Probable herbal medication induced fulminant hepatic failure

A 4-year-old male child was admitted to a regional hospital for investigation of acute hepatitis.His past medical history was unremarkable.Two weeks before his admission, he developed 48 h of vomiting, as did his two younger twin sisters.There was associated fever but no cough, rhinorrhea, rash or diarrhoea.His sisters stopped vomiting.The patient received a single dose of paracetamol and his illness resolved completely.Four days later his vomiting recurred.On this occasion, he was given an herbal mixture containing 20 g of burnt clay, unknown quantities of ginger, licorice, mandarin skin, Chinese date, Inula britannica (flower), bitter orange, codonopsiz root and 'haematitium' (comprising zinc, tin, iron, magnesium and diferric trioxide).The patient was given 10 mL of the mixture three times a day for 3 days.His siblings were not given any of the mixture.The vomiting stopped for a few days after drinking the mixture but then recurred.He was seen by his local medical officer and was found to have jaundice and cervical lymphadenopathy.He was commenced on a cephalosporin antibiotic.The family also commenced him on homeopathic Ipecacuanha drops and tablets.Investigations performed showed an acute hepatitic picture (Table 1).Ten days after ingestion of the mixture, he was transferred to our institution.Clinically, he had mild jaundice and no signs of encephalopathy.He had no evidence of hepatosplenomegaly or signs of chronic liver disease.His liver function tests showed a marked increase of transaminases but normal synthetic function (Table 1).He was extensively investigated in an attempt to determine the aetiology of his acute hepatitis.Serology for Hepatitis A, B and C, Epstein-Barr virus (EBV), cytomegalovirus (CMV), human immunodeficiency virus (HIV), Syphilis, Parvovirus Mycoplasma, Coxsackie and Echovirus were negative.EBV, CMV and VZ IgG were positive consistent with past infection.Hepatitis A, Rubella and Measles IgG were detected indicating past vaccination.A urine drug screen was negative.Smooth muscle antibodies, antinuclear antibody (ANA) and liver-kidney muscle (LKM) autoantibodies were normal.Copper and alpha-1 antitrypsin levels were within normal limits.Caeruloplasmin levels were increased consistent with an acute hepatitis.An abdominal ultrasound showed normal liver architecture, but a complex pericholecystic collection without gallstones.Liver biopsy showed a severe acute hepatitis with portal-toportal bridging necrosis and a significant number of eosinophils raising the possibility of a drug-induced hepatitis (Fig. 1).Electron microscopy showed a normal number and appearance of peroxisomes and no evidence of a specific lysosomal storage