To the Editor: We wish to report a case of acute liver failure associated with the use of a herbal preparation that contained several ingredients, including Cimicifuga racemosa (black cohosh).

In January 2003, a 52-year-old woman was referred to our unit with acute liver failure. She had taken a herbal preparation for three months (for severe tinnitus), but ceased four weeks before admission. The preparation was made and provided by a pharmacist. The preparation was supplied in a 200 mL bottle and contained a mixture of the fluid extracts of Nepeta hederacea (ground ivy) 80 mL, Hydrastis canadensis (golden seal) 20 mL, Ginkgo biloba (ginkgo) 40 mL, Avena sativa (oats seed) 40 mL and Cimicifuga racemosa (black cohosh) 20 mL. According to the information supplied by the pharmacist, one gram of herb was contained in each 1 mL of extract, with the exception of golden seal, for which 0.5 g of herb was contained in each millilitre. The oats seed fluid extract was supplied by Southern Cross Herbal School (Gosford, NSW), and all other fluid extracts were supplied by the Herbal Extract Company of Australia (Sydney, NSW). The patient took a total of 600 mL over the 3-month period (7.5 mL bd orally as required). Before developing symptoms of liver failure, the patient had taken no other medications and had no risk factors for the acquisition of viral hepatitis.

On arrival, she was deeply jaundiced but not encephalopathic. Liver span was reduced and there were no signs of chronic liver disease. The international normalised ratio was 3.0 (normal, 1.0–1.2), and she had serum concentrations of albumin, 26 g/L (normal, 35–50 g/L); bilirubin, 368 μmol/L (normal, < 18 μmol/L); alkaline phosphatase, 230 U/L (normal, 35–104 U/L); alanine aminotransferase, 1380 U/L (normal, < 55 U/L); and g glutamyl-transpeptidase, 134 U/L (normal, < 45 U/L). Extensive investigation excluded other recognised causes of acute liver failure.

Her condition deteriorated over the following week, with the development of hepatic encephalopathy and hepatorenal failure. She underwent liver transplantation in early February 2003, and had an uneventful postoperative course. Examination of the explanted liver revealed massive hepatic necrosis.

Following transplantation, the pharmacist supplied samples of the individual extracts to the Therapeutic Goods Administration (Canberra) for analysis. The analysis revealed no undeclared pharmaceutical drugs. Assay of the individual extracts of golden seal, ginkgo and black cohosh revealed the listed ingredients to be present. The presence of ground ivy and oats seed in the extracts has not yet been confirmed owing to the lack of a suitable reference standard.

It is not possible to determine the individual ingredient, or mixture of ingredients, that resulted in acute liver failure in this patient. However, this is the third case of acute liver failure associated with black cohosh ingestion to be reported recently in Australia.1 In this instance, liver failure progressed despite cessation of the herbal therapy, and transplantation was required, suggesting that a process of irreversible liver injury had been initiated before treatment was ceased. It should be noted that ground ivy contains pulegone, a known hepatotoxin. However, the concentration of pulegone in ground ivy is accepted to be vastly less than in pennyroyal, where pulegone-induced hepatotoxicity has been reported.2 To our knowledge, there are no reports of golden seal, oats seed or ginkgo causing hepatotoxicity.

The popularity of herbal therapies is due in part to their perceived lack of side effects. It is important for the medical and broader community to be aware of the potential toxicity of these preparations. In any patient presenting with unexplained hepatitis it is essential to determine if there has been exposure to herbal therapies, since early cessation of treatment may be life saving.