Epub: Seror et al; for the Club Rhumatismes et Inflammation Section of the SFR. Pattern of demyelination occurring during anti-TNF-α therapy: a French national survey. Rheumatology. 2013 Jan .
Objective. To determine the pattern of demyelinating disorders (DDs) occurring during anti-TNF-α therapy.
Methods. Between June 2005 and April 2008, 1800 French rheumatologists and internists were contacted to report cases of DDs occurring in patients treated with anti-TNF-α.
Results. After a median of 10.2 (1.5-39.9) months of treatment, 33 patients developed DDs: 22 had CNS and 11 peripheral nervous system (PNS) involvement. Underlying diseases were RA (n = 16), AS (n = 11), PsA (n = 4), JIA (n = 1) and PM (n = 1). Anti-TNF-α was infliximab (n = 15), etanercept (n = 12) or adalimumab (n = 6). CNS involvement was encephalic lesions (n = 16), transverse myelitis (n = 8) or retrobulbar optic neuritis (n = 5). Cerebrospinal fluid (CSF) analysis in 16 patients and MRI in 20 patients were abnormal. All patients discontinued anti-TNF-α. Fifteen patients required steroids. Twenty patients initially improved. Five patients developed multiple sclerosis. PNS involvement was chronic (n = 9) or acute inflammatory demyelinating polyneuropathy (n = 2). CSF analysis revealed an increased protein level in nine patients. Nerve conduction studies confirmed DD in all these patients. Anti-TNF-α was discontinued in 10 patients and 8 received i.v. immunoglobulins. Two patients relapsed after introduction of another anti-TNF-α. Overall, a causal relationship between anti-TNF-α and DD was considered as probable in 31 patients and definite in 2 who had positive rechallenge.
Conclusion. Causal relationship between anti-TNF-α and induction of DD remains unclear, but in some cases the chronology of clinical events is suggestive. Nevertheless, DD might persist despite treatment discontinuation, suggesting that anti-TNF-α could trigger the demyelinating process, which further evolves independently.
People treated with Lemtrada can develop autoimmune thyroid disease, it appears that people with arthritis treated with anti-tumour necrosis factor develop demyelinating disease and multiple sclerosis. This is further evidence that overall blockade of TNF is not a good idea in MS. Most experimental data may suggest that TNF blockade could be good, however I think this shows that TNF does lots of different things some could be good and others bad and balance is that its removal at least from the peripheral compartment is bad news. This can tell us something about biology. Following Lemtrda administration there is a cytokine storm, quelled by steroids, that reactive old demylinated lesions