The incidence of food allergy is increasing in children. The incidence in children aged five or less is 3.5%.1 Clinical findings usually appear within the first few years of life with the addition of new foods to the diet. Food-related clinical findings may or may not be IgE mediated. Although most commonly seen as urticaria and angio-oedema in the clinic, they can also produce anaphylaxis, atopic dermatitis, and various gastrointestinal and respiratory symptoms.1
The distribution of the foods that cause food allergy differs between countries according to how frequently they are ingested with the diet.1 The most common causes of food allergies in children are milk, eggs, soya, wheat and nuts. Egg is the most common food that causes an Ig-E mediated reaction.1 Combinations of food allergies may also be seen. The most common combinations of food allergens were included ‘egg-milk’, ‘egg-wheat’, and ‘milk-wheat’.2
Legumes are an important source of proteins and are commonly found in the diet of developing countries and in the Mediterranean diet. The legumes most commonly ingested are lentil, chickpeas, beans and peas. The most commonly reported legume allergy is for lentil, followed by that for chickpeas.3 These are quite commonly consumed in our country and added to the diet within the first year of life. However, there are no clear data on legume allergies in our country and in other countries.
We present a child who has IgE-mediated reaction to chickpea and egg.
A 19-month-old male presented at our clinic because of facial and labial swelling and redness within 30minutes after eating chickpeas when he was 12 and 14 months old. He also defined a red skin lesion raised from the skin within one hour of eating food containing eggs twice in the past.
The patient had been delivered by the spontaneous vaginal route at term with a birth weight of 4050 gr. He had received mother's milk for 18 months and formula had been added at the 5th month and cow's milk at the 15th month. The patient did not want to eat eggs. Eggs had been added to his diet in yolk form when he was eight months old and as egg white when one year old. The patient had received a diagnosis of atopic eczema while three months old and had used steroid ointments. He also had a history of diarrhoea lasting for 3 months following the gastroenteritis he had suffered when 6.5 months old. The family history revealed no consanguinity of allergic disease in the family. The physical examination was normal.
Laboratory test results were as follows: haemogram, IgG, IgA, IgM were normal. IgE level was 172 IU/mL, there were 4% eosinophils on the peripheral smear, and egg-specific IgE was 17.5 IU/mL. The skin prick test (SPT) (induration/hyperaemia) revealed the following sensitivities: histamine 6x5/28mm, egg white 6x6/15mm, egg yolk 5x5/13mm, boiled chickpea water 9x9/22mm and chickpea itself 9x9/25mm. We found no sensitivity to soya, pea, peanut or bean antigens on the SPT. A double-blind placebo-controlled food loading test was performed with eggs and urticaria and angio-oedema appeared five minutes after the second egg dose. A double-blind placebo-controlled food loading test was not performed as the family was not willing.
The case was followed-up after elimination of chickpeas and eggs from his diet. An adrenaline auto-syringe (epi-pen junior 0.15mg/ml) was provided for the patient. The family was educated on epi-pen usage and the anaphylaxis action plan.
The one-year follow-up revealed that the patient had not eaten any chickpeas or eggs and had not had any reactions. There was no skin lesion related to atopic eczema. The repeated SPT showed continuing chickpea (8x6/20mm) and egg (6x5/15mm) sensitivity.
Lentil and chickpea allergy is seen most commonly in the Mediterranean and Central Asia while soya and nuts from the same family commonly cause allergy in the USA, UK and Southeast Asia.5 A study from the Mediterranean country Spain reports legume allergy as the fifth most common food allergy.6 There are no clear data regarding legume allergy in our country. However, a 17-year-old case with lentil or food-dependent exercise-induced anaphylaxis and concurrent chickpea anaphylaxis has been reported.7 A case that underwent liver transplantation and had lentil allergy following the transplant has also been reported.8
Food allergy develops in the first two years of life: lentil allergy in the first 15 months and chickpea allergy in the first 18 months.2 This duration is especially related to the time the food enters the diet. Our patient had first shown signs related to chickpeas when it was added to the diet at 12 months of age.
Clinical findings of food allergy can consist of the oral allergy syndrome, urticaria, angio-oedema, rhinitis, asthmatic attack, anaphylaxis or even death.5 Urticaria/angio-oedema had developed within 30minutes following chickpea and egg ingestion in our case. The symptoms usually develop following oral ingestion but may also appear following contact or by inhalation during cooking.3,4 Both of the reactions suffered by our case in relation to food had developed following oral ingestion.
A reaction may also develop following the first encounter with the food, as seen in our patient. Although the reason is not clear, prenatal sensitisation may be due to encountering the substance via the mother's milk before birth or previous ingestion of it without realising.3 There may be sensitisation to other foods as well in children with legume allergy. A study from Spain has found the concurrence of allergies to eggs, fish and tree nut legumes.3 Our case also had IgE-mediated food allergy related to eggs.
Lentils, chickpeas, beans and peas are consumed cooked. Both lentils and peas preserve their allergenic features after being boiled.3,9 The SPT has revealed that the swelling was larger with the boiled preparation compared to the commercial preparation for both lentils and chickpeas. Boiled chickpea preparation values have been reported as follows: sensitivity 97%, specificity 85%, positive predictive value 89%, and negative predictive value 89%.3 We performed an SPT with boiled chickpea water and the chickpea itself on our patient as we did not have the commercial chickpea preparation available. We found positivity with both.
Eliminating the food from the diet is required for food allergies. We eliminated both chickpeas and eggs from our patient's diet. We also provided an anaphylaxis action plan and adrenaline auto-syringe training to his family. Follow-up a year later with full elimination of eggs and chickpeas showed continuing chickpea and egg sensitivity on the SPT. Full elimination in the patient's diet is therefore continuing.
We wanted to use this case to emphasise concurrent legume and egg allergies, both consumed often in our country.
