H. Koga
Kurume University
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Publication
Featured researches published by H. Koga.
British Journal of Dermatology | 2015
Norito Ishii; Kwesi Teye; Shunpei Fukuda; R. Uehara; T. Hachiya; H. Koga; Atsunari Tsuchisaka; Sanae Numata; Bungo Ohyama; Chiharu Tateishi; Daisuke Tsuruta; Minao Furumura; S. Hattori; Tamihiro Kawakami; Chika Ohata; Takashi Hashimoto
Despite the established pathogenic role of anti‐desmoglein (Dsg) antibodies in classical pemphigus, the significance of autoantibodies to another desmosomal cadherin, desmocollin (Dsc) is at present unknown. No consistent immunoassay for immunoglobulin (Ig) G autoantibodies to Dscs has been developed.
British Journal of Dermatology | 2015
Ayaka Ohzono; Ryosuke Sogame; Xiaoguang Li; Kwesi Teye; Atsunari Tsuchisaka; Sanae Numata; H. Koga; Tamihiro Kawakami; Daisuke Tsuruta; Norito Ishii; Takashi Hashimoto
Although there are many reports of sporadic patients with paraneoplastic pemphigus (PNP), only a few systematic studies on large cohorts of patients with PNP have been reported.
British Journal of Dermatology | 2014
Amrinder J. Kanwar; Keshavamurthy Vinay; Gitesh U. Sawatkar; Sunil Dogra; Ranjana W. Minz; Neil H. Shear; H. Koga; Norito Ishii; Takashi Hashimoto
Rituximab is a promising therapy in pemphigus. However, there is no consensus on optimum dose.
British Journal of Dermatology | 2012
H. Koga; Bungo Ohyama; Daisuke Tsuruta; Norito Ishii; Takahiro Hamada; Teruki Dainichi; Yohei Natsuaki; Ryosuke Sogame; Shunpei Fukuda; Tadashi Karashima; J. Tada; M. Yamashiro; H. Uezato; Po Tak Chan; Takashi Hashimoto
Background Oral mucosal lesions develop in pemphigus vulgaris, but not in pemphigus foliaceus. This clinical phenomenon is explained by the ‘desmoglein (Dsg) compensation theory’. Dsg3 and Dsg1 are major autoantigens for pemphigus vulgaris and pemphigus foliaceus, respectively. Dsg3 is overexpressed and Dsg1 is weakly expressed on the oral mucosa. Thus, on the oral mucosa, suppression of Dsg3 function by anti‐Dsg3 autoantibodies is not compensated by weakly expressed Dsg1 in pemphigus vulgaris, while suppression of Dsg1 function by anti‐Dsg1 autoantibodies is perfectly compensated by richly expressed Dsg3 in pemphigus foliaceus.
British Journal of Dermatology | 2016
Takashi Hashimoto; Daisuke Tsuruta; H. Koga; Shunpei Fukuda; Bungo Ohyama; A. Komai; Tadashi Karashima; Chika Ohata; Kwesi Teye; Norito Ishii
Although many new disease entities of autoimmune bullous disease (AIBD) have recently been recognized, satisfactory immunological diagnostic methods and comprehensive classifications for various AIBDs have not been established.
British Journal of Dermatology | 2015
Naomi Tani; Y. Kimura; H. Koga; T. Kawakami; Chika Ohata; Norito Ishii; Takashi Hashimoto
Systematic study of pemphigoid gestationis (PG) has not been performed owing to its rarity.
British Journal of Dermatology | 2006
Ryohei Ogura; H. Koga; Masanori Kinoshita; Yukie Takashima
Certain enzymes participating in the degradation of DNA have been measured in cow snout epidermis, liver, kidney and intestinal epithelium. High activities were found in epidermis compared to other tissues.
British Journal of Dermatology | 2014
Y. Zenke; T. Nakano; H. Eto; H. Koga; Takashi Hashimoto
Linear IgA bullous dermatosis (LABD) is a rare autoimmune bullous disease, which is defined by the histopathological finding of subepidermal vesicles with neutrophilic infiltration and linear IgA deposits in the basement membrane zone, revealed by immunofluorescence study. We present a case of LABD in which vancomycin (VCM) administration triggered LABD, and immunoblot analysis showed IgA antibodies reactive to the 145‐ and 165‐kDa α3 subunits of laminin‐332. This is the first report of VCM‐associated LABD in which the target antigen was laminin‐332. In the present case, we were compelled to continue administration of VCM along with systemic steroids, which eventually led to the attenuation of the symptoms, normalization of the serum IgA level, and negative results on both indirect immunofluorescence of 1 mol L−1 NaCl‐split skin and immunoblot analysis.
British Journal of Dermatology | 2013
Y. Majima; H. Yagi; Chiharu Tateishi; Stephanie Groth; Enno Schmidt; Detlef Zillikens; H. Koga; Takashi Hashimoto; Yoshiki Tokura
63:607–41. 4 Esposito G, Auricchio L, Rescigno G et al. Transglutaminase 1 gene mutations in Italian patients with autosomal recessive lamellar ichthyosis. J Invest Dermatol 2001; 116:809–12. 5 Esposito G, Tadini G, Paparo F et al. Transglutaminase 1 deficiency and corneocyte collapse: an indication for targeted molecular screening in autosomal recessive congenital ichthyosis. Br J Dermatol 2007; 157:808–10. 6 Akiyama M, Takizawa Y, Kokaji T, Shimizu H. Novel mutations of TGM1 in a child with congenital ichthyosiform erythroderma. Br J Dermatol 2001; 144:401–7. 7 Esposito G, De Falco F, Brazzelli V et al. Autosomal recessive congenital ichthyosis and congenital hypothyroidism in a Tunisian patient with a nonsense mutation in TGM1. J Dermatol Sci 2009; 55:128–30. 8 Hackett BC, Fitzgerald D, Watson RM et al. Genotype–phenotype correlations with TGM1: clustering of mutations in the bathing suit ichthyosis and self-healing collodion baby variants of lamellar ichthyosis. Br J Dermatol 2010; 162:448–51. 9 Fachal L, Rodrı́guez-Pazos L, Ginarte M et al. Multiple local and recent founder effects of TGM1 in Spanish families. PLoS ONE 2012; 7:e33580. 10 Maślanka J. Demographic changes in Portugal at the turn of the 21st century. Bulletin of Geography (Socio-economic series) 2007; 8:83–98.
British Journal of Dermatology | 2014
Kazuhiro Yoshimura; Norito Ishii; Takahiro Hamada; T. Abe; Fumitake Ono; Keiko Hashikawa; Shunpei Fukuda; Bungo Ohyama; H. Koga; Ryosuke Sogame; Kwesi Teye; Toyoko Ochiai; H. Nakajima; K. Nakajima; Shigeruko Iijima; M. Kanzaki; K. Kojima; T. Nagatani; Wataru Fujimoto; Tadashi Karashima; Takekuni Nakama; Chika Ohata; Minao Furumura; Daisuke Tsuruta; Takashi Hashimoto
Drug‐induced pemphigus (DIP) shows clinical, histopathological and immunological features of pemphigus. However, little is known about immunological profiles in DIP.