LONG-TERM TREATMENT OF MULTIPLE SCLEROSIS WITH CORTICOTROPHIN

To determine long-term treatment (LTT) of neuromyelitis optica (NMO), we retrospectively reviewed therapies of 26 patients with NMO followed in five French neurological departments. To assess LTT efficacy, the probability of relapse free after LTT was analysed. Patients were divided into two groups according to the first treatment receiving interferon beta (IFN Group, seven patients) or immunosuppressants (IS Group, 19 patients). The probability of relapse was significantly lower in the IS Group (P = 0.0007). From our results, interferon beta is not recommended, and one of the best current therapeutic options for NMO appears to be immunosuppressants. Multiple Sclerosis 2007; 13: 256–259. http://msj.sagepub.com

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Secondary myelodysplastic syndrome following long-term treatment with azathioprine in patients with multiple sclerosis

Multiple Sclerosis Journal ◽

10.1191/135248506ms1307cr ◽

2006 ◽

Vol 12 (3) ◽

pp. 363-366 ◽

Cited By ~ 13

Author(s):

Norman Putzki ◽

Sabine Knipp ◽

T im Ramczykowski ◽

Susanne Vago ◽

Ulrich Germing ◽

...

Keyword(s):

Multiple Sclerosis ◽

Term Treatment ◽

Immunosuppressive Drug ◽

Term Therapy ◽

Secondary Myelodysplastic Syndrome ◽

Long Term Treatment ◽

Complete Blood Counts ◽

Long Term Therapy ◽

Dose Dependent

Azathioprine (Aza) is a widely used immunosuppressive drug in multiple sclerosis (MS) treatment. Recently, the incidence of secondary myelodysplastic syndromes (sMDS) associated with a poor prognosis was found to be elevated in patients treated with Aza for non-malign disorders. Three hundred and seventeen MS patients were retrospectively analysed and complete blood counts were examined for those exposed to Aza. We identified one case of sMDS (cumulative dose 627 g) in a young patient and two further malignancies (cumulative doses 27 g and 54 g) in the Aza group ( n=81; 3.7%). In the non-Aza ( n=236) group, five malignancies (2.1%, P=0.419) were identified. Including our patient, four cases of sMDS after long-term Aza therapy in MS have been reported so far. Cases suggest a time- and dose-dependent risk of sMDS in long-term therapy of MS with Aza. Long-term Aza therapy needs careful monitoring.

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Glatiramer acetate antibodies, gene expression and disease activity in multiple sclerosis

Multiple Sclerosis Journal ◽

10.1177/1352458511420268 ◽

2011 ◽

Vol 18 (3) ◽

pp. 305-313 ◽

Cited By ~ 14

Author(s):

F Sellebjerg ◽

CJ Hedegaard ◽

M Krakauer ◽

D Hesse ◽

H Lund ◽

...

Keyword(s):

Multiple Sclerosis ◽

Transcription Factors ◽

Disease Activity ◽

Glatiramer Acetate ◽

Immunological Response ◽

Term Treatment ◽

Pcr Analysis ◽

Enhanced Mri ◽

Long Term Treatment

Background: Glatiramer acetate (GA) treatment suppresses disease activity in multiple sclerosis (MS). The immunological response to treatment may differ in patients who are stable on GA therapy and patients with breakthrough disease activity, but the results of previous studies are inconsistent. Objectives: We studied the immunological response to GA and its relationship with disease activity. Methods: Anti-GA antibodies in plasma and the expression of genes encoding cytokines and T-cell-polarizing transcription factors in blood cells were analysed by flow cytometric bead array and polymerase chain reaction (PCR) analysis in 39 untreated and 29 GA-treated relapsing–remitting MS patients. Definition of breakthrough disease was based on the occurrence of relapses, disability progression, or gadolinium (Gd)-enhanced MRI. Results: The expression of T helper type 1 (Th1) and Th17 cytokines and transcription factors was reduced during long-term treatment, but there was no relationship between the expression of cytokines and transcription factors and anti-GA antibodies. High expression of mRNA encoding GATA3 and lymphotoxin-β (LT-β) was associated with low disease activity in Gd-enhanced MRI studies. None of the variables studied were associated with clinical disease activity. GA treatment resulted in the development of IgG and IgG4 anti-GA antibodies during the first months of treatment, persisting during long-term treatment. Conclusions: The observed relationship between the expression of mRNA encoding GATA3 and LT-β expression and MRI disease activity deserves further analysis in future studies. The development of anti-GA antibodies was observed in all patients treated with GA, but this was not related with measures of cellular immunity, clinical or MRI disease activity.

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