Multiple Sclerosis with Optic Neuritis in Crohnʼs Disease Patient Taking Adalimumab

Abstract

Neurologic events presumably due to demyelination have been reported with anti-TNFα therapy, such as infliximab and etanercept. In addition, a clinical trial of Lenercept, a TNF receptor-p55 immunoglobulin fusion protein, was terminated when the patients in the treatment group had more flares of multiple sclerosis (MS) than the control group. There have not been any reports of MS in Crohn's disease (CD) patients taking adalimumab. Case report: A 37 year old woman with a 20 year history of CD was refractory to mesalamine treatment and did not tolerate 6-mercaptopurine (hepatotoxicity) or infliximab (delayed-type hypersensitivity). She began taking adalimumab in August 2005 and developed left-sided paroxysmal headaches, scalp tenderness, left hand numbness and weakness, and left buttock numbness in April 2006. An MRI revealed focal T2 hyperintesities in the periventricular and subcortical regions of the brain, as well as the cervical and thoracic spinal cord. Adalimumab was discontinued, and she was treated with intravenous methylprednisolone and discharged home. Over the next two months, her headaches, left upper extremity weakness, and left buttock numbness improved, but she developed blurry vision in her left eye consistent with optic neuritis. Discussion: Our patient developed MS while receiving adalimumab for her CD. There is only 1 reported case in the literature of a patient developing demyelinating disease during adalimumab treatment in the literature. On adalimumab for psoriasis, that patient developed distal lower extremity paresthesia and foot drop which completely resolved 4 weeks after adalimumab was discontinued. This is the first reported case of a patient receiving adalimumab for CD developing MS and optic neuritis, and the first time adalimumab associated demyelinating disease has been confirmed by MRI. Interestingly, there is an increased risk of demyelinating disease in patients with inflammatory bowel disease (IBD) even in the absence of anti-TNFα biologic therapy. Further studies will be needed to determine if the incidence of demyelinating disorders observed in IBD patients treated with anti-TNFα therapy is higher than that in IBD patients not receiving these medications.