Department of Pediatrics, Süleyman Demirel University School of Medicine, Cunur, Isparta, Turkey.
Email: [email protected] 
   

There are no published data on drug-induced autoimmune hepatitis caused by albendazole. We present here a patient with autoimmune hepatitis (AIH) induced by albendazole prescribed for hydatid cyst. A six-year-old girl was referred to our outpatient clinic with the diagnosis of liver hydatid cyst. Her physical examination and routine laboratory analyses were unremarkable. Albendazole treatment (15 mg/kg/day) was given for two weeks to perform puncture, aspiration, injection and re-aspiration (PAIR). But she was lost to follow up and she was admitted with abdominal pain after 2 months. AST, ALT, and GGT were 663, 800, and 92 IU/L, respectively. Laboratory investigations to exclude infectious, autoimmune, and metabolic liver disease were normal. The elevated transaminase levels returned to the normal range after cessation of albendazole. At 9th month, abdominal ultrasound revealed a progressive increase in the size of the　cyst. Treatment with PAIR technique was considered. Albendazole treatment (15 mg/kg/day) was initiated again 2 weeks before the PAIR procedure. She had mild elevation of transaminase levels at time of the procedure, but albendazole was continued for a week. Three weeks later, AST and ALT were 496 and 468 IU/L. ANA titers became positive (1:100; granular pattern). The pattern of liver enzyme derangement in the child is depicted in Fig. 1. Liver biopsy showed widespread portal lymphoplasmacytic inflammation with extensive interface (piecemeal) necrosis. Prednisolone and azathioprine were started. Transaminase levels rapidly decreased to normal ranges in two weeks. One month later, she had no complaints; physical examination and laboratory parameters were all normal. The steroid dose was tapered. Four months later, laboratory findings and clinical features were also normal. Afterwards, the dose of azathioprine was also tapered.

Fig. 1 The pattern of liver enzyme derangement in the patient.

AIH can be triggered in susceptible persons by an external factor. Previous data suggest [2] that drug-induced AIH makes up a significant proportion, approximately 9%, of AIH cases [1]. Björnsson, et al. [2] suggested that a substantial number of patients who were found to develop drug-induced liver injury were diagnosed with AIH during follow-up.

Our patient had transaminitis recurring every time after treatment of albendazole. In the first episode, elevated transaminase levels rapidly returned to the normal ranges following the cessation of albendazole. Also, ANA was negative and IgG level was in normal range. Hence, she was diagnosed as drug-induced hepatotoxicity due to albendazole. AIH was considered during second episode as ANA became positive, IgG level raised, and liver biopsy showed histologic features of AIH. Rapid response to immunosuppressive drugs supported our diagnosis, as well.

To our knowledge, this is the first report of AIH induced by albendazole. We speculate that drug-induced AIH may be prevented by avoiding use of drugs which have previously caused hepatotoxicity in a given patient.

2. Björnsson E,　Talwalkar J,　Treeprasertsuk S,　Neuhauser M, Lindor K. Drug induced autoimmunehepatitis: Clinical characteristics and prognosis. Hepatology. 2010;51: 2040-8.