Acute Ackee Fruit Intoxication: Disease-Characteristics Report

Executive summary

Acute ackee fruit intoxication—classically Jamaican vomiting sickness—is an acquired, potentially fatal foodborne metabolic poisoning caused mainly by hypoglycin A (HGA) in immature Blighia sapida fruit. It produces an acquired multiple-acyl-CoA-dehydrogenase-deficiency phenotype: impaired mitochondrial fatty-acid oxidation deprives fasting patients of ketones and gluconeogenic energy, causing recurrent vomiting, profound hypoketotic hypoglycemia, encephalopathy, seizures, coma, hepatic steatosis/injury, and sometimes death. Children and undernourished or fasting persons are especially vulnerable. The evidence base is unusual: landmark human observations are old, modern human cohorts are scarce, and much current mechanistic, biomarker, and therapeutic evidence comes from rats, mice, and naturally poisoned horses. Accordingly, animal values below must not be used as human reference intervals.

Table: This table summarizes the strongest available evidence for acute ackee fruit intoxication across clinical, mechanistic, diagnostic, epidemiologic, preventive, and animal-model domains. It prioritizes direct human evidence and clearly labels extrapolations from horse, rat, mouse, and other comparative studies.

1. Disease information

Definition and synonyms

The disorder is an acute exogenous intoxication, not a Mendelian disease. Synonyms include ackee poisoning, ackee fruit poisoning, acute ackee intoxication, hypoglycin A poisoning, toxic hypoglycemic syndrome, and Jamaican vomiting sickness. The classic syndrome consists of gastrointestinal illness, severe hypoglycemia, and central nervous-system depression after consumption of unripe ackee; severe disease includes seizures, coma, and death. Mature arils from fruit that has opened naturally are ordinarily consumed safely. (latif2017newdevelopmentof pages 2-3, latif2017newdevelopmentof pages 1-2)

Identifiers and coding

• MONDO: no disease-specific MONDO identifier was substantiated in the retrieved sources; do not assign one without checking the current MONDO release.
• OMIM/Orphanet: not applicable as disease-specific inherited-disorder identifiers; no dedicated entry was substantiated.
• MeSH: best represented under broad concepts such as plant poisoning, foodborne intoxication, hypoglycemia, and hypoglycins; a dedicated descriptor was not substantiated.
• ICD: coding is generally under toxic effects of ingested berries/other noxious food substances or plant poisoning, with intent and encounter extensions where required. The precise ICD-10-CM/ICD-11 code should be validated against the jurisdiction and release rather than inferred from literature.

The report is assembled from aggregated disease-level literature, human case reports and autopsies, outbreak investigations, analytical-method studies, and animal experiments—not individual EHR data.

2. Etiology, risk, and protective factors

Cause

The initiating exposure is ingestion of toxic ackee material, especially an immature, forcibly opened, damaged, or improperly prepared fruit. HGA occurs in arils and seeds; hypoglycin B is a less potent γ-glutamyl conjugate concentrated in seeds. One clinical review reports approximately 100-fold more HGA in unripe than ripe fruit, although toxin concentration varies with maturity and processing. (latif2017newdevelopmentof pages 2-3, latif2017newdevelopmentof pages 1-2)

Suggested chemical annotations are hypoglycin A, hypoglycin B, methylenecyclopropylpyruvate, methylenecyclopropylacetate/MCPA, MCPA-CoA, MCPA-carnitine, and MCPA-glycine; exact ChEBI identifiers should be release-validated.

Risk factors

• Environmental/dietary: unripe or unopened ackee, seeds or attached membrane, contaminated cooking liquid, inadequate washing, and unregulated processing.
• Physiological: childhood, low body mass, overnight fasting, malnutrition, depleted glycogen, and delayed glucose treatment plausibly increase vulnerability. Historical disease was strongly seasonal and concentrated in children when other foods were scarce. (scott1916onthevomiting pages 56-58, scott1916onthevomiting pages 58-62)
• Clustering: multiple members of a household may become ill after sharing fruit. (scott1916onthevomiting pages 56-58)
• Sex: historical work found no clear sex preference. (scott1916onthevomiting pages 56-58)

Historical ethnic differences are more parsimoniously explained by dietary access and exposure than inherited susceptibility. No reproducible human susceptibility locus or pharmacogenomic association has been established.

Protective factors

Primary protection consists of eating only fruit that has opened naturally, discarding seeds and the attached pink/red membrane, washing arils thoroughly, using validated processing controls, and avoiding prolonged fasting—particularly in children. Regulated products and hazard-analysis systems reduce exposure; a clinical review cites an FDA import/HACCP ceiling of 100 ppm HGA. (latif2017newdevelopmentof pages 1-2)

No genetic protective variant is known. Gene–environment interaction remains hypothetical: variants affecting fatty-acid oxidation or toxin disposition could modify severity, but this has not been demonstrated in human ackee poisoning.

3. Phenotypes

Percentages are unavailable from modern, adequately sized cohorts; frequencies therefore remain qualitative.

Symptoms generally begin within 6–48 hours, although historical fulminant cases began near two hours after exposure. Severe cases may die within 48 hours; survivors commonly improve over days and may recover within approximately one week. (latif2017newdevelopmentof pages 2-3, scott1916onthevomiting pages 56-58, scott1916onthevomiting pages 58-62)

Quality-of-life instruments such as EQ-5D or SF-36 have not been studied. Acute impact is nevertheless major: inability to eat or function, emergency hospitalization, seizures, ventilation/critical care, and risk of neurologic injury or death.

4. Genetic and molecular information

There is no established causal gene, pathogenic germline or somatic variant, inheritance pattern, chromosomal lesion, penetrance estimate, modifier gene, or disease-specific epigenetic abnormality. WES, WGS, panels, CMA, karyotyping, FISH, mitochondrial sequencing, and repeat-expansion testing are not routine diagnostic tests.

Mechanistically relevant human proteins include mitochondrial acyl-CoA dehydrogenases—especially ACADM/MCAD and IVD—and electron-transfer flavoprotein pathways. These are inhibited by toxin metabolites rather than altered genetically. Thus, intoxication phenocopies inherited MADD/glutaric acidemia type II but must not be represented as an ETF-pathway genetic disorder. Comparative work supports inhibition of multiple acyl-CoA dehydrogenases and consequent abnormal acylcarnitines and organic acids. (bochnia2015hypoglycinacontent pages 1-2, boemer2017acylcarnitinesprofilebest pages 15-16, boemer2017acylcarnitinesprofilebest pages 16-16)

5. Environmental information

The disease is entirely exposure driven. Blighia sapida is the relevant plant; unripe fruit is the principal source. Diet, food scarcity, harvesting before natural opening, and unsafe preparation govern risk. There is no infectious agent, person-to-person transmission, radiation association, or conventional occupational syndrome, although harvesters, processors, and food inspectors have exposure-control responsibilities.

6. Mechanism and pathophysiology

Ordered causal chain

1. Ingestion of immature/improperly prepared ackee leads to absorption of HGA and related methylenecyclopropyl compounds.
2. HGA metabolism leads to methylenecyclopropyl intermediates and MCPA-CoA, the active inhibitory metabolite.
3. MCPA-CoA leads to irreversible or functionally sustained inhibition of several mitochondrial acyl-CoA dehydrogenases, including MCAD and IVD, producing acquired MADD. (bochnia2015hypoglycinacontent pages 1-2, boemer2017acylcarnitinesprofilebest pages 15-16, boemer2017acylcarnitinesprofilebest pages 16-16)
4. Blocked β-oxidation leads to reduced acetyl-CoA, reducing equivalents, ATP, and ketogenesis, while accumulating acyl-CoAs.
5. Energy/cofactor depletion leads to impaired hepatic gluconeogenesis and depleted glucose availability, producing hypoketotic hypoglycemia. (latif2017newdevelopmentof pages 2-3, latif2017newdevelopmentof pages 3-4)
6. Accumulated acyl-CoAs branch into acylcarnitines/acylglycines and ω-oxidation, resulting in characteristic acylcarnitinemia, dicarboxylic aciduria, and metabolic acidosis. Rat studies identify glutaric, adipic, unsaturated dicarboxylic acids, MCPA-glycine, and isovalerylglycine; their diagnostic interpretation in humans is partly extrapolative. (boemer2017acylcarnitinesprofilebest pages 15-16)
7. Hepatic lipid oxidation failure leads to triglyceride accumulation and hepatocellular energy failure, resulting in micro-/macrovesicular fatty change and potentially acute liver injury.
8. Neuroglycopenia leads to vomiting-associated lethargy, seizures, encephalopathy, and coma; a separate direct neurotoxic contribution is reported but less firmly resolved in humans. (latif2017newdevelopmentof pages 2-3, latif2017newdevelopmentof pages 3-4)
9. Severe systemic energy failure branches to renal, pancreatic, cardiac, and pulmonary injury, resulting in multiorgan failure and death in fulminant cases. (scott1916onthevomiting pages 56-58)

Upstream processes are exposure, toxin bioactivation, and enzyme inhibition; downstream processes are metabolic energy failure, alternative metabolite formation, steatosis, neuroglycopenia, and organ injury.

Suggested GO annotations include fatty-acid beta-oxidation (GO:0006635), mitochondrial fatty-acid beta-oxidation (GO:0006635 with mitochondrial context), gluconeogenesis (GO:0006094), ketone-body biosynthetic process (GO:0046951), cellular response to hypoglycemia, and lipid-storage process. Principal cells are hepatocytes (CL:0000182), neurons (CL:0000540), renal tubular epithelial cells, pancreatic acinar cells, and cardiomyocytes (CL:0000746). Principal compartment: mitochondrion (GO:0005739), especially mitochondrial matrix (GO:0005759).

No ackee-specific human transcriptomic, proteomic, lipidomic, single-cell, spatial-transcriptomic, CRISPR-screen, or multi-omics dataset was substantiated. Targeted metabolomics is currently the relevant molecular-profiling modality.

7. Anatomical structures affected

The liver is the principal metabolic organ; the brain is the principal clinically vulnerable organ. Historical fatal pathology demonstrated diffuse fatty liver, renal tubular fatty degeneration/nephritis, pancreatic necrobiosis, myocardial fat droplets, and pulmonary/visceral congestion. (scott1916onthevomiting pages 56-58)

Suggested anatomy annotations include liver (UBERON:0002107), brain (UBERON:0000955), kidney (UBERON:0002113), pancreas (UBERON:0001264), heart (UBERON:0000948), and lung (UBERON:0002048). At cell level, hepatocytes and renal tubular epithelial cells are central. At subcellular level, mitochondria are primary; cytosolic lipid droplets are secondary. Lateralization is not relevant.

8. Temporal development

The disease is acute and monophasic after a discrete meal. A useful clinical staging scheme is:

1. Latent/early phase: hours after ingestion; nausea, malaise, vomiting.
2. Metabolic phase: recurrent vomiting, hypoglycemia, low ketones, aciduria/acidosis.
3. Neurologic/organ-injury phase: altered consciousness, seizures, rising aminotransferases/creatinine.
4. Recovery or fulminant phase: improvement over several days after glucose/support, or coma, multiorgan failure, and death—often within 48 hours in severe cases. (latif2017newdevelopmentof pages 2-3, latif2017newdevelopmentof pages 3-4)

There is no chronic relapsing course unless exposure recurs. The crucial therapeutic window is before prolonged neuroglycopenia and hepatic energy failure; glucose should not await confirmatory toxicology.

9. Inheritance and population epidemiology

Inheritance, anticipation, mosaicism, founder effects, consanguinity, carrier frequency, and penetrance are not applicable.

Reliable contemporary incidence and prevalence per 100,000 are unavailable. Historical Jamaican reports described seasonality, household clusters, disproportionate pediatric disease, and mortality estimates as high as 80–90%, but these figures predate modern critical care and should not be treated as current case-fatality rates. (scott1916onthevomiting pages 58-62)

A secondary retrieved source reports 60 intoxications in Haiti during 2000–2001; the primary outbreak report should be consulted before database ingestion. Disease is concentrated where ackee grows or is imported, particularly Jamaica, Haiti, and parts of West Africa. Historical racial/ethnic patterns likely reflected food practices and poverty rather than proven biology. No current sex ratio is established.

10. Diagnostics

Clinical diagnosis

Diagnosis is based on compatible exposure plus acute vomiting and hypoketotic hypoglycemia, with neurologic or hepatic abnormalities. Immediate tests should include serial bedside glucose, blood gas, electrolytes, bicarbonate/anion gap, lactate, serum/urine ketones, AST/ALT, bilirubin, INR, creatinine, urea, ammonia, CK, urinalysis, ECG, and continuous neurologic monitoring where severe.

Specific and omics-based tests

Confirmation can use LC-MS/MS or GC-MS measurement of HGA, MCPA-glycine, MCPA-carnitine, related acylcarnitines, acylglycines, and urinary organic acids. The clinical report describes urinary MCPAA detection by GC-MS and HGA/metabolite measurement in blood and urine. (latif2017newdevelopmentof pages 2-3)

Horse data demonstrate the principle but not human cutoffs: affected horses had serum HGA 387.8–8,493.8 μg/L and urine HGA 143.8–926.4 μg/L, versus controls below 10 μg/L; serum MCPA-carnitine was 0.17–0.65 mmol/L, versus below 0.01 in controls. (bochnia2015hypoglycinacontent pages 1-2)

A 2023 derivatization-free UPLC-MS/MS method achieved an HGA quantification limit of 1.12 μg/L in milk, 85–106% recovery across milk/urine, and ≤20% precision; none of 68 samples from 35 German dairy farms contained quantifiable analytes. This is an exposure-surveillance advance, not a validated human diagnostic threshold. The authors’ abstract states: “The determination of HGA, MCPrG, and their glycine and carnitine metabolites in blood and urine is a useful tool for screening for potential exposure to these toxins.” DOI: https://doi.org/10.1007/s00216-023-04607-9, published March 2023.

Differential diagnosis

Important alternatives are inherited fatty-acid-oxidation disorders/MADD, Reye syndrome, sepsis, malaria or meningoencephalitis in endemic settings, insulin/sulfonylurea exposure, starvation, alcohol-related hypoglycemia, adrenal insufficiency, inborn organic acidemias, acetaminophen or other hepatotoxic poisoning, and litchi-associated MCPG/HGA encephalopathy. Historical cases were mistaken for meningitis or yellow fever. (scott1916onthevomiting pages 58-62)

Imaging, EEG, biopsy, and genetic testing are not routine; use them for complications or unresolved alternatives. There is no asymptomatic population screening program.

11. Outcome and prognosis

Outcome depends on dose, maturity of fruit, age/body mass, nutritional state, depth/duration of hypoglycemia, hepatic injury, and speed of glucose administration. Nonfatal cases can recover rapidly or within approximately one week; prolonged seizures, coma, acute liver failure, renal injury, aspiration, and death are principal complications. (latif2017newdevelopmentof pages 2-3, latif2017newdevelopmentof pages 3-4)

Historical 80–90% mortality estimates represent selected early severe outbreaks and are not generalizable to current treated patients. No validated human prognostic score, long-term survival curve, disability estimate, or quality-of-life dataset exists. Serial glucose, neurologic status, pH/lactate, INR, aminotransferases, creatinine, and ammonia are practical severity markers, but none is a validated ackee-specific prognostic biomarker.

12. Treatment

Immediate clinical algorithm

1. Stabilize airway, breathing, and circulation; check glucose immediately.
2. Administer IV dextrose promptly for symptomatic or documented hypoglycemia, then continue glucose-containing fluids/titrated infusion with frequent checks; recurrent hypoglycemia is expected.
3. Correct dehydration, electrolytes, acid–base disturbance, and temperature; stop fasting and provide carbohydrate when safe.
4. Treat seizures conventionally while correcting glucose; protect the airway if consciousness is impaired.
5. Monitor liver enzymes, bilirubin, INR, ammonia, creatinine, urine output, CK, ECG, and neurologic status; transfer severe cases to intensive care or a liver-capable center.
6. Contact a poison center/medical toxicologist and retain food, blood, and urine for targeted testing.

Human evidence supports early dextrose and supportive care; one review characterizes IV dextrose as extremely effective when administered early. (latif2017newdevelopmentof pages 3-4)

Suggested NCIt intervention concepts are dextrose administration, intravenous fluid therapy, electrolyte replacement, anticonvulsant therapy, mechanical ventilation, intensive-care management, and liver transplantation when fulminant failure meets standard criteria.

Unproven therapies

Glycine, methylene blue, and carnitine have experimental rationales. Mouse studies support early glucose and methylene blue; rat-hepatocyte experiments did not establish carnitine as an antidote. No controlled human efficacy data support these agents, and they should not replace dextrose/supportive care. (latif2017newdevelopmentof pages 3-4)

No ackee-specific gene, cell, RNA, immunologic, targeted, or surgical therapy exists. A ClinicalTrials.gov search retrieved no relevant ackee/HGA interventional trial. Pharmacogenomic guidance and response-rate estimates are unavailable.

13. Prevention

• Primary: consume only naturally opened, fully mature fruit; never force open immature pods; discard seeds and membrane; wash arils; use approved processors and validated HACCP controls. (latif2017newdevelopmentof pages 1-2)
• Secondary: recognize household clusters rapidly, test glucose in every exposed symptomatic person, and treat before encephalopathy. Assess children who shared the meal even if symptoms are initially mild.
• Tertiary: prevent recurrent hypoglycemia, aspiration, seizures, cerebral injury, liver failure, and renal failure through monitoring and critical care.
• Public health: trace and withdraw implicated lots, communicate safe harvesting/preparation practices, train clinicians in endemic regions, and maintain analytical capacity for HGA/MCPA compounds.

Vaccination, antimicrobial prophylaxis, genetic counseling, prenatal testing, carrier screening, and newborn screening are not applicable.

14. Other species and natural disease

HGA-containing Acer seeds/seedlings cause equine atypical myopathy, a naturally occurring, often fatal acquired MADD in horses. This is a mechanistically strong analogue but differs clinically: horses predominantly develop severe rhabdomyolysis, whereas human ackee intoxication is dominated by vomiting, hypoglycemia, encephalopathy, and liver injury. Horse exposure studies show that clinically normal co-grazers can contain HGA, demonstrating that exposure does not equal disease. (bochnia2015hypoglycinacontent pages 1-2)

A 2023 dairy study addressed possible carry-over into milk; its 68 field samples from 35 farms were negative at the assay’s quantification limits. This does not exclude exposure under different conditions. No zoonotic transmission occurs; susceptibility reflects shared plant toxins, not infection.

Suggested taxonomy annotations include Homo sapiens (NCBI Taxon 9606), Equus caballus (9796), Mus musculus (10090), Rattus norvegicus (10116), and Danio rerio (7955). Breed-specific susceptibility is not established.

15. Model organisms and recent research

Established models

• Rat: HGA dose-response and hepatocyte systems reproduce hypoglycemia, abnormal fatty-acid oxidation, dicarboxylic aciduria, and enzyme inhibition. They are valuable for mechanism and antidote testing but incompletely model human vomiting/encephalopathy.
• Mouse: unripe-ackee exposure models have tested early glucose and methylene blue; timing and dosing limit translation.
• Horse natural model: provides abundant blood/urine metabolomics and tissue pathology for acquired MADD. It strongly supports HGA causality and MCPA-conjugate biomarkers, but its muscle-dominant phenotype differs from human disease. In one study, HGA and MCPA conjugates clearly separated diseased horses, exposed healthy co-grazers, and unexposed controls. (bochnia2015hypoglycinacontent pages 1-2)
• Zebrafish embryo: a 2024 study developed a Sapindaceae-poisoning platform to screen therapeutic compounds (Wouters et al., Molecules, October 2024; DOI: https://doi.org/10.3390/molecules29204954). This is a preclinical screening system, not evidence of human efficacy.
• Historical guinea-pig/rabbit experiments: results were inconclusive because of limited extracts, solvent effects, and species selection. (scott1916onthevomiting pages 40-43)

No standardized knockout, knock-in, humanized mouse, organoid, or patient-derived iPSC model specific to ackee intoxication was identified. Genetic ETF/ETFDH/ACADM models may illuminate downstream energy failure but model inherited enzyme defects rather than toxin bioactivation.

Evidence interpretation and research gaps

The most authoritative conclusion is that acute ackee intoxication is a preventable exposure-induced mitochondrial energy crisis requiring immediate glucose and supportive care. The major gaps are contemporary prospective human cohorts, validated human toxin/metabolite reference ranges, dose–response data, standardized diagnostic criteria, controlled antidote trials, long-term neurodevelopmental follow-up, and modern incidence/case-fatality surveillance. Recent work has advanced sensitive mass-spectrometric exposure measurement and preclinical screening rather than changing clinical management.

Representative exact abstract quotation from the 2018 analytical/model literature is: “Hypoglycin A (HGA) toxicity, following ingestion of material from certain plants, is linked to an acquired multiple acyl-CoA dehydrogenase deficiency.” DOI: https://doi.org/10.1371/journal.pone.0199521, published July 2018. (medina2018detectionofequine pages 10-11)

Where PMIDs were not verified in the retrieved records, DOI URLs are provided rather than risking incorrect PMID assignment.

References

1. (latif2017newdevelopmentof pages 2-3): Summaya Abdul Latif and Pooja Luthra. New development of hypoglycemia in a previously poorly-controlled type 2 diabetic: ackee fruit-induced hypoglycemia. International Journal of Diabetes and Clinical Research, Dec 2017. URL: https://doi.org/10.23937/2377-3634/1410073, doi:10.23937/2377-3634/1410073. This article has 2 citations.

2. (latif2017newdevelopmentof pages 1-2): Summaya Abdul Latif and Pooja Luthra. New development of hypoglycemia in a previously poorly-controlled type 2 diabetic: ackee fruit-induced hypoglycemia. International Journal of Diabetes and Clinical Research, Dec 2017. URL: https://doi.org/10.23937/2377-3634/1410073, doi:10.23937/2377-3634/1410073. This article has 2 citations.

3. (scott1916onthevomiting pages 56-58): H. Harold Scott. On the 'vomiting sickness' of jamaica. Annals of Tropical Medicine and Parasitology, 10:1-78, Apr 1916. URL: https://doi.org/10.1080/00034983.1916.11684104, doi:10.1080/00034983.1916.11684104. This article has 54 citations.

4. (scott1916onthevomiting pages 58-62): H. Harold Scott. On the 'vomiting sickness' of jamaica. Annals of Tropical Medicine and Parasitology, 10:1-78, Apr 1916. URL: https://doi.org/10.1080/00034983.1916.11684104, doi:10.1080/00034983.1916.11684104. This article has 54 citations.

5. (bochnia2015hypoglycinacontent pages 1-2): M. Bochnia, J. Ziegler, J. Sander, A. Uhlig, S. Schaefer, S. Vollstedt, M. Glatter, Steffen Abel, S. Recknagel, G. Schusser, M. Wensch-Dorendorf, and A. Zeyner. Hypoglycin a content in blood and urine discriminates horses with atypical myopathy from clinically normal horses grazing on the same pasture. PLoS ONE, 10:e0136785, Sep 2015. URL: https://doi.org/10.1371/journal.pone.0136785, doi:10.1371/journal.pone.0136785. This article has 75 citations and is from a peer-reviewed journal.

6. (boemer2017acylcarnitinesprofilebest pages 15-16): François Boemer, Johann Detilleux, Christophe Cello, Hélène Amory, Christel Marcillaud-Pitel, Eric Richard, Gaby van Galen, Gunther van Loon, Laurence Lefère, and Dominique-Marie Votion. Acylcarnitines profile best predicts survival in horses with atypical myopathy. PLoS ONE, 12:e0182761, Aug 2017. URL: https://doi.org/10.1371/journal.pone.0182761, doi:10.1371/journal.pone.0182761. This article has 36 citations and is from a peer-reviewed journal.

7. (boemer2017acylcarnitinesprofilebest pages 16-16): François Boemer, Johann Detilleux, Christophe Cello, Hélène Amory, Christel Marcillaud-Pitel, Eric Richard, Gaby van Galen, Gunther van Loon, Laurence Lefère, and Dominique-Marie Votion. Acylcarnitines profile best predicts survival in horses with atypical myopathy. PLoS ONE, 12:e0182761, Aug 2017. URL: https://doi.org/10.1371/journal.pone.0182761, doi:10.1371/journal.pone.0182761. This article has 36 citations and is from a peer-reviewed journal.

8. (medina2018detectionofequine pages 10-11): Sonia González Medina, Carolyne Hyde, Imogen Lovera, and Richard J. Piercy. Detection of equine atypical myopathy-associated hypoglycin a in plant material: optimisation and validation of a novel lc-ms based method without derivatisation. PLoS ONE, 13:e0199521, Jul 2018. URL: https://doi.org/10.1371/journal.pone.0199521, doi:10.1371/journal.pone.0199521. This article has 24 citations and is from a peer-reviewed journal.

9. (latif2017newdevelopmentof pages 3-4): Summaya Abdul Latif and Pooja Luthra. New development of hypoglycemia in a previously poorly-controlled type 2 diabetic: ackee fruit-induced hypoglycemia. International Journal of Diabetes and Clinical Research, Dec 2017. URL: https://doi.org/10.23937/2377-3634/1410073, doi:10.23937/2377-3634/1410073. This article has 2 citations.

10. (scott1916onthevomiting pages 40-43): H. Harold Scott. On the 'vomiting sickness' of jamaica. Annals of Tropical Medicine and Parasitology, 10:1-78, Apr 1916. URL: https://doi.org/10.1080/00034983.1916.11684104, doi:10.1080/00034983.1916.11684104. This article has 54 citations.

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