Mir Amir Aghdashi 1 , Mohsen Khadir 2 , Roshan Dinparasti-Saleh 2 Show Affiliations »
Abstract
BACKGROUND: Up to 44% of patients treated with infliximab and 7% of patients treated with etanercept reported to have anti-drug antibodies within the first 6 months of treatment. Recently, anti-TNF-α therapies have been reported to be employed in the induction of the druginduced lupus erythematous. OBJECTIVE: The aim of the present study was to investigate the relationship between anti-TNFα antibodies and various manifestations of lupus erythematous. METHODS: We enrolled a total of 56 cases divided into 28 known cases of rheumatoid arthritis and 28 cases of ankylosing spondylitis patients and 56 controls. The case group was divided into 4 groups according to the underlying disease (RA or AS) and treatment regimen (infliximab or etanercept). ANA and anti-dsDNA levels and lupus criteria were assessed at the beginning of the study and 4 months after the initiation of anti-TNFα. RESULTS: 36% and 21% of RA patients treated with infliximab, were ANA and anti-dsDNA positive after 4 months (P=0.003, P=0.025). 28% and 7% of RA patients treated with etanercept, were ANA and anti-dsDNA positive after 4 months (P=0.009, P=0.15). 21% and 7% of AS patients treated with infliximab, were ANA and anti-dsDNA positive, respectively (P=0.025, P=0.15). 14% and 7% of AS patients treated with etanercept, were ANA and anti-dsDNA positive, respectively (P=0.63, P=0.15). Three patients who were positive for auto-antibodies developed three criteria for SLE. CONCLUSION: Infliximab potentially may increase both ANA and anti-dsDNA levels in rheumatoid arthritis, but only ANA in ankylosing spondylitis patients. In general, clinicians should consider different clinical symptoms of ATIL, which may be present as a lupus-like syndrome similar to idiopathic SLE or classical DIL. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
BACKGROUND: Up to 44% of patients treated with infliximab and 7% of patients treated with etanercept reported to have anti-drug antibodies within the first 6 months of treatment. Recently, anti-TNF-α therapies have been reported to be employed in the induction of the druginduced lupus erythematous . OBJECTIVE: The aim of the present study was to investigate the relationship between anti-TNFα antibodies and various manifestations of lupus erythematous . METHODS: We enrolled a total of 56 cases divided into 28 known cases of rheumatoid arthritis and 28 cases of ankylosing spondylitis patients and 56 controls. The case group was divided into 4 groups according to the underlying disease (RA or AS) and treatment regimen (infliximab or etanercept). ANA and anti-dsDNA levels and lupus criteria were assessed at the beginning of the study and 4 months after the initiation of anti-TNFα. RESULTS: 36% and 21% of RA patients treated with infliximab , were ANA and anti-dsDNA positive after 4 months (P=0.003, P=0.025). 28% and 7% of RA patients treated with etanercept, were ANA and anti-dsDNA positive after 4 months (P=0.009, P=0.15). 21% and 7% of AS patients treated with infliximab , were ANA and anti-dsDNA positive, respectively (P=0.025, P=0.15). 14% and 7% of AS patients treated with etanercept, were ANA and anti-dsDNA positive, respectively (P=0.63, P=0.15). Three patients who were positive for auto-antibodies developed three criteria for SLE . CONCLUSION: Infliximab potentially may increase both ANA and anti-dsDNA levels in rheumatoid arthritis , but only ANA in ankylosing spondylitis patients . In general, clinicians should consider different clinical symptoms of ATIL , which may be present as a lupus-like syndrome similar to idiopathic SLE or classical DIL. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
Entities: Chemical
Disease
Gene
Species
Keywords:
Lupus erythematosus; ankylosing spondylitis; anti-TNF-α therapies; etanercept; infliximab; rheumatoid arthritis.
Year: 2020
PMID： 31057111 DOI： 10.2174/1573397115666190506152729
Source DB: PubMed Journal: Curr Rheumatol Rev ISSN： 1573-3971