Lactic acidosis during telbivudine treatment for HBV: A case report and literature review

Figure 1 Progression of serum hepatitis B virus DNA and aminotransferase. Telbivudine was introduced when alanine aminotransferase (ALT) and hepatitis B virus (HBV) DNA level was both high. The indication was clear and sufficient, and lactic acidosis happened after 11 mo of antiviral treatment when liver function was controlled well. HBV DNA continued to be normal after telbivudine was stopped and changed to tenofovir soon after.

Figure 2 Progression of serum creatine kinase level. Creatine kinase (CPK) elevated at the very beginning of lactic acidosis and returned to normal range quickly. AST: Aspartate aminotransferase.

Figure 3 A refractory lactic acidosis case and the fluctuation of blood lactate level. Symptoms lasted more than 3 mo and recovered slowly after 16 times of hemodialysis and small dosage of glucocorticoid helped to resolve the persistent serum lactate elevation.

Figure 4 Histopathology of muscle biopsy specimens showed mitochondrial toxicity. A: Many regenerating and necrotic muscle fibers, mild nuclear proliferation and necrosis around muscle fibers (HE, magnification × 200); B: Part of muscle fibers filled with fatty droplets (HE, magnification × 400); C: Ragged red fibers under envelope of shrinking muscle cells (modified Gomori trichrome stain, magnification × 200); D: The figure revealed the structural disorders of mitochondria. The myocytes different in size; Type I and Type II muscle fibers showed mosaic arrangement (nicotinamide-adenine dinucleotid, magnification × 200).