. restricta, M. globosa, and M. sympodialis with non-culture methods. These results were in agreement with those found with samples from non-lesion skin areas of MF patients and healthy subjects. This study clarified that MF is caused by Malassezia species that are part of the cutaneous microflora and not by exogenous species.


Journal of Dermatology | 2010

Cutaneous Malassezia microbiota of healthy subjects differ by sex, body part and season.

Narifumi Akaza; Hirohiko Akamatsu; Yasuyuki Sasaki; Shiori Takeoka; Masataka Kishi; Hiroshi Mizutani; Akiyo Sano; Keiko Hirokawa; Satoru Nakata; Kayoko Matsunaga

Malassezia is a component of normal cutaneous resident microbiota. The aim of this study was to quantitatively clarify the differences in cutaneous Malassezia microbiota in healthy subjects by sex, body part and season. Samples were collected from the forehead, cheek, upper chest and upper back of 20 healthy men and 20 healthy women (average age 32 years) in summer and winter by the swab method. Malassezia DNA was analyzed using a real‐time PCR system. As a result, in sex, body parts and season, men, the upper trunk and summer showed the highest total numbers of cutaneous Malassezia species on average. There were also differences depending on the analytical method. The predominant species were M. restricta on the face of men, M. globosa and M. dermatis on the upper trunk of men, and M. globosa and M. sympodialis on the upper trunk of women. This study clarified that the cutaneous Malassezia microbiota of healthy subjects differed by sex, body part and season.


Contact Dermatitis | 2014

Allergic contact dermatitis caused by 3-o-ethyl-L-ascorbic acid (vitamin C ethyl).

Akiko Yagami; Kayoko Suzuki; Yusuke Morita; Yohei Iwata; Akiyo Sano; Kayoko Matsunaga

No abstract available Keywords: 3-o-ethyl-l-ascorbic acid; allergic contact dermatitis; cosmetics; skin-lightening agent; vitamin C ethyl.


Allergology International | 2014

A New Reliable Method for Detecting Specific IgE Antibodies in the Patients with Immediate Type Wheat Allergy due to Hydrolyzed Wheat Protein: Correlation of Its Titer and Clinical Severity

Masashi Nakamura; Akiko Yagami; Kazuhiro Hara; Akiyo Sano; Tsukane Kobayashi; Michiko Aihara; Michihiro Hide; Yuko Chinuki; Eishin Morita; Reiko Teshima; Kayoko Matsunaga

BACKGROUND Immediate-type wheat allergy caused by a specific hydrolyzed wheat protein (HWP-IWA), Glupearl 19S (GP19S), typically develops food-dependent exercise-induced anaphylaxis (FDEIA), but is different from conventional FDEIA, or simple wheat allergy in many aspects. The skin prick test (SPT) is considered to be the most effective method for diagnosis of HWP-IWA. As SPT is a relatively qualitative method, we developed quantitative and high-throughput test method for HWP-IWA. METHODS An enzyme-linked immunosorbent assay (ELISA)-based GP19S-specific IgE assay was tested using sera from 14 HWP-IWA and five conventional wheat-dependent exercise-induced anaphylaxis (CO-WDEIA) patients, as well as five healthy subjects. Then a validation study at five different institutions was carried out using sera from 10 HWP-IWA and five CO-WDEIA patients, as well as five healthy subjects different from the previous studies. RESULTS The mean unit values converted from measured absorbance of ELISA were 68.3, 1.3 and 1.1 respectively. Furthermore, the validation study revealed reproducible results across all five institutions, with the standard deviation (SD) being 0.3-0.4 for the healthy group, 0.2-0.6 for the CO-WDEIA group, and 3.8-9.6 for HWP-IWA group except for one case. One case of HWP-IWA was excluded from analysis due to the high SD of 53.3 units, indicating that samples with a unit value > 100.0 will affect inter-laboratory reproducibility. CONCLUSIONS Our findings suggest that the ELISA-based GP19S-specific IgE assay can be used to test HWP-IWA using venous blood samples, except for those with a unit value > 100.0.


Dermatology | 2010

Cutaneous Malassezia microbiota in atopic dermatitis patients differ by gender and body part.

Narifumi Akaza; Hirohiko Akamatsu; Yasuyuki Sasaki; Shiori Takeoka; Masataka Kishi; Hiroshi Mizutani; Akiyo Sano; Keiko Hirokawa; Satoru Nakata; Kayoko Matsunaga

Background:Malassezia is a particularly important factor in the occurrence of atopic dermatitis (AD).Aim: The aim of this study was to quantitatively clarify the Malassezia species isolated from AD patients by gender, body part and analytical method in detail. Methods: The subjects were 20 AD males and 47 AD females. Samples were collected from lesion and nonlesion areas on the face and upper trunk of AD patients. Malassezia DNA was analyzed using a real-time PCR system. Results: The cutaneous Malassezia microbiota in AD patients differed by gender, body part and analytical method. Conclusions: The present results indicate the possibility that the influence of Malassezia antigens is different according to gender and body part.


Contact Dermatitis | 2013

Allergic contact dermatitis caused by phenylethyl resorcinol [4-(1-phenylethyl)-1,3-benzenediol], a skin-lightening agent in cosmetics.

Michi Gohara; Akiko Yagami; Kayoko Suzuki; Yusuke Morita; Akiyo Sano; Yohei Iwata; Takashi Hashimoto; Kayoko Matsunaga

Allergic contact dermatitis caused by phenylethyl resorcinol [4-(1-phenylethyl)-1,3-benzenediol], a skin-lightening agent in cosmetics Michi Gohara1,2, Akiko Yagami1, Kayoko Suzuki3, Yusuke Morita1, Akiyo Sano1, Yohei Iwata1, Takashi Hashimoto2 and Kayoko Matsunaga1 1Department of Dermatology, Fujita Health University School of Medicine, Aichi, 470-1192, Japan, 2Department of Dermatology, Kurume University School of Medicine, Fukuoka, 830-0011, Japan, and 3Department of Dermatology, Kariya Toyota General Hospital, Aichi, 448-8505, Japan


Journal of Dermatology | 2015

Rhododendrol-induced leukoderma accompanied by allergic contact dermatitis caused by a non-rhododendrol skin-lightening agent, 5,5′-dipropylbiphenyl-2,2′-diol

Akiko Yagami; Kayoko Suzuki; Akiyo Sano; Masayuki Takahashi; Tsukane Kobayashi; Yusuke Morita; Aki Ando; Yohei Iwata; Kayoko Matsunaga

Dear Editor, In 2013, a number of consumers who used rhododendrol-containing cosmetics developed leukoderma at the site of application of the cosmetic in Japan and Taiwan. Here, we report the first case of rhododendrol (4-[4-hydroxyphenyl]-2-butanol; C10H14O2, Chemical Abstracts Service [CAS] no. 501-96-2, molecular weight [MW] = 166.22)-induced leukoderma accompanied by allergic contact dermatitis caused by 5,50-dipropylbiphenyl-2,20diol (C18H22O2, CAS no. 20601-85-8, MW = 270.37). A 64-year-old housewife suffered from itchy erythema on the face for 2 years and noticed leukoderma at the same sites. The leukoderma gradually extended to her neck and forearms. For 2 years, she had been using skin-lightening cosmetics that contained 5,50-dipropylbiphenyl-2,20-diol or rhododendrol. When she presented at our hospital, she had leukoderma surrounded by pigmentation and itchy erythema on her face. The leukoderma was prominent on the face, and also affected her neck and forearms. Because we initially suspected allergic contact dermatitis caused by the cosmetics, we performed patch testing using her cosmetics and patch test allergens related to cosmetics after obtaining written informed consent. Finn Chambers (Smart Practice, Phoenix, AZ, USA) were used for the test, and the results were read according to the International Contact Dermatitis Research Group standards. On days 3, 4 and 7, the patient showed a positive reaction (+) to her skin lotion (as is) containing 5,50-dipropylbiphenyl-2,20-diol. In the ingredient patch test of this skin lotion, she also showed positive reactions ([+?] on day 4 and [+] on day 7) to 5,50-dipropylbiphenyl-2,20-diol (0.5% pet.) and negative reactions to rhododendrol (2% pet). All three healthy control subjects did not react to 5,50-dipropylbiphenyl-2,20-diol and rhododendrol. Rhododendrol was synthesized in Japan as a new skinlightening agent that suppresses melanogenesis formation. Cosmetics that contained 2% rhododendrol had been sold in 10 Asian countries. The symptoms of depigmentation had been confirmed in approximately 16 000 (2%) of 800 000 estimated users of cosmetic products containing rhododendrol (The Japanese Dermatological Association Special Committee on the Safety of Cosmetics Containing Rhododendrol, 2014 [in Japanese]). On the other hand, Suzuki et al. reported the first case of allergic contact dermatitis caused by the skin-lightening agent, 5,50-dipropylbiphenyl-2,20-diol. Because 5,50-dipropylbiphenyl-2,20-diol was a skin lightening agent as well as rhododendrol, we could not deny the possibility that the leukoderma of our patient’s face and neck was caused by 5,50-dipropylbiphenyl-2,20-diol. However, based on the sites of her lesions of leukoderma, we reached the diagnosis of rhododendrol-induced leukoderma accompanied by allergic contact dermatitis from 5,50-dipropylbiphenyl-2,20-diol. After discontinuing the cosmetics containing 5,50-dipropylbiphenyl-2,20-diol and rhododendrol, her erythema and leukoderma improved (Fig. 1). Sasaki et al. elucidated that rhododendrol Figure 1. Clinical course of leukoderma in the patient. (Top) Clinical appearance of her neck at the first visit to our department. There was leukoderma surrounded by pigmentation on her neck. (Bottom) Clinical appearance of the neck 1 year after the first visit. The leukoderma had gradually improved.


Journal of Dermatology | 2015

Case of anaphylactic reaction to soy following percutaneous sensitization by soy‐based ingredients in cosmetic products

Akiko Yagami; Kayoko Suzuki; Masashi Nakamura; Akiyo Sano; Yohei Iwata; Tsukane Kobayashi; Mari Suzuki; Kazuhiro Hara; Reiko Teshima; Kayoko Matsunaga

1 Aihara Y, Kotoyori T, Takahashi Y, Osuna H, Ohnuma S, Ikezawa Z. The necessity for dual food intake to provoke food-dependent exercise-induced anaphylaxis (FEIAn): a case report of FEIAn with simultaneous intake of wheat and umeboshi. J Allergy Clin Immunol 2001; 107: 1100–1105. 2 Komoto K, Kimura Y, Horio T. A case of umeboshi-dependent exercise-incudes anaphylaxis. Jpn J Dermatoallergol 2003; 11: 62–66. (in Japanese). 3 Inomata N, Okazaki F, Moriyama T et al. Identification of peamaclein as a marker allergen related to systemic reactions in peach allergy. Ann Allergy Asthma Immunol 2014; 112: 175–177. 4 Bianchi A, Rienzo Businco AD, Bondanini F, Mistrello G, Carlucci A, Tripodi S. Rosaceae-associated exercise-induced anaphylaxis with positive SPT and negative IgE reactivity to Pru p 3. Eur Ann Allergy Clin Immunol 2011; 43: 122–124. 5 Miceli Sopo S, Monaco S, Giorgio V, Calvani M, Mistrello G, Onesimo R. Food-dependent exercise-induced anaphylaxis (FDEIA) by nectarine in a paediatric patient with weakly positive nectarine prick-byprick and negative specific IgE to Pru p3. Allergol Immunopathol 2013; 41: 201–203.


Allergology International | 2015

Occupational food allergy due to parvalbumin and phaseolin induced by epicutaneous sensitization

Akiko Yagami; Kayoko Suzuki; Masashi Nakamura; Akiyo Sano; Tsukane Kobayashi; Yohei Iwata; Masaru Arima; Kazuhiro Hara; Kayoko Matsunaga

Sensitization in food allergy is traditionally thought to occur via the intestinal tract. In recent years, it has been proposed that the primary mechanism for the development of food allergies is epicutaneous sensitization.1,2 In Japan, numerous cases of wheat allergy that developed from epicutaneous sensitization to hydrolyzed wheat protein (Glupearl 19S) in soap (sold by Yuuka Co., Ltd., Fukuoka, Japan) have been reported; this finding suggests that food allergies may be caused by epicutaneous sensitization.3 A 25-year-old man with atopic dermatitis (LDH: 321 U/L, TARC level: 2208 pg/ml, SCORAD index: 24) and pollinosis visited our hospital for investigation of food allergy and hand eczema. He had worked as a sushi chef and handled raw fish with his bare hands. After one year, he experienced itchiness in his hands after touching multiple types of fish, and intraoral itchiness, respiratory difficulty, diarrhea and abdominal pain occurred after consuming them. Consequently, he changed his job and become a Japanese sweets maker. He touches white bean paste (white kidney beans) with his bare hands for making Japanese sweets in daily work. After 6 months in this job, he felled itchy on his hands after touching white bean paste, and the hand eczema had worsened. When he consumed white bean paste, he began to experience the same symptoms as consuming fish. He had no history of food allergy before working in the aforementioned occupations. We considered the possibility that his food allergies were induced by epicutaneous sensitization. The total IgE level was 841 IU/mL. The levels of specific IgE antibodies by ImmunoCAP (Phadia Inc., Tokyo, Japan) were: class 2 for codfish, flatfish, salmon, mackerel, sardine and horse mackerel, class 3 for soybeans and class 4 for kidney beans. On the other hand, specific IgE antibodies for wheat, gluten, u-5 gliadin, latex and anisakis were not detected. In skin prick test, he showed positive reactions for several kinds of fish (raw, as is) such as young yellowtail, horse mackerel, salmon roe, flatfish, sardine and white kidney bean.4 The tests for prawns, octopus, spiral shellfish, anisakis and black bean paste with azuki beans were negative. The positive control (1% of histamine dihydrochloride, Wako Pure Chemical Industries, Ltd., Osaka, Japan) exhibited a reaction of 3 3 mm. The negative control (physiological saline) exhibited no reaction. The skin prick test reaction was considered positive if a wheal 3 mm diameter appeared after 15e20 min of application. The fluorescence intensities of specific IgE antibodies to


Contact Dermatitis | 2013

Allergic contact dermatitis caused by N,N‐diethyl‐p‐phenylenediamine used in water quality analysis

Yusuke Morita; Kayoko Suzuki; Akiko Yagami; Mamiko Isami; Akiyo Sano; Yusuke Yokoyama; Kayoko Matsunaga

A 28-year-old woman with mild atopic dermatitis started work as an analyst of water quality 2 years previously, where she came into direct contact with chemicals, including DPD, without using gloves. Before starting this job, she had a 1-year history of hand dermatitis with erythema. After she started the new job, the hand dermatitis worsened; there was an itchy erythematous rash with small blisters, and erythema appeared on her arms, legs, and neck. She had never dyed her hair. We performed patch testing with the Japanese baseline series and chemicals used at her workplace, using Finn Chambers® (SmartPractice, Phoenix, AZ, USA) mounted on Scanpor® tape (Norgesplaster AS, Vennesla, Norway). The tests were applied to the upper part of her back for 2 days, and read on D2, D3, and D7, according to International Contact Dermatitis Research Group criteria. The patient showed a positive reaction to DPD at the following concentrations: 1% aqua (D3, +; D7, +); 0.1%

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Akiko Yagami

Fujita Health University

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Yohei Iwata

Fujita Health University

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Masaru Arima

Fujita Health University

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Yasuto Kondo

Fujita Health University

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Yusuke Morita

Fujita Health University

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