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Practitioner's Corner
J Investig Allergol Clin Immunol 2019; Vol. 29(5): 378-398
© 2019 Esmon Publicidad
Induction of Oral Tolerance in a Case of Severe
Allergy to Coconut
Hernández-Santana GL
1
, Rodríguez-Plata E
1
, González-
Colino CE
1
, Martínez-Tadeo JA
1
, Bartolomé B
2
, García-
Robaina JC
1
, Pérez-Rodríguez E
2
1
Allergy Department, Hospital Universitario La Candelaria, Santa
Cruz de Tenerife, Spain
2
SpainResearch andDevelopment Department, Roxall, Bilbao, Spain
J Investig Allergol Clin Immunol 2019; Vol. 29(5): 380-381
doi: 10.18176/jiaci.0405
Key words:
Oral tolerance induction. Allergy. Coconut.
Palabras clave:
Inducción a la tolerancia oral. Alergia. Coco.
Food allergyhas increased in frequency in the last 2-3decades.
Some studies report a prevalence of up to 10% [1] depending
on the study population (age range, dietary habits, allergen
exposure, geographic location) and on the evaluation method
used. In addition, more globalized dietary habits mean that it
is increasingly frequent to find patients sensitized to allergens
that are not part of traditional Western cuisine, such as coconut.
Several cases of coconut allergy have been reported. Most
were systemic reactions and anaphylaxis [2-7]. We present the
case of a patient who underwent oral desensitization to treat
coconut allergy.
A 47-year-old Thai woman living in Tenerife (Canary
Islands, Spain) was assessed at our unit for suspected
coconut allergy. She had a previous history of severe allergic
rhinoconjunctivitis and sensitization to house dust mite that
were treated with specific immunotherapy, to which she
responded well. The patient reported her first coconut allergy
episode 4 years earlier. She presented with dysphonia, dyspnea,
and palmoplantar pruritus immediately after eating grated
coconut and subsequently reduced her intake of coconut, albeit
not entirely. She occasionally experienced oropharyngeal
pruritus after eating small amounts of coconut-containing
foods, until she experienced a second episode of anaphylaxis
with coconut milk curry and was referred to our unit.
Skin testswerepositive for commercial coconut extract (8mm),
Aroy-D coconut milk (8 mm), Dunn coconut milk (7 mm), and
dehydratedcoconut (8mm)witha4-mmhistamine-inducedwheal.
Coconut-specific IgE measured using the ImmunoCAP
System (Thermo Fisher) was 17.7 kUA/L.
Oral challenge with coconut milk Aroy-D was not
performed owing to positive results in the rub test, namely,
palmoplantar and oral pruritus and dysphonia that required
treatment with adrenaline.
SDS-PAGE immunoblotting with coconut pulp extract and
coconut milk extract was performed according toLaemli [8]. IgE-
binding proteins of approximately 70 kDa, 66 kDa, 43/40 kDa,
26.5 kDa, 22 kDa, and 17 kDa were detected in coconut pulp
extract, and bands of 45 kDa, 40 kDa, 37 kDa, 26 kDa, 24 kDa,
and 20.5 kDa were revealed in coconut milk extract.
Table.
Protocol, Adverse Reactions, and Treatment
First Phase
Dilution
a
Dose, mL
Amount of Protein, g
Reaction
Treatment
Day 1
1/100
1
0.00016
No
1/100
2
0.00032
No
1/100
4
0.00064
No
1/100
8
0.00128
No
1/10
1.6
0.00256
No
Day 2
1/10
1.6
0.00256
Pharyngeal pruritus
None
1/10
3.2
0.00512
No
1/10
6
0.0096
No
1/1
1.2
0.0192
No
1/1
2.5
0.04
Pharyngeal pruritus
None
Day 3
1/1
2.5
0.04
No
1/1
7.5
0.12
Pharyngeal pruritus
Desloratadine 5 mg
Day 4
1/1
7.5
0.12
No
Day 5
1/1
10
0.16
No
Day 6
1/1
15
0.24
No
Second Phase
b
Dose, mL
Amount of Protein, g
Reaction
Treatment
Day 7
2
0.136
No
Day 8
4
0.272
No
Day 9
6
0.4
No
a
Dilution of coconut milk (Aroy-D) (60% coconut in water).
b
Grated coconut (Hacendado).
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