PT  - JOURNAL ARTICLE
AU  - Xu, Hongliang
AU  - Wang, Zhaoxia
AU  - Zheng, Lemin
AU  - Zhang, Wei
AU  - Lv, He
AU  - Jin, 
Suqin
AU  - Yuan, Yun
TI  - Lamivudine/telbivudine-associated neuromyopathy: neurogenic damage, mitochondrial dysfunction and mitochondrial DNA depletion
AID  - 10.1136/jclinpath-2013-202069
DP  - 2014 Nov 01
TA  - Journal of Clinical Pathology
PG  - 999--1005
VI  - 67
IP  - 11
4099  - http://jcp.bmj.com/content/67/11/999.short
4100  - http://jcp.bmj.com/content/67/11/999.full
SO  - J Clin Pathol2014 Nov 01; 67
AB  - Aims Myopathy or neuropathy has been associated with lamivudine/telbivudine therapy in hepatitis B patients. We aim to describe the pathological changes of lamivudine/telbivudine-associated neuromyopathy. Methods We retrospectively recruited six patients who were diagnosed with nucleotide analogues-associated myopathy or neuropathy. Muscle and nerve biopsy were performed, and the specimens were prepared for the light microscopy and electron microscopy. Genomic DNA was extracted from frozen muscle specimens, and the mitochondrial DNA (mtDNA) content was quantified by real-time PCR. Results Recovery of the myopathy can be achieved after the discontinuation or changing the drugs to entecavir. Muscle and nerve biopsy revealed similar changes under either the light or electronic microscopy in all the subjects. Quantitative real-time PCR revealed decrease of mtDNA content in the affected muscle. Conclusions MtDNA depletion results in mitochondrial dysfunction in the lamivudine/telbivudine-associated neuromyopathy. Myopathy was characterised by mitochondrial dysfunction accompanied with neurogenic damage due to axonal neuropathy. Ultrastructure changes of mitochondria included vacuolisation, simplification of the cristae and homogenised matrix.