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Liver is the major site where metabolism of various drugs takes place and hence it is prone for injury from various chemical and toxic agents¹. Albendazole is a synthetic nitroimidazole with a broad spectrum of antinematode activity with anticestodal and some antiprotozoal action. Albendazole binds irreversibly to the nematodal isoform of ß-tubulin, blocking microtubule assembly, disrupting tegumental integrity, inhibiting motility, and impeding glucose uptake by the worm. Detectable levels are achieved in serum, cerebrospinal fluid, cyst fluid, and bile, with a serum half-life of 8 to 15 hours depending upon the dose.

Its common adverse effects are transient epigastric distress, diarrhoea, headache, nausea, dizziness, and insomnia. Abdominal discomfort, headache, fever, fatigue, alopecia are few side effects that are seen after long term use of this drug. Although it is metabolised in liver abnormal liver function tests are not common². 

We present 2 cases of acute hepatitis induced by albendazole. We ruled out other possible causes of acute hepatitis based on current and past medical history, drug history and laboratory analysis. Our diagnosis of drug induced liver injury was supported by the council for International Organization of Medical Sciences-Rousseau Uclaf Causality Assessment Method (CIOMS-RUCAM)3.

A 5 year old girl presented with complaints of yellowish discolouration of eyes and passage of clay coloured stools for 1 week. There was no history of fever, pain abdomen, pruritis, vomiting, loss of appetite and loose stools. There was history of intake of albendazole 5 days prior to onset of symptoms, was prescribed prophylactically by a local physician. There was history of previous hospitalisation with similar complaints 1 year back (after around 1 week of ingestion of albendazole). Laboratory records for the previous episode were not available. Icterus was noted. Abdominal examination revealed palpable liver 2 cm below right costal margin, having soft consistency and round margins and normal span. Spleen was not palpable. There was no free fluid in abdomen. Rest of the systemic examination was unremarkable.

A 7 year old girl presented with yellowish discolouration of eyes and vomiting for 4 days. There was no history of abdominal pain, clay coloured stools and pruritis, and there was no history of travel to endemic areas for viral hepatitis. There was history of intake of albendazole 4 days prior to onset of symptoms. The child had history of similar episodes from two year back  and it occurred after ingestion of albendazole with duration of interval between intake of albendazole and onset of symptoms being around one week. On general  examination there was no significant finding apart from icterus.

Investigations in both cases (Table 1) helped to rule out other causes of acute hepatitis and a possibility of albendazole induced hepatitis was considered in both cases  which was further supported by CIOMS-RUCAM score of 7  in both cases which corresponds to a probable correlation of drug induced liver injury due to albendazole.  Both the patients were managed conservatively and showed improvement during hospital stay. 

Drug induced hepatitis is defined as hepatitis caused by some medication with or without prescription which may include traditional alternative or natural medications³. Drug induced hepatitis is of two types, predictable which implies  a  high  incidence  of  hepatic  injury  in exposed  persons,  with  dose  dependence. The other type is idiosyncratic which   is  uncommon  and  unpredictable,  but accounts  for  the  majority  of  adverse  reactions and is possibly  related  to  genetic  polymorphisms,  with  production  of  toxic  intermediates1. Drug induced liver injuries are mainly of three types: hepatocellular, chloestatic and combined⁴. 

In our case 1, injury was of combined type whereas in case 2 it was predominantly of hepatocellular type. Drug induced liver injury  is diagnosed after excluding all other possible causes of acute hepatitis and there is no absolute criteria for its diagnosis. The CIOMS RUCAM scale was used to evaluate the probability of toxic hepatitis which showed a “probable” correlation with a score of 7. The CIOMS/RUCAM  scale is used to establish causal relationship between the offending drug and liver damage. The scale involves  scoring system which categorizes the suspicion into “definite or highly probable” (score > 8), “probable” (score 6-8), “possible” (score 3-5), “unlikely” (score 1-2) and “excluded” (score = 0). 

Toxic hepatitis due to albendazole which has broad anti-parasitic spectrum is rare and most of the cases have been reported after its prolonged usage⁵. Hepatitis after single dose exposure is uncommonly reported⁶. As albendazole is a common deworming agent so one should be aware of this rare but significant adverse effect and detailed drug history in a patient of acute hepatitis should always be obtained. In India albendazole is given as a part of national deworming program and millions of children are given this drug simultaneously, few of whom may develop this uncommon but known complication. This  adverse effect should always be taken into consideration while evaluating a child with acute hepatitis with unknown etiology.