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Ackee Fruit Toxicity (also known as Jamaican vomiting sickness) is an syndrome caused by ingestion of unripened Ackee which contains the high levels of the toxin hypoglycin A. Effects of the toxin cause a rapidly progressive encephalopathy similar to Reye syndrome. Symptoms include vomiting, personality changes, confusion, seizures, loss of consciousness and possibly death.

Pathophysiology
When ingested, hypoglycin A is metabolized to produce methylenecyclopropylacetic acid (MCPA). MCPA acts to inhibit the beta-oxidation of fatty acids in two ways. First, it interferes with the transport of long-chain fatty acids into the mitochondria. Also, it inhibits acyl-CoA dehydrogenases, so that only unsaturated fatty acids can be fully oxidized. Fatty acids accumulate in the liver in a microvesicular pattern that can be seen on biopsy. In the absence of fatty acid metabolism, the body becomes dependent on glucose and glycogen for energy. Octreotide can be used to reduce secretion of insulin by the pancreas, preventing severe hypoglycemia.

Inhibition of beta-oxidation of fatty acids, however, also depletes a necessary cofactor for gluconeogenesis. Once the liver glycogen stores are depleted, the body cannot synthesize glucose, and severe hypoglycemia results.

A similar outbreak of lethal hypoglycemic encephalopathy has been linked to consumption of lychee fruit in Muzaffarpur, India. Urinalysis of children affected by the disease has shown all affected have elevated levels of hypoglycin suggesting the same underlying pathophysiology as Jamaican vomiting sickness.

Disease course
Abdominal discomfort begins two to six hours after eating unripe ackee fruit, followed by sudden onset vomiting. In severe cases, profound dehydration, seizures, coma, and death may ensue. Children and those who are malnourished are more susceptible to the disease.

In popular culture
The disease appears in an ER episode, "Great Expectations", where the symptoms are not recognized by Dr. Carter.