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Onset of lupus like syndrome in patients with spondyloarthritis treated with anti-TNF-α

DOI: 10.1186/1755-7682-5-7

Keywords: Antinuclear antibodies, Lupus-like syndrome, Anti-TNFα therapy, Anti-dsDNA, Psoriasis

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Abstract:

We studied 57 patients with SpA who received more than 1 year of anti-TNFα therapy (infliximab, adalimumab or etanercept). Patients were analyzed for the development of LLS, in addition to measuring ANA levels ≥ 1:160 and Anti-dsDNA (measured by IIF).In total, 7.01% of patients treated with anti-TNFα had titers of ANA ≥ 1:160, whereas 3.5% of patients had serum levels of dsDNA. However, only one patient (1.75%; n = 1) experienced clinical symptoms of LLS; this was a female patient with a history of psoriatic arthritis.The presence of LLS secondary to anti-TNFα therapy in patients with SpA is observed less frequently compared with patients with RA. LLS was only detected in a patient with a history of psoriasis since youth, who developed psoriatic arthritis after 27 years of age and had received anti-TNFα therapy for > 2 years. This may be because LLS is an entity clearly associated with innate immunity, with little central role of B and T cells.Lupus Like Syndrome (LLS) is an autoimmune disease characterized by the appearance of at least one serological marker and one non serological marker of systemic lupus erythematosus (SLE) (according to ACR criteria) in patients who previously had not; the syndrome commonly is associated with use of drugs such as procainamide and hydralazine, [1-3] although other causes exist, for example, in the context of a paraneoplastic syndrome (malignant neoplasms) [4-6]. After approval by the FDA of anti-TNFα therapy in RA and rheumatic diseases to such as spondyloarthritis, the emergence of this syndrome has been described under the name of lupus-like syndrome [7-10] and other ones under the name DILE (drug-induced lupus erythematosus), but classification criteria are not yet well defined and, worse still, there are few published data on its occurrence in spondyloarthritis [8,9].The mechanism by which the therapy against tumor necrosis factor anti-TNFα induces LLS is not yet well understood [10]. One hypothesis states that the binding of

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