Literature DB >> 21897603

YMDD motif mutation after lamivudine therapy.

Seyed Mohammad Jazayeri1, Seyed Mohammad Miri, Seyed Moayed Alavian.   

Abstract

Entities:  

Year:  2011        PMID: 21897603      PMCID: PMC3159254          DOI: 10.4103/0973-6247.83252

Source DB:  PubMed          Journal:  Asian J Transfus Sci        ISSN: 0973-6247


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Sir, We have read the article entitled “Probing rate of YMDD motif mutant in lamivudine treatment of Iranian patients with chronic hepatitis B virus infection” by Ghandehari et al.[1] There are some points that seem to be helpful. Hepatitis B virus (HBV) infection is the main cause of liver disease in our region and Isfahan (Central of Iran) is low endemicity for HBV infection.[2] The most of HBV infected in Iran are HBeAg negative,[3] but in Ghandehari et al.'s work the most cases (76%) were HBeAg positive. In the Materials and Method section, the authors did not refer to the trade characteristics of ELISA kit. Published data indicated that not all ELISA tests could find HBsAg in chronic patients due to either HBsAg mutants[4] or very low levels of HBV DNA.[5] Also, in the Results section they did not differentiate between serology and DNA detection, and no tables were included in the results, thus discriminating this correlation seems to be impossible for the readers. What was the aim of study? If the goal was finding the YMDD mutations in the patients who received lamivudine, where were the clinical criteria (histology, serology and biochemistry) for differentiating between patients who contained the mutations and those who did not? This paper does not allocate molecular finding to the above clinical points of view. Finding YMDD in 12% or 14% of patients while they were PCR and HBsAg negative indicated that the methodology used by the authors was inaccurate, although the selection bias of the patient studies could not be ruled out. Further, published and unpublished data from Iran indicated a higher rate of drug resistance among patients after 48 weeks of antiviral therapy.[6] Taken together, the authors should have used other more sensitive serologic and molecular approaches. In the Discussion section, the authors concluded that a significant difference existed between YMDD mutation and lamivudine therapy. What does this mean? As mentioned above, the authors did not differentiate between these two groups of patients. Thus, how did they make this conclusion? There are also some mistakes in the abstract, as YMDD results were included in the Conclusion section of the Abstract. Also, there are two different percentages (12% and 14%) for the rate of these mutations in the patients.
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Review 1.  Persistent hepatitis B virus infection in subjects without hepatitis B surface antigen: clinically significant or purely "occult"?

Authors:  C Bréchot; V Thiers; D Kremsdorf; B Nalpas; S Pol; P Paterlini-Bréchot
Journal:  Hepatology       Date:  2001-07       Impact factor: 17.425

2.  Molecular, immunological and clinical properties of mutated hepatitis B viruses.

Authors:  C Kreutz
Journal:  J Cell Mol Med       Date:  2002 Jan-Mar       Impact factor: 5.310

3.  Probing rate of YMDD motif mutant in lamivudine treatment of Iranian patients with chronic hepatitis B virus infection.

Authors:  Freshte Ghandehari; Abasali Pourazar; Mehrnaz Shanehsaz Zadeh; Nahid Tajedin
Journal:  Asian J Transfus Sci       Date:  2011-01
  3 in total

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