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Letters to the Editor
2 (
2
); 206-207

Author's reply

Department of Medicine and HIV/AIDS Centre for North East India, Military Hospital, Shillong, Meghalaya, India
Department of Medicine, AFMC and Command Hospital, Pune Complex, Pune, India
Department of Pathology, Military Hospital, Shillong, Meghalaya, India

Address for correspondence: Dr. Amitabh Sagar, Department of Medicine and HIV/AIDS Centre, North East India, Military Hospital, Shillong, Meghalaya - 793 001, India. E-mail: amitthephysician@gmail.com

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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.

Disclaimer:
This article was originally published by Medknow Publications and was migrated to Scientific Scholar after the change of Publisher.

Sir,

Thank you for giving us an opportunity to reply to the letter.[1] Our views are, firstly, we had followed-up a total of 147 patients with a mean of 3.83 years, which translates to 563.5 patient years. The average duration of symptoms to appear in zidovudine myopathy varies in different studies. The most prominent of them by Peters et al. recorded an average of 270 days, or 0.74 years, and the average incidence of the problem ranges from 8 to 50%.[23] Taking an average of 13% as the incidence of the problem and with a confidence interval of 5 and confidence level 95%, the sample size required will be 384 patients. Hence, our sample size was adequate. With a higher incidence of the problem (tending toward 50%), the required sample size will shrink further. Secondly, mitochondria contain DNA. In toxic mitochondrial disorders due to nucleoside reverse transcriptase inhibitors like zidovudine, there is also some evidence that clinical involvement of a given organ, like blood, skeletal muscle, myocardium and liver, parallels mitochondrial DNA depletion.[4] This mitochondrial DNA damage has also been implicated for selective lactic acidosis and lipodystrophy for stavudine and zidovudine to a lesser degree in Australian whites compared to the US and European cohorts.[4] Hence, we postulated a racial variance for zidovudine myopathy. Thirdly, our study includes cases with a mean follow-up of 3.83 years on antiretroviral therapy, which is almost two- to three-times the follow-up period of comparable studies on the subject. The living conditions, compliance with drugs, follow-up and survival was comparable with the western population; hence, the higher prevalence in the latter may not be linked to an increase in the survival associated with iatrogenic conditions.

References

  1. , . Zidovudine-induced myopathy. J Neurosci Rural Pract. 2011;2:206.
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  2. , , , , , . Mitochondrial myopathy associated with chronic zidovudine therapy in AIDS. Q J Med. 1993;86:5-15.
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  3. , , , , , , . Early features of zidovudine-associated myopathy: Histopathological findings and clinical correlations. Acta Neuropathol. 1995;90:1-6.
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  4. Mitochondrial toxicity and HIV disease meeting report. Available from: http://www.hivforum.org
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