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Neurology 2002;59:1275-1277
© 2002 American Academy of Neurology
Brief Communications

Ubiquinone and nicotinamide treatment of patients with the 3243A->G mtDNA mutation

A. M. Remes, MD PhD, E. V. Liimatta, MD, S. Winqvist, Psych Lic, U. Tolonen, MD PhD, J. A. Ranua, MD, K. Reinikainen, MD PhD, I. E. Hassinen, MD PhD and K. Majamaa, MD PhD

From the Departments of Neurology (Drs. Remes, Winqvist, and Majamaa), Medical Biochemistry and Molecular Biology (Drs. Remes, Liimatta, Hassinen, and Majamaa), and Biocenter (Drs. Remes and Majamaa), University of Oulu; Department of Clinical Neurophysiology (Dr. Tolonen), University Hospital of Oulu; Department of Neurology (Dr. Ranua), Seinäjoki Central Hospital, Seinäjoki; and Neurological Projects, Research Center, Orion Pharma (Dr. Reinikainen), Espoo, Finland.

Address correspondence and reprint requests to Prof. Kari Majamaa, Department of Neurology, University of Oulu, P.O. Box 5000, FIN-90014 Oulu, Finland; e-mail: kari.majamaa{at}oulu.fi

The efficacy and safety of ubiquinone (Q10) and nicotinamide were evaluated in a 6-month open-label trial in patients with the 3243A->G mitochondrial DNA mutation. Blood lactate and pyruvate concentrations decreased, but there was little clinical improvement. Q10 and nicotinamide were well tolerated, but two patients died suddenly and unexpectedly during the trial. These deaths may have been unrelated to treatment. The unpredictable course of the disease makes evaluation of the clinical response difficult.




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K Majamaa-Voltti, J Turkka, M-L Kortelainen, H Huikuri, and K Majamaa
Causes of death in pedigrees with the 3243A>G mutation in mitochondrial DNA
J. Neurol. Neurosurg. Psychiatry, February 1, 2008; 79(2): 209 - 211.
[Abstract] [Full Text] [PDF]


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