Antegren

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J Neurol. 2004 Apr;251(4):407-13. Related Articles, Links

Effect of natalizumab on conversion of gadolinium enhancing lesions

to T1 hypointense lesions in relapsing multiple sclerosis.

Dalton CM, Miszkiel KA, Barker GJ, MacManus DG, Pepple TI, Panzara

M, Yang M, Hulme A, O'Connor P, DH.

Institute of Neurology, London, UK.

BACKGROUND: Natalizumab, a humanized monoclonal anti-adhesion

molecule antibody, reduces the frequency of new gadolinium (Gd)

enhancing lesions and relapses in multiple sclerosis (MS). Its

effect on evolution of new Gd enhancing lesions to T1 hypointense

lesions is unknown. METHODS: 213 patients were randomized to receive

3 mg/kg or 6 mg/kg natalizumab or placebo monthly for 6 months and

then followed for a further 6 months. A subset of patients who had

one or more new gadolinium enhancing lesions from Month 0 to Month 6

and available electronic data were analysed. Each new Gd enhancing

lesion that developed during treatment (months 1-6) was investigated

for conversion to a new T1 hypointense lesion at month 12. Lesions

were classified as large or small if their cross-sectional area was

greater or less than 20mm(2). Because of the similarity of both

doses of natalizumab on the frequency of new Gd enhancing lesions,

the two natalizumab arms were combined in all analyses. RESULTS:

Compared with the placebo group, the natalizumab group exhibited

significant decreases in: (i) the proportion of patients with new Gd

enhancing lesions that evolved to T1-hypointense lesions (10/38 [26

%] versus 27/40 [68 %]; p < 0.01); (ii) the proportion of patients

who developed large T1 hypointense lesions (2/38 [5 %] versus 16/40

[40 %]; p < 0.01); (iii) the proportion of new Gd enhancing lesions

that became T1 hypointense (11/75 [15 %] versus 118/466 [25 %]; p =

0.045); (iv) the mean proportion per patient of new Gd enhancing

lesions that converted to T1-hypointense lesions (0.15 versus 0.28;

p = 0.005), and (v) the odds ratio (OR) of converting from Gd

enhancing to T1-hypointense lesions (OR = 0.48; 95% CI = 0.24, 0.94,

p = 0.031)). CONCLUSION: Natalizumab significantly suppresses the

evolution of new Gd enhancing to T1-hypointense lesions. This may

reflect several mechanisms including reduced cell migration across

the blood brain barrier, reduced T cell activation within lesions,

an inhibitory effect on subsequent axonal damage within the new

central nervous system lesion, and a reduced likelihood of recurrent

lesion inflammation.