TY - JOUR
T1 - D-penicillamine-induced pancreatic islet autoantibody production is independent of the immunogenetic background
T2 - A lesson from patients with Wilson's disease
AU - Kauschansky, Arieh
AU - Frydman, Moshe
AU - Assa, Sara
AU - Kwon, Oh Joong
AU - Israel, Shoshana
AU - Lazard, Daniel
AU - Sprecher, Elliot
AU - Bloch, Konstantin
AU - Brautbar, Chaim
AU - Vardi, Pnina
PY - 1998/12
Y1 - 1998/12
N2 - D-penicillamine (D-PA) was reported to induce various immunological abnormalities including production of autoantibodies to insulin. These abnormalities were mainly described in patients with primary immunological disorders such as rheumatoid arthritis. In order to clarify whether D-PA- induced immune disorders are restricted to patients genetically prone to develop autoimmune diseases or to a direct drug effect, we tested for the presence of various autoantibodies and for molecular HLA typing in 17 patients with Wilson's disease treated with this drug. In 2/17 patients, low- titer (10 JDFU) circulating islet cell autoantibodies (ICA) were detected, while another patient was positive for the presence of insulin autoantibodies. None of the sera tested showed reactivity for glutamic acid decarboxylase or ICA512. Five of twelve patients were positive for anti- single-stranded DNA autoantibody. Molecular HLA typing of the autoantibody- positive subjects showed that they carry HLA haplotypes not associated with insulin-dependent diabetes. The insulin response to intravenous glucose tolerance test in two patients with autoantibodies was found to be normal. A second blood testing of the autoantibody-positive patients 5 months following initial evaluation revealed conversion to negativity in all three. Our results suggest that D-PA-induced autoantibodies in patients with Wilson's disease are independent of the immunogenetic background characteristics of diabetes.
AB - D-penicillamine (D-PA) was reported to induce various immunological abnormalities including production of autoantibodies to insulin. These abnormalities were mainly described in patients with primary immunological disorders such as rheumatoid arthritis. In order to clarify whether D-PA- induced immune disorders are restricted to patients genetically prone to develop autoimmune diseases or to a direct drug effect, we tested for the presence of various autoantibodies and for molecular HLA typing in 17 patients with Wilson's disease treated with this drug. In 2/17 patients, low- titer (10 JDFU) circulating islet cell autoantibodies (ICA) were detected, while another patient was positive for the presence of insulin autoantibodies. None of the sera tested showed reactivity for glutamic acid decarboxylase or ICA512. Five of twelve patients were positive for anti- single-stranded DNA autoantibody. Molecular HLA typing of the autoantibody- positive subjects showed that they carry HLA haplotypes not associated with insulin-dependent diabetes. The insulin response to intravenous glucose tolerance test in two patients with autoantibodies was found to be normal. A second blood testing of the autoantibody-positive patients 5 months following initial evaluation revealed conversion to negativity in all three. Our results suggest that D-PA-induced autoantibodies in patients with Wilson's disease are independent of the immunogenetic background characteristics of diabetes.
KW - D-penicillamine
KW - Insulin autoantibodies
KW - Islet cell autoantibodies
KW - Wilson's disease
UR - http://www.scopus.com/inward/record.url?scp=0032374076&partnerID=8YFLogxK
U2 - 10.1006/clin.1998.4609
DO - 10.1006/clin.1998.4609
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C2 - 9837698
AN - SCOPUS:0032374076
SN - 0090-1229
VL - 89
SP - 279
EP - 283
JO - Clinical Immunology and Immunopathology
JF - Clinical Immunology and Immunopathology
IS - 3
ER -