Exacerbation of chronic inflammatory demyelinating polyradiculoneuropathy during interferonβ-1b therapy in a patient with childhood-onset multiple sclerosis

Interferonβ-1b (IFNβ-1b) is commonly used for relapsing-remitting multiple sclerosis (MS). We report a 23-year-old woman with childhood onset relapsing-remitting MS treated with IFNβ-1b who developed overt chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) immediately after therapy. A baseline conduction study before IFNβ-1b therapy revealed decreased motor conduction velocities and prolonged F wave latencies in several nerves, but there was no neurological sign indicating neuropathy. The existence of subclinical demyelinating neuropathy before IFNβ-1b treatment was suggested, although the clinical criteria for CIDP were unfulfilled. Following two months of IFNβ-1b therapy, numbness of her right upper and lower limbs progressively worsened and all tendon reflexes were depressed. Electrophysiologically, F waves were not evoked in any limbs except for the left ulnar and tibial nerves, which showed marked prolongation of F wave latencies. Moreover, subclinical hyperthyroidism developed in association with high titers of anti-thyroglobulin and anti-thyroid peroxydase antibodies, which were negative before IFNβ-1b therapy. These findings indicated that peripheral demyelination worsened at the nerve roots after IFNβ-1b therapy. In addition to the development of autoimmune thyroid disease, the patient now fulfilled the criteria for probable CIDP. Along with the results of a previous report demonstrating IFNβ-induced CIDP development in patients with childhood MS, this case underscores IFNβ as a potential risk factor for CIDP in patients with childhood onset MS.