Datasets:

---

Recag

/

Rp_CommonC_340

like 0

ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvODE3MzI1LW92ZXJ2aWV3\nDrugs & Diseases > Emergency Medicine\nHypoglycemic Plant Poisoning\nAuthor: Nathan Reisman, MD; Chief Editor: Sage W Wiener, MD more...\nSections Hypoglycemic Plant Poisoning\nLaboratory Studies\nPrehospital Care\nEmergency Department Care\nGI decontaminant\nSomatostatin analogs\nAntianxiety Agent\nMore than 270 plant species have been identified as having hypoglycemic potential. Many of these plants are used in developing countries in the treatment of diabetes. The most well known of these plants are listed below:\nHerb fenugreek ( Trigonella foenum-graecum)\nBitter melon gourd ( Momordica charantia)\nClimbing ivy gourd ( Coccinia indica)\nMamijava ( Enicostemma littorale)\nAsian ginseng ( Panax ginseng)\nAmerican ginseng ( Panax quinquefolius)\nSiberian ginseng ( Eleutherococcus senticosus)\nAckee tree ( Blighia sapida)\nPrickly pear ( Opuntia robusta)\nYellow bells ( Tecoma stans [family Bignoniaceae])\nMost of the plants studied have shown minimal-to-moderate effects on glucose regulation, with the exception of ackee fruit and bitter melon. Bitter melon produces hypoglycemia via steroidal saponins (charantin, insulinlike peptides, and alkaloids), but it has never been reported to result in fatality. Methylenecyclopropylglycine (MCPG) and hypoglycin A (HGA) are naturally-occurring amino acids found in some soapberry fruits. Fatalities have been reported worldwide as a result of HGA ingestion, and exposure to MCPG has been implicated recently in the Asian outbreaks of hypoglycemic encephalopathy. [1]\nThis article focuses on the potentially fatal effects produced by ackee fruit ingestions due to HGA contained in the fruit. [2] In addition, several references regarding other plants with hypoglycemic effects have been included.\nAckee fruit is produced biannually by the tropical evergreen tree, Blighia sapida. Although indigenous to West Africa, it is commonly found in the Caribbean islands, Central America, South America, and southern Florida. In South America, the fruit has been used to treat colds, fever, and diseases as varied as edema and epilepsy, though no clinical trials support these uses. In Jamaica, ackee fruit is a food staple, commonly prepared like scrambled eggs or boiled with fish. The fruit itself is 10 cm wide and weighs 100 g. It houses 3 glossy, black seeds contained within a straw- to red-colored husk and covered by a thick, oily appearing yellow aril. The outer aril is closed in unripe ackee fruit. Upon ripening, the aril spontaneously opens.\nUnripe fruit and the water used to cook it are toxic and cause Jamaican vomiting sickness when ingested (see Ackee Fruit Toxicity). [3, 4] Fatal epidemics of this illness have been well studied in Haiti, West Africa, and Jamaica. These epidemics tend to coincide with food shortages. The disease is characterized by profound hypoglycemia and intractable vomiting. Before widespread recognition of the hypoglycemia produced by this illness, the mortality rate approached 80%.\nFor patient education resources, see the First Aid and Injuries Center, as well as Food Poisoning, Poisons, and Activated Charcoal.\nTwo water-soluble toxins are present in unripe ackee fruit, hypoglycin A and hypoglycin B. Hypoglycin A is L-alpha-amino-beta-[methylene cyclopropyl]propionic acid. Hypoglycin A is found in both the aril and the seeds of the unripe fruit. Hypoglycin B is a gamma-L-glutamyl derivative of hypoglycin A and is found only in the seeds of the fruit.\nHypoglycin A is metabolized by transamination and oxidative decarboxylation to form methylenecyclopropylacetic acid (MCPA). MCPA then forms nonmetabolizable carnitine and coenzyme A (CoA) esters, rendering them unavailable for other metabolic reactions. Hypoglycemia results because CoA and carnitine are required for long-chain fatty acid oxidation, and oxidation is required for gluconeogenesis. Thus, hypoglycemia results from an inability to perform gluconeogenesis. This inhibition of fatty acid metabolism also results in the accumulation of unusual dicarboxylic acids that are subsequently excreted in the urine such as 2-ethyl malonate, 2-methyl succinate, glutarate, and adipate.\nAdditionally, MCPA inhibits acyl-CoA dehydrogenases. Inhibition of butyryl CoA dehydrogenase stops the oxidation of long-chain fatty acids at the level of hexanoyl CoA and butyryl CoA, causing decreased production of nicotinamide adenine dinucleotide (NADH) and acetyl CoA. Their lowered concentration further inhibits gluconeogenesis. Hypoglycin A does not affect insulin release or serum insulin levels in animal models.\nIt is postulated that increased concentrations of glutaric acid may have an inhibitory effect on glutamic acid decarboxylase, causing a decrease in GABA production and an increase in concentration of glutamate. This mechanism can explain the proconvulsive effect of hypoglycin A.\nCauses include ingestion of unripe ackee fruit, canned ackee fruit, ackee fruit that has been forcibly opened or water in which unripe ackee fruit has been cooked.\nThe true incidence of ackee poisoning is unknown. Ackee fruit sales are illegal in the United States, likely leading to underreporting. Cases have been reported after consumption of fruit illegally shipped or transported by travelers. Several isolated, nonfatal cases have been reported in Ohio, Connecticut, and New York.\nIn 2000, the US lifted a decades-old ban on the importation of ackee fruit. More recently, the Food and Drug Administration (FDA) is considering modifying the importation of ackee. Research by Whitaker et al has led to evaluation of sampling plans to detect hypoglycin A in ackee fruit. This research will help the FDA to develop a cost-effective monitoring program to reduce lots of misclassified product and to increase consumer safety. [5, 6]\nJamaica: Although endemic to Jamaica, the epidemiology of ackee poisoning is not well characterized. The true incidence is likely underreported. Incidence has been estimated at 2 cases per 100,000 annually for persons younger than 15 years and 0.4 case per 100,000 persons annually for those older than 15 years. [7]\nWest Africa: Based on recent epidemics, the incidence in children aged 2-6 years is estimated to be about 40 cases per 100,000 population.\nOther: Most cases occur in developing nations in Africa and the Caribbean. Incidence rates in other areas have not been well studied.\nReported cases in Africa, Jamaica, and Haiti occurred in blacks.\nIn reported cases, no difference in sex distribution was noted.\nPoisoning is more common in persons younger than 15 years, and severe poisoning is more common in the pediatric population.\nPrognosis is good if unripe ackee fruit ingestion is promptly recognized and appropriately managed; however, deaths do occur. Ackee poisoning has killed an estimated 5,000 people since 1886. Children are more likely than adults to experience fatal complications of ackee poisoning. The most well-studied epidemics have been in Haiti, Jamaica, and West Africa.\nJamaica: Large-scale poisonings reach epidemic proportions typically during the winter months. Between January 1989 and July 1991, 28 patients reported symptoms of ackee poisoning. Six of 28 patients died. The most common symptoms were vomiting, coma, and seizures. Seven of the patients had confirmed hypoglycemia. Most of the cases occurred between January and March. [7]\nWest Africa: In 1998, in Burkina Faso, an epidemic of fatal encephalopathy was linked to ackee poisoning. Between January and May of 1998, 29 children aged 2-6 years died. The clinical presentation was similar to that of Jamaican vomiting sickness and toxic hypoglycemic syndrome; the most common symptoms included hypotonia, convulsions, and coma. [8]\nHaiti: From November 2000 to March 2001, 60 cases with symptoms consistent of ackee poisoning (ie, continuous vomiting, abdominal pain, loss of consciousness, convulsions within 24 h) were recorded in 2 districts of Haiti's Northern Province. Retrospective analysis confirmed 31 of the 80 cases were related to consumption of ackee fruit. The mean age of the victims ranged from 6 months to 88 years, with a median of 7 and an average of 16. The case-fatality rate was 52%. [9]\nIsenberg SL, Carter MD, Hayes SR, Graham LA, Johnson D, Mathews TP, et al. Quantification of Toxins in Soapberry (Sapindaceae) Arils: Hypoglycin A and Methylenecyclopropylglycine. J Agric Food Chem. 2016 Jul 13. 64 (27):5607-13. [Medline]. [Full Text].\nAdelia C. Bovell-Benjamin, Jerry Roberts. Naturally Occurring Toxicants: Presence in Selected Commonly Consumed Fruits. https://www.sciencedirect.com/. Available at https://www.sciencedirect.com/science/article/pii/B978012800605400013X. Accessed: 2016.\nBarceloux DG. Akee fruit and Jamaican vomiting sickness (Blighia sapida Köenig). Dis Mon. 2009 Jun. 55(6):318-26. [Medline].\nSurmaitis R, Hamilton RJ. Ackee Fruit Toxicity. 2018 Jan. [Medline]. [Full Text].\nWhitaker TB, Saltsman JJ, Ware GM, Slate AB. Evaluating the performance of sampling plans to detect hypoglycin A in ackee fruit shipments imported into the United States. J AOAC Int. 2007 Jul-Aug. 90(4):1060-72. [Medline].\nUS Department of Agriculture. Improve the Detection of Quality Attributes and Chemical Agents in Agricultural Commodities. Last updated November 9, 2009. Available at http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=215290. Accessed: November 10, 2009.\nCDC. Toxic hypoglycemic syndrome--Jamaica, 1989-1991. MMWR Morb Mortal Wkly Rep. 1992 Jan 31. 41(4):53-5. [Medline]. [Full Text].\nMeda HA, Diallo B, Buchet JP, Lison D, Barennes H, Ouangre A, et al. Epidemic of fatal encephalopathy in preschool children in Burkina Faso and consumption of unripe ackee (Blighia sapida) fruit. Lancet. 1999 Feb 13. 353(9152):536-40. [Medline].\nJoskow R, Belson M, Vesper H, Backer L, Rubin C. Ackee fruit poisoning: an outbreak investigation in Haiti 2000-2001, and review of the literature. Clin Toxicol (Phila). 2006. 44(3):267-73. [Medline].\nPitkin F and Randall S. Laboratory Patterns in Hypoglycin A Toxicity. Archives of Clinical and Biomedical Research. 10 April 2017. 1(3):76-84. [Full Text].\nHumphries LK, Eiland LS. Treatment of acute seizures: is intranasal midazolam a viable option?. J Pediatr Pharmacol Ther. 2013 Apr. 18(2):79-87. [Medline]. [Full Text].\nHolsti M, Sill BL, Firth SD, Filloux FM, Joyce SM, Furnival RA. Prehospital intranasal midazolam for the treatment of pediatric seizures. Pediatr Emerg Care. 2007 Mar. 23(3):148-53. [Medline].\nBarennes H, Valea I, Boudat AM, Idle JR, Nagot N. Early glucose and methylene blue are effective against unripe ackee apple (Blighia sapida) poisoning in mice. Food Chem Toxicol. 2004 May. 42(5):809-15. [Medline].\nGaillard Y, Carlier J, Berscht M, et al. Fatal intoxication due to ackee (Blighia sapida) in Suriname and French Guyana. GC-MS detection and quantification of hypoglycin-A. Forensic Sci Int. 2011 Mar 20. 206(1-3):e103-7. [Medline].\nNathan Reisman, MD Clinical Assistant Professor, Department of Emergency Medicine, SUNY Downstate Medical Center\nSage W Wiener, MD Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center; Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center\nSage W Wiener, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, Society for Academic Emergency Medicine\nJohn T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals\nJohn T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists\nB Zane Horowitz, MD, FACMT Professor, Department of Emergency Medicine, Oregon Health and Sciences University School of Medicine; Medical Director, Oregon Poison Center; Medical Director, Alaska Poison Control System\nB Zane Horowitz, MD, FACMT is a member of the following medical societies: American College of Medical Toxicology\nMichael Hodgman, MD Assistant Clinical Professor of Medicine, Department of Emergency Medicine, Bassett Healthcare\nMichael Hodgman, MD is a member of the following medical societies: American College of Medical Toxicology, American College of Physicians, Medical Society of the State of New York, and Wilderness Medical Society\nJennifer Coles Schecter, MD Resident Physician, Department of Emergency Medicine, Lahey Clinic, Burlington, MA\nencoded search term (Hypoglycemic Plant Poisoning) and Hypoglycemic Plant Poisoning\nSeafood Toxicity\nBotulinum Toxin in Pain Management\nBotulinum Toxin Injections in Plastic Surgery\nPathophysiology and Etiology of Lead Toxicity\nBotulinum Toxin for Laryngeal Dystonia\nLocal Anesthetic Toxicity\nDietary Supplement Causes Widespread Selenium Poisoning\nManagement of Tourette's Syndrome Reviewed\nAtopic Dermatitis: Five Promising Targeted Therapies\nUrinary Incontinence: Not Just a Flow Issue\nAccording to Emergency Physicians\nUS Air Ambulances: Expensive, Risky, and Regulation-Averse\nDoc Gets New Heart, Loses Residency in 5 Weeks\nEmergency Reversal of Anticoagulation\nSepsis in Pregnancy: Recognition and Resuscitation\nFast Five Quiz: Drug Overdoses\nDiseases & Conditions Seafood Toxicity\nDiseases & Conditions Ethylene Glycol Toxicity\nProcedures Botulinum Toxin\nProcedures Botulinum Toxin in Pain Management"