Acute Hepatotoxicity After Ingestion of Morinda citrifolia (Noni Berry) Juice in a 14-year-old Boy


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Morinda citrifolia, commonly known as the noni berry, is a tropical fruit that has been used for more than 2000 years as a Polynesian herbal remedy (1). Since 1996, it has been sold widely in the United States as a general remedy for a wide array of health problems including cancer, diabetes, HIV/AIDS, gastric ulcers, hypertension, infections, depression, and chronic fatigue (2,3). We report a case of acute hepatotoxicity after ingestion of an energy drink containing noni berries in a previously healthy 14-year-old boy.CASE REPORTA previously healthy 14-year-old boy presented with a 1-week history of fatigue and a 2-day history of scleral icterus. Initial presentation at the patient's pediatrician's office demonstrated that the patient's alanine aminotransferase (ALT) was elevated to 3000 U/L with a direct bilirubin of 4.4 mg/dL and international normalized ratio of 1.6. Further questioning revealed that the patient had 2 episodes of nonbilious, nonbloody emesis and 2 days of diarrhea without hematochezia or melena. No change in mental status, acute bleeding, recent travel, sick contacts, or fever was reported. Medications within the last 6 months included ibuprofen taken approximately 2 times weekly for headaches. The patient had no history of acetaminophen, alcohol, tobacco, or any illicit drug use. Home, education, activities, drug use and abuse, sexual behavior, suicidality, and depression examination was negative. In regard to animal exposure, the patient resided on a farm and reported exposure to sheep, chickens, snakes, and mice. The only dietary change was ingestion of 10 two-oz bottles of an over-the-counter antioxidant drink during the course of 2 months (∼600 mL total) for improving energy during the current track and field season. The last ingestion of the antioxidant drink occurred on the day of admission to the hospital. Ingredients of the antioxidant drink were aloe vera, acai berry, muscadine grape, mangosteen, noni berry, gogi berry, pomegranate, blueberry, green tea extract, and plant-derived vitamins and minerals. The ingested dose of noni berry was approximately 91 mg/kg. His family history was significant for Hashimoto thyroiditis and migraines. There was no previous report of liver disease in the family.On presentation, the patient had significant scleral icterus and a palpable liver edge approximately 1 to 2 cm beyond the costal margin. The patient was lucid and answered all questions appropriately. Body mass index for sex, height, and weight was at the 30th percentile. Laboratory analysis revealed aspartate aminotransferase 1584 U/L; ALT 2860 U/L; γ-glutamyltransferase 141 U/L; total and direct bilirubin of 4.4 mg/dL and 3.4 mg/dL, respectively; normal ammonia of 22 umol/L; and elevated prothrombin time at 19.4 seconds and international normalized ratio of 1.7. A workup for etiology of acute hepatitis, inclusive of viral hepatitis panel, cytomegalovirus/Epstein-Barr virus polymerase chain reaction, serum ceruloplasmin and copper, serum iron, α-1-antitrypsin genotype, HIV, herpes simplex virus, anti-nuclear antibody, anti-smooth muscle antibody, and anti-liver-kidney-microsome antibody, was negative. An abdominal ultrasound with Doppler was consistent with hepatitis and did not show any signs of biliary tree obstruction.A liver biopsy revealed acute hepatitis with portal inflammation and periportal necrosis, hepatocellular cholestasis with focal ductular proliferation, and presence of numerous eosinophils (Figs 1 and 2). No plasma cells were found. Qualitative copper and iron stains were negative.The classification of hepatotoxic agents may be divided in general into those drugs that cause a known histological response and those that produce an idiosyncratic response, either because the drug produces the toxic response in a small percentage of the population or its hepatotoxic effects are poorly described.

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