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Featured researches published by Natsuko Fujita.


Journal of The European Academy of Dermatology and Venereology | 2009

Urinary biomarker of oxidative stress in patients with psoriasis vulgaris and atopic dermatitis

Kozo Nakai; Kozo Yoneda; Reiko Maeda; Asuka Munehiro; Natsuko Fujita; Ikumi Yokoi; Junko Moriue; Tetsuya Moriue; Hiroaki Kosaka; Yasuo Kubota

Background  The involvement of oxidative stress in the pathogenesis of various skin disorders has been suggested for decades. However, few clinical studies have assessed oxidative stress in skin diseases. The easiest and least invasive method to assess oxidative stress in patients may be the measurement of oxidation products in urine.


Journal of Dermatology | 2009

Nodular cystic fat necrosis in a patient with diabetes mellitus.

Yasuo Kubota; Kozo Nakai; Tetsuya Moriue; Ikumi Yokoi; Natsuko Fujita; Izumi Miyamoto; Kozo Yoneda

Dear Editor, Nodular cystic fat necrosis (NCFN), first described by Przyjemski et al. in 1977, is a distinct, benign subcutaneous lesion characterized histologically by encapsulated fat necrosis showing membranocystic change. We report a case of nodular cystic fat necrosis in a patient with diabetes mellitus. An 81-year-old Japanese man presented multiple asymptomatic subcutaneous nodules on his back and extremities with a 2-year history. On physical examination, approximately 30 mobile, firm subcutaneous nodules measured 10–15 mm in diameter were scattered at the extensor aspect of the lower back, upper arm and thigh. (Fig. 1a,b) His general condition was good. He had no history of trauma. Clinical differential diagnosis included lipoma, angiolipoma, post-traumatic lipogranuloma, subcutaneous type sarcoidosis and Rothmann–Makai syndrome. He was also diagnosed with diabetes mellitus and had suffered from diabetic retinopathy for more than 10 years. Laboratory data revealed that his fasting blood sugar (FBS) level was 121 mg/dL and hemoglobin A1c was 6.1%. Histologically, the excised cutaneous mass showed well-demarcated encapsulated fat necrosis and marked lipomembranous changes. The lipomembrane was positive for periodic acid-Schiff staining (Fig. 2a,b). Two months after the first visit, the nodules decreased in size slightly with good control of FBS and HbA1c levels although no medication for skin lesions was used. Nodular cystic fat necrosis shows a distinctive spectrum of clinical and histological features. Names such as nodular cystic fat necrosis, mobile encapsulated lipoma and encapsulated fat necrotic nodules have been offered to designate the lesion. Most of the lesions are mobile subcutaneous nodules in regions vulnerable to trauma, such as the elbows, knees and shins. The histology is characterized by encapsulated fat necrosis and lipomembranous change in which multiple, non-viable adipocytes are surrounded by condensed fibrous tissue. The etiology of NCFN is still unclear. Its pathogenesis seems to be related to trauma, rapid vascular insufficiency and subsequent fibrous capsule formation. Many previously reported patients, however, had no history of trauma, as was the same with our patient. The lesion must be distinguished histologically from lipoma, angiolipoma, α-1-antitrypsin deficiency-associated panniculitis and pancreatic fat necrosis.


British Journal of Dermatology | 2010

Seborrhoeic keratoses and acanthosis nigricans in a long‐term survivor of thanatophoric dysplasia

Kozo Nakai; Kozo Yoneda; Tetsuya Moriue; Asuka Munehiro; Natsuko Fujita; Junko Moriue; Ikumi Yokoi; Reiji Haba; S. Itoh; Yasuo Kubota

therapy, there was a marked recession of the palmoplantar hyperkeratoses. The suberythroderma, however, showed no response in either intensity or spread. After obtaining consent from the patient, who weighed 78 kg, and ruling out relevant infections (tuberculosis, viral hepatitis, HIV infection), we initiated therapy with ustekinumab 45 mg given as a single subcutaneous injection. After 4 weeks, the erythema had almost completely faded (Fig. 1). We repeated the administration of ustekinumab 45 mg subcutaneously after 4 weeks and continued it at 12week intervals. The patient was completely free of symptoms after ustekinumab therapy for a total of 16 weeks. The aetiopathogenesis of PRP remains unknown. The currently preferred explanation is a T cell-mediated autoimmunological event based on a possibly infection-reactive hypersensitivity reaction. The rather inconclusive data thus far support the hypothesis that PRP is not a single, uniform entity, but rather describes phenotypically similar states of different pathogenetic inflammation patterns. This would also explain the very different and ultimately individual response of the disease to the known therapy options. Due to the histological and clinical overlap of PRP with psoriasis vulgaris, parallels have been drawn regarding the therapeutic options including established antipsoriatic systemic therapies considered for the treatment of PRP. The extent to which knowledge of the cellular regulation of inflammatory processes in psoriasis can be applied to PRP is, however, unclear. Nonselective immunosuppressive therapy approaches show efficacy in individual cases of both diseases. TNF-a blockers and the anti-CD11a mAb efalizumab as antipsoriatics have also been found basically effective in PRP. In light of this, efficacy of ustekinumab as an anti-p40 mAb to block interleukin (IL)-12 ⁄ IL-23 could be expected, especially as ustekinumab is known to act very early at the regulatory T-cell (TH17) level, thus suppressing activation of further T-cell cascades. Although the present single case report does not enable additional statements on the pathogenetic processes of PRP, it does become clear from the apparent effectiveness of ustekinumab that an overlap with psoriasis vulgaris can also be postulated in this case. Additional clinical studies must show how reliable the therapeutic effects of ustekinumab are in PRP. Perhaps this will become a new treatment option for PRP, at least in therapy-resistant patients.


British Journal of Dermatology | 2010

Bevacizumab-induced hand-foot syndrome: circumscribed type

Asuka Munehiro; Kozo Yoneda; Kozo Nakai; Toshio Demitsu; Tetsuya Moriue; Junko Moriue; Ikumi Yokoi; Natsuko Fujita; N. Matsuura; Sinya Ishikawa; Hiroyasu Yokomise; Yasuo Kubota

compared with placebo. Indeed, the limited recommendations for the use of TNF-a blockers in BD are primarily based upon this single study. At present no formal guidelines exist to support clinicians in the use of biologics in other forms of oral mucosal disease. Furthermore, given this lack of evidence, it would seem unlikely that formal guidelines and recommendations for such use could be developed at present. Dermatologists are ideally placed to participate in the clinical care of patients with treatment-resistant ⁄refractory inflammatory oral mucosal disease, either as the sole specialist physician or in consultation with colleagues from other specialties (e.g. oral medicine, ophthalmology, and maxillofacial ⁄otorhinolaryngological surgeons). In this context, collective and individual experience of biologic agents, and the provision of formal guidelines for their use in specific indications, may serve as a basis for judicious use and ⁄or advice to colleagues with limited experience of these agents. Individual experience of off-label use in other dermatoses may also be relevant. Clearly great caution must be used when discussing ‘off-label’ use of any agent, chiefly for patient safety but also for economical considerations. Nevertheless, using established guidelines as a framework for individual case selection, certain proposals could be made for clinical decisionmaking regarding the use of ‘biologics’ in select patients with severe treatment-resistant oral mucosal disease. An appropriate reference point may be the recently updated recommendations from the British Association of Dermatologists for use of biologics in psoriasis. It should be explicitly stated that this author in no form suggests that such guidelines be used to validate off-label usage. Yet, they do represent authoritative guidance on their recommended use in dermatology, and, as such may serve as the best available resource to guide similar use on an individual trial basis as appropriate. Similar dermatology guidelines and those developed for rheumatology, including those for BD, may also assist. Each emphasizes strict eligibility criteria which include: (i) severe disease, as measured by objective measurements such as disease indices and quality of life scores and (ii) patients who are refractory to ⁄ intolerant of conventional systemic therapy or where such therapy is contraindicated. At a minimum, similar criteria (including the use of the best available objective measurements for the specific mucosal condition) should be met before one should consider use of biologics in oral disease. Biological class and agent-specific contraindications and cautions should be followed, with appropriate pretreatment clinical and laboratory assessments and continued monitoring throughout treatment. As patients must be able to provide informed consent and use of biologics must be fully documented, the strong recommendation for patient registration in the British Association of Dermatologists’ Biologic Interventions Register (BADBIR) is one that could be extended for all biologic use (including oral mucosal disease). Finally, it is essential that any use of biologics be conducted and ⁄or supervised by clinicians experienced in these agents. In this matter, dermatologists may be most suitable. I . O’NE I L L de l’immeuble 3, Centre d’Affaires Poincaré, 3 Rue Poincaré, 06000, Nice, France E-mail: [email protected]


Journal of The European Academy of Dermatology and Venereology | 2009

Narrow-band ultraviolet B decreases serum interleukin-2 receptor levels in patients with poikiloderma vasculare atrophicans

Kozo Nakai; Kozo Yoneda; Tetsuya Moriue; Izumi Miyamoto; Natsuko Fujita; Ikumi Yokoi; Yasuo Kubota

© 2008 The Authors JEADV 2009, 23, 835–862 Journal compilation


Journal of Dermatology | 2012

Pinch and ligation method: a new non-surgical approach to viral warts.

Tetsuya Moriue; Kozo Yoneda; Junko Moriue; Kozo Nakai; Ikumi Yokoi; Natsuko Fujita; Asuka Munehiro; Reiko Maeda; Yasuo Kubota

thoic acid. After the application of a synthetic retinoid, 0.1% adapalene gel, blister formation was not observed at the tumor site, and only the keratotic plaque remained for 1 full year. In this tumor, acantholysis generate multiple small blisters which extend into a large hemorrhagic blister. We think that acceleration of acantholysis by retinoid causes blister collapse easily and prevents formation of a hemorrhagic blister. Although a synthetic retinoid cannot remove the tumor, it can be an alternative treatment that improves patient satisfaction and may also be applied to other benign tumors with acantholysis.


Journal of The European Academy of Dermatology and Venereology | 2009

Caveolae in Fabry telangiectagia.

Kozo Nakai; Kozo Yoneda; Tetsuya Moriue; Natsuko Fujita; Yasuo Kubota

References 1 Shimomura Y, Wajid M, Ishii Y et al. Disruption of P2RY5, an orphan G protein-coupled receptor, underlies autosomal recessive woolly hair. Nat Genet 2008; 40: 335–339. 2 Petukhova L, Sousa EC Jr, Martinez-Mir A et al. Genome-wide linkage analysis of an autosomal recessive hypotrichosis identifies a novel P2RY5 mutation. Genomics 2008; 92: 273–278. 3 Shimomura Y, Wajid M, Petukhova L, Shapiro L, Christiano AM. Mutations in the lipase H gene underlie autosomal recessive woolly hair ⁄ hypotrichosis. J Invest Dermatol 2009; 129: 622–628. 4 Shimomura Y, Garzon MC, Kristal L, Shapiro L, Christiano AM. Autosomal recessive woolly hair with hypotrichosis caused by a novel homozygous mutation in the P2RY5 gene. Exp Dermatol 2009; 18: 218– 221. 5 Horev L, Tosti A, Rosen I et al. Mutations in lipase H cause autosomal recessive hypotrichosis simplex with woolly hair. J Am Acad Dermatol 2009; 61: 813–818. 6 Pasternack SM, Von Kügelgen I, Aboud KA et al. G protein-coupled receptor P2Y5 and its ligand LPA are involved in maintenance of human hair growth. Nat Genet 2008; 40: 329–334. 7 Kazantseva A, Goltsov A, Zinchenko R et al. Human hair growth deficiency is linked to a genetic defect in the phospholipase gene LIPH. Science 2006; 314: 982–985. 8 Yanagida K, Masago K, Nakanishi H et al. Identification and characterization of a novel lysophosphatidic acid receptor, p2y5 ⁄ LPA6. J Biol Chem 2009; 284: 17731–17741. 9 Tariq M, Ayub M, Jelani M et al. Mutations in the P2RY5 gene underlie autosomal recessive hypotrichosis in 13 Pakistani families. Br J Dermatol 2009; 160: 1006–1010. 10 Petukhova L, Shimomura Y, Wajid M, Gorroochurn P, Hodge SE, Christiano AM. The effect of inbreeding on the distribution of compound heterozygotes: a lesson from lipase H mutations in autosomal recessive woolly hair ⁄ hypotrichosis. Hum Hered 2009; 68: 117–130.


European Journal of Dermatology | 2009

Giant pilomatricoma and psoriasis vulgaris with myotonic dystrophy

Kozo Nakai; Kozo Yoneda; Reiko Maeda; Ikumi Yokoi; Natsuko Fujita; Asuka Munehiro; Tetsuya Moriue; Yasuo Kubota


European Journal of Dermatology | 2009

Primary cutaneous nocardiosis in a patient with Evans’ Syndrome

Tetsuya Moriue; Kozo Yoneda; Junko Moriue; Kozo Nakai; Ikumi Yokoi; Natsuko Fujita; Izumi Miyamoto; Katsuharu Kittaka; Hiroaki Dobashi; Yasuo Kubota


Nishi Nihon Hifuka | 2012

Comparative Study of Two Types of Emollients Containing 0.3% Heparinoid on the Clinical Efficacy, Usability and Satisfaction in Patients with Atopic Dermatitis

Yasuo Kubota; Tetsuya Moriue; Junko Moriue; Kozo Nakai; Ikumi Yokoi; Natsuko Fujita; Asuka Munehiro; Reiko Maeda; Emiko Ishikawa; Youichiro Hosokawa; Ayako Koura; Kozo Yoneda

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Kozo Yoneda

Osaka Ohtani University

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