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Coconut Allergy Revisited

  • Texas Children's Hospital & Baylor College of Medicine

Abstract and Figures

Despite concerns voiced often by food-allergic patients, allergy to coconut is rare, not directly associated with nut allergy and few cases are reported so far in the literature. We present an interesting case of coconut allergy in a child that was previously tolerant to coconut and regularly exposed via both the skin and gastrointestinal route.
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Case Report
Coconut Allergy Revisited
Katherine Anagnostou 1,2
1Department of Pediatrics, Section of Immunology, Allergy and Rheumatology, Texas Children’s Hospital,
Feigin Center, 1102 Bates Avenue, Suite 330, MS: BCM320, Houston, TX 77030, USA;; Tel.: +1-832-824-1319
2Department of Pediatrics, Section of Immunology, Allergy and Rheumatology, Baylor College of Medicine,
Houston, TX 77030, USA
Received: 19 September 2017; Accepted: 28 September 2017; Published: 29 September 2017
Despite concerns voiced often by food-allergic patients, allergy to coconut is rare, not
directly associated with nut allergy and few cases are reported so far in the literature. We present an
interesting case of coconut allergy in a child that was previously tolerant to coconut and regularly
exposed via both the skin and gastrointestinal route.
Keywords: food allergy; coconut allergy; anaphylaxis; allergic reaction; skin prick tests
A common concern of food allergic patients (especially those allergic to nuts) is whether they can
safely consume coconut products. Despite coconut allergy being rare, there is a misconception that
if a patient is allergic to nuts, they are at high risk of experiencing allergic reactions to coconut; as a
consequence, nut-allergic patients are not uncommonly advised to avoid coconut.
Coconut (Cocos nucifera) is a fruit (not a nut) that belongs to the Aracaceae (palms) plant family.
The term is derived from the 16th-century Portuguese and Spanish word ‘coco’ meaning ‘head’ or
‘skull’. The oil and milk derived from coconut are commonly used in cooking and frying, as well as in
soaps, cosmetics and other skin care products.
Reports of immunoglobulin E (IgE)-mediated coconut allergy are rare and only a handful of cases
have been reported in the literature in adults and children [
]. However, despite the low prevalence
of coconut allergy, reactions tend to be systemic and all cases reported so far have involved anaphylactic
reactions. In the United States, coconut must be disclosed as an ingredient on package labels.
We report a case of coconut allergy in a school-age child, who presented with a history of recurrent
allergic reactions to coconut. At the age of 6 years, the patient experienced generalized urticaria to
coconut oil applied on the skin. Prior to this reaction, coconut oil had been applied multiple times
a week on the skin, since the age of 2 weeks old, without any problems. The patient was also
eating coconut regularly without allergic reactions. A second episode of skin reaction (widespread
hives) was noted two weeks after the first one, again following application of coconut oil on the
skin. Soon after these two episodes, the patient complained of a ‘scratchy throat’ after eating coconut.
The parents also report one episode when the child ate a few spoonfuls of coconut ice-cream and,
20–30 min later, complained of throat itching and severe abdominal pain with subsequent vomiting
and diarrhea. There were no respiratory symptoms on that occasion. The reaction was treated
successfully with antihistamines. At the age of 6 and a half, the patient ate an oatmeal/raisin cookie
that also contained coconut. Throat itching developed and was treated successfully with antihistamines.
More recently however, while at school, the patient inadvertently ate another oatmeal/raisin cookie
containing coconut and developed a scratchy throat. This was followed by vomiting and wheeze. Both
bronchodilators and antihistamines were administered and the patient was taken to a medical facility.
By the time of arrival, the wheeze had resolved and all other symptoms of anaphylaxis had also settled,
so no further treatment was required.
Children 2017,4, 85; doi:10.3390/children4100085
Children 2017,4, 85 2 of 3
In terms of atopic background, the patient did not report any other food allergies and had
been eating peanuts, almonds, hazelnuts, cashews, pistachios, pecans and walnuts regularly without
any problems or reactions. With regards to nasal allergies, parents reported mild, occasional, nasal
congestion, not requiring treatment. No food pollen syndrome symptoms to any fresh fruits or
raw vegetables were reported. The child had experienced allergic reactions to cats in the past with
skin and upper respiratory/eye symptoms. With regards to respiratory symptoms, bronchodilators
were prescribed at the age of 6 years, following an upper respiratory infection with persistent
cough. These were not required on a regular basis. Mild infantile eczema was noted shortly after
birth, mostly in the form of dry skin, for which coconut oil was applied. On examination in clinic,
mild flexural eczema was noted on the antecubital fossae and popliteal fossae, well controlled with
regular moisturizer.
Skin prick testing to coconut commercial extract showed a strongly positive result (20 mm wheal).
Cat and dog skin test results were also positive (see Table 1below).
Table 1.
Skin prick testing results. Measurements represent the mean of 2 diameters. Test results to
other aeroallergens (including pollens and house dust mite) were negative (data not shown).
Allergen Wheal/Flare (mm)
Control positive skin prick test 12/20
Control negative skin prick test 0/0
Coconut 20/26
Cat 15/20 P
Dog 6/8 P
Mold mix #1 4/4
Mold mix #2 3/3
P: Pseudopod formation.
Coconut allergens have previously been identified as Coc n2, a 7S globulin; and Coc n4, an 11S
globulin [
]. Cross-reactivity between coconut and tree nuts/lentils has been described in the
literature (due to the 7S and 11S globulins) [
], but a retrospective study from the US has previously
reported that children with sensitization or allergy to peanuts or tree nuts are not more likely to be
sensitized or allergic to coconut [
]. We note that the official allergen nomenclature subcommittee, the
International Union of Immunological Societies (IUIS,, currently includes
only the 7S globulin allergen, also known as vicilin-like, and named Coc n1 for coconut.
What is interesting in our case is that coconut allergy developed in a child that was regularly
exposed to coconut allergen previously without reaction. This involved skin exposure in the form of
coconut oil since the age of two weeks and subsequently also via the oral route, tolerating coconut and
coconut-containing products, until the age of 6 years. This pattern of coconut allergy development has
not been reported previously in children, to our knowledge. It has been shown however, for peanut
allergy, that sensitization may occur via the skin (without concurrent oral exposure), due to topical
exposure from a very early age [
]. In our case, there was confirmed oral tolerance to coconut for
some years prior to reactions occurring.
In summary, we report a case of coconut allergy, presenting in a 6-year-old child, despite previous
regular exposure to coconut via both the cutaneous and oral route. Our knowledge in coconut allergy is
limited as only a very small number of patients are affected. Given the increasing use of commercially
available coconut products, it is important to be aware of the allergenic potential of coconut, even if
the allergen has previously been tolerated.
Conflicts of Interest:
The authors declare no conflict of interest. The founding sponsors had no role in the design
of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, and in the
decision to publish the results.
Children 2017,4, 85 3 of 3
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... In addition, several other studies have reported allergy/ anaphylaxis following ingestion of fresh coconut, coconut milk, and other coconut containing food with the total of 10 cases reported across all studies [4][5][6][7][8][9][10][11][12][13]. Allergy to coconut oil is rare and only two cases have been reported [5,14]. Further, several other cases of contact dermatitis have been reported as a result of sensitization to coconut oil derived surfactants; cocamide DEA (diethanolamine), cocamidopropyl betane, and TEA-PGE-3 (triethanolamine-phenyl glycidyl ether-3) cocamide sulphate [15][16][17][18][19][20][21][22][23]. ...
... Most of the patients who are allergic to coconut milk can consume coconut oil. However, there is one case report where the patient was allergic to both coconut milk and coconut oil [5]. ...
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... In a study of children with allergy to tree nut, coconut sensitization was reported to be approximately 30% in 298 children 7 and approximately 20% in another study of 191 children with sesame and tree nut allergy, with a 25% patient-reported rate of allergic reactions. 1 Although reaction characteristics have been described in published case reports and case series, [8][9][10][11][12][13][14] diagnostic cutoffs associated with reactions on specific immunoglobulin E (sIgE) and skin prick testing (SPT) have not been established. ...
... Specifically, products with higher amount of allergen, such as pure coconut oil, should be the focus of counseling. There is only 1 case report suggesting ingestion of coconut might not be tolerogenic in someone applying coconut topically, 10 but we believe that this case report reflects the need for frequent ingestion, several times per week, to maintain tolerance in high-risk individuals. Although none of our patients had documented allergic contact dermatitis to coconut, this and irritant dermatitis have been described as risks of topical coconut and possibly coconut derivatives. ...
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... In the present clinical trial, VCO was used as an antifungal agent for the treatment of DS associated with oral candidiasis in older people with removable prostheses. It is proposed as an alternative antifungal treatment, with no or low toxicity, no side effects, and low cost, which helps to recover the oral-dental health of older people [21,22]. ...
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... The allergic reaction is currently attributed to a 7S and an 11S globulin protein called Coc n2 and Coco n4. 7S globulins have already been described as allergens in walnuts and hazelnuts, so that some patients who are allergic to tree nuts show cross-reactions to coconuts [3][4][5][6]. As there is no causative immunotherapy in the clinical routine for food allergies so far, the only way to prevent an allergic reaction for people who are affected is to strictly avoid the allergenic food. ...
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So far, only a few cases of immunoglobulin E (IgE)-mediated coconut allergies have been described in the literature. Due to a growing consumption of coconut-containing foods in occidental countries, the number of coconut allergies may also increase. As there is no causative immunotherapy in clinical routine, appropriate food labelling is particularly important, also with regard to cross-contamination, to prevent serious health consequences. The purpose of this study was to develop a DNA-based detection method for coconut (Cocos nucifera). Initially, three sets of coconut-specific primers were designed and tested. A TaqMan™ probe was then developed to identify and quantify coconut by real-time PCR assay. With 27 other plant and animal species, the specificity of the primer/probe system was tested and cross reactivity was excluded. In a dilution series, a limit of detection of 1 pg/µL was determined. Thus, the developed real-time PCR assay is a suitable method to detect coconut in food.
... The sample was diluted to 0.01% (w/w) total solid and adjusted in the certain range of pH (Anagnostou, 2017 cell containing an aliquot of the sample was placed in Nano patica SZ-100, Horiba. ζ-Potential was calculated from particle electrical mobility using Smulochowski's model. ...
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Cross‐flow ultrafiltration has been reported as a promising technique to concentrate the coconut protein in the liquid by‐product called coconut skimmed effluent, which is produced from coconut oil wet process. However, the cake developed on the membrane surface always causes a measurable resistance, which extremely impedes the filtration efficiency. This study investigated the cross‐flow filtration performance under different operational conditions, which included membrane molecular weight cut‐off (10 and 30 kDa), transmembrane pressure (0.1, 0.2, and 0.3 MPa) and cross‐flow velocity (0.5, 1.0, and 1.5 l/min), and molecular electrostatic interaction by adjusting the feed suspension pH (2.0, 4.0, 6.3, 9.0). The results showed that there was no substantial difference in the filtration performance between 10 kDa and 30 kDa membrane because the number of molecules, in which the particle size was larger than 30 kDa, was high. Furthermore, the results confirmed that the permeate flux increased with the cross‐flow velocity but decreased with the transmembrane pressure due to the cake layer compressibility. For the suspension chemistry effects, although a thick cake layer was developed on the membrane when the feed suspension pH was very close to pI (pH 4.0), the permeate flux was surprisingly greater than the other pH conditions. Practical Application This research was carried out by focusing on the evaluation of the alternative method other than the traditional one, such as precipitation or centrifugation, for coconut protein concentration. The membrane ultrafiltration, which is widely used to improve the quality of many dairy products, has been applied to the coconut suspension and filtration performances including fouling behavior under various conditions have been investigated. The results obtained could provide extensive information for the operational optimization of the coconut liquor cross‐flow filtration process considering the hydrodynamic factors. Furthermore, since the experiment was conducted with a real polydispersed biopolymer mixture, its unique characteristics that depend on the change of pH would be able to extend the knowledge including the influence of the electrostatic interaction on the cake formation of such plant‐based protein–polysaccharide mixture.
Résumé La noix de coco est responsable de rares réactions allergiques, parfois anaphylactiques. Nous rapportons le cas de 2 enfants ayant consulté dans 2 centres d’allergologie d’Île de France. Le premier enfant, âgé de 14 ans, a présenté une réaction de grade 2 (classification d’Astier), après consommation d’une cuillère d’un gâteau à la coco. Le prick test natif coco est positif à 16 mm, (témoin : 10 mm). L’IgE spécifique est supérieure à 100 kU/L. Il a également présenté une réaction de contact avec un gel douche à la coco. Le deuxième enfant, âgé de 9 ans, a une allergie avérée à l’arachide, au sésame, et aux fruits à coques. Après ingestion de lait de coco dans une préparation culinaire, il a présenté une réaction de grade 2. Le Prick test natif est positif à 6 mm pour la coco (témoin : 3 mm). L’IgE spécifique est à 3,12 kU/L. Plusieurs cas d’anaphylaxies sévères à la noix de coco ont été décrites dans la littérature, ainsi que des allergies de contact. Les protéines allergisantes identifiées sont des protéines de stockage et une profiline. Une allergie à la noix de coco et des co-sensibilisations éventuelles doivent être recherchées car, bien que rares, elles peuvent être sévères. La sensibilisation par voie cutanée a été décrite, car la coco est contenue dans de nombreux produits cosmétiques. Une augmentation de son utilisation dans les produits alimentaires et les cosmétiques fait craindre une recrudescence de cette allergie dans le futur.
This study focuses on the addition of tapioca starch as a stabilizer in the formulation of yogurt-like products made from coconut milk. Yogurt-like products supplemented with tapioca starch at 0.5, 1.0, 1.5 and 2.0% (w/w) or without tapioca starch were stored at 4 °C for 14 days, and analyzed for pH changes, lactic acid bacteria viability, syneresis, rheological properties, whiteness index and sensory properties using 9-point hedonic scale. The results showed that the addition of tapioca starch did not affect the number of lactic acid bacteria during storage. Syneresis decreased with increasing concentration of tapioca starch, while the storage modulus (G' or solid-like property) increased when the concentration of tapioca starch increased. Whiteness index was not affected by supplementation of tapioca starch at the end of storage. The sensory evaluation indicated that addition of tapioca starch from 1.0% led to higher liking scores, especially texture attribute. The product made with 1.0% tapioca starch was selected based on sensory scores for proximate analysis. The product contained 71.31% moisture, 1.91% protein, 6.01% carbohydrate, 20.22% fat and 0.55% ash. This study suggested that yogurt-like product made from coconut milk can be obtained using tapioca starch as a stabilizer.
Stutius LM, Sheehan WJ, Rangsithienchai P, Bharmanee A, Scott JE, Young MC, Dioun AF, Schneider LC, Phipatanakul W. Characterizing the relationship between sesame, coconut, and nut allergy in children. Pediatr Allergy Immunol 2010: 21: 1114–1118. © 2010 John Wiley & Sons A/S Sesame and coconut are emerging food allergens in the United States. We sought to examine whether children allergic to peanuts and tree nuts are at increased risk of having an allergy to sesame or coconut. We performed a retrospective chart review of children who underwent skin prick testing (SPT) to sesame and coconut and identified 191 children who underwent SPT to sesame and 40 to coconut. Sensitization to sesame was more likely in children with positive SPT to peanuts (odds ratio [OR] = 6.7, 95% confidence interval [CI] [2.7–16.8], p < 0.001) and tree nuts (OR = 10.5, 95% CI [4.0–27.7], p < 0.001). Children with histories of both peanut and tree nut reaction were more likely to have a history of sesame reaction (OR = 10.2, 95% CI [2.7–38.7], p < 0.001). Children with sensitization or allergy to peanuts or tree nuts were not more likely to be sensitized or allergic to coconut. In conclusion, children with peanut or tree nut sensitization were more likely to be sensitized to sesame but not coconut. Children with clinical histories of both peanut and tree nut allergy were more likely to be allergic to sesame.
Two patients with tree nut allergy manifested by life-threatening systemic reactions reported the subsequent onset of systemic reactions after the consumption of coconut. Herein, the IgE-binding proteins from coconut are described, and in vitro cross-reactivity with other nuts is investigated. The IgE-binding profile of coconut endosperm tissue extract was analyzed by SDS-PAGE followed by immunoblotting. Immunoblot inhibition studies with walnut, almond, peanut, and coconut were performed. Sera IgE from both patients recognized reduced coconut allergens with molecular weights of 35 and 36.5 kd. IgE from 1 patient also bound a 55-kd antigen. Preabsorption of sera with nut extracts suppressed IgE binding to coconut proteins. Preabsorption of sera with coconut caused the disappearance of IgE binding to protein bands at 35 and 36 kd on a reduced immunoblot of walnut protein extract in 1 patient and suppression of IgE binding to a protein at 36 kd in the other patient. The reduced coconut protein at 35 kd was previously shown to be immunologically similar to soy glycinin (legumin group of seed storage proteins). The clinical reactivity in these 2 patients is likely due to cross-reacting IgE antibodies primarily directed against walnut, the original clinical allergy reported, and most likely to a walnut legumin-like protein. Coconut allergy in patients with tree nut allergy is rare; these are the first 2 patients ever reported, and therefore there is no general indication to advise patients with tree nut allergy to avoid coconut.
The prevalence of peanut allergy appears to have increased in recent decades. Other than a family history of peanut allergy and the presence of atopy, there are no known risk factors. We used data from the Avon Longitudinal Study of Parents and Children, a geographically defined cohort study of 13,971 preschool children, to identify those with a convincing history of peanut allergy and the subgroup that reacted to a double-blind peanut challenge. We first prospectively collected data on the whole cohort and then collected detailed information retrospectively by interview from the parents of children with peanut reactions and of children from two groups of controls (a random sample from the cohort and a group of children whose mothers had a history of eczema and who had had eczema themselves in the first six months of life). Forty-nine children had a history of peanut allergy; peanut allergy was confirmed by peanut challenge in 23 of 36 children tested. There was no evidence of prenatal sensitization from the maternal diet, and peanut-specific IgE was not detectable in the cord blood. Peanut allergy was independently associated with intake of soy milk or soy formula (odds ratio, 2.6; 95 percent confidence interval, 1.3 to 5.2), rash over joints and skin creases (odds ratio, 2.6; 95 percent confidence interval, 1.4 to 5.0), and oozing, crusted rash (odds ratio, 5.2; 95 percent confidence interval, 2.7 to 10.2). Analysis of interview data showed a significant independent relation of peanut allergy with the use of skin preparations containing peanut oil (odds ratio, 6.8; 95 percent confidence interval, 1.4 to 32.9). Sensitization to peanut protein may occur in children through the application of peanut oil to inflamed skin. The association with soy protein could arise from cross-sensitization through common epitopes. Confirmation of these risk factors in future studies could lead to new strategies to prevent sensitization in infants who are at risk for subsequent peanut allergy.
Total globulins extracted with 0.4 M NaCl in buffer from coconut endosperm separated into two peaks on gel filtration: peak I corresponding to 11S globulin or cocosin and peak II to 7S globulin with native molecular weights of 326 000 and 156 000, respectively. The percent composition of total globulins was estimated to be 11S, 86% and 7S, 14%. On SDS-PAGE, cocosin resolved into two closely migrating bands at approximately 34 000 (acidic polypeptide) and another set of 2 bands at 24 000 (basic polypeptide). Each set consisted of one darkly stained band and one lightly stained band. The 7S globulin consisted of three bands of 16 000, 22 000, and 24 000. Three isoforms of cocosin were identified after anion exchange chromatography. Cocosin, but not the 7S, was found to have disulfide bonds. Using periodic acid-Schiff's reagent, all of the bands of cocosin on SDS-PAGE were positive for carbohydrate. However, when con A-peroxidase was used, only the basic polypeptide stained positively for carbohydrate. For the 7S globulin, no carbohydrate group was detected using the PAS and con A-peroxidase tests. The 7S globulin was easily extracted with 0.10-0.15 M NaCl, whereas cocosin was extracted with 0.35 M NaCl. The N-terminal amino acid sequences of the 34 k band and 24 k band of cocosin were SVRSVNEFRXE and GLEETQ, respectively, and that of the 7S was EQEDPELQK.
Coconut (Cocos nucifera) is a monocotyledonous plant of the Arecaceae family. Allergy to coconut is infrequent, with only 5 cases reported so far in the medical literature. To identify coconut allergens in 2 patients allergic to this food. We describe 2 patients allergic to coconut: an adult pollen-allergic patient monosensitized to coconut who presented with severe oropharyngeal symptoms and a child with a previous allergy to walnut, not allergic to pollen, who developed anaphylaxis on coconut ingestion. Both patients had positive skin prick test results and serum specific IgE (CAP) to coconut. IgE sodium dodecyl sulfate-polyacrylamide gel electrophoresis immunoblotting was performed to identify the allergens involved, and a strong IgE binding band detected in both patients was further analyzed by matrix-assisted laser desorption/ionization time-of-flight mass spectroscopy (MALDI-TOF MS). Stability to pepsin digestion of the coconut extract and its cross-reactivity with tree nuts were studied. An immunoblot showed an almost identical profile of IgE binding proteins in the coconut extract in both patients who reacted strongly to a band of approximately 29 kDa. The peptide analysis by MALDI-TOF MS of this band obtained the sequence GHGKREDPEKR. The protein with the highest correlation with this peptide was found to be a 7S globulin from Elaeis guineensis, another oil palm species also belonging to the Arecaceae family. The 29-kDa band was digested by pepsin in less than 1 minute. Cross-reactivity among coconut, walnut, and hazelnut was demonstrated by CAP inhibition in patient 2. We have identified a 7S storage protein as a novel coconut allergen.
The medical literature reports few cases of severe allergic reactions to coconut. We encountered a patient with anaphylaxis to coconut and oral symptoms to tree nuts. To identify cross-reactive antibodies between coconut and other tree nuts. We performed commercial radioallergosorbent tests to coconut and various tree nuts using the patient's serum. Skin prick testing was performed to fresh coconut and commercial extracts of coconut, almond, Brazil nut, cashew, pecan, walnut, and hazelnut. Proteins from fresh coconut, commercial coconut extract, and tree nuts were extracted. Immunoblot and inhibition assays were performed to evaluate for cross-reacting IgE antibodies between similar-sized allergens in coconut and hazelnut. Positive skin test results occurred to the coconut and multiple tree nut extracts. In vitro serum specific IgE was present for coconut, hazelnut, Brazil nut, and cashew. Immunoblots demonstrated IgE binding to 35- and 50-kDa protein bands in the coconut and hazelnut extracts. Inhibition assays using coconut demonstrated complete inhibition of hazelnut specific IgE, but inhibition assays using hazelnut showed only partial inhibition of coconut specific IgE. Our study demonstrates the presence of cross-reactive allergens between hazelnut (a tree nut) and coconut (a distantly related palm family member). Because there are many potentially cross-reactive allergens among the tree nuts, we recommend patients with coconut hypersensitivity be investigated for further tree nut allergies.