TY - JOUR
T1 - Exacerbation of chronic inflammatory demyelinating polyradiculoneuropathy during interferonβ-1b therapy in a patient with childhood-onset multiple sclerosis
AU - Matsuse, Dai
AU - Ochi, Hirofumi
AU - Tashiro, Kenshi
AU - Nomura, Takuo
AU - Murai, Hiroyuki
AU - Taniwaki, Takayuki
AU - Kira, Jun Ichi
PY - 2005/1
Y1 - 2005/1
N2 - 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.
AB - 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.
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U2 - 10.2169/internalmedicine.44.68
DO - 10.2169/internalmedicine.44.68
M3 - Article
C2 - 15704667
AN - SCOPUS:13844314064
VL - 44
SP - 68
EP - 72
JO - Internal Medicine
JF - Internal Medicine
SN - 0918-2918
IS - 1
ER -