In my view, anti TNF induced Lupus should only come to attention when it is severe enough to cause symptoms, i. e. with more progressive disease. One of the characteristic features of anti TNF induced lupus is that most (if not all) diseae manifestation should resolve upon drug withdrawal.
So it basically comes to the bottom-line: I can't actually think of any cirucmstances to continue anti TNF treatment with anti-TNF induced Lupus (ATIL). If another agent of the same class will also cause ATIL is to my knowledge, not exactly known.
Some investigators have suggested that TNF-α antagonists do not need to be discontinued if the patient has isolated induction of autoantibodies without any clinical manifestations of lupus (Ramos-Casals, Brito-Zeron etal. 2007; Kerbleski and Gottlieb 2009). In another study, 4 of 5 patients tolerated an alternative TNF inhibitor (adalimumabfor 3 patients, etanercept for 1) without recurrence of ATIL after discontinuation of infliximab (Wetter and Davis 2009).In any case, your position favors the security in the present real world. We will see in the future. Thanks !
In fact, I have a RA woman with isolated induccion of antibodies and good response to anti-TNF during sever al years.
Which antibodies? Finding positive ANA is quite common and should not lead to discontinuation if there are no clinical signs of lupus. Does she have symptoms? Or just positive antibodies?
Hi Joan
I agree with Peter . If patient has only ANA positive: You do not need to stop Anti TNF treatment. But if patient developed clinical features suggestive of Lupus : then you need to stop it. Best regards
We are speaiking about isolated ANA antibodies, with/witout anti DNA antibodies without clinical features. In this case we all agree, Regards
say, a patient of ank spond is well controlled on anti tnf, and develops ANA positivity. the anti tnf should be continued till the ATIL causes any symptoms which can't be managed without stopping anti-tnf. the ATIL should remit with cessation of the anti-tnf
Induction of ANA positivity may occur; however, true drug-induced lupus although possible is uncommon. Interestingly, a new article I believe out of the Barcelona group just came out actually looking at TNF inhibition for the treatment of lupus; I will try to locate this reference; there are also a couple of case reports (see The Rheumatologist) where TNF inhibition helped lupus as well,
It seems, at present, that in lupus there are two signatures: IFN-I(antiglomerulonephritis antibodies) and TNF@(arthritis, anemia), a balance between monocytes/macrophages and neutrophis. This could explain the different subsets of lupus and, consequently, the different treatment approaches(Zhuang H et al.Toll_like receptor-7...A & R.2014;66:140-161).
There, in the TNF lupus signature, anti-TNF therapy could have a chance.
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