Commentary on a review on the mechanism of Ackee-induced vomiting sickness

A recent review article concluded that glutamic acid probable plays a central role in the vomiting and neurological features of ackee poisoning. The present article draws attention to misconceptions in the basis of that hypothesis, and reviews important evidence suppporting a different role (AU)

Effects of ackee fruit extracts on bronchomotor tone in rats

The unripe ackee fruit, when eaten, is known to cause serious clinical manifestations, including vomiting, hypoglycaemia and acidosis. The effects, of various extracts from the arilli of the unripe fruit (including hypoglyin-A) on the lungs from rats were examined in an in vitro preparation. All the extracts were found to induce moderately severe broncho-constriction, indicating a possible contribution of these effects to the observed toxicity of ackee (AU)

A re-examination of the mechanism of ackee-induced vomiting sickness

The hypoglycemia seen in ackee poisoning almost certainly results from the presence of hypoglycin A in the aril. However, the mechanism underlying the vomiting and neurologic disorders have not been properly established. We have, in this review, re-established the latter and proposed that the vomiting and neurological features of ackee poisoning probably result from the excitotoxic properties of glutamic and aspartic acids derived directly and indirectly from ackee intake (AU)

Fatty acids generate dicarboxylic acids in hypoglycin poisoning - abstract

We investigated the metabolic origin of certain dicarboxylic acids which appears in urine of hypoglycin poisoned subjects (Jamaican vomiting sickness). These include hexanedioic (adipic), octanedioic (suberic) and decanedioic (sebacic) acids which, with unsaturated variants, are also excreted in some rare congenital diseases (glutaric acidaemia Type II, generalized dicarboxlic acidaemias), and in ketosis. Long-chain fatty acids have been established as precursors only in the case of diabetic, ketotic rats. In one report, evidence for this origin was negative for the case of hypoglycin poisoning, but no alternative precursors appear likely and the problem has remained unresolved since 1972. The present work utilized palmitic acid labelled either with Tritium, or with 14c at various atoms of the molecule as a tracer in hypoglycin-treated rats. Suberate and sebacate, isolated from urines by gas liquid chromatography, were found to be radioactively labelled, and hence, significant conversion of fatty acid to dicarboxylic acid was demonstrated. A further conclusion emerged from the relative labelling yielded by [1-14C] - and [16-14C] palmitic acid. After chain shortening by 3 -4 cycles of fatty acid á-oxidation, w-oxidation appears to intervene as a consequence of inhibition of the former process by the hypoglycin metabolite methylenecyclopropylacetyl-CoA. This sequence is in contrast to the ketotic animal, in which initial w-oxidation of fatty acid apparently precedes bilateral á-oxidation. In fasted hypoglycin-poisoned rats, excretion of each of these compounds is not insignificant, being about 7 - 33 mg/24 hr(1 - 4 mg/mg creatinine) (AU)

Biosynthesis of L-á-(methylenecyclopropyl)-alanine (hypoglycin) in Blighia sapida

Threonine and C(1) units from methionine contribute to form an intermediate in the biosynthesis of L-á-(methylenecyclopropyl)-alanine, the toxic amino acid hypoglycin in Blighia sapida. Thereafter, the pathway followed duplicates that for leucine biosynthesis, utilizing identical or analogous enzymes

Reye's syndrome - a case report

A single case fulfilling the clinical and pathological criteria of Reye's syndrome is reported. The possible aetiology of the syndrome, the diferential diagnosis with special reference to toxic hypoglycaemia induced by ackee and renta yams, and the treatment of the disease are discussed. This report represents to our knowledge the first case of Reye's syndrome thus documented in Jamaica (AU)

Some non-infective diseases endemic in the West Indies

The West Indies, and associated parts of the Caribbean area, are extremely diverse and afford interesting examples for the study of geographical medicine. Short accounts are given of some conditions whose aetiologies have been relatively recently clarified, including vomiting sickness of Jamaica, veno-occlusive disease of Jamaica, blackfat pulmonary fibrosis of Guyana, and epidemic acute glomerulonephritis of Trinidad. The aetiology of tropical sprue, which is common in Puerto Rico and absent from Jamaica remains to be explained although a hypothesis has been put forward. Further work is needed to establish the geographical distribution of idiopathic cardiomegaly and the spinal neuropathies and associated syndromes of retrebublar neuritis and sensorineural deafness before their aetiologies can be understood (AU)

The determination of hypoglycin-A in blood and plasma

Hypoglycin-A, the causative agent of vomiting sickness, was added to samples of human blood plasma and whole haemolysed blood and the quantitative recovery of the compound by means of comparison of the amino acid profiles before and after bromination of the samples was investigated. The method was found to be suitable for the estimation of the compound in blood or plasma down to a level of about 1 æmole/100ml. Analyses of blood samples from cases of suspected ackee poisoning, using the method reported, proved negative. The implications of this are discussed (AU)

Jamaican vomiting sickness: biochemical investigation of two cases

We identified methylenecyclopropylacetic acid, a known metabolite of hypoglycin A, in the urine of two patients with Jamaican vomiting sickness. Excretion of unusual dicarboxylic acids such as 2-ethylmalonic, 2-methylsuccinic, glutaric, adipic and dicarboxylic acids with eight and 10 carbon chains were also detected in both patients. The amounts of these dicarboxylic acids were 70 to 1000 times higher than normal. These metabolities have also been identified in urine of hypoglycin-treated rats. This evidence links hypoglycin A to Jamaican vomiting sickness as its causative agent. Urinary excretion of short-chain fatty acids was also increased up to 300 times higher than normal. These results indicate that, despite their clinical and histological similarities, the cause and biochemical mechanisms of Jamaican vomiting sickness differ distinctly from those of Reye's syndrome in which these abnormal urinary metabolities are not appreciably increased.(AU)

Jamaican vomiting sickness: a theoretical investigation

Jamaican vomiting sickness has been investigated for over sixty years, and yet this acute disease remains an epidemiological mystery. In this article, we have critically examined the toxin hypotheses emphasized in the literature - particularly the ackee and yam theories of causation. Because of the inadequacies of the conventional toxin hypotheses, we suggest that more attention should be given to a malnutrition hypothesis and a psychogenic hypothesis. Jamaican vomiting sickness (JVS), a reportedly culture bound syndrome, may very well have multiple causation. That is, toxin, malnutrition, and psychogenic etiologies may be operative independently and sometimes jointly in the epidemics and family outbreaks of acute and often fatal Jamaican vomiting sickness. (AU)