Brain, Vol. 126, No. 6, E1,
June 2003
© 2003 Guarantors of Brain
doi: 10.1093/brain/awg140
Letters to the Editor |
Glatiramer acetate treatment in Devic’s neuromyelitis optica
Department of Clinical Neurology, Multiple Sclerosis Center, Neurological Institute ‘IRCCS C.Mondino’, Pavia, Italy.
Correspondence to: Roberto Bergamaschi. E-mail: roberto.bergamaschi{at}mondino.it
Lucchinetti et al. (2002
) have recently depicted the pathological pattern of Devic’s neuromyelitis optica (NMO), characterized by perivascular deposition of immunoglobulins (especially IgM), complement activation and eosinophilic infiltration. This pattern is strongly suggestive of a Th-2 response, adding new evidences to the hypothesis that NMO is a disease entity distinct from multiple sclerosis, considered a ‘Th-1 disease’. In this respect, Gold and Linington (2002) argue that a therapy with glatiramer acetate (GA), leading to the augment of Th-2-type responses, would be problematic in NMO patients. A direct experience of mine is in contrast with the previous suggestion. A relapsing NMO patient, started in 1979 with optic neuritis, had 14 relapses in the subsequent 15 years, invariably involving optic nerve and spinal cord. CSF was normal, as well as repeated brain MRI, while spinal MRI showed a large lesion extended from C3 to C6. In 1994, she started GA, after which she had only two relapses within the first 2 years of treatment, and from then on she remained relapse free. Therefore, relapse-rate decreased from 0.93/year (before GA treatment) to 0.25/year; in addition, the very large cervical cord lesion appeared to be reduced. Of course, the observation of only one patient is not conclusive, as the long remission could be spontaneous and not necessarily related to the treatment. However, if the improvement were related to the therapy, a possible explanation for this discrepancy (that is a beneficial effect on a ‘Th-2 disease’ obtained with a drug favouring the shift from Th-1 towards Th-2), could come from the findings of Ziemssen et al. (2002). These authors report that GA-specific T-helper 1- and 2-type cells produce the brain-derived neurotrophic factor (BDNF), with possible effects on neuronal survival and myelin repair. Therefore, GA-Th-2 activation could have a neuroprotective role in NMO course.
I think that the use of GA in NMO should not be definitely rejected, especially considering the poor prognosis and the unsatisfactory response and tolerance to immunosuppressive therapies already used in NMO. New trials for the assessment of GA effect and, especially, of its relationships with the production of neurotrophic factors in NMO, are required.
References
Bergamaschi R, Uggetti C, Tonietti S, Egitto MG, Cosi V. A case of relapsing neuromyelitis optica treated with glatiramer acetate. J Neurol In press 2003.
Gold R, Linington C. Devic’s disease: bridging the gap between laboratory and clinic. Brain 2002; 125: 1425–7.
Lucchinetti CF, Mandler RN, McGavern D, et al. A role for humoral mechanisms in the pathogenesis of Devic’s neuromyelitis optica. Brain 2002; 125: 1450–61.
Ziemssen TZ, Kümpfel T, Klinkert WEF, Neuhaus O, Hohlfeld R. Glatiramer acetate-specific T-helper 1- and 2-type cell lines produce BDNF: implications for multiple sclerosis therapy. Brain 2002; 125: 2381–91.
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