Two cases of telbivudine-induced myopathy in siblings with chronic hepatitis B
A 28-year-old man who received telbivudine therapy for chronic hepatitis B presented with progressive weakness of both lower legs and difficulty in ascending stairs over the past 4 months. And also, he was unable to lift up a dumbbell and do pushups due to weakness in both arm. He was diagnosed with CHB 3 years ago and started taking 600 mg of telbivudine once daily for 9 months to control HBV activation. Since taking telbivudine, the serum viral DNA level gradually decreased from 100,000 IU/mL to 222 IU/mL, and the serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were also normalized. However, he showed muscle weakness since taking telbivudine. Although there was no symptoms such as dysphagia, cramps, or sensory abnormality, the patient suffered from progressive and generalized weakness, especially of his legs, and had difficulty climbing stairs. He exhibited motor weakness (grade 4) of the hip flexor, making it difficult for him to stand up from the sitting position, but there was no sign of abnormal deep tendon reflex, muscle atrophy, or hypertrophy on physical examination. He had not taken any other medications that would be regarded as a cause of his symptoms while taking telbivudine. Laboratory examinations showed AST of 59 IU/L, ALT of 26 IU/L, total bilirubin of 0.9 mg/dL, blood urea nitrogen (BUN) of 15.4 mg/dL, and serum creatinine of 0.7 mg/dL. His serum CK level was elevated up to 788 IU/L (44-245 IU/L). Electromyography (EMG) was performed and showed a few positive sharp waves with polyphasic myopathic motor unit action potentials in the right vastus medialis, tibialis anterior, and biceps brachii muscles, which is consistent with the active stage of generalized myopathy (). We planned to perform a muscle biopsy for confirmation, but he refused to have a muscle biopsy. The serum CK level was elevated up to 728 IU/L, 4 months prior to this visit. At that time, he felt general weakness, but he did not stop taking telbivudine. Because most of telbivudine-related CK elevations were transient and increased CK levels decreased to normal range without any interruption. However, his symptoms persisted and CK elevation was also shown. Thus, he was diagnosed him with telbivudine-induced myopathy based on the clinical clues and EMG findings and decided to change the anti-viral agent to 0.5 mg entecavir once daily. He revisited our clinic at one month after telbivudine withdrawal, and his clinical symptoms subsequently improved to the extent that he was able to climb stairs easily. The serum CK level was also decreased to 326 IU/L.