title: A prospective analysis of anti-desmoglein antibody profiles in patients with rheumatoid arthritis treated with thiol compounds.
abstract: BACKGROUND
  Drug-induced pemphigus is mainly caused by drugs containing sulfhydryl (thiol) groups in their molecules.
  
  
  OBJECTIVE
  To understand the serial alteration of anti-desmoglein (Dsg) antibody profile in patients with rheumatoid arthritis (RA) receiving thiol compounds.
  
  
  METHODS
  Anti-Dsg1 or -Dsg3 antibodies were analysed twice in a 1.6-year interval, in the same series of RA patients.
  
  
  RESULTS
  Eleven of 204 serum samples (5.4%) and 6 of 139 samples (4.3%) from the same RA group showed a positive reaction against Dsg1 or Dsg3 in the first and second screening tests, respectively. The positive rates were higher than those in patients with collagen diseases including systemic lupus erythematosus, Sjögren syndrome, mixed connective tissue disease, and systemic sclerosis. In comparison with the results in the first and second screening tests, one RA patient newly gained anti-Dsg3 antibody, and at least 4 patients lost the antibodies in 1.6 years. Three patients produced antibodies to Dsg1 and/or Dsg3 in a similar fashion as did in the first screening tests. Only one RA serum sample exhibited an intercellular reactivity to human skin or monkey esophagus by immunofluorescence, and another sample bound to a 130 kDa protein suggestive of Dsg3 by immunoblotting. Most anti-Dsg antibodies in RA patients recognized EDTA-resistant epitopes of Dsg different from EDTA-sensitive epitopes recognized by pemphigus sera.
  
  
  CONCLUSIONS
  RA patients receiving any of the thiol compounds may gain autoantibodies to non-conformational epitopes of either Dsg1 or Dsg3, and that such autoantibodies alone are not capable of inducing acantholysis.
authors.affiliation: Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry Pharmaceutical Sciences, Kita-ku, Okayama 700-8558, Japan.
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Mikiko
authors.initials: M
authors.lastname: Takata-Michigami
authors.forename: Yoshiko
authors.initials: Y
authors.lastname: Hisamatsu
authors.forename: Takenobu
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Toshihisa
authors.initials: T
authors.lastname: Hamada
authors.forename: Kazuyasu
authors.initials: K
authors.lastname: Fujii
authors.forename: Wataru
authors.initials: W
authors.lastname: Fujimoto
authors.forename: Koji
authors.initials: K
authors.lastname: Taneichi
authors.forename: Yumi
authors.initials: Y
authors.lastname: Aoyama
authors.forename: Keiji
authors.initials: K
authors.lastname: Iwatsuki
mesh_terms: D000051:Acantholysis / Q000097:blood / Q000276:immunology; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000188:drug therapy* / Q000276:immunology; D001323:Autoantibodies / Q000097:blood* / Q000276:immunology; D051183:Desmoglein 1 / Q000276:immunology*; D051184:Desmoglein 3 / Q000276:immunology*; D005260:Female; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000276:immunology; D008297:Male; D008875:Middle Aged; D008947:Mixed Connective Tissue Disease / Q000097:blood / Q000276:immunology; D010392:Pemphigus / Q000097:blood / Q000209:etiology / Q000276:immunology; D017285:Polymyositis / Q000097:blood / Q000276:immunology; D011446:Prospective Studies; D012595:Scleroderma, Systemic / Q000097:blood / Q000276:immunology; D012859:Sjogren's Syndrome / Q000097:blood / Q000276:immunology; D013438:Sulfhydryl Compounds / Q000009:adverse effects / Q000627:therapeutic use*; D055815:Young Adult
chemical_list: D001323:Autoantibodies; C495297:DSG1 protein, human; C071894:DSG3 protein, human; D051183:Desmoglein 1; D051184:Desmoglein 3; D013438:Sulfhydryl Compounds