CIDP+ avonex and interferone

Interferon beta-1a in chronic inflammatory demyelinating polyneuropathy: case report.

Villa AM, Garcea O, Di Egidio M, Saizar R, Sica RE.

Division Neurologia, Hospital Ramos Mejia, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina.

Here we report on a patient who had a relapsing form of pure sensory ataxic CIDP and who failed to respond to intravenous human immunoglobulin. He was put on INF beta1a for 3 years. During this period he suffered no relapses while his condition stabilized.

PMID: 15476092 [PubMed - in process]

: Interferon beta-1a as an investigational treatment for CIDP.

Vallat JM, Hahn AF, Leger JM, Cros DP, Magy L, Tabaraud F, Bouche P, Preux PM.

Department of Neurology, Dupuytren University Hospital, Limoges, France. vallat@unilim.fr

A total of 20 treatment-resistant patients with CIDP were enrolled in the study. The tolerability of IFNbeta-1a in patients with CIDP was similar to that seen with its use in MS. Seven patients (35%) showed clinical improvement, 10 (50%) had stable disease, and 3 (15%) continued to deteriorate. Significant improvements from baseline were observed in NDS in both the intent-to-treat and per protocol analyses (p=0.0005).
PMID: 12707419 [PubMed - indexed for MEDLINE]

Neurology. 2003 May 27;60(10):1697-9.

Contrasting effects of IFNbeta and IVIG in children with central and peripheral demyelination.

Pirko I, Kuntz NL, Patterson M, Keegan BM, Weinshenker BG, Rodriguez M.

Department of Neurology, Mayo Clinic, Rochester, MN 55902, USA.

Reported are three children with MS who responded dramatically to interferon-beta (IFNbeta) therapy. While on immunomodulatory therapy, they developed chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) that responded to IV immunoglobulin (IVIG) administration. These cases emphasize two interesting observations:

1) IFNbeta treatment did not prevent development of CIDP;

2) CIDP in the context of MS responded to IVIG, even though IVIG had no therapeutic effect on the central demyelinating disease.

PMID: 12771272 [PubMed - indexed for MEDLINE]

Intern Med. 2005 Jan;44(1):68-72.

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

Matsuse D, Ochi H, Tashiro K, Nomura T, Murai H, Taniwaki T, Kira J.

Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka.

We report a 23-year-old woman with childhood onset relapsing-remitting MS treated with IFNbeta-1b who developed overt chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) immediately after therapy.

A baseline conduction study before IFNbeta-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 IFNbeta-1b treatment was suggested, although the clinical criteria for CIDP were unfulfilled. Following two months of IFNbeta-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 antithyroid peroxydase antibodies, which were negative before IFNbeta-1b therapy. These findings indicated that peripheral demyelination worsened at the nerve roots after IFNbeta-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 IFNbeta-induced CIDP development in patients with childhood MS, this case underscores IFNbeta as a potential risk factor for CIDP in patients with childhood onset MS.

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