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Letters to the Editor
Dear Editor, ECHINACEA-INDUCED ACUTE LIVER FAILURE IN A CHILD We report, for the first time, severe acute liver failure in a child likely secondary to echinacea toxicity. A 2-year-old European female, unimmunised but previously well, presented with acute onset of jaundice, lethargy, loose stools and anorexia over a 2-week period. She was noted to have pale stools and dark urine. Initially there was no history of drug ingestion or exposure to herbal or alternative therapies. There was no history of travel or recent contact with anyone with hepatitis or diarrhoeal illness. On examination, the patient was afebrile and jaundiced. There was no clubbing, oedema or palmar erythema. Abdominal examination revealed a soft, non-tender abdomen with a smooth liver edge palpable 1 cm below the costal margin. Admission blood tests were consistent with an acute hepatitis with a bilirubin of 155 (conjugated 100), alanine aminotransferase 4021, aspartate aminotransferase 4246, γ-glutamyl transpeptidase 77, alkaline phosphatase 474, lactate dehydrogenase 1249 and international normalized ratio 2.2. Her full blood count was normal. Abdominal ultrasound scan was normal, and a liver biopsy showed marked hepatocyte swelling with spotty necrosis and inflammatory infiltrate with eosinophils present. The initial impression was either an acute infectious process or an adverse drug reaction. Serological tests were negative for hepatitis A, B and C and other viruses, and tests of autoimmune hepatitis were all negative. The patient was unwell over the first 7 days of her admission, with continued synthetic dysfunction. She slowly improved and was discharged 2 weeks after admission. On review of history, her mother recalled giving her two herbal remedies containing echinacea prior to the onset of her symptoms. These were Kiwiherb Children’s Echinature (3.5 mg echinacea in 5 mL solution), 0.5–1.0 mL daily for 2 weeks, and Healtheries Boost Immunity (containing vitamin C 1 g, zinc 7.5 mg and echinacea 200 mg), half a tablet daily for 2 weeks. Total daily dose equated to 100.7 mg of echinacea. We believe the echinacea was the cause of the patient’s acute liver failure, as it was temporally related to the ingestion, there was no evidence of any infective or autoimmune cause, and she made a steady recovery once she stopped taking the drug. On review of the literature we found one documented case with a similar pattern of hepatitis considered to be secondary to echinacea in an adult.1 There is little standardisation of preparations of echinacea or regulation of their use.2 This case serves to remind practitioners of the potential significance of complementary medicines and the importance of carefully asking for details of all nonprescribed therapies.
Dr Jennifer Anne Lawrenson1 Dr Tony Walls2 Professor Andrew S Day3 1 Resident Medical Officer, 2Consultant in Paediatric Infectious Diseases, 3Professor in Paediatric Gastroenterology, Department of Paediatrics, Christchurch Public Hospital, Canterbury District Health Board, Christchurch, New Zealand
References 1 Kocman O, Hulagu S, Senturk O. Echinacea-induced severe acute hepatitis with features of cholestatic autoimmune hepatitis. Eur. J. Intern. Med. 2008; 19: 148–52. 2 Toselli F, Matthias A, Gillam EM. Echinacea metabolism and drug interactions: the case for standardisation of a complementary medicine. Life Sci. 2009; 85: 97–106.
Dear Editor, NEWBORN PULSE OXIMETRY SCREENING We read with great interest Bhola’s recent paper on pulse oximetry screening.1 We congratulate the authors and agree wholeheartedly with the conclusions. We have recently published a similar study2 (using the PulseOx protocol3) that examined screening in a UK setting. Both datasets are comparable – from tertiary units over a similar time period. Bhola reported 18 801 babies over 42 months, and we reported 25 859 babies over 40 months. We too found that pulse oximetry (i) is an effective method of identifying both congenital heart defects (CHDs) and important non-cardiac conditions (ii) can be undertaken without additional staff and (iii) does not overload clinical services, particularly echocardiography. However, there are some important differences between the two studies that are worth exploring. Although the baseline pass thresholds were the same (>94%), Bhola used only post-ductal saturations, whereas we used both pre- and post-ductal (additional pass threshold – difference of
Letters to the Editor
Dear Editor, ECHINACEA-INDUCED ACUTE LIVER FAILURE IN A CHILD We report, for the first time, severe acute liver failure in a child likely secondary to echinacea toxicity. A 2-year-old European female, unimmunised but previously well, presented with acute onset of jaundice, lethargy, loose stools and anorexia over a 2-week period. She was noted to have pale stools and dark urine. Initially there was no history of drug ingestion or exposure to herbal or alternative therapies. There was no history of travel or recent contact with anyone with hepatitis or diarrhoeal illness. On examination, the patient was afebrile and jaundiced. There was no clubbing, oedema or palmar erythema. Abdominal examination revealed a soft, non-tender abdomen with a smooth liver edge palpable 1 cm below the costal margin. Admission blood tests were consistent with an acute hepatitis with a bilirubin of 155 (conjugated 100), alanine aminotransferase 4021, aspartate aminotransferase 4246, γ-glutamyl transpeptidase 77, alkaline phosphatase 474, lactate dehydrogenase 1249 and international normalized ratio 2.2. Her full blood count was normal. Abdominal ultrasound scan was normal, and a liver biopsy showed marked hepatocyte swelling with spotty necrosis and inflammatory infiltrate with eosinophils present. The initial impression was either an acute infectious process or an adverse drug reaction. Serological tests were negative for hepatitis A, B and C and other viruses, and tests of autoimmune hepatitis were all negative. The patient was unwell over the first 7 days of her admission, with continued synthetic dysfunction. She slowly improved and was discharged 2 weeks after admission. On review of history, her mother recalled giving her two herbal remedies containing echinacea prior to the onset of her symptoms. These were Kiwiherb Children’s Echinature (3.5 mg echinacea in 5 mL solution), 0.5–1.0 mL daily for 2 weeks, and Healtheries Boost Immunity (containing vitamin C 1 g, zinc 7.5 mg and echinacea 200 mg), half a tablet daily for 2 weeks. Total daily dose equated to 100.7 mg of echinacea. We believe the echinacea was the cause of the patient’s acute liver failure, as it was temporally related to the ingestion, there was no evidence of any infective or autoimmune cause, and she made a steady recovery once she stopped taking the drug. On review of the literature we found one documented case with a similar pattern of hepatitis considered to be secondary to echinacea in an adult.1 There is little standardisation of preparations of echinacea or regulation of their use.2 This case serves to remind practitioners of the potential significance of complementary medicines and the importance of carefully asking for details of all nonprescribed therapies.
Dr Jennifer Anne Lawrenson1 Dr Tony Walls2 Professor Andrew S Day3 1 Resident Medical Officer, 2Consultant in Paediatric Infectious Diseases, 3Professor in Paediatric Gastroenterology, Department of Paediatrics, Christchurch Public Hospital, Canterbury District Health Board, Christchurch, New Zealand
References 1 Kocman O, Hulagu S, Senturk O. Echinacea-induced severe acute hepatitis with features of cholestatic autoimmune hepatitis. Eur. J. Intern. Med. 2008; 19: 148–52. 2 Toselli F, Matthias A, Gillam EM. Echinacea metabolism and drug interactions: the case for standardisation of a complementary medicine. Life Sci. 2009; 85: 97–106.
Dear Editor, NEWBORN PULSE OXIMETRY SCREENING We read with great interest Bhola’s recent paper on pulse oximetry screening.1 We congratulate the authors and agree wholeheartedly with the conclusions. We have recently published a similar study2 (using the PulseOx protocol3) that examined screening in a UK setting. Both datasets are comparable – from tertiary units over a similar time period. Bhola reported 18 801 babies over 42 months, and we reported 25 859 babies over 40 months. We too found that pulse oximetry (i) is an effective method of identifying both congenital heart defects (CHDs) and important non-cardiac conditions (ii) can be undertaken without additional staff and (iii) does not overload clinical services, particularly echocardiography. However, there are some important differences between the two studies that are worth exploring. Although the baseline pass thresholds were the same (>94%), Bhola used only post-ductal saturations, whereas we used both pre- and post-ductal (additional pass threshold – difference of
