Angela Regina DO
Department Of Emergency Medicine
North Shore University Hospital
Case: 35 year old man presents to the emergency department complaining of nausea and vomiting about 3 hours after a traditional Jamaican meal. He is lethargic and your nurse calls you about a finger stick “Lo” on the machine. His aunt admits to smuggling the ingredients from Jamaica.
Between 1880 and 1955 there were a variety of case reports associating an illness and death with ingestion of unripe ackee fruit ingestion.
In 1954 near Montego Bay, Jamaica there were 151 cases with 32 deaths.
In 1954, two toxic constituents were isolated from the arils of unripe ackee fruit by Hassall et al.
In 1976, Tanaka et al confirmed that unripe ackee fruit is the cause of Jamaican vomiting sickness via the toxin Hypoglycin A.
Distribution and Ecology
Ackee tree is native to West Africa and was introduced to Jamaica and has naturalized in southern California and Florida.
Unripened fruit is oblong shaped and the color changes as it ripens from green to yellow, to yellow-red and then to red. Opens and exposes a black seed with thick oily arils, which are used in cooking.
Ackee is the national fruit of Jamaica.
Hypoglycin B - the gamma glutamyl conjugate of hypoglycin A
Mechanism of Toxicity
Hypoglycin A is metabolized to methylene cyclopropyl acetic acid, which competitively inhibits the carnitine–acyl coenzyme (CoA) transferase system. This prevents importation of long-chain fatty acids into the mitochondria, preventing their β-oxidation to precursors of gluconeogenesis.
The reduction in fatty acid metabolism causes an increased use of glucose, and the blockade of the substrate for hepatic gluconeogenesis causes hypo- glycemia after the depletion of NADH and hepatic glycogen stores.
Increased concentrations of glutaric acid may inhibit glutamic acid decarboxylase, which produces GABA from glutamic acid. This not only depletes GABA but also increases concentrations of excitatory glutamate to produce seizures.
Triphasic clinical course, with initial vomiting and weakness followed by an apparent improvement and recovery phase. Finally vomiting returns with seizures, coma and death.
Initital symptoms appear by 4 hours after ingestion.
Mortality was 80% prior to utilization of glucose infusions in 1954.
Testing of the fruit for HGA concentrations is done by liquid chromatography, with a level of 100 mcg/g being the cut off for a level of concern.
Laboratory findings in intoxicated patients are notable for profound hepatic aminotransferase and bilirubin abnormalities, and aciduria and acidemia without ketonemia.
Carboxylic and other organic acid substrates build up in the urine and serum as a result of the metabolic disturbances. Detection of these acids (propionic, isobutyric, n-butyric, isovaleric, n-hexanoic, glutaric, adipic, suberic, sebacic) can help corroborate the diagnosis.
1973 FDA banned ackee fruit from entering the United States, but in 1990 the FDA established a program where producers could send information on their fruit to receive an exception from the ban.
Treatment is supportive, with glucose and fluid replacement essential.
Benzodiazepines can be given for seizures.
There is minimal data on the use of L-Carnitine.
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