An 18-year-old woman presented to the emergency department (ED) with symptoms of nausea, vomiting, diarrhea, and abdominal pain. She reported that these symptoms started two days prior, shortly after consuming a fruit known as ackee. Since the onset of illness, she had been unable to tolerate any oral intake. Before arriving at our ED, the patient sought care at an urgent care clinic, where she was prescribed ondansetron without improvement.

Upon physical examination, the patient was noted to have dry mucous membranes. Abdominal exam was benign. Most pertinently, her point of care glucose was 24 mg/dL.

Brief History of Toxic Hypoglycemic Syndrome

Ackee, the national fruit of Jamaica, is a dietary staple; however, consuming unripe ackee can lead to Toxic Hypoglycemic Syndrome (THS), also known as Jamaican Vomiting Syndrome. THS is generally characterized by the acute onset of profuse vomiting within six to 48 hours of ingestion of the unripe ackee, with subsequent hypoglycemia.¹ In severe cases altered mental status, seizures, coma, or even death have been observed.² The persistent consumption of ackee has been shown to cause acute liver injury, however, abstaining from eating the fruit can lead to improvement in liver health.³ Additionally, it has been demonstrated that ackee toxicity is dose-dependent; individuals who consume multiple unripe fruits or ackee seeds tend to develop more severe symptoms. Similarly, death is more prevalent in children with Toxic Hypoglycemic Syndrome compared to adults.¹ An estimated 5000 fatalities were attributed to what was then called Jamaican Vomiting Syndrome between 1886 and 1950.⁴ The association between ackee ingestion and the illness was initially recognized in 1875 and officially documented in 1904.⁵ Despite being endemic to Jamaica, cases of THS have been reported across the world, with the first case in the United States documented in 1993.⁶

The aril (flesh), rind, and seeds of ackee contain heat-stable hypoglycin A and hypoglycin B. The fully ripened aril is the only edible portion of the fruit, as concentration of these toxins drastically decreases in the flesh of ripened ackee fruit. It’s crucial to note that the seeds and the rind of ackee should never be consumed, as they contain toxic levels of hypoglycin, even when the fruit is ripe. Studies indicate that THS is primarily caused by the toxin hypoglycin A. While the mechanism of hypoglycin A is not thoroughly understood, research demonstrates that its metabolism leads to the production of methylene cyclopropyl acetic acid (MCPA-CoA), which inhibits long-chain fatty acid beta-oxidation and ultimately causes depletion of glycogen stores.⁷