Club Rhumatismes et Inflammation.: Systemic lupus erythematosus induced by anti-tumour necrosis factor alpha therapy: A French national survey

Rheumatology Department, Hôpital Robert Ballanger, Aulnay sous Bois, France.
Arthritis research & therapy (Impact Factor: 3.75). 02/2005; 7(3):R545-51. DOI: 10.1186/ar1715
Source: PubMed

ABSTRACT The development of drug-induced lupus remains a matter of concern in patients treated with anti-tumour necrosis factor (TNF) alpha. The incidence of such adverse effects is unknown. We undertook a retrospective national study to analyse such patients.
Between June and October 2003, 866 rheumatology and internal medicine practitioners from all French hospital centres prescribing anti-TNF in rheumatic diseases registered on the website of the 'Club Rhumatismes et Inflammation' were contacted by email to obtain the files of patients with TNF-induced systemic lupus erythematosus. Twenty-two cases were collected, revealing two aspects of these manifestations. Ten patients (six patients receiving infliximab, four patients receiving etanercept) only had anti-DNA antibodies and skin manifestations one could classify as 'limited skin lupus' or 'toxidermia' in a context of autoimmunity, whereas 12 patients (nine patients receiving infliximab, three patients receiving etanercept) had more complete drug-induced lupus with systemic manifestations and at least four American Congress of Rheumatology criteria. One patient had central nervous system manifestations. No patients had lupus nephritis. The signs of lupus occurred within a mean of 9 months (range 3–16 months) in patients treated with infliximab and within a mean of 4 months (range 2–5 months) in patients treated with etanercept. In all cases after diagnosis was determined, anti-TNF was stopped and specific treatment introduced in eight patients: two patients received intravenous methylprednisolone, four patients received oral steroids (15–35 mg/day), and two patients received topical steroids. Lupus manifestations abated within a few weeks (median 8 weeks, standard deviation 3–16) in all patients except one with longer-lasting evolution (6 months). At that time, cautious estimations (unpublished data from Schering Plough Inc. and Wyeth Inc.) indicated that about 7700 patients had been exposed to infliximab and 3000 to etanercept for inflammatory arthritides in France. It thus appears that no drug was more implicated than the other in lupus syndromes, whose incidence was 15/7700 = 0.19% with infliximab and 7/3800 = 0.18% with etanercept.
Clinicians should be aware that lupus syndromes with systemic manifestations may occur in patients under anti-TNF alpha treatment.

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Available from: Xavier Mariette, Dec 23, 2013
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    • "However, TNF antagonists, which are the most potent agents in preventing joint damage in RA when used in combination with methotrexate (MTX), can induce production of autoantibodies characteristic to SLE such as antinuclear antibodies (ANA) or anti-DNA antibodies [6] [7]. Less frequently but more importantly, TNF antagonists can cause lupus manifestations in RA [6] [7] [8] [9] [10] and rhupus syndrome [11]. Abatacept is a fully human, soluble fusion protein that consists of the extracellular domain of human cytotoxic T-lymphocyte antigen 4 (CTLA-4) and the Fc portion of IgG1, which selectively modulates the CD80/CD86:CD28 costimulatory signals and interactions between activated T cells and antigen presenting cells (APCs). "
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    • "0.5-1% develop high affinity IgG antibodies to ds DNA (Charles et al, 2000). The development of clinical lupus-like syndromes in anti-TNF treated patients is rare and in those who do develop this, manifestations are for the main part mild (De Bandt et al, 2005). The development of lupus nephritis as a complication of TNF-induced lupus has been reported but is extremely rare (Mor et al, 2005) (Stokes et al, 2005) (Neradova et al, 2009). "
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    • "At the last follow-up, 8 months after re-starting steroids, his neurological condition was unchanged. Arguments for a causative role of PM are that DHS has been previously described in PM [2], dermatomyositis [3], and as focal myositis of the extensor neck muscles [4] [5] [6] [7] [8], and that DHS responded well to steroids. Arguments for a mitochondrial disorder (MID) are that there was basal ganglia calcification, hypoacusia , diabetes, short stature, osteoporosis, recurrent hyponatremia, hyperlipidemia, myocardial thickening despite normal blood pressure and short stature and hypoacusis in his mother, albinism, visual impairment, nystagmus and hypothyroidism in his daughter , and that MID has been previously reported to cause DHS [9] [10]. "
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