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For those of us who enjoy the Mediterranean diet

Introduction

Chickpea (Cicer arietinum), a member of the Fabaceae family, is an essential source of plant-based proteins, fibers, vitamins, and minerals. Its consumption has increased significantly with the rise of vegetarian, vegan, and “plant-based” diets. However, in regions where it is a staple food —the Mediterranean, Middle East, and India— chickpea has also been recognized as a relevant cause of food allergies.

The clinical interest lies in its main storage proteins, vicilin (7S globulin) and legumin (11S globulin), which are potent allergens resistant to heat and digestion, explaining the persistence and severity of reactions.

Protein composition of chickpea

The protein content ranges between 18–24%, dominated by:

Globulins (65–70%)

Vicilin (7S globulin): protein of 150–180 kDa, highly resistant to gastric hydrolysis; considered the major allergen.

Legumin (11S globulin): hexamer of 320–400 kDa, with multiple IgE-binding epitopes.

Albumins (10–15%): water-soluble, generally involved in mild reactions.

Prolamins and glutelins: present in small amounts, with limited clinical relevance but potential cross-reactivity with other legumes.

Pathophysiology of allergy

Chickpea allergy is a classic IgE-mediated immune phenomenon, different from enzymatic intolerances such as lactose deficiency or A1/A2 beta-casein sensitivity.

1. Sensitization: resistant epitopes of vicilin and legumin cross the intestinal mucosa and are presented by dendritic cells.

2. Production of specific IgE: CD4+ T cells activate B lymphocytes, which differentiate into plasma cells producing chickpea-specific IgE.

3. Re-exposure: antigen–IgE binding on mast cells and basophils triggers release of histamine, tryptase, and leukotrienes.

4. Clinical manifestations: ranging from mild skin symptoms to anaphylaxis.

Clinical manifestations

Cutaneous: urticaria, angioedema, pruritus.

Respiratory: rhinitis, food-induced asthma.

Gastrointestinal: abdominal pain, diarrhea, vomiting.

Anaphylaxis: reported in severe cases after consumption of hummus or curry.

In children, chickpea allergy often coexists with sensitization to peanuts, soy, or lentils. In adults, it may be misinterpreted as chronic digestive intolerance or irritable bowel syndrome.

Diagnosis

Skin prick test: positive reaction to chickpea extract.

Specific serum IgE: detection against purified vicilin/legumin.

Oral food challenge (OFC): the gold standard, though carrying risk of severe reactions.

Cross-reactivity

High sequence and structural homology exists between chickpea proteins and those of peanut, lentil, and soy. Patients allergic to one legume may react to several, a clinically significant issue in vegetarian populations.

Management strategies

1. Strict avoidance
Currently, the only fully effective strategy is avoiding chickpeas and their derivatives (flour, hummus, falafel, soups, and processed foods containing them).

2. Food processing

Fermentation and germination: partially reduce allergenicity by hydrolyzing globulins.

High pressure and autoclaving: denature conformational epitopes, significantly decreasing IgE reactivity in experimental studies.

3. Immunotherapy

Oral immunotherapy (OIT): under investigation, with promising results in peanut and milk allergy; not yet standardized for chickpea.

Anti-IgE (omalizumab): approved for severe food allergies, may be an option for patients with legume-induced anaphylaxis.

4. Treatment of acute reactions

Antihistamines: for urticaria and mild symptoms.

Corticosteroids: for persistent reactions.

Intramuscular epinephrine: first-line treatment in anaphylaxis.

Prognosis

In children, chickpea allergy may resolve over time, though persistence into adulthood is not uncommon. Coexistence with other food allergies complicates long-term outcomes. Research in food processing and immunotherapy suggests a hopeful future with the possibility of inducing tolerance.

Conclusion

Chickpea allergy is centered on its storage proteins vicilin (7S) and legumin (11S), responsible for potentially severe reactions. Unlike milk, where A1/A2 beta-casein variants explain non-immunological sensitivities, chickpea represents a classical model of IgE-mediated plant protein allergy.

Diagnosis requires specific testing, and strict avoidance remains the cornerstone of management, though food processing, oral immunotherapy, and anti-IgE biologics provide an encouraging horizon.

Raul Ayala, MD