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Multiple Sclerosis
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Levocarnitine administration in multiple sclerosis patients with immunosuppressive therapy-induced fatigue

C Lebrun

Department of Neurology, Hôpital Pasteur, 30 voie romaine, 06002 Nice, France, lebrun.c{at}chu-nice.fr

H Alchaar

Department of Neurology, Hôpital Pasteur, 30 voie romaine, 06002 Nice, France

M Candito

Department of Biology, Hôpital Pasteur, 30 voie romaine, 06002 Nice, France

V Bourg

Department of Neurology, Hôpital Pasteur, 30 voie romaine, 06002 Nice, France

M Chatel

Department of Neurology, Hôpital Pasteur, 30 voie romaine, 06002 Nice, France

Nutritional factors and comedications are among the postulated causes of fatigue, a highly prevalent symptom in the multiple sclerosis (MS) population, with serious impact on patients’ quality of life. Deficiency of carnitine may play a role by reducing energy production through fatty acid oxidation and numerous MS therapies can induce fatigue syndrome. The aim of this prospective open-labelled study was to collect and study serum carnitine levels in MS patients with and without disease-modifying treatment-induced fatigue syndrome. We investigated whether restoration of the carnitine pool might improve treatment-induced fatigue in MS patients. In our study, there was no statistical difference in fatigue frequency between treated and untreated patients (P=0.5). Matched to age, gender and treatments, carnitine levels were lower for MS treated patients compared to untreated MS patients (P<0.05) or controls (P<0.001). Consecutive patients with low plasma carnitine levels who experienced fatigue were substituted. Treatment consisted of oral levocarnitine, 3-6 g daily. All patients achieved normal plasma carnitine levels. For 63% of patients treated with immunosuppressive or immunomodulatory therapies, oral levocarnitine adjunction decreased fatigue intensity, especially in patients treated with cyclophosphamide and interferon beta.

Key Words: carnitine • cyclophosphamide • fatigue • interferon • mitoxantrone • multiple sclerosis

Multiple Sclerosis, Vol. 12, No. 3, 321-324 (2006)
DOI: 10.1191/135248506ms1275oa
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