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Zidovudine-induced myopathy
Address for correspondence: Dr. Prof. Viroj Wiwanitkit, Wiwanitkit House, Bangkhae, Bangkok - 10160, Thailand. E-mail: wviroj@yahoo.com
This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
This article was originally published by Medknow Publications and was migrated to Scientific Scholar after the change of Publisher.
Sir,
I read the recent publication on zidovudine-induced myopathy with a great interest.[1] Sagar et al., concluded that “Zidovudine myopathy may be a constraint for use of the drug in the Western population; however, it is a well-tolerated drug as regards myopathy in our study on Indian patients.”[1] I have some comments on this work. First, the number of subjects in this study is very small and might have a limitation in further interpretation Second, the actual mechanism of zidovudine myopathy is believed to be due to a zidovudine-induced mitochondrial DNA depletion.[2] The corresponding mechanisms include azidothymidine (AZT) -induced oxidative stress, direct inhibition of mitochondrial bioenergetic machinery, and mitochondrial depletion of L-carnitine.[3] Based on these mechanisms, there should be no race difference of this zidovudine adverse effect. The higher prevalence in the Western population might be due to the reason that is given by Authier et al., that “lengthening of the survival of HIV-infected individuals has been associated with an increasing prevalence of iatrogenic conditions”.[4]
References
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- Mechanisms of zidovudine-induced mitochondrial toxicity and myopathy. Pharmacology. 2008;82:83-8.
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- Skeletal muscle involvement in human immunodeficiency virus (HIV)-infected patients in the era of highly active antiretroviral therapy (HAART) Muscle Nerve. 2005;32:247-60.
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