Seler – przyczyną ciężkiego wstrząsu anafilaktycznego

KOMUNIKAT O WYNIKACH BADAŃ

Seler – przyczyną ciężkiego wstrząsu anafilaktycznego

Krzysztof Pałgan 1 , Magdalena Götz-Żbikowska 1 , Marta Tykwińska 1 , Katarzyna Napiórkowska 1 , Zbigniew Bartuzi 1

1. Department of Allergology, Clinical Immunology and Internal Diseases, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, Poland

Opublikowany: 2012-03-14
GICID: 01.3001.0003.0868
Dostępne wersje językowe: pl en
Wydanie: Postepy Hig Med Dosw 2012; 66 : 132-134

 

Streszczenie

Przedstawiono przypadek 28-letniej pacjentki, u której wystąpił ciężki wstrząs anafilaktyczny po spożyciu surowego selera. Chora była w trakcie immunoterapii alergenowej (brzoza 50% i tra­wy 50%). Wstrząs wystąpił po 15 minutach po spożyciu selera. W terapii zastosowano adrenali­nę, glikokortykosteroidy oraz antazolinę.
Celem pracy jest zwrócenie uwagi na jednoczesne występowanie alergii wziewnej oraz pokar­mowej. W tego typu przypadkach rozważany jest udział reakcji krzyżowych, których znaczenie jest omawiane w pracy.

Słowa kluczowe:seler • wstrząs anafilaktyczny • reakcje krzyżowe

Summary

Background: We present a case of anaphylactic shock induced by celery ingestion in a 28-year old woman with pollinosis during allergen (50% birch, 50% grass) immunotherapy.
Case Report:
 A female patient, aged 28 was admitted to the clinic due to a serious anaphylactic reaction. The event took place 15 min after ingesting fresh celery. She recovered after routine treatment with adrenaline, corticosteroids and antazoline.
Conclusions:
 Our case shows the possibility of simultaneous occurrence of hypersensitivity to inhaled aller­gens and food. In such cases, it is considered part of cross-reactivity We discuss the importance of cross- reactivity associated with sensitization to pollen and vegetable foods.

Key words:celery • anaphylactic shock • cross-reactivity

It is a problem – sighed the celery
J. Brzechwa

Introduction

Analysis of the incidence of severe anaphylactic reactions after foods shows that in the past two decades the inciden­ce of food allergy has significantly increased [1]. The in­cidence of food hypersensitivity, allergic type, occurs in 2.4-4% of adults and in children ranges from 5-8% [5].

Celery (Apium graveolens), because of its taste and nutri­tional value, occupies an important position in the human diet. This vegetable contains twice as much vitamin C as citrus fruit and also contains vitamins B, PP, E and folic acid, as well as being a source of phosphorus, calcium, po­tassium and zinc [14]. However, in patients showing hyper­sensitivity, celery, like most vegetables and fruits, can cause symptoms. Particularly common celery can cause anaphy­lactic reactions in persons allergic to mugwort and birch pollen. It is estimated that as many as 71-95% of cases of pollinosis caused by birch show sensitivity for cellery [4].

Apium graveolens is one of the most important plant food allergen sources in the adult Central European. The most important celery allergens are PR-10 protein (Api g 1), non-specific lipid transfer proteins – LTP1 (Api g 2), pro­filin (Api g 4) and flavoprotein (Api g 5). Api g 2 and Api g 4 allergies are potentially dangerous for allergic indivi­duals because these allergens may induce an anaphylactic reaction as a result of cross-reactions between foods and inhaled allergens [7].

Case Report

A female patient, aged 28 was admitted to the Clinic of Department of Allergology, Clinical Immunology and Internal Diseases of the Collegium Medicum in Bydgoszcz due to a serious anaphylactic reaction after ingestion of raw celery. Originally there appeared abdominal pain located in the upper abdomen, generalized pruritic hives, swelling of the eyelids and lips, and general weakness and short­ness of breath. These symptoms occurred about 15 minu­tes after ingestion of raw celery. In the physical examina­tion, in addition to these abnormalities the following were observed: decrease in blood pressure to 60/40 mmHg, ta­chycardia (120/min.), tachypnöe (25 breaths/min.). The medical history taken from this patient revealed that for about three years the patient had had symptoms of seaso­nal allergic rhinitis, while after eating raw apples symp­toms in the oral cavity, such as burning, and swelling of the lips and cheeks, typical allergy symptoms of the oral cavity (oral allergy syndrome, OAS). Until then, she had not consumed raw celery. The skin tests showed an aller­gy to tree pollen (birch, alder, hazel), grass, weeds, fun­gi, moulds and apple. For 4 months the patient had been given Phostal® (Stallergen) desensitization vaccine (50% birch, 50% grass), the last dose of vaccine having been gi­ven 14 days before the onset of acute anaphylactic reaction.

Laboratory tests using Pharmacia UniCAP showed an ele­vated total IgE value of 287.27 IU/ml, while specific IgE against antigens of celery was 0.70 kU/l (class I), mixed early grasses 3.70 kU/l (class III), a mix of early trees, 1,20 kU/l (class II). A complete blood count revealed periphe­ral blood leukopenia (2.34 G/l), and a slight increase in the concentration of C-reactive protein (1.72 mg/l). The study showed β tryptase concentration of 18,6 µg/l.

Treatment consisted of epinephrine 1 mg im, dexametha­sone 16 mg im, antazoline 100 mg im, and 0.9% NaCl 500 ml. After this treatment normal blood pressure returned, shortness of breath was relieved and the patient felt better. After 24 hours the described skin lesions cleared.

Discussion

Epidemiological studies on the incidence of allergic hyper­sensitivity to birch pollen (Betula verrucosa) showed that this kind of pollinosis is the most common in Scandinavia, northern Russia and in Central Europe [9]. Birch pollen, after grass pollen, is the most common cause of pollinosis in Poland. The largest concentration of birch pollen is found in March-April [13]. A specific aspect of allergy to birch pollen is cross-reactions with other plants. According to Neudecker [11] the incidence of such reactions with birch pollen ranges from 50-93%. Since the description in 1948 of the first case of disease symptoms in the gastrointesti­nal tract in a child sensitized to tree pollens, research has been ongoing to explain this phenomenon. There is a hy­pothesis which suggests the participation of lectins in this type of reaction, because of the occurrence of this type of particles in both pollen and fruits and vegetables[17]. Rougé et al. [15] believe that lectin has the ability to con­nect to the IgE molecule and thus may trigger the release of histamine from mast cells. More convincing, however, are numerous studies discussing the importance of cross­-reactions in the presence of symptoms of the gastrointe­stinal tract in patients with pollinosis [3].

There are suggestions that a more than 70%-similarity of proteins present in pollen and foods causes the cross-re­activity. Although in the case of the birch allergen Bet v 1 and Api g 1 of celery there is only 40% amino acid sequ­ence similarity, there nevertheless occur cross-reactions and symptoms in the gastrointestinal tract in patients suf­fering from pollinosis [6]. The presented case shows that such reactions can even lead to the occurrence of dange­rous anaphylaxis. Cross-reactions may occur not only be­tween birch and celery allergens, but between birch pol­len and apple, birch-mugwort and celery, or birch-plantain and celery [10]. In connection with this, the groupings of birch-apple, birch-celery, birch-mugwort-celery and final­ly birch-plantain-celery have been described [8]. A tho­rough analysis of the co-occurrence of food allergies and inhalation allergies revealed a large number of foods that can cause cross-reactions with pollen [11,12]. Therefore, Yagami [17] proposed to identify such reactions as pollen­-food syndrome – PFS). The PFS would include OAS and severe anaphylactic reactions, as well.

Diagnosis of this case once again proves that taking a me­dical history plays an important role in the diagnosis of al­lergy. Virtually immediate symptoms in the circulatory and respiratory systems were indicators of the onset anaphylac­tic shock. The performed laboratory tests, and especially β tryptase levels, confirmed an acute anaphylactic reaction [16]. The development of the early-phase response is asso­ciated with immediate degranulation of mast cells. In addi­tion to histamine and other mediators, tryptase is also re­leased from mast cells. According to Arnold and Wiliams [2] elevated levels of this enzyme protein are a good mar­ker of acute anaphylactic reaction.

Analyzing this case, the question arises whether there is an association between the occurrence of anaphylaxis and the conducted allergen immunotherapy. However, the inte­rval which occurred between the last dose of allergen im­munotherapy, and the incident of shock is likely to exclu­de a causal relationship.

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The authors have no potential conflicts of interest to declare.

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