West African lychee fruit toxicity

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Akaimu, also known as West African lychee fruit (Blighia sapida), is a fruit from the soapberry family, like lychee and longan. Native to tropical West Africa.

Although long considered poisonous and potentially deadly, fruit arils are renowned for their delicious taste when ripe, prepared and cooked properly, and are a feature of various Caribbean cuisines. The ackee is the national fruit of Jamaica and is considered a delicacy .

Fruit toxicity

Ingestion of unripe lychee fruit may cause a metabolic syndrome known as "Jamaican Vomiting Sickness."

Clinical manifestations may include profuse vomiting, altered mental status, and hypoglycemia. Severe cases have been reported to cause seizures, hypothermia, coma and death.

Medical treatment is mainly supportive care with intravenous fluids and glucose.

Etiology

The West African lychee fruit is divided into three parts when mature, each part consists of a large black seed and a fleshy yellow aril. The arils are the edible parts of the fruit and initially contain high concentrations of hypoglycine toxin. However, over time, as the fruit ripens, hypoglycine levels drop to a range that allows for safe human consumption.

Toxic effects occur only when ingesting unripe ackee fruits. Distinguishing between ripe and unripe ackee fruits is necessary to prevent any potential adverse health effects.

Ripe ackee fruits can be identified by their yellowish-red to red color and open appearance (the seeds are easily visible).

Immature fruits are green to yellow and closed in appearance (the seeds are difficult to see).

Cooking unripe fruit does not reduce its potential toxicity. The seeds are still poisonous and should not be ingested. Risk factors for ackee fruit poisoning include eating unripe ackee, purchasing tampered ackee, or reusing water previously used to cook unripe ackee.

Epidemiology

The Blighia sapida tree is native to West Africa. It was imported to Jamaica in 1778 and has remained the country's national fruit and an important part of the Jamaican diet. The epidemiology of the disease has not been established in Jamaica, but mortality and morbidity are considered under-reported. Cases of this disease are higher during the Jamaican winter, when the fruit is still unripe. Blighia sapida is also found in southern Florida, several Caribbean countries, and Central America. West African lychee fruits imported into the United States are regulated by the U.S. Food and Drug Administration (FDA) to restrict products containing dangerous amounts of hypoglycine A toxin. Only a few cases of poisoning have been reported in the United States. Pediatric patients and those who are malnourished are at greatest risk for toxicity.

pathophysiology

West African lychee fruit contains hypoglycine A and hypoglycine B. Hypoglycine A is the toxin responsible for the leading cause of vomiting sickness in Jamaica. The exact mechanism of hypoglycemia is unknown; however, hypoglycemia is likely due to inhibition of gluconeogenesis. Metabolism of hypoglycine also produces the toxic by-product methylenecyclopropylacetic acid (MCPA-CoA), which inhibits long-chain fatty acid beta-oxidation and leads to depletion of glycogen stores. Because the minimum toxic dose is not yet known, it is impossible to predict what symptoms a patient will experience after ingestion. Low glycine may be hepatotoxic with liver pathology resembling a Reyes syndrome-like pattern. Long-term ingestion of lychee fruit has been reported to cause cholestatic jaundice in adults.

Pharmacokinetics

The onset of hypoglycemia is delayed for several hours, but once it occurs it progresses rapidly. There is a chance of death within approximately 12 to 48 hours.

history and body

Gastrointestinal (GI) symptoms usually appear within 6 to 48 hours after ingesting unripe ackee fruits, but may appear sooner in severe cases. There may be a significant recovery period (approximately 10 hours) after the initial gastrointestinal symptoms. It is important to note that although vomiting is common, the absence of vomiting does not exclude the diagnosis. Diarrhea is usually absent, which may help differentiate Jamaican vomiting syndrome from other acute gastrointestinal infections. Seizures may be a predictor of disease severity, as they are reported in 85% of deaths. Other neurologic manifestations may include altered mental status, tremor, and paresthesia. To accurately identify recent ackee intake, a patient's recent dietary history may be required. Toxicity is dose-dependent; therefore, it is important to quantify intake. Recovery, if it occurs, will occur within a week of ingestion.

Evaluate

Patients with clinical suspicion of Jamaican vomiting sickness should be evaluated in hospital and admitted for observation. Intravenous fluids and glucose should be obtained if needed. Diagnostic evaluation should include blood glucose, serum electrolytes, liver function tests, renal function, lactate, ketones, and blood gases. Symptomatic patients require close monitoring of laboratory tests, especially glucose and serum electrolytes. An early electrocardiogram may show evidence of electrolyte abnormalities before laboratory diagnostic results are obtained. Hypoglycine and its metabolite MCPA can be detected in blood and urine; however, they may not be detected after rapid elimination. Other diagnostic tests that may help confirm the diagnosis include elevated serum/urinary carnitine concentrations and elevated urinary dicarboxylic acid concentrations.

Treatment/Management

Treatment is mainly supportive, as there is currently no antidote for hypoglycine A.

Patients need to be closely monitored for hypoglycemia and should receive glucose therapy.

A glucose bolus may be given initially, followed by an infusion, which may be titrated to maintain euglycemia.

Intravenous fluids should be provided to prevent dehydration and antiemetics should be used to relieve symptoms.

Vomiting and dehydration may cause electrolyte abnormalities, and electrolytes should be replenished.

Benzodiazepines may be used to treat epileptic seizures, but caution should be exercised in excluding hypoglycemia as a cause of seizures.

If a patient experiences potential toxicity within a few hours of ingestion, gastrointestinal decontamination, including activated charcoal and gastric lavage, may be considered. There is insufficient evidence that gastrointestinal decontamination consistently improves patient outcomes. Syrup of ipecac has no effect after acute ingestion.

Riboflavin and glycine have been used therapeutically because they are thought to antagonize hypoglycine A.

Methylene blue has also been proposed as a treatment option for potentially fatal encephalopathy.

The true effectiveness of these supplements is unknown. Medical toxicologists can assist with management and can be contacted through local poison control centers. Patients with persistent hypoglycemia, seizures, metabolic acidosis, altered mental status, or malperfusion are likely to require admission to the intensive care unit (ICU). Education about the health hazards of consuming unripe lychee fruit may reduce future incidence of the disease.