ABSTRACT
INTRODUCTION: Tumor necrosis factor- (TNF) blockers are efficient in the treatment of autoimmune disorders such as inflammatory bowel disease and rheumatoid arthritis, but can induce CNS adverse effects including retrobulbar optic neuritis or aggravation of multiple sclerosis. OBSERVATION: We report a case of progressive demyelinating polyneuropathy after initiation of Adalimumab (Humira). Corticosteroid and intravenous immunoglobulins were ineffective but the neuropathy improved within six months after adalimunab discontinuation. DISCUSSION: This case, and other reports recently published suggest that anti-TNF alpha drugs can induce demyelinating neuropathy. CONCLUSION: Clinicians should be on the lookout for signs evocating neuropathy in patients given anti TNF alpha.
Subject(s)
Anti-Inflammatory Agents/adverse effects , Antibodies, Monoclonal/adverse effects , Polyradiculoneuropathy/chemically induced , Tumor Necrosis Factor-alpha/adverse effects , Adalimumab , Adrenal Cortex Hormones/therapeutic use , Aged , Anti-Inflammatory Agents/therapeutic use , Antibodies, Monoclonal/therapeutic use , Antibodies, Monoclonal, Humanized , Arthritis, Rheumatoid/complications , Arthritis, Rheumatoid/drug therapy , Electric Stimulation , Electromyography , Electrophysiology , Female , Humans , Immunoglobulins, Intravenous/therapeutic use , Polyradiculoneuropathy/drug therapy , Polyradiculoneuropathy/pathology , Tumor Necrosis Factor-alpha/therapeutic useABSTRACT
A 35 year-old man developed a syndrome with muscle cramp, myokimia, generalized, fasciculations, excessive sweating, sleep disorders and severe impairment. It was a syndrome of continuous muscle fiber activity--or Isaacs syndrome--with central disorders (this may be called "Maladie de Morvan"). Previous reports have suggested that Isaac's syndrome might be an autoimmune disorder. Moreover, high doses intravenous immunoglobulins were given resulting in a substantial improvement six months after the onset of this treatment.