Abstract

The unripe fruit of the ackee tree (Blighia Sapida), contains significantly high concentrations of the hypoglycin (L-α - amino-β -[methylene cyclopropyl] propionic acid) a toxin implicated in over 5000 deaths worldwide. Methylenecyclopropane acetyl CoA (MCPA-CoA) a metabolite of hypoglycin A, inhibits several coenzyme A dehydrogenases which are essential for gluconeogenesis resulting in depletion of glucose reserves and the inability of cells to regenerate glucose; eventually leading to hypoglycaemia. This study aimed at reviewing literature on the hypoglycin A toxicity, add to the body of tests already established by the WHO in detecting hypoglycin toxicity based on the patterns we have observed and to provide physicians with a simple panel of tests that will aid in the speedy detection of hypoglycin A toxicity for more timing therapeutic intervention. This review covers the description, pathophysiology, epidemiology, and clinical presentation. In addition, data on patients diagnosed with hypoglycin A toxicity was collected and analysed for significant trends. Analysis of data determined that 86%, 97% and 79% of patients demonstrated significant increase in phosphorous (95% CI of 1.74-2.73), anion gap (95% CI 24.26-29.05) and AST (95% CI 37.97-73.06) respectively. On the other hand, 95%, and 92% of patients demonstrated significant decrease in bicarbonate (95% CI of 13.02-16.56) and Lymphocytes count 95% CI of 7.49-12.81 respectively. Significantly low random plasma glucose levels, in conjunction with elevated levels of Phosphorus, Anion gap, and AST, as well as decreased levels of bicarbonate, and an absolute lymphocyte count could prove an effective screening for Hypoglcyin A toxicity in affected regions.

Highlights

  • Introduction and Review of LiteratureThe ackee fruit (Blighia sapida) has its origins in West Africa and is indigenous to the Caribbean

  • Results were recorded for each patient with major emphasis on U&Es (BUN, creatinine, and electrolytes), liver function tests (LFTs), and complete blood count (CBC)

  • An increased trend was observed for anion gap and the decreased levels of bicarbonate are consistent with the hyperemesis induced by the toxic process

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Summary

Introduction

The ackee fruit (Blighia sapida) has its origins in West Africa and is indigenous to the Caribbean. Consumption of the fruit is mainly in Haiti, some parts of West Africa, and Jamaica- where ackee is a component of the national dish. The fruit is composed of a pod, the seed, and the aril (the part which is consumed). In 1954, Hassal et al were the first to isolate 2 toxic compounds in their crystalline form. These compounds were called hypoglycin A and hypoglycin B because of their hypoglycaemic activity [1]. Of the two toxic compounds only hypoglycin A can be found in the aril of the fruit. Ill effects occur only when the immature fruit is consumed” according to Goldson [2]

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