Allergy syndrome, oral T78.4

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 29.10.2020

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Contact urticaria syndrome; OAS; oral allergy syndrome

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Allergic, IgE-mediated food allergy, in which mucosal contact urticaria develops only a few minutes after consumption of raw vegetables or fruit. It is caused by a type I allergy to various foods. The most common OAS-causing foods are: apples, raw vegetables, carrots, celery, almonds, nuts, kiwi, pumpkin seeds, chicken protein, citrus fruits, cinnamon et al. which also trigger localized to generalized urticarial reactions on contact with the intact dermis. The OAS is the most common food allergy.

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In the general population up to 10% are affected.

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The cause is a secondary food allergy in the context of a cross-allergy with pollen allergens (e.g. Bet v 1 homologous allergens, profilins). After penetration of the allergen into the skin or mucous membrane, IgE-mediated degranulation of dermal or mucosal mast cells occurs and mediators, i.e. inflammation-promoting substances such as histamine, are released.

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Most frequently occurring in cases of sensitization to birch, grass and mugwort pollen (see below pollinosis) (see below cross-reactions). Also affected are persons who have ample (intensive) skin contact with food due to their profession or hobby, e.g. cooks, fish sellers, bakers, vegetable sellers etc.

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In most cases all places of contact with the corresponding allergen are affected, these are mostly the hands, forearms, oral cavity, lips.

Clinical features
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Immediately after eating the food, a furry feeling in the oral cavity, followed by swelling of the lips and tongue, hoarseness, laryngeal tightness (laryngeal edema), difficulty swallowing and difficulty breathing. Rare gastrointestinal complaints such as stomach cramps, vomiting and nausea. Occasionally erythema and vesicles develop. In rare cases anaphylaxis symptoms occur (especially when celery and soya are consumed).

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Total serum IgE normal or elevated; specific IgE elevated.

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Careful anamnesis, rubbing and if necessary prick test with the suspected allergen. Determination of the specific IgE.

Internal therapy
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  • For itching peroral application of non-sedative H 1 antagonists such as desloratadine or levocetirizine. In case of severe symptoms: Antihistamines i.v. such as Dimetinden (e.g. Fenistil) 1-2 times/day 1 amp. or Clemastin (e.g. Tavegil) 2-4 mg, later switch to oral anthistamine. Glucocorticoids in medium dosages such as prednisolone (e.g. Solu Decortin H) 80-100 mg initial i.v. with gradual dose reduction depending on the clinic and later conversion to an oral preparation such as methylprednisolone (e.g. Urbason) or prednisolone.
  • Generalized form with mucosal involvement and angioedema: volume substitution, glucocorticoids in high doses i.v. like prednisolone (e.g. Solu Decortin H) 250-500 mg/day, possibly even higher. After clinical findings, repeated administration may be necessary. Gradual dose reduction according to clinical findings 250-150-100-75-50-25 mg/day and switch to oral preparation such as methylprednisolone (e.g. Urbason).
    Antihistamines initial e.g. Dimetinden (e.g. Fenistil) 4 mg i.v. (conversion to oral medication up to 6 mg/day, reduction according to clinic) or Clemastine (e.g. Tavegil) 2-4 mg/day.
  • For laryngeal glottis oedema: additional adrenalin (suprarenin 1:1000) 0.3-0.5 ml s.c. repeated administration possible. In highly acute cases: After diluting 1 ml of the commercially available epinephrine solution (1:1000) to 10 ml or using a pre-filled epinephrine syringe (1:10 000), 0.5-1.0 ml (= 0.05-0.1 mg epinephrine) is first injected slowly i.v. (0.1 mg/min.) under pulse and blood pressure control. Cave! A maximum dose of 1 mg adrenaline should not be exceeded as a rule. Oxygen administration 4-6 l/min. Intubation if possible and necessary; otherwise coniotomy, Ultima ratio: tracheotomy.
  • Especially in cases of respiratory distress and concomitant obstructive respiratory disease terbutaline sulphate (e.g. Bricanyl) 0.5-2.0 mg i.v. or fenoterol (e.g. Berotec dosage aerosol) 1 time 1-2 strokes.
  • Generalized form with angioedema and anaphylactic shock: Stage-specific shock therapy, see also Urticaria, acute.

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Cheap. Patients can often name the triggering antigen and seek early medical treatment in case of recurrence due to repeated exposure.

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In case of cross-reacting OAS (e.g. birch pollen sensitization), SCIT promises an improvement of oral allergy symptoms. S.a. food allergy.

Diet/life habits
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Strict avoidance of the triggering allergens

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  • Cave! Toxic reactions, e.g. by enzyme-containing food or hot spices, can cause false positive reactions in the rubbing test. In case of doubt, healthy control persons should always be tested as well. Many allergens change or denature by heating! For the rubbing test always use the anamnestically relevant allergen.

  • An oral allergy syndrome can be relevant for a patient, e.g. a cook, from an occupational dermatological point of view (see below occupational skin disease / case report).

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  1. Amlot PL, Kemeny DM, Zachary C, Parkes P, Lessof MH (1987) Oral allergy syndrome (OAS): symptoms of IgE-mediated hypersensitivity to foods. Clin Allergy 17: 33
  2. Cadot P et al (2003) Oral allergy syndrome to chicory associated with birch pollen allergy. Int Arch Allergy Immunol 131: 19-24
  3. De Waard-van der Spek FB et al (1998) Diagnostic tests in children with atopic dermatitis and food allergy. Allergy 53: 1087-1089
  4. Osterballe M et al (2003) Diagnostic value of scratch-chamber test, skin prick test, histamine release and specific IgE in birch-allergic patients with oral allergy syndrome to apple. Allergy 58: 950-953
  5. Schwarz I et al (2016) Mucosal diseases from an allergological point of view. Dermatologist 67:780-785
  6. Sloane D, Sheffer A (2001) Oral allergy syndrome. Allergy Asthma Proc 22: 321-325
  7. Wakelin SH (2001) Contact urticaria. Clin Exp Dermatol 26: 132-136


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Last updated on: 29.10.2020