GSC Biological and Pharmaceutical Sciences, 2020, 13(01), 067-077
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Intoxication of the immature fruit of the ackee (Blighia sapida Koenig): Summary
and development
Armand Kouassi Kakpo 1, *, Jacques Ahouassa 1, Majella Chrysante Djohossou 1, Stanislas Djossou 1, Carolle
Abiola Adjalla 1, Claudia Aurelie Fagla 1, Armel Thomas Elegbede 1 and Moutawakilou Gomina 2
1 Pediatric service of the L’Abbraccio hospital of Sokponta, Glazoué, Republic of Benin.
2 Unit for Training and Research in Biochemistry, Faculty of Medicine, University of Parakou, Parakou, Republic of Benin.
Publication history: Received on 27 September 2020; revised on 09 October 2020; accepted on 13 October 2020
Article DOI: [Link]
Abstract
Deaths linked to the consumption of plants are sometimes overlooked by health personnel in tropical environments.
Parts of several plants are recognized as potentially toxic, including the fruit of the ackee.
This review paper aimed to synthesize data on the toxicity of the fruit of the ackee (Blighia sapida) and a brief overview
on the measures of management of its acute intoxication.
This was a documentary and analytical study. We made an analysis/synthesis of the articles relating to the poisoning
with the immature fruit of the ackee. The PubMed, AJOL and Google scholar databases were used.
The ackee is a plant native to West-Africa. Known by several names, lissètin in Fon in Benin, atsia in Evé in Togo, Finzan
in Bambara in Mali, its aril contains lipids, proteins, carbohydrates, vitamins and trace elements. Hypoglycin is present
in two forms A (2-methylene-cyclopropane-alanine) and B found in immature fruit, a very toxic compound which
disrupts β-oxidation of fatty acids. Acute immature fruit poisoning, manifests as an acute hypoglycemic encephalopathy,
gastrointestinal signs, hydro-electrolyte disturbances, metabolic acidosis and liver damage. The detection of urinary
dicarboxylic acids is pathognomonic. Its treatment is symptomatic. A crude gastrointestinal and hepatic
symptomatology characterizes chronic intoxication.
The ackee is a tree whose unripe fruit is of acute lethal toxicity. Treatment of acute intoxication is symptomatic.
Keywords: Ackee; Hypoglycin; Hypoglycemia; Urinary dicarboxylic acid; Poisoning.
1. Introduction
In the health context that is ours today, where any infant death must be a source of questioning, it becomes indisputable
to wonder especially about the causes of those who are preventable. In addition to the causes which are classically
incriminated (malaria, infections, etc.), there are many others, such as poisoning, especially in our rural areas, which
kill children, outside of the radar of official statistics. In the Republic of Benin and as in the West African sub-region,
several plants and fruits constitute an essential food resource [1, 2]. Given their physicochemical properties, some
constitute edible poisons that cause sometimes collective infant deaths [3, 4].
Corresponding author: Armand Kouassi Kakpo
Pediatric service of the L’Abbraccio hospital of Sokponta,Glazoué, Republic of Benin.
Copyright © 2020 Author(s) retain the copyright of this article. This article is published under the terms of the Creative Commons Attribution Liscense 4.0.
GSC Biological and Pharmaceutical Sciences, 2020, 13(01), 067–077
The ackee (Blighia sapida), is a tree whose fruit is highly prized by people in certain regions of Benin and the world [1].
The history of this plant relates to cases of death linked to the consumption of its fruit [4]. The first poisoning in Africa
dates back to 1984 in Côte d'Ivoire, where mysteriously more than 70 deaths have been recorded [3, 5]. Investigations
were needed later to clear the pesticides that were initially implicated. This fruit is said to contain a substance called
hypoglycin, responsible for these deaths [6]. Several other cases of morbidity due to the consumption of the aril of
Blighia sapida have been recorded worldwide [7]. Cases continue in our countries and deserve a closer look.
This synthesis aimed to take stock of the toxicity of the unripe fruit of the apple tree and the measures for managing its
acute intoxication.
2. Botanical aspects of Blighia sapida
The ackee (Blighia sapida) is a medium-sized tree in the Sapindaceae family native to West Africa. The plant is said to
have been introduced from Guinea to the Antilles, and to Jamaica in 1789, thanks to the slave trade [2, 5, 7, 8]. It is a
species close to the "lychee" (Litchi chinensis). The ackee belongs to the reign of the plantae, to the division of
magnoliaphyta and to the order of sapindales [2]. It is a beech tree, with prominent roots at the base of the trunk. Its
foliage is massive, with a dense crown of spreading branches and carried by a robust trunk (Figure 1) [2, 7, 9]. The
leaves are fifteen centimeters long. They are oval in shape, ending in a point; dark green in color and shiny at the upper
base. The flowers are small, greenish or white in color. They measure less than a centimeter and are arranged in axillary
clusters. The fruits, the size of a small pear, are pink to red in color, oval in shape, marked by three protruding ribs five
to six centimeters long, sometimes longer (Figure 2). They contain one to three kernels the size of a nutmeg, black in
color and shiny [9]. These stones are topped with a mass of ivory, white or cream-colored flesh, which has a nutty or
avocado flavor. The black seed has a detestable taste (Figure 3) [7]. Blighia sapida is cultivated in tropical regions for its
fruit which is widely consumed [10]. It is found in the countries of West Africa [2, 9, 11]. The different parts of the tree
are used for several purposes: consumption, manufacture of soaps, pharmacopoeia [1, 12, 13]. He is very well known
among the Malinkés, who call him finzan, from which comes the name which is sometimes given to him in French,
"fisanier". Several other names are used to designate it: finsan fig, sweetbread, fricassee tree. It has various vernacular
names (Table 1).
Figure 1 Blighia sapida shrub. (Photo Kakpo, 2017)
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Figure 2 Not fully ripe fruit of Blighia sapida (Photo Kakpo, 2017)
Figure 3 Fully ripe fruit of Blighia sapida [6]
Figure 4 Fully ripe fruit of Blighia sapida. (Photo Kakpo, 2020)
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Table 1 Vernacular names of the ackee [3, 7]
Language Vernacular name
Tagwana Kou, kohou, koum
Djimini Kokougo
Baoulé Kaa
Shien Pagwé
Attie Baza
Agni Founzan, Foufoué, Baza
Koulango Songo
Wobé Goihien
Bobo Finsan
Bambara Finzan
Haoussa Fisa, Gwanja Kousa
Ashanti Achin, akyen, akye
Twi Ankye, akye, fufuo
Fanti Twitakwada
Losso Peso
Ga Hatschi, Ayigbeatia
Basari Bugpom
Konkomba Bugpob
Malinké Finzan
Ebrié Atuanbi
Gouro Tia
Gagou Sen
Onitscha Okwocha
Yorouba Ishin, ishinjife, ishinoka
Bété Newgouei
Dioula Finzan
Mooré Finzan
Kabure Peso
Tschandjo Peso
Chumbulu Kake
Awuna Adza, atsia
Ewe Adza, atsia
Kuatchi Keka
Krobo Kngatscho
Ibo Okpu
Boki Otusi‐shet
Kukuruku Awai
Jekri Abikotor
Ijaw Ilipa
Owerri Okpuocha
Nupe Ila, ella
Sobo Ukperehren
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Fulani Feso
Adja Atjan
Ditamari, somba Nufugodom, Moufodom
Batombu Diremou
Natemba Foulama
Kabyé Kposso
Koto KoléKpezo
Moba Gbeng
Portuguese castanheiro da África
Fon Lissètin, Sissitin
English ackee, akee, akeeapple, achee, vegetable brain
3. Phytochemical composition of Blighia sapida aril
The main components of the aril of this fruit are lipids, which constitute more than 40%, an oil level comparable to that
of peanuts [7, 11, 13]. Proteins are also well represented with 20% while carbohydrates are low, representing less than
10% [14]. Aril is also rich in vitamin C and contains various other vitamins and minerals, mainly magnesium, sodium,
calcium and phosphorus [7, 8, 10, 15, 16]. However, the aril contains, when the fruit is not ripe, a toxic compound,
hypoglycin, which exists in two forms A (Figure 5) and B (Figure 6) [2, 8, 17]. It is an amino acid not included in the
composition of proteins, isolated (as well as its gamma-glutamyl derivative, hypoglycin B) for the first time in 1955 by
Hassal and Reyle [7]. Hypoglycin A is a water-soluble and thermostable compound, therefore not denatured by cooking.
Fruit cooking water is more toxic than the fruit itself [7]. It is formed from an alanine residue linked to a methylene-
cyclopropane group and whose systematic name is 2‐methylene-cyclopropane-alanine. Hypoglycin A is very high (1000
ppm) in the unripe fruit, and its concentration decreases with ripening, until it drops below 100 ppm in the ripe fruit.
Figure 5 Structure of hypoglycin A [17, 18]
Figure 6 Structure of hypoglycin B [17, 18]
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Table 2 presents the quantified composition of the fruit seed of Blighia sapida.
Table 2 Phyto-chemical composition of the aril of the Blighia sapida fruit [6, 12]
Quantity/100 g Composition of 1 kg of dried aril
Humidity (water) 57,60 g 6,84±1,13%
Lipids 18,78 g 45,32±2,90%
Carbohydrates 9,55 g 24,43±2,24%
Protein 8,75 g 11,99±1,12%
Fibers 3,45 g 3,21±0,34%
Phosphate 0,098 g -
Calcium 0,083 g 139,67±0,85 (mg/100 g)
Ascorbic acid 0,065 g -
Iron 0,00552 g 17,33±0,24 (mg/100 g)
Niacin 0,00374 g -
Riboflavin 0,00018 g -
Thiamine 0,00010 g -
Potassium - 1503,3±1,89 (mg/100 g)
Magnesium - 215,33±1,03 (mg/100 g)
Sodium - 53,17±1,03 (mg/100 g)
Zinc - ± 0 (mg/100 g)
4. Blighia sapida fruit poisoning
4.1. Pathophysiology
Hypoglycin A is found in seeds and arils, while hypoglycin B is only found in seeds. This difference explains the fact that
intoxications related to hypoglycin B are rare because the seed is not also consumed. Once ingested, hypoglycin A is
metabolized in the liver to methylene-cyclopropyl-Acetyl-Coenzyme A (MCPA-CoA) [5]. This compound disrupts the
catabolism of fatty acids in the mitochondria, preventing their oxidation (by inhibiting β-oxidation) and the resulting
energy production [10]. MCPA-CoA binds in particular irreversibly to coenzyme A, carnitine and carnitine
acyltransferases, reducing their bioavailability and consequently inhibiting β-oxidation of fatty acids [10]. The site
where hypoglycine toxicity manifests has been identified as acyl-CoA dehydrogenases which catalyze the first stage of
fatty acid oxidation [7]. The process of inhibiting acyl-CoA dehydrogenases by MCPA-CoA is initiated by a deprotonation,
followed by a break in bond, leading to the formation of a conjugated carbanion. This carbanion binds covalently to the
coenzyme Flavin Adenine Dinucleotide (FAD), which causes enzyme inactivation. The energy that the body needs can
then only be produced from carbohydrates [3, 12]. The hypoglycemic coma observed is therefore due to an abnormally
exaggerated catabolism of carbohydrates since lipids are almost no longer a source of energy [5].
In addition to the decrease in blood sugar, hypoglycin causes a digestive syndrome made of uncontrollable vomiting,
without diarrhea. It also causes convulsions, especially in young children. It is also a riboflavin or vitamin B2 antagonist.
Consumption of high level of ackee fruit arils can cause vitamin deficiency, [5]. Figure 7 shows schematic summary of
the different mechanisms that lead to this hypoglycemia.
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Figure 7 Metabolism and metabolic effects of the ackee fruit toxin, hypoglycin [19]
4.2. Signs
4.2.1. Acute poisoning
Still called emetising disease of Jamaica, acute hypoglycin A poisoning usually appears late in the meal. The affected
subjects are very often young children who cannot identify the ripe fruits of the unripe. The weight/amount of toxin
ratio also influences the severity of this disease in children. The clinical picture is that of an acute hypoglycemic often
fatal encephalopathy. Depending on the extent of intoxication, the time for onset of symptoms may be delayed by several
hours. Once started, the progression of symptoms is quite rapid and often of uncertain outcome. The clinical signs
observed are diverse and sometimes inconsistent. There is often a deceptive lull before the fatal development. This
period of calm must be known to the nursing staff so as not to lower their guard. Death occurs on average in 12 to 24
hours after the onset of signs [2, 3, 7]. The clinical signs observed are of three groups: general signs, gastrointestinal
signs and neurological signs.
General signs
They are represented by impairment of the general condition with weakness, hypotonia, pallor and often intense thirst.
Body temperature is normal or hypothermia can occur. Tachycardia and tachypnea are also observed in some cases [7].
Gastrointestinal signs
These signs boil down to persistent nausea and vomiting [20]. They are the first alarming symptoms of poisoning. They
can be followed by a period of very deceptive lull. Cramps, abdominal pain and diarrhea are often absent [3].
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Neurological signs
Neurological signs often start with headache. Above all, generalized convulsions are observed, sometimes preceded by
clonic spasms or localized contractions of the limbs, then coma occurs.
From a biological point of view, the manifestations are of several orders [7, 20, 21]:
• A biological sign characteristic of intoxication with ackee fruit, hypoglycemia generally occurs a few hours
after the onset of symptoms. Often very severe, it can reach values lower than 0.2 g/L;
• Metabolic acidosis following the accumulation of dicarboxylic acids;
• A hydro-electrolyte imbalance, a consequence of intense vomiting;
• The accumulation of lipids following the inhibition of β-oxidation in the liver cells will cause hepatotoxicity,
manifested by: an increase in total and conjugated bilirubin as well as alkaline phosphatases, a syndrome
of hepatic cytolysis (increased aminotransferases);
• Excessive elimination of dicarboxylic acids in the urine is a pathognomonic sign of poisoning in the ackee
fruit; in particular, ethylmalonic, glutaric and adipic acids. Their detection and dosage makes it possible to
establish the diagnosis of certainty;
• Some post-mortem liver biopsies revealed massive micro-vesicular steatosis, surrounded by macro-
vesicular steatosis affecting more than 90% of hepatocytes, without necrosis or associated inflammatory
lesions. Cases of fulminant hepatitis have been described as linked to the consumption of the ackee fruit
[22]
4.2.2. Chronic poisoning
Chronic poisoning by the ackee fruit is poorly documented. The literature mentions the possibility of cholestatic
jaundice, observed following the repeated consumption of the ackee fruit. It is clinically characterized by pruritus,
intermittent diarrhea, and localized abdominal pain in the hepatic region [23]. Liver tests show increased levels of total
and conjugated bilirubin, alkaline phosphatases, and aminotransferases [14]. At liver biopsy, central lobular necrosis is
observed [23]. A typical equine myopathy, a relatively rare disease touching horses consuming the seeds or seedlings
of some maples, is known to be caused by hypoglycin A [21].
4.3. Supported
It often comes down to symptomatic treatment, depending on the clinical and biological manifestations observed. This
care begins at the place of intoxication and must continue in a hospital environment.
4.3.1. First steps at the scene of intoxication
If the poisoning is recent and the patient is still conscious, he should be vomited immediately. This gesture can reduce
the digestive absorption of the toxic and therefore limit its effects. It should be given to bite into pieces of sugar or to
drink any glucose-containing substance to prevent hypoglycemia.
The transfer of unconscious patients must be done urgently and in a lateral safety position. The circumstances of
discovery (notion of ingestion of unripe ackee fruit or the presence of unripe ackee fruit in or near the family concession)
are very important for diagnosis and management.
4.3.2. In a hospital environment
Symptomatic treatment must be implemented upon admission to the hospital. It consists of taking charge of
hypoglycemia, convulsions, hydro-electrolyte imbalances and possible coma.
Hypoglycemia
The correction of hypoglycemia is the first emergency of this therapy. It is done by the infusion of glucose serum (SG):
1cc/kg of SG 30% or 3 to 5cc/kg of SG 10% [7, 21, 24-28]. Glucagon can be used from 0.5 to 1 mg intramuscularly or
subcutaneously. A relay to the 10% glucose serum in vein guard or an oral intake of slow sugar depending on the
patient's condition must be systematic. Other authors suggest the use of cortisone [3]. When the venous route is
impossible, a glucose solution must be provided by oral route or by a nasogastric tube. The response to treatment should
be checked after 30 minutes. Highly concentrated solutions should be avoided as much as possible as they can lead to a
state of hyper-osmolarity as well as reaction hypoglycemia in reaction to an increased secretion of insulin.
The glucose intake usually required to maintain acceptable blood sugar is 3 to 5 mg/kg/min [7, 24-28].
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Convulsions
Intravenous or intra-rectal administration of diazepam at a dose of 0.5 mg/kg allows the convulsions to subside,
possibly repeated after half an hour if the attacks do not subside. If convulsions persist, the use of phenobarbital and
then clonazepam (RIVOTRIL®) is indicated [7, 24-28].
Maintenance of vital functions
Clearance of the airways, ventilation, vascular filling, oxygenation and if necessary intubation to provide assisted
ventilation are measures to be taken. These gestures are very important and are done according to the child's weight
and age [24-28].
Gastric lavage
Gastric lavage is never the emergency for which priority should be given, since it is an evacuating treatment aimed at
reducing the digestive absorption of the toxic. In all cases, vital failures must be corrected before practicing gastric
lavage. The earliness and effectiveness of initial symptomatic treatment are more important than gastric lavage.
Gastric lavage requires certain conditions, in particular the good mastery of the technique by the nursing staff, the
commitment or not of the vital prognosis, the duration of the ingestion which must not exceed three hours and the
absence of ingestion of corrosive substances or derivatives of the associated oil. Make sure that a vacuum cleaner is
available in case the child vomits. From a practical point of view, put the child on the left side, head down; measure the
length of the probe to be inserted. The introduction of the probe is done by mouth. You just have to make sure it's in the
stomach. The actual washing is carried out with saline serum at the rate of 10 cc/kg which is sent by the probe and
which is removed immediately. The volume of liquid discharged should be approximately equal to that administered.
Washing is stopped as soon as the liquid without gastric residue is obtained [24].
Care-nursing
They boil down to the prevention of bedsores, phlebitis and the administration of eye drops.
Monitoring sheet
It must include the following points: general information concerning the patient, vital signs (indicated by the score
obtained on the coma scale or degree of consciousness, temperature, respiratory rate, pulse and weight), water balance,
presence of clinical signs, presence of signs of complication, results of examinations, treatments administered, new signs
or new complications.
5. Conclusion
The ackee is a tree whose unripe fruit is deadly toxic. Hypoglycin, a non-standard amino acid found abundantly in its
unripe fruit, is responsible for the main manifestations of acute intoxication, by blocking the fatty acid oxidation. The
dangerous nature of its immature fruit is not known. The management of acute intoxication is essentially focused on
the correction of hypoglycemia and the maintenance of vital functions.
Compliance with ethical standards
Acknowledgments
We say our sincere thanks to all the staff of the Sokponta L’Abbraccio hospital for their daily sacrifice and to
its promoters for the love they never stop showing to the populations in this an area of Benin.
Our sincere thanks to Dr Selim rashed, Associate clinical professor in pediatrics Montreal university, Assistant
Professor in Tropical Diseases, McGill University, for your contribution to this article and for all that you do in
medicine in Benin and Africa.
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Disclosure of conflict of interest
No conflict financial authors declared
References
[1] Ekue RM, Assogbadjo AE, Mensah GA, Codjia JT. Overview of the ecological distribution and the traditional
agroforestry system around the ackee (Blighia sapida) in the Sudanese environment in North Benin. Benin
Agronomic Research Bulletin. 2004; 44: 34-44.
[2] Aubry P. Poisoning by toxic plants in tropical and inter-tropical zones. Medicine tropical. 2012; 1-11.
[3] Moya lP. Cases of fatal poisoning by the aril of the fruit of Blighia sapida koenig (sapindaceae) in Côte d'Ivoire.
Ethnomedicine Bulletin. 1985; 33: 67-71.
[4] Camille SB, Donna AM. Structural characterization of hypoglycin B, a diastereomeric dipeptide from the ackee
fruit (Blighia sapida Koenig) by NMR experiments. Magnetic resonance chemistry. 2009; 47(11): 1004-6
[5] Moyal P. General information: natural products can be toxic, case of Cote d'Ivoire. Phytoma, defense of cultures.
1986; 383: 6.
[6] Atolani O, Olatunji GA, Fabiyi OA. Blighia sapida; the plant and its hypoglycinsan overview. Journal of Scientific
Research. 2009; 2 (39): 15-25.
[7] Valea I. Effect of methylene blue on acute poisoning by immature fruit of the strawberry tree (Blighia sapida,
sapindaceae): experimental study in mice. Thesis in pharmacology. 2002; 78.
[8] Ouattara H, Meite A, Kouame P, Kati-Coulibaly S. Impact of Blighia sapida aril powder level in diet on the growth
and the well-being of albino wistar rats. African Journal of Food Science. 2016; 10(9): 161-71.
[9] Orwa C, Mutua A, Kindt R, Jamnadass R, Anthony S. Agroforestree Database: a tree reference and selection guide
version 4.0.2009. Juillet 2018.
[10] Ouattara H, Meite A, Amonkan KA, Kouame KG, Kati-Coulibaly S. Aril of Blighia sapida (K. Koenig, 1778):
nutritional potential, toxic and deficient effects linked to its consumption, depending on the harvest stage and
the degree of consumption. Int J Biol Chem. Sci. 2011; 5 (1): 392-401.
[11] Aloko S, Azubuike CP, Coke AB. Physicochemical properties and lubricant potentials of Blighia sapida
Sapindaceaeae seed oil in solid dosage formulations. Tropical Journal of Pharmaceutical Research. 2017; 16 (2):
305-11.
[12] Ouattara H, Niamké B, Dally T, Kati-Coulibaly S. Nutritional composition studies of sun dried Blighia sapida (k.
koenig) aril from Côte d’Ivoire. Journal of Applied Biosciences. 2010; 32: 1989 – 94.
[13] Dossou MK, Codjia JT, Biaou G. Uses, functions and perceptions of the resource species Blighia sapida (ackee or
false mahogany) in north-western Benin. Benin Agronomic Research Bulletin. 2004; 45: 17-28.
[14] Azor AA, Abiodun AA, Kolade JJ, Afolabi T, Adesina AO. Haematolo-gical and hepatic indices of cockerels fed
treated dietary Blighia sapida seeds. Biokemistri. 2012; 24(2): 72-6.
[15] Dossou VM, Agbenorhevi JK, Combey S, Afi-Koryoe S. Ackee (Blighia sapida) Fruit Arils: Nutritional,
Phytochemicals and Antioxidant Properties. International Journal of Nutrition and Food Sciences. 2014; 3(6):
534-7.
[16] Dossou V, Agbenorhevi J, Alemawor F, Oduro I. Physicochemical and functional properties of full fatand defatted
Ackee (Blighia sapida) Aril Flours. American Journal of Food Science and Technology. 2014; 2 (6): 187-91.
[17] Gaillard Y, Carliera J, Mazoyer MC, Guittonc FJ, Fanton L. Fatal intoxication due to ackee (Blighia sapida) in
Suriname and French Guyana. GC–MS detection and quantification of hypoglycin-A. Forensic Science
International. 2011; 206: 103–7.
[18] Grande-Tovar CD, Delgado-Ospina J, Puerta LF, Rodríguez GC, Sacchetti G, Paparella A, Chaves-López C. Bioactive
micro-constituents of ackee arilli (Blighia sapida [Link]). An Acad Bras Cienc 91. 2019; 91(3): 1-15.
e20180140.
76
GSC Biological and Pharmaceutical Sciences, 2020, 13(01), 067–077
[19] Joskow R, Belson M, Vesper H, Backer L, Rubin C. Ackee Fruit Poisoning: An Outbreak Investigation in Haiti 2000–
2001, and Review of the Literature, Clinical Toxicology. 2006; 44(3): 267-73.
[20] Anderson-Foster NE, Adebayo AS, Justiz-Smith N. Physico-chemical properties of Blighia sapida (ackee) oil
extract and its potential application as emulsion base. African Journal of Pharmacy and Pharmacology. 2012;
6(3): 200-10.
[21] Gillman JH, Hegeman AD, Sharp RG. Clarifying the role of maples in atypical 289 myopathy. Equine Veterinary
76
Journal. 2014; 46: 135-6.
[22] Dianne E. G, Irini Scordi-Bello, Matthew S, Sander F, Jonathan Y, Maria Isabel F, Swan N. T. Fulminant hepatic
failure attributed to ackee Fruit Ingestion in a Patient with Sickle Cell Trait. Corporation Case Reports in
Transplantation. 2012; 1-4
[23] Larson J, Vender R, Camuto P. Cholestatic jaunice due to ackee fruit poisoning. American Journal of
Gastroenterology. 1994; 89(9): 1577-8.
[24] Bellaïche M. Pham A. Pédiatrie. 10e Ed. Paris: Editions Vernazobres-Grego. 2017.
[25] Bourrous M, Hindi M. Guide pratique des principales urgences pédiatriques. Thèse de doctorat en médecine.
Faculté de médecine et de pharmacie de l’Université Cadi Ayyad, Maroc. 2019.
[26] WHO. Pediatric hospital care: management of common ailments in small hospitals. WHO Publishing: 2007.
[27] Turgeon J, Hervouet-Zeiber C, Overtchkine P, Bernard Bonnin A. Gautthier M. Dictionary of Pediatrics, Weber. 3e
Ed. Canada: Edition Chenelière. 2015.
[28] Médecins sans frontières. Clinical and therapeutic guide. Edition. 2016; 363
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