Long-term course of demyelinating neuropathies occurring during tumor necrosis factor-alpha-blocker therapy.
OBJECTIVE
To report the long-term follow-up (mean, 41 months; range, 25-55 months) of patients with demyelinating neuropathy occurring after tumor necrosis factor-alpha (TNF-alpha) blocker treatment (infliximab [Remicade], etanercept [Enbrel], and adalimumab [Humira]).


BACKGROUND
Demyelinating neuropathy is a rare adverse event of anti-TNF-alpha therapy. Improvement usually occurs after drug interruption and/or in association with usual treatments for demyelinating neuropathies.


METHODS
Case report with review of the previously published cases.


METHODS
University hospital in Le Kremlin-Bicêtre, France: tertiary reference center for peripheral neuropathies and national reference center for rare peripheral neuropathies (www.nnerf.fr).


METHODS
Five patients (4 men, mean age, 47 years) who developed a demyelinating neuropathy during anti-TNF-alpha therapy.


METHODS
Development of neuropathy.


RESULTS
Neuropathy developed early (8 months) after treatment introduction. Various clinical patterns were encountered, including pure sensory neuropathy. Immunomodulating treatments were always required for neuropathy control. Chronic demyelinating neuropathy developed either after change of anti-TNF-alpha drug or spontaneously after treatment discontinuation without any drug reintroduction.


CONCLUSIONS
Influence of anti-TNF-alpha treatment continuation on the long-term course of neuropathy is variable, suggesting that anti-TNF-alpha treatment withdrawal is not always necessary for neuropathy control.
Department of Neurology, Assistance Publique-Hôpitaux de Paris, Université Paris Sud, France. pierre.lozeron@bct.aphp.fr
Pierre
P
Lozeron
Christian
C
Denier
Catherine
C
Lacroix
David
D
Adams
D000068879:Adalimumab; D000328:Adult; D000893:Anti-Inflammatory Agents / Q000009:adverse effects* / Q000627:therapeutic use; D000911:Antibodies, Monoclonal / Q000009:adverse effects* / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D015535:Arthritis, Psoriatic / Q000188:drug therapy*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy*; D003424:Crohn Disease / Q000188:drug therapy*; D003711:Demyelinating Diseases / Q000139:chemically induced* / Q000175:diagnosis; D004359:Drug Therapy, Combination; D000068800:Etanercept; D005260:Female; D005500:Follow-Up Studies; D017497:Hidradenitis Suppurativa / Q000188:drug therapy*; D006801:Humans; D007116:Immunization, Passive; D007074:Immunoglobulin G / Q000009:adverse effects* / Q000627:therapeutic use; D007166:Immunosuppressive Agents / Q000009:adverse effects* / Q000627:therapeutic use; D000069285:Infliximab; D008233:Lymphotoxin-alpha / Q000037:antagonists & inhibitors*; D008297:Male; D008875:Middle Aged; D009460:Neurologic Examination / Q000187:drug effects; D010951:Plasma Exchange; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D013167:Spondylitis, Ankylosing / Q000188:drug therapy*; D016896:Treatment Outcome
D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D007074:Immunoglobulin G; D007166:Immunosuppressive Agents; D008233:Lymphotoxin-alpha; D018124:Receptors, Tumor Necrosis Factor; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept