A RARE AND UNFORTUNATE CASE OF PARESTHESIAS SECONDARY TO INFLIXIMAB

Abstract Introduction The tumor necrosis factor-α (TNF-α) antagonists infliximab, adalimumab, and etanercept have been approved for treatment of inflammatory bowel disease (IBD). We describe a rare manifestation of a demyelinating neuropathy affecting the peripheral nervous system in a patient on Infliximab for the treatment of Crohn’s disease following progression of his disease. Case Report A 34-year-old male with a past medical history of Crohn’s disease presented for progressive and worsening diffuse numbness and paresthesias over two months in almost all of his extremities except the right side of his face, his sternum and center of his back. His symptoms were well controlled on mesalamine for 16 years until he had a progression of his disease which was seen on endoscopy and colonoscopy so he was switched to treatment with infliximab. He had finished induction with a third infusion two months prior to onset of parasthesias leading to control of symptoms. However, he started to experience non bloody diarrhea and diffuse, dull abdominal pain, weight loss of 15 pounds, gait dysfunction, lower extremity weakness, bilateral knee erythema and tenderness, and tight and stiff muscles, which were not typical for his Crohn’s disease flare-ups. On physical exam, his vitals were unremarkable and there was decreased sensation to light touch. He also had paresthesias as well as weakness most pronounced in his lower extremities. Laboratory tests and Imaging with CT, MRI, EMG, and Lumbar Puncture were all negative. The patient had 70% improvement of his symptoms following discontinuation of Infliximab, although his symptoms never completely resolved in his feet despite additional treatment with B12, thiamine, gabapentin, prednisone, and baclofen. Conclusion Due to the chronological progression and manifestation of the neurological symptoms with infliximab therapy for our patient, it is very likely that this drug triggered or caused his demyelinating neuropathy. There are only a few case reports in the literature and small review studies demonstrating Guillain-Barre Syndrome, demyelinating polyneuropathy, and neurologic disease due to infliximab. Various clinical patterns have been described. Chronic demyelinating neuropathy developed either after change of anti–TNF-α drug or spontaneously after treatment discontinuation without any drug reintroduction. There have been case reports describing treatment of demyelinating polyneuropathy related to TNF-alpha inhibitors with IVIG 1 or 2 g/kg with good results. Gabapentin has also been tried for treatment. Influence of anti–TNF-α treatment continuation on the long-term course of neuropathy is variable, suggesting that anti–TNF-α treatment withdrawal is not always necessary for neuropathy control. For future cases, our case highlights the importance of close inpatient and outpatient follow up for patients on infliximab.