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Coconut Allergy Revisited

Authors:
  • 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;
Aikaterini.Anagnostou@bcm.edu; 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
Abstract:
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 [
1
4
]. 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 www.mdpi.com/journal/children
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 [
5
,
6
]. Cross-reactivity between coconut and tree nuts/lentils has been described in the
literature (due to the 7S and 11S globulins) [
4
,
7
,
8
], 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 [
9
]. We note that the official allergen nomenclature subcommittee, the
International Union of Immunological Societies (IUIS, http://www.allergen.org), 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 [
10
]. 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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2017 by the author. Licensee MDPI, Basel, Switzerland. This article is an open access
article distributed under the terms and conditions of the Creative Commons Attribution
(CC BY) license (http://creativecommons.org/licenses/by/4.0/).
... Another allergy study from the United States has reported 69 patients with allergic reactions to coconut, including 2 during breastfeeding, 10 20:14 after contact, and 57 following ingestion, with 50% of the patients who developed allergy after ingestion having mild/moderate anaphylaxis [3]. 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]. ...
... 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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Background Despite the low prevalence of IgE sensitivity to fresh or boiled coconut milk and coconut oil, those may contain allergens of which the clinical significance remains undetermined. This study aimed to identify and compare allergens in fresh coconut milk (FCM), boiled coconut milk (BCM), unrefined wet-processed coconut oil (WPCO), and dry-processed coconut oil (DPCO) using sera from patients with allergy to coconut milk. Methods The study included 18 patients with immediate hypersensitivity to coconut milk, including five who developed anaphylaxis. Sensitization was assessed by skin prick test and ImmunoCAPs using commercially available coconut extracts. Immunoblotting was performed to identify and compare allergen profiles. Results Total sIgE levels and overall IgE reactivity of patients with anaphylaxis were higher compared to patients with allergy. Twelve allergens ranging from 5 to 128 kDa including six novel allergens with 5, 12, 47, 87, 110, and 128 kDa were visualized in immunoblots with FCM. Similarly, nine allergens of 5, 12, 17, 32, 35, 47, 87, 110, and 128 kDa were detected in BCM. One allergen (110 kDa) was discerned in all four extracts. Higher IgE prevalence was detected with three allergens of 55, 87, and 110 kDa. Conclusions Allergens of BCM and unrefined coconut oil (WPCO and DPCO) were determined for the first time. Novel allergens of 87 and 110 kDa and the 55 kDa allergen have the highest potential to be used in Component Resolved Diagnostics. Further, these findings demonstrate that, patients who have an allergy to coconut milk could also react to boiled coconut milk and unrefined coconut oil.
... O óleo e o leite derivados do coco são comummente usados na culinária, bem como na produção de sabonetes, cosméticos e outros produtos de higiene pessoal. São raros os casos descritos na literatura de alergia ao coco mediada por IgE (1,2,3,4). No entanto, apesar da baixa prevalência de alergia ao coco, estão descritas reações anafiláticas e não anafiláticas, sendo as segundas mais prevalentes (1,2,3,4,5,6). ...
... São raros os casos descritos na literatura de alergia ao coco mediada por IgE (1,2,3,4). No entanto, apesar da baixa prevalência de alergia ao coco, estão descritas reações anafiláticas e não anafiláticas, sendo as segundas mais prevalentes (1,2,3,4,5,6). Os autores apresentam o caso clínico de um doente com alergia alimentar ao coco, com início de sintomas em idade adulta. ...
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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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... The list of fruits mentioned in the oral care product labels is presented in Table 4. Coconut (N = 7) and strawberry (N = 11) were the most prevailing fruits in the oral care products surveyed. Although coconut reactions are sporadic, the presence of coconut should not be neglected since there is evidence of allergy to this fruit, which tends to provoke systemic responses, such as anaphylaxis 30 . Strawberry is a fruit that does not cause many allergic reactions. ...
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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.
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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.
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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.
Article
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.
Article
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.
Article
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.