TY - JOUR
T1 - A prospective analysis of anti-desmoglein antibody profiles in patients with rheumatoid arthritis treated with thiol compounds
AU - Yamamoto, Tetsuya
AU - Takata-Michigami, Mikiko
AU - Hisamatsu, Yoshiko
AU - Yamamoto, Takenobu
AU - Hamada, Toshihisa
AU - Fujii, Kazuyasu
AU - Fujimoto, Wataru
AU - Taneichi, Koji
AU - Aoyama, Yumi
AU - Iwatsuki, Keiji
N1 - Funding Information:
This work was supported by the grant from the Ministry of Health, Labour and Welfare (Research for Intractable Diseases).
PY - 2010/9
Y1 - 2010/9
N2 - Background: Drug-induced pemphigus is mainly caused by drugs containing sulfhydryl (thiol) groups in their molecules. Objectives: 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. Conclusion: 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.
AB - Background: Drug-induced pemphigus is mainly caused by drugs containing sulfhydryl (thiol) groups in their molecules. Objectives: 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. Conclusion: 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.
KW - Desmoglein
KW - Non-pathogenic
KW - Pemphigus
KW - Rheumatoid arthritis
KW - Thiol
UR - http://www.scopus.com/inward/record.url?scp=77956178349&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=77956178349&partnerID=8YFLogxK
U2 - 10.1016/j.jdermsci.2010.06.007
DO - 10.1016/j.jdermsci.2010.06.007
M3 - Article
C2 - 20650613
AN - SCOPUS:77956178349
SN - 0923-1811
VL - 59
SP - 170
EP - 175
JO - Journal of Dermatological Science
JF - Journal of Dermatological Science
IS - 3
ER -
