Refractory oral ulcers with multiple immunoglobulin G/immunoglobulin A autoantibodies without skin lesions  Teruki Dainichi, MD, Bungo Ohyama, MD, Norito.

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Presentation transcript:

Refractory oral ulcers with multiple immunoglobulin G/immunoglobulin A autoantibodies without skin lesions  Teruki Dainichi, MD, Bungo Ohyama, MD, Norito Ishii, MD, Zenichi Yamaguchi, MD, Shinichiro Yasumoto, MD, Takashi Hashimoto, MD  Journal of the American Academy of Dermatology  Volume 62, Issue 4, Pages 712-715 (April 2010) DOI: 10.1016/j.jaad.2008.09.055 Copyright © 2008 American Academy of Dermatology, Inc. Terms and Conditions

Fig 1 Oral lesions in the present case. A, Ulcers distributed on the palate. Histologic features of a biopsy specimen obtained from a lesion on the buccal mucosa, stained with hematoxylin–eosin (scale bar, 100 μm). B, The specimen showed subepithelial blister formation with infiltration of lymphocytes and plasma cells in the lamina propria. Direct immunofluorescence showed linear deposition of both (C) immunoglobulin G and (D) immunoglobulin A antibodies along the basement membrane zone. Indirect immunofluorescence with the patient's serum using 1M sodium chloride split-skin sections demonstrated (E) immunoglobulin G antibodies reactive with both epidermal and dermal sides and (F) immunoglobulin A antibodies reactive with the epidermal side. Journal of the American Academy of Dermatology 2010 62, 712-715DOI: (10.1016/j.jaad.2008.09.055) Copyright © 2008 American Academy of Dermatology, Inc. Terms and Conditions

Fig 2 Immunoblot analyses. A, Immunoglobulin G (IgG) antibodies of control bullous pemphigoid serum reacted with the recombinant protein (RP) of the BP180 NC16a domain (arrow; lane 1), while normal control serum did not react (lane 2). IgG (lane 3) and immunoglobulin A (IGA; lane 4) antibodies of the serum of the present case reacted with this recombinant protein. B, IgG antibodies of control anti-BP180 type mucous membrane pemphigoid serum reacted with the recombinant protein of BP180 C-terminus (arrow; lane 1), while IgG (lane 2) and IgA (lane 3) antibodies of the serum of the present case did not react with this recombinant protein. Asterisks show the nonspecific protein bands. C, IgA antibodies of control linear IgA bullous dermatosis serum reacted with the 120-kDa linear IgA dermatosis antigen LAD-1 (arrow) in cultured HaCaT cell supernatant. Both IgG (lane 2) and IgA (lane 3) antibodies of the serum of the present case also reacted with the LAD-1. D, IgG antibodies of control antilaminin 5 mucous membrane pemphigoid serum reacted with all of the 165-kDa α3, 145-kDa α3, 140-kDa β3, and 105 kDa γ2 subunits of laminin 332 (formerly laminin 5) in purified laminin 332 (lane 1). IgG antibodies of the serum of the present case reacted with the 105 kDa γ2 subunit (lane 2). Journal of the American Academy of Dermatology 2010 62, 712-715DOI: (10.1016/j.jaad.2008.09.055) Copyright © 2008 American Academy of Dermatology, Inc. Terms and Conditions