Most Common Allergic Diseases: Historical Reflections in Understanding Bergmann K-C, Ring J (eds): History of Allergy. Chem Immunol Allergy. Basel, Karger, 2014, vol 100, pp 109–119 DOI: 10.1159/000358616
History of Food Allergy
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Brunello Wüthrich Faculty of Medicine, University of Zurich, Zurich, Switzerland
In this chapter we will first consider whether there is real evidence on the basis of literature for early descriptions in antiquity of pathogenic reactions after food intake that could be comparable to allergy, for instance in the scriptures of Hippocrates or Lucretius. On this topic we are skeptical, which is in agreement with the medical historian Hans Schadewaldt. We also assert that it is unlikely that King Richard III was the first food-allergic individual in medical literature. Most probably it was not a well-planned poisoning (‘allergy’) with strawberries, but rather a birth defect (‘… his harm was ever such since his birth’) that allowed the Lord Protector to bring Mylord of Ely to the scaffold in the Tower, as we can read in The History of King Richard III by Thomas More (1478– 1535; published by his son-in-law, Rastell, in 1557). In 1912, the American pediatrician Oscar Menderson Schloss (1882–1952) was probably the first to describe scratch tests in the diagnosis of food allergy. Milestones in the practical diagnosis of food allergy are further discussed, including scratch tests, intradermal tests, modified prick tests and prick-to-prick tests. False-negative results can be attributed to the phenomenon of a ‘catamnestic reaction’ according to Max Werner (1911–
1987), or to the fermentative degradation of food products. Prior to the discovery of immunoglobulin E, which marked a turning point in allergy diagnosis, and the introduction of the radioallergosorbent test in 1967, several more or less reliable techniques were used in the diagnosis of food allergy, such as pulse rate increase after food intake according to Coca, the leukopenic index, drop in basophils or drastic platelet decrease. The ‘leukocytotoxic test’ (Bryan’s test), today called the ‘ALCAT’ test, shows no scientific evidence. The double-blind placebo-controlled food challenge test remains the gold standard in the diagnosis of food allergy. For the future, component-resolved diagnostics with the use of recombinant molecular allergens or chip arrays, such as the ISAC technique, hold a lot of promise. With regard to the clinical situation, a subjective selection is given, touching on the pollen-associated food allergies (‘birchmugwort-celery-spice syndrome’), as well as the new phenomenon of lethal food allergies that have appeared since the 1980s. Finally, rare ways of elicitation of a ‘derivative allergy’, first described by Erich Fuchs (1921–2008), for example by kissing, as well as ‘oral allergy syndrome’ and oral hyposensitization are considered. © 2014 S. Karger AG, Basel
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Abstract
In classic antiquity the teaching of the four humors led to the term ‘idiosyncrasy’, which was probably used for unexpected allergic reactions. In this context, Hippocrates and Lucretius are quoted as first descriptors of ‘idiosyncratic’ reactions to food. This will be briefly discussed here. Hippocrates (460–375 BC), the father of medicine, is assumed to have given the first description of cheese allergy. In chapter 20 of the Corpus Hippocraticum (‘About Antique Medicine’) from the 5th century BC, we can read, according to Hans Schadewaldt: Cheese occasionally could be a ‘dangerous food’, because it causes discomfort in those who fill themselves with it. [1]
And the following: Also wine in high amounts consumed might usually cause complaints. But with the cheese there is the special situation that it causes pain only in certain individuals whose constitution of humors is not compatible with cheese, who so to speak are enemies to cheese.
Unfortunately there is no description of the nature of the complaints suffered by individuals after the consumption of cheese or wine. It is impossible to really evaluate whether these conditions were allergic or due to enzymatic intolerance (lactase deficiency or histamine intolerance). Most likely it was an exaggerated dose that led to the symptoms. The therapy of this condition was clear-cut and effective: ‘Don’t eat cheese.’ The following often-quoted verse from Titus Lucretius Carus (109–150 BC) is usually taken as the first description of food allergy: What is normal food for one, may be strong poison for another one. [2]
However, when we read literally the corresponding verses in his epos De natura rerum [3], the quotation is: Nunc aliis alius qui sit cibus ut videamus expediam, quareve aliis quod triste et amarum est; hoc tamen esse aliis possit perdulce videri. Tantaque in his rebus distantia differitasque est, ut quod aliis cibus est aliis fiat acre venenum, at capris adipes et cocturni cibus auget!
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Again, according to Schadewaldt [4], Lucretius made note of an observation that certain animals are able to eat certain weeds without damage to their health, but the same plants are poisonous to other animals. In detail, he describes that hemlock, for example, is a poison for humans, but provides good nutrition for goats and quails, probably due to different enzymatic metabolic processes in different species. Furthermore, Lucretius describes differences in taste between animals and human beings – ‘the leaves of olive trees obviously are delicious food for bearded goats, but for humans of utter bitterness’: Quippe videre licet pinquescere saepe cicuta barbigeras pecudes, homini quae est acre venenum.
Now we turn to Shakespeare and the character of Richard III, purportedly the first food-allergic individual in medical literature (fig. 1); but what is the truth? We read in act 3, scene 4: My lord of Ely, when I was last in Holborn I saw good strawberries in your garden there. I do beseech you send for some of them. Marry and will, my lord, with all my heart. Where is my lord the Duke of Gloucester? I have sent for these strawberries.
After the herald arrived, the monarch ostentatiously ate one of the strawberries and continued with the trial. One hour later he caused consternation among the assembly of lords when he revealed his arm by pushing back the sleeve of his shirt, and said: I pray you all, tell me what they deserve That do conspire my death with devilish plots Of damned witchcraft, and that have prevail’d Upon my body with their hellish charms? … Then be your eyes the witness of their evil. Look how I am bewitch’d; behold, mine arm Is like a blasted sapling wither’d up.
Obviously, it was not an acute strawberry-induced urticaria that afflicted King Richard III, as we allergists like to claim, but was probably a birth defect that brought Mylord of Ely to the scaffold of the Tower.
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Food Allergy in Antiquity and the Middle Ages: Myth or Reality?
Fig. 1. King Richard III of England (1452–
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First Documentation of Food Allergy – Skin Test as Diagnostic Routine Method The first scientific report of food allergy can be found from the beginning of the 20th century [5]. In 1912, the American pediatrician Oscar Menderson Schloss [6] (1882–1952; fig. 2) was the first to diagnose food allergy by skin tests. He could prove that a case of allergy was due to the consumption of egg, since a scarification test (scratch test) with hen’s egg white was positive. He was also able to test isolated fractions of hen’s egg white and to note that ovomucoid apart from ovoglobulin and ovomucin were the strongest elicitors of allergic skin reactions. He also tested oatmeal and almonds. His paper is a milestone in the history of allergy. Following a further publication [7], the scratch test, which was originally introduced by Blackley in 1873 for the detection of pollen allergy [5], became the routine method in the diagnosis of food allergy. In 1908, Mendel and Mantoux introduced the intradermal test as a tuberculin test, which was then used by Cooke and van der Veer in 1916 for testing aeroallergens [5]. With this method, Karl Prausnitz (1876–1963) and Heinz Küstner (1897–1963) succeeded in passively transferring fish allergy using the serum of an allergic individual [8]. Soon it became apparent that intradermal tests with foods could be false negative, either with exclusively gastrointestinal symptoms because the skin was not the ‘shock
History of Food Allergy
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organ’, or because the relevant allergens were denatured during the extract production. Some authors mentioned that fermentative metabolites could have sensitizing properties [9–11]. The observation of Max Werner (1911–1987) is of interest when he stated a ‘catamnestic skin reaction’ [12] where intradermal tests with food allergens only became positive after a 10- to 14-day elimination diet, an observation which was confirmed by other authors [13]. The modified prick test was developed by Helmtraut Ebruster and published in 1959 in relation to aeroallergens [14]. Using the knowledge of the 1970s that skin tests with commercial extracts from foods and vegetables often yielded false-negative results, in the examination of these allergens the prick-to-prick test method was increasingly used besides scratch tests with native material [15, 16]. The test needle was first pricked into the fresh fruit or vegetable and then pricked into the skin of the patient (fig. 3).
Other Test Methods for Food Allergy Prior to the Discovery of Immunoglobulin E Since cutaneous testing with food allergens often remained unreliable (either false negative or false positive), besides attempts at re-exposure, other test methods were employed. However, these were also not totally reliable. Examples include the increase in pulse rate according to Coca after food exposure
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1485). He probably was not the first documented patient with strawberry allergy. Fig. 2. Oscar Menderson Schloss (1882– 1952), the first author to describe the ‘scratch test’ and the first documented case of food allergy.
Fig. 3. Prick-to-prick tests with raw apples and vegetables.
Radioallergosorbent Test – Significant Progress in the Diagnosis of Immunoglobulin E-Mediated Food Allergies The discovery of immunoglobulin (Ig) E as a new class of immunoglobulins with reagin activity and the development of sensitive and quantitative in vitro methods like the radioimmunosorbent test for the determination of total serum IgE [27], or the radioallergosorbent test (RAST) for detection of circulating antibodies with IgE specificity [28], without doubt represents a major advancement in allergy diagnosis, including food allergy. By using highly purified cod fish allergen extracts in children with allergic symptoms after fish consumption, 100% concordance be-
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tween history, RAST and skin test was found [29]. The spectrum of available food species for IgE determination was gradually extended; however, it was also recognized that the diagnostic reliability of RAST as a skin test is limited. Positive IgE detection only measures sensitization against the food, but does not prove clinical relevance, indicating the occurrence of allergy symptoms after exposure. In contrast, the lack of detection of serum IgE antibodies against foods by RAST or other modified in vitro techniques, such as the ImmunoCAP FEIA (fluor enzyme immunoassay), cannot exclude a certain kind of food as the cause of the elicitation of symptoms. Many food extracts are poorly standardized. Degradation of allergenic proteins during the extraction process represents a common phenomenon, resulting in too low concentrations of allergens in the final extracts. On the other hand, similar molecular structures in foods and aeroallergens (pollen, house dust mite, latex, etc.) give rise to multiple positive results in skin tests and RASTs due to cross-reacting IgE antibodies [30].
Component-Resolved Diagnostic Techniques A new promising strategy to distinguish crossreactions from genuine co-sensitizations as possible therapeutic consequences can be seen in the use of recombinant allergens which are already available for the ImmunoCAP System (Phadia, Thermo Fisher, Uppsala, Sweden). The component-resolved diagnostics, namely the detection of the specific IgE against molecular marker proteins within foods, is able to distinguish relevant from irrelevant sensitizations [31]. At the same time, allergologic research in
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[17], the leukopenic index [18], drop in basophil leukocytes [19], the platelet drop [20, 21] and – in patients with exclusively gastrointestinal symptoms – complex exposure tests at the small intestine [22]. At the end of the 1950s, Black and Bryan developed a leukocytotoxic test (Bryan’s test) for the detection of allergies against foods and additives based on the microscopic evaluation of activation-induced alterations or autolysis of leukocytes after adding food or food extracts to the blood. This test was not registered for proving allergies in the USA because of unreliability [23, 24]. The ALCAT test (antigen leukocyte cellular antibody test) or leukocyte activation test, which even nowadays is still advertised as a diagnostic method for qualitative determination of food intolerances, is nothing more than a modified Bryan test. Many national and international societies state that this test cannot be used in the diagnosis of food allergy [25, 26].
Double-Blind Placebo-Controlled Food Challenge – The Gold Standard and the Diagnosis of Food Allergy Oral provocation tests are often the last diagnostic opportunity to detect actual food allergy or intolerance. The so-called double-blind placebo-controlled food challenge (DBPCFC) is regarded as the only scientifically accepted detection method of food allergy or intolerance [30]. Even if the DBPCFC is the gold standard of clinical studies, this procedure is rather complex for routine diagnosis and only used in special allergy centers since provocation tests can always implicitly lead to generalized anaphylactic reactions.
Fatal Food Allergies A fatal reaction after a food challenge was published in 1926 [33]: an 18-month-old infant with atopic eczema and three episodes of generalized allergic reaction after the consumption of a few spoons of pease pudding was tested under in-patient conditions at a pediatric hospital during the lunch break when the head nurse gave a carrot/pea mixture to the infant. Immediately after the application the child developed angioedema, cyanosis and shock, and died in spite of intensive emergency treatment. The first case of a spontaneous fatal allergic food reaction was published 25 years ago [34]. A 24-year-old female patient with peanut allergy died after eating a cake. The Canadian pa-
History of Food Allergy
tient had repeatedly eaten and tolerated hazelnut cake with marzipan and almond icing. However, a short time after eating a few bites of the cake she suddenly developed a severe allergic reaction leading to suffocation and death. The forensic autopsy of this extraordinary case revealed that the paste used for the icing of the cake contained ‘arachides’, a name for peanuts that was not known to the English-speaking baker. Fatal or potentially fatal or life-threatening allergic reactions to foods in infants and children are unfortunately no rarity any more, especially in adolescents and young adults. Since the end of the 1990s, a series of fatal cases have been published in the USA, mostly after exposure to hidden food allergens, commonly peanuts, but also other tree nuts, Brazil nut and cashew nut, and also cow’s milk, hen’s egg, fish and crustacea (lobster, crabs) [35–37]. The lay press regularly reports such fatalities [38]. It is estimated that in the USA approximately 120 fatal cases occur each year due to anaphylactic reactions against foods. Hidden allergens, for example peanut allergens in sweets or chocolate, often make avoidance strategies difficult or impossible in spite of improved declaration rules.
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Pollen-Associated Food Allergies and the ‘Oral Allergy Syndrome’ At the end of the 1970s, Scandinavian allergists reported that 30–50% of patients with pollinosis against birch, hazel or alder pollen suffer from untoward symptoms like itch in the lips or the palate after eating raw apples. Similar symptoms were reported after consumption of other fruits, raw carrots or celery [39, 40]. A sensitization was proven by scratch or prick-to-prick tests with fresh materials [15, 16, 40, 41]. The most common symptoms in this oral ‘contact urticaria syndrome’ [42] or ‘oral allergy syndrome’ [43, 44] often start immediately after contact with certain foods, especially apples, raw vegetables, celery, nuts, hazel nuts and almonds. They are not necessarily only itch or swelling of the lips and tongue, or in the cavum oris or the palate, but can also be hoarseness due to discrete laryngeal edema, difficulties in swallowing and dyspnea. Furthermore, sneezing, rhinorrhea, obstruction of the nose ventilation and conjunctivitis can be observed.
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recent decades has identified marker allergens for certain disease conditions, respective of clinical symptoms, for example wheat-dependent exerciseinduced anaphylaxis (WDEIA) with s-IgE against rTri-α-omega-5-gliadin. With the immuno solidphase allergen chip (ISAC), we now have a test system for in vitro diagnosis that allows the analysis of a large number of allergen components in a single step. Using the ISAC technology, many relevant allergy elicitors can be measured in one analysis with a rather small volume of patient serum [32]. Due to the magnitude of the results and relatively high costs, the ISAC test should only be used by allergists or physicians with special knowledge in the field.
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celery is not the urticariogenic substance, because it did not yield any reaction.’ While the first botanic taxonomical associations with Rosaceae (the rose family) and Apiaceae (or Umbelliferae; known as carrot or parsley family) were suspected, it soon became apparent that several allergens, especially Bet v 1 and Bet v 2 (profilin), in birch pollen were responsible for these cross-reactivities [59–61] (fig. 4). The thermostable allergen in mugwort pollen and celery is yet to be identified; however, a lipid-transfer protein is most likely [62].
‘Derivative Allergy’ – A Rare Pathway of Elicitation of Food Allergy The elicitation of food allergy via a mediator in the form of a second person (mother, partner) was described as the phenomenon of ‘derivative allergy’ in 1954 by Erich Fuchs [63]. The first report of a kissinduced oral allergy syndrome described a birch pollen-allergic woman who developed symptoms after kissing her boyfriend, who had eaten an apple. An even more severe reaction occurred in a highly sensitized peanut-allergic man after kissing his girlfriend, who again had eaten a few peanuts 2 h previously [55, 64–68]. In one case it was possible to use the saliva of a man, who had eaten a suspected fruit, to elicit positive skin prick tests in his birch and grass pollen-allergic girlfriend, but only when the saliva was used within 5 min after the consumption of the fruit (e.g. kiwi), probably due to the instability of the birch pollen cross-reactive kiwi allergen [66]. This phenomenon is not at all rare: out of 379 allergic individuals with severe life-threatening reactions to peanuts and tree nuts, 20 (5.3%, 4 males, 16 females) reported to have suffered from a reaction after kissing. The symptoms ranged from oral allergy syndrome, lip swelling, massive angioedema and lid swelling to dyspnea with expiratory wheezing in 4 cases [68]. In most cases the symptoms occurred between less than 1 min and 30 min after the kiss, but occasionally also after some hours (indicating the stability of peanut and tree nut allergens). Recently, the media reported a fatal anaphylaxis in a 15-yearold Canadian girl with severe peanut allergy after kissing a friend who had eaten a peanut butter sand-
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Classical immediate symptoms of gastrointestinal food allergy like gastric cramps, vomitus, nausea, abdominal pain, colic or diarrhea are rare in patients with oral allergy syndrome [13, 45]. Recent investigations using molecular allergens in patients with oral allergy syndrome showed that a sensitization to birch pollen often reflects the thermolabile major antigen Bet v 1 [46, 47]. Birch pollen-associated food allergy has been shown to occur in 40–93% of birch pollen-allergic individuals in various studies. At the beginning of the 1980s, several authors from Finland [45], Sweden [48], Germany [49], Austria [50], France [51, 52] and Switzerland [13, 53] independently reported anaphylactic reactions or shock fragments after the consumption of celery in association with birch, mugwort pollen or spice allergy. The term, ‘celery-mugwort-spice syndrome’ or ‘celery-carrot-mugwort-spice syndrome’ was proposed [53–56]. It was stressed that in these patients the consumption of celery root (celeriac), either boiled, raw or used as a spice in soups, was able to elicit severe reactions in contrast to cases of birch pollen-associated celery allergy, in which only raw celery, and not cooked celery, induced symptoms, mainly oral allergy syndrome. The first publication of a celery allergy comes from Zurich [57] and was proven for the first time using DBPCFC in 2000 [58]. In 1926, Werner Jadassohn and Margarete Zaruski described a young woman who developed urticaria, dyspnea and fever at three different times after eating celery. Other ‘idiosyncrasies’ were unknown, except for a mild hay fever [57]. After application of celery juice to the skin treated with abrasive paper or scratching, wheals with red flares occurred, while the application of the same celery juice to healthy skin did not induce reactions. The allergen was regarded as ‘coctostabile’ since the affect was not diminished after 5 min of boiling. The pellets developed during boiling and dialysis were as effective in the skin test as the supernatants. According to Prausnitz and Küstner the transfer was positive in 18 out of 20 volunteers, including with celery dialysate, while when the serum was heated for over half an hour to 56 ° C the sensitizing properties were lost. The authors postulated that: ‘our antigen most likely is not a protein and probably not a very high molecular substance and that the substance apiol from
Apiaceae (or Umbellifereae) celeriac (celery root) cooked celery spice celery stalk, cooked Solanaceae chili pepper red pepper tomato potato raw
Asteraceae
Mugwort pollen (Asteraceae or Compositae)
artichoke tarragon camomile wormwood
ragweed dandelion sunflower chrysanthemum
2
Piperaceae green pepper black pepper
Cucurbitaceae melon cucumber, pumpkin
Apiaceae (or Umbellifereae) celery root (or celeriac) raw dill aniseed fennel carrot raw lovage coriander parsley cumin
Labiatae basil majoram oregano thyme
Rosaceae Betulaceae hazelnut
Birch pollen (Betulaceae)
apple raw peach raw apricot raw almond
pear raw plum raw cherry raw strawberries raw
Exotic fruits kiwi litchi
Fig. 4. Birch and mugwort pollen-associated food allergy.
History of Food Allergy
Food-Induced/Food-Dependent ExerciseInduced Anaphylaxis In 1979, American authors observed a phenomenon in which an allergic sensitization was elicited in a marathon runner only after the concomitant exposure of physical exercise and food, while exercise alone or consumption of the food alone were each tolerated without reaction [71]. The term ‘food-de-
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wich [69]. Also, a case of food allergy elicited by sexual intercourse was reported as ‘connubial allergy’ [70]. The eliciting allergen was from Brazil nuts which had been eaten by a man prior to intercourse with his girlfriend, who was severely allergic to nuts. Prick tests with sperm were negative before and positive after Brazil nut consumption. Thus, foods eaten by other persons can endanger the life or the quality of life of food-allergic individuals.
2 1
1 Years
0
a
3
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Start OMD 1:10 250 ml
1
K
50 g Gruyère
SPT ±
SPT – Cheese fondue
Pasta
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**
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pendent exercise-induced anaphylaxis’, or FDEIA, was coined in 1983 [72]. FDEIA is quite common today, especially after wheat (WDEIA; see above) [73] and has to be differentiated from exercise-induced anaphylaxis [74] and idiopathic anaphylaxis [75].
Oral Desensitization – Long Controversial, but Now Established On several occasions since the 1980s we have published, initially in the German literature [13, 76– 79] and later in international medical literature [80, 81], the possibility of oral desensitization in food allergy, especially with untreated cow’s milk. Some authors have repeated our results [82–84]. However, the European Academy of Allergy and Clinical Immunology, EAACI, did not accept this technique, since there were no placebo-controlled studies and
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SPT milk –; SPT cheese –
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thus no ‘scientific evidence regarding efficacy’(!). Experts violently rejected this stance [85]. Meanwhile, the method was re-discovered by pediatricians who did not even quote the first articles in the literature [86–89]. In severe allergy oral desensitization with food can be performed, however, under utmost caution: the treatment has to be started with adequate dilutions of the allergen and under emergency conditions. Lack of success may be explained by very low tolerance thresholds on the one hand, or a too rapid increase on the other hand. After reaching the maintenance dose it is important that the tolerated food is consumed every day since even short intervals can break the tolerance. This first phase may be called tolerance induction; the later application over months or years then leads to true desensitization and can be proven in negative test results in skin tests and RAST against milk proteins such as casein (fig. 5). In a series of 16 patients with IgE-mediated
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Class
3
Class
[skin prick tests (SPT) and specific IgE (RAST) results] under oral desensitization with cow’s milk in 2 patients with severe allergic reactions after intake of a small amount of cheese or hidden diary products. a Case 1, 29-year-old female: SPT with cheese (Gruyère) +++; RAST to milk class 4. Oral milk desensitization (OMD) started with a drop of 1: 100 milk:water dilution, increasing the dose to 250 ml of undiluted milk daily without any interruption. After 2 years the SPT and RAST became negative and the patient could eat a cheese fondue and other dairy products without any problems. * = Dyspnea, eyelid edema. b Case 2, 45-year-old female: SPT with raw cow’s milk ++; RAST to milk class 4. After 6 months under a strict elimination diet, OMD was started with a drop of 1: 10 milk:water dilution, increasing to 250 ml of undiluted milk daily without any interruption. The SPT became negative after 4 years, and the RAST only after 5.5 years, so that the daily intake of 250 ml milk was stopped and the patient could drink milk and eat dairy products. After 6 years, the patient could eat a cheese fondue. ** = Urticaria, cramps; K = ketotifen.
SPT milk –; SPT cheese +++
4
Fig. 5. Clinical and immunological course
cow’s milk allergy, in 50% of cases complete tolerance to cow’s milk and cheese was induced after a 3- to 5-year treatment program [80]. In 4 patients (25%) partial tolerance could be induced; these patients were able to consume at least 1 dl of cow’s milk every day together with some cheese, but not hard cheese. In 4 patients (25%) oral hypersensitization had to be stopped because of repeated allergic
reactions occurring even with low doses and concomitant therapy with antihistamines or ketotifen [80]. Acknowledgement I would like to thank Johannes Ring for the English translation.
2 References
History of Food Allergy
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27 Johansson SGO, Bennich H, Wide L: A new class of immunoglobulin in human serum. Immunology 1968;14:265–272. 28 Wide L, Bennich H, Johansson SGO: Diagnosis of allergy by an in vitro test for allergen antibodies. Lancet 1967;ii:1105–1107. 29 Aas K, Lundvist U: The radioallergosorbent test with a purified allergen from cod fish. Clin Allergy 1973;3:255. 30 Bruijnzeel-Koomen C, Ortolani C, Aas K, Bindslev-Jensen C, Björstén B, MoneretVautrin D, Wüthrich B: Adverse reactions to food. Allergy 1995;50:623–635. 31 Ballmer-Weber BK, Scheurer S, Fritsche P, Enrique E, Cistero-Bahima A, Haase T, Wüthrich B: Component-resolved diagnosis with recombinant allergens in patients with cherry allergy. J Allergy Clin Immunol 2002;110:167–173. 32 Ott H, Baron JM, Heise R, Ocklenburg C, Stanzel S, Merk HF, Niggemann B, Beyer K: Clinical usefulness of microarray-based IgE detection in children with suspected food allergy. Allergy 2008;63:1521–1528. 33 von Stark K: Primäre spezifische Allergie und idiosynkratrischer Schock. Monatsschr Kinderheilkd 1926;32:119–127. 34 Evans S, Skea D, Dolovitch J: Fatal reaction to peanut antigen in almond icing. Can Med Assoc J 1988;139:232–233. 35 Yunginger JW, Sweeney KG, Sturner WQ, Giannandrea LA, Teigland JD: Fatal foodinduced anaphylaxis. JAMA 1988; 260: 1450–1452. 36 Sampson HA, Mendelson L, Rosen JP: Fatal and near-fatal anaphylactic reactions to food in children and adolescents. N Engl J Med 1992;327:380–384. 37 Wüthrich B: Lethal or life-threatening allergic reactions to food. Invest Allergol Clin Immunol 2000;10:59–65. 38 Wüthrich B: Lethal or life-threatening food anaphylaxis: notes from the ‘lay press’. Allergy Clin Immunol Int 2003; 15: 175–180.
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1 Schadewaldt H: Magen-Darmallergie; in Schadewaldt H (ed): Geschichte der Allergie. Deisenhofen, Dustri, 1983, vol 4, pp 37–51. 2 Panzani R: Cypress and food allergy: was it suspected in antiquity? J Asthma 1985; 22; 223–226. 3 Lucretius TC: De natura rerum; in Güthling O (ed): Von der Natur der Dinge, ed 2, revised. Leipzig, Reclam, 1927. 4 Schadewaldt H: Geschichte der Allergie. Deisenhofen, Dustri, 1983, vol 1, p 22. 5 Schadewaldt H: Geschichte der Allergie. Deisenhofen, Dustri, 1983, vol 1, pp 403– 404. 6 Schloss O: A case of food allergy. Idiosyncrasy to eggs, almonds and oats, due to anaphylaxis. Arch Paediat 1912;29:219. 7 Schloss OM: Allergy to common food. Arch Paediat 1915;32:349. 8 Prausnitz K, Küstner H: Studien über die Überempfindlichkeit. Zbl Bakt 1921; 86: 160. 9 Cooke RA: Protein derivatives as factors in allergy. Ann Int Med 1942;16:71. 10 Blamoutier P: Allergie digestive: sensibilisation à un produit de désintégration de la protéine alimentaire. Presse Méd 1945; 53: 162. 11 Wüthrich B, Schwarz-Speck M: Milch- und Hühnerei-Eiweiss-Allergie: Ausfall der Hautteste mit Gesamtextrakten und mit Hydrolysaten. Dermatologica 1970; 141: 102–112. 12 Werner M: Über die katamnestische Hautreaktion. Acta Allergol 1959;14:51–65. 13 Wüthrich B: Nahrungsmittelallergie. Allergologie 1981;4:320–328. 14 Bergmann KC, Aberer W: Aus der Geschichte der Allergologie: Frau Helmtraut Ebruster – die vergessene Autorin des modifizierten Pricktests. Allergologie 2011; 34:599–600. 15 Storck H, Wüthrich B: Allergie-Diagnostik (in vivo) bei allergischen Erkrankungen der Haut und innerer Organe; in Braun-Falco
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53 Wüthrich B, Hofer T: Nahrungsmittelallergie: das ‘Sellerie-Beifuss-Gewürz-Syndrom’: Assoziation mit einer MangofruchtAllergie? Dtsch Med Wochenschr 1984;109: 981–986. 54 Wüthrich B, Dietschi R: Das ‘SellerieKarotten-Beifuss-Gewürz-Syndrom’: Hauttest- und RAST-Ergebnisse. Schweiz Med Wochenschr 1985;115:358–364. 55 Stäger J, Wüthrich B: Association de l’allergie au céleri à l’allergie aux épices. Résultats des RAST aux épices chez des patients présentant une allergie au céleri. Rev Fr Allergol 1987;27:137–141. 56 Wüthrich B, Stäger J, Johansson SGO: Celery allergy associated with birch and mugwort pollinosis. Allergy 1990:45:566–571. 57 Jadassohn W, Zaruski M: Idiosynkrasie gegen Sellerie. Arch Derm Syph 1926;151:93– 97. 58 Ballmer-Weber BK, Vieths S, Luttkopf D, Heuschmann P, Wuthrich B: Celery allergy confirmed by double-blind, placebo-controlled food challenge: a clinical study in 32 subjects with a history of adverse reactions to celery root. J Allergy Clin Immunol 2000; 106:373–378. 59 Bauer L, Ebner C, Hirschwehr R, Wüthrich B, Pichler W, Fritsch R, Scheiner O, Kraft D: IgE cross-reactivity between birch pollen, mugwort pollen and celery is due to at least three distinct cross-reacting allergens: immunoblot investigation of the birch-mugwort-celery syndrome. Clin Exp Allergy 1996;26:1161–1170. 60 Jensen-Jarolim E, Leitner A, Hirschwehr R, Kraft D, Wüthrich B, Scheiner O, Graf J, Ebner C: Characterization of allergens in Apiaceae spices: anise, fennel, coriander and cumin. Clin Exp Allergy 1997; 27: 1299– 1306. 61 Leitner A, Jensen-Jarolim E, Grimm R, Wüthrich B, Ebner H, Scheiner O, Kraft D, Ebner C: Allergens in pepper and paprika: immunologic investigation of the celerybirch-mugwort-spice syndrome. Allergy 1998;53:36–41. 62 Ballmer-Weber BK, Hoffmann A, Wüthrich B, Lüttkopf D, Pompei C, Wangorsch A, Kästern M, Vieths S: Influence of food processing on the allergenicity of celery: DBPCFC with celery spice and cooked celery in patients with celery allergy. Allergy 2002;57:228–235. 63 Fuchs E: Durch Zwischenträger vermittelte Kontaktallergie: ‘derivative Allergie’. Dtsch Med Wochenschr 1954;79:473. 64 Wüthrich B: Oral allergy syndrome to apple after a lover’s kiss. Allergy 1997; 52: 235– 236. 65 Wüthrich B, Däscher M, Borelli S: Kiss-induced allergy to peanut. Allergy 2001;56:913.
66 Mancuso G, Berdondini RM: Oral allergy syndrome from kiwi fruit after a lover’s kiss. Contact Dermatitis 2001;45:41. 67 Steensma DP: The kiss of death: a severe allergic reaction to a shellfish induced by a good-night kiss. Mayo Clin Proc 2003; 78: 221–222. 68 Hallett R, Haapanen LA, Teuber SS: Food allergies and kissing. N Engl J Med 2002; 346:1833–1834. 69 Boyfriend’s kiss causes girl’s death: 15-yearold had allergy to the peanut butter he had eaten. Edmonton J, Nov 26, 2005. 70 Bansal AS, Chee R, Nagendran V, Warner A, Hayman G: Dangerous liaison: sexually transmitted allergic reaction to Brazil nuts. J Invest Allergol Clin Immunol 2007; 17: 189–191. 71 Maulitz RM, Pratt DS, Schocket AL: Exercise-induced anaphylactic reaction to shellfish. J Allergy Clin Immunol 1979; 63: 433– 434. 72 Kidd JM, Cohen SH, Sosman AJ, Find J: Food-dependent exercise-induced anaphylaxis. J Allergy Clin Immunol 1983;71:407– 411. 73 Wüthrich B, Hofer T: Nahrungsmittelbedingte, anstrengungsinduzierte Anaphylaxie bei starker Sensibilisierung auf Getreideproteine, insbesondere auf Omega5-Gliadin, und bei fraglichem Hausstaubmilben-Krustazeen-Syndrom. Allergologie 2010;33:205–210. 74 Sheffer AL, Austen KF: Exercise-induced anaphylaxis. J Allergy Clin Immunol 1984; 73:699—703. 75 Lenchner K, Grammer LC: A current review of idiopathic anaphylaxis. Curr Opin Allergy Clin Immunol 2003;3:305–311. 76 Wüthrich B, Hofer T: Nahrungsmittelallergien. 3. Therapie: Eliminationsdiät, symptomatische, medikamentöse Prophylaxe und spezifische Hyposensibilisierung. Schweiz Med Wochenschr 1986;116:1401– 1410, 1446–1449. 77 Wüthrich B: Therapie von NahrungsmittelAllergien; in Braun-Falco O, Schill WB (eds): Fortschritte der Praktischen Dermatologie und Venerologie. Berlin, Springer, 1987, vol 11, pp 439–440. 78 Wüthrich B: Neuere Aspekte zur Diagnostik und Therapie der Nahrungsmittelallergie. Dargestellt anhand ausgewählter Fallbeispiele von Milchallergie. Allergologie 1987;10:370–376. 79 Wüthrich B, Stäger J: Allergie au lait de vache chez l’adulte et désensibilisation spécifique au lait par voie orale. Méd Hyg 1988;46:1899–1905.
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39 Hannuksela M, Lahti A: Immediate reactions to fruits and vegetables. Contact Dermatitis 1977;3:79–84. 40 Lahti A, Hannuksela M: Hypersensitivity to apple and carrot can be reliably detected with fresh material. Allergy 1978; 33: 143– 146. 41 Kleinhans D: Apfel-Allergie: Vergleichende Hauttestungen mit kommerziellen Testlösungen und der nativen Frucht. Akt Dermatol 1978;4:71–75. 42 Kremser M, Lindemayr W: Zur Häufigkeit sogenannter ‘Apfelallergie’ (‘ApfelkontaktUrtikariasyndrom’) bei Patienten mit Birkenpollenallergie. Z Hautkr 1983; 58: 543–552. 43 Amlot PL, Kemeny DM, Zachary C, Parkes P, Lessof MH: Oral allergy syndrome (OAS): symptoms of IgE-mediated hypersensitivity to foods. Clin Allergy 1987;17:33–42. 44 Ortolani C, Ispano M, Pastorello E, Bigi A, Ansaloni R: The oral allergy syndrome. Ann Allergy 1988;61:47–52. 45 Kauppinen K, Kousa M, Reunala T: Aromatic plants – a cause of severe attacks of angioedema and urticaria. Contact Dermatitis 1980;6:251–254. 46 Ebner C, Birkner T, Valenta R, Rumpold H, Breitenbach M, Scheiner O, Kraft D: Common epitopes of birch pollen and apples: studies by Western and Northern blot. J Allergy Clin Immunol 1991;88:588–594. 47 Ebner C, Hirschwehr R, Bauer L, Breiteneder H, Valenta R, Ebner H, Kraft D: Identification of allergens in fruits and vegetables: IgE cross-reactivities with the important birch pollen allergens Bet v 1 and Bet v 2 (birch profilin). J Allergy Clin Immunol 1995;95:962–969. 48 Forsbeck M, Ros AM: Anaphylactoid reaction to celery. Contact Dermatitis 1979; 5: 191. 49 Thiel C, Fuchs E: Über korrelative Beziehungen bei Kräuterpollen- und Gewürzallergenen. Berichtsband. 3. Kölner RAST Symposium. Berlin, Grosse, 1981, pp 178–185. 50 Kremser M, Lindemayer JW: Sellerieallergie (Sellerie-Kontakturtikaria Syndrom) und Zusammenhänge mit Allergien gegen Pflanzenallergene. Wiener Klin Wochenschr 1983;23:838–843. 51 Déchamp C, Michel J, Deviller P, Perrin LF: Anaphylactic shock to celery and sensitization to ragweed and mugwort: crossed or concomitant allergy? (in French). Presse Med 1984;13:871–874. 52 Pauli G, Bessot JC, Dietermann-Molard A, Braun PA, Thierry R: Celery sensitivity: clinical and immunological correlations with pollen allergy. Clin Allergy 1985; 15: 273–279.
80 Wüthrich B: Oral desensitization with cow’s milk in cow’s milk allergy. Pro!; in Wüthrich B, Ortolani C (eds): Highlights in Food Allergy. Basel, Karger, 1996, pp 236–240. 81 Bucher C, Wüthrich B: Oral desensitization in cow’s milk allergy. Ital J Allergy Clin Immunol 2000;10:119–120. 82 Bauer A, Ekanayake Mudiyanselage S, Wigger-Alberti W, Elsner P: Oral rush desensitisation to milk. Allergy 1999;54:894–895. 83 Patriarca G, Nucera E, Roncallo C, Pollastrini E, Bartolozzi F, De Pasquale T, Buonomo A, Gasbarrini G, Di Campli C, Schiavino D: Oral desensitizing treatment in food allergy: clinical and immunological results. Aliment Pharmacol Ther 2003;17:459–465.
84 Meglio P, Bartone E, Plantamura M, Arabito E, Giampietro PG: A protocol for oral desensitization in children with IgE-mediated cow’s milk allergy. Allergy 2004; 59: 980– 987. 85 Bahna SL: Oral desensitization with cow’s milk in IgE-mediated cow’s milk allergy. Contra!; in Wüthrich B, Ortolani C (eds): Highlights in Food Allergy. Basel, Karger, 1996, pp 233–235. 86 Niggemann B, Staden U, Rolinck-Werninghaus C, Beyer K: Specific oral tolerance induction in food allergy. Allergy 2006; 61: 808–811. 87 Staden U, Rolinck-Werninghaus C, Brewe F, Wahn U, Niggemann B, Beyer K: Specific oral tolerance induction in food allergy in children: efficacy and clinical patterns of reaction. Allergy 2007;62:1261–1269.
88 Staden U, Blumchen K, Blankenstein N, Dannenberg N, Ulbricht H, Dobberstein K, Ziegert M, Niggemann B, Wahn U, Beyer K: Rush oral immunotherapy in children with persistent cow’s milk allergy. J Allergy Clin Immunol 2008;122:418–419. 89 Nowak-Wegrzyn A, Bloom KA, Sicherer SH, Shreffler WG, Noone S, Wanich N, Sampson HA: Tolerance to extensively heated milk in children with cow’s milk allergy. J Allergy Clin Immunol 2008; 122: 342–347.
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Prof. em. Dr. med. Brunello Wüthrich Im Ahorn 18 CH–8125 Zollikerberg (Switzerland) E-Mail bs.wuethrich @ bluewin.ch
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Brunello Wüthrich Faculty of Medicine, University of Zurich, Zurich, Switzerland
In this chapter we will first consider whether there is real evidence on the basis of literature for early descriptions in antiquity of pathogenic reactions after food intake that could be comparable to allergy, for instance in the scriptures of Hippocrates or Lucretius. On this topic we are skeptical, which is in agreement with the medical historian Hans Schadewaldt. We also assert that it is unlikely that King Richard III was the first food-allergic individual in medical literature. Most probably it was not a well-planned poisoning (‘allergy’) with strawberries, but rather a birth defect (‘… his harm was ever such since his birth’) that allowed the Lord Protector to bring Mylord of Ely to the scaffold in the Tower, as we can read in The History of King Richard III by Thomas More (1478– 1535; published by his son-in-law, Rastell, in 1557). In 1912, the American pediatrician Oscar Menderson Schloss (1882–1952) was probably the first to describe scratch tests in the diagnosis of food allergy. Milestones in the practical diagnosis of food allergy are further discussed, including scratch tests, intradermal tests, modified prick tests and prick-to-prick tests. False-negative results can be attributed to the phenomenon of a ‘catamnestic reaction’ according to Max Werner (1911–
1987), or to the fermentative degradation of food products. Prior to the discovery of immunoglobulin E, which marked a turning point in allergy diagnosis, and the introduction of the radioallergosorbent test in 1967, several more or less reliable techniques were used in the diagnosis of food allergy, such as pulse rate increase after food intake according to Coca, the leukopenic index, drop in basophils or drastic platelet decrease. The ‘leukocytotoxic test’ (Bryan’s test), today called the ‘ALCAT’ test, shows no scientific evidence. The double-blind placebo-controlled food challenge test remains the gold standard in the diagnosis of food allergy. For the future, component-resolved diagnostics with the use of recombinant molecular allergens or chip arrays, such as the ISAC technique, hold a lot of promise. With regard to the clinical situation, a subjective selection is given, touching on the pollen-associated food allergies (‘birchmugwort-celery-spice syndrome’), as well as the new phenomenon of lethal food allergies that have appeared since the 1980s. Finally, rare ways of elicitation of a ‘derivative allergy’, first described by Erich Fuchs (1921–2008), for example by kissing, as well as ‘oral allergy syndrome’ and oral hyposensitization are considered. © 2014 S. Karger AG, Basel
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Abstract
In classic antiquity the teaching of the four humors led to the term ‘idiosyncrasy’, which was probably used for unexpected allergic reactions. In this context, Hippocrates and Lucretius are quoted as first descriptors of ‘idiosyncratic’ reactions to food. This will be briefly discussed here. Hippocrates (460–375 BC), the father of medicine, is assumed to have given the first description of cheese allergy. In chapter 20 of the Corpus Hippocraticum (‘About Antique Medicine’) from the 5th century BC, we can read, according to Hans Schadewaldt: Cheese occasionally could be a ‘dangerous food’, because it causes discomfort in those who fill themselves with it. [1]
And the following: Also wine in high amounts consumed might usually cause complaints. But with the cheese there is the special situation that it causes pain only in certain individuals whose constitution of humors is not compatible with cheese, who so to speak are enemies to cheese.
Unfortunately there is no description of the nature of the complaints suffered by individuals after the consumption of cheese or wine. It is impossible to really evaluate whether these conditions were allergic or due to enzymatic intolerance (lactase deficiency or histamine intolerance). Most likely it was an exaggerated dose that led to the symptoms. The therapy of this condition was clear-cut and effective: ‘Don’t eat cheese.’ The following often-quoted verse from Titus Lucretius Carus (109–150 BC) is usually taken as the first description of food allergy: What is normal food for one, may be strong poison for another one. [2]
However, when we read literally the corresponding verses in his epos De natura rerum [3], the quotation is: Nunc aliis alius qui sit cibus ut videamus expediam, quareve aliis quod triste et amarum est; hoc tamen esse aliis possit perdulce videri. Tantaque in his rebus distantia differitasque est, ut quod aliis cibus est aliis fiat acre venenum, at capris adipes et cocturni cibus auget!
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Again, according to Schadewaldt [4], Lucretius made note of an observation that certain animals are able to eat certain weeds without damage to their health, but the same plants are poisonous to other animals. In detail, he describes that hemlock, for example, is a poison for humans, but provides good nutrition for goats and quails, probably due to different enzymatic metabolic processes in different species. Furthermore, Lucretius describes differences in taste between animals and human beings – ‘the leaves of olive trees obviously are delicious food for bearded goats, but for humans of utter bitterness’: Quippe videre licet pinquescere saepe cicuta barbigeras pecudes, homini quae est acre venenum.
Now we turn to Shakespeare and the character of Richard III, purportedly the first food-allergic individual in medical literature (fig. 1); but what is the truth? We read in act 3, scene 4: My lord of Ely, when I was last in Holborn I saw good strawberries in your garden there. I do beseech you send for some of them. Marry and will, my lord, with all my heart. Where is my lord the Duke of Gloucester? I have sent for these strawberries.
After the herald arrived, the monarch ostentatiously ate one of the strawberries and continued with the trial. One hour later he caused consternation among the assembly of lords when he revealed his arm by pushing back the sleeve of his shirt, and said: I pray you all, tell me what they deserve That do conspire my death with devilish plots Of damned witchcraft, and that have prevail’d Upon my body with their hellish charms? … Then be your eyes the witness of their evil. Look how I am bewitch’d; behold, mine arm Is like a blasted sapling wither’d up.
Obviously, it was not an acute strawberry-induced urticaria that afflicted King Richard III, as we allergists like to claim, but was probably a birth defect that brought Mylord of Ely to the scaffold of the Tower.
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Food Allergy in Antiquity and the Middle Ages: Myth or Reality?
Fig. 1. King Richard III of England (1452–
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First Documentation of Food Allergy – Skin Test as Diagnostic Routine Method The first scientific report of food allergy can be found from the beginning of the 20th century [5]. In 1912, the American pediatrician Oscar Menderson Schloss [6] (1882–1952; fig. 2) was the first to diagnose food allergy by skin tests. He could prove that a case of allergy was due to the consumption of egg, since a scarification test (scratch test) with hen’s egg white was positive. He was also able to test isolated fractions of hen’s egg white and to note that ovomucoid apart from ovoglobulin and ovomucin were the strongest elicitors of allergic skin reactions. He also tested oatmeal and almonds. His paper is a milestone in the history of allergy. Following a further publication [7], the scratch test, which was originally introduced by Blackley in 1873 for the detection of pollen allergy [5], became the routine method in the diagnosis of food allergy. In 1908, Mendel and Mantoux introduced the intradermal test as a tuberculin test, which was then used by Cooke and van der Veer in 1916 for testing aeroallergens [5]. With this method, Karl Prausnitz (1876–1963) and Heinz Küstner (1897–1963) succeeded in passively transferring fish allergy using the serum of an allergic individual [8]. Soon it became apparent that intradermal tests with foods could be false negative, either with exclusively gastrointestinal symptoms because the skin was not the ‘shock
History of Food Allergy
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organ’, or because the relevant allergens were denatured during the extract production. Some authors mentioned that fermentative metabolites could have sensitizing properties [9–11]. The observation of Max Werner (1911–1987) is of interest when he stated a ‘catamnestic skin reaction’ [12] where intradermal tests with food allergens only became positive after a 10- to 14-day elimination diet, an observation which was confirmed by other authors [13]. The modified prick test was developed by Helmtraut Ebruster and published in 1959 in relation to aeroallergens [14]. Using the knowledge of the 1970s that skin tests with commercial extracts from foods and vegetables often yielded false-negative results, in the examination of these allergens the prick-to-prick test method was increasingly used besides scratch tests with native material [15, 16]. The test needle was first pricked into the fresh fruit or vegetable and then pricked into the skin of the patient (fig. 3).
Other Test Methods for Food Allergy Prior to the Discovery of Immunoglobulin E Since cutaneous testing with food allergens often remained unreliable (either false negative or false positive), besides attempts at re-exposure, other test methods were employed. However, these were also not totally reliable. Examples include the increase in pulse rate according to Coca after food exposure
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1485). He probably was not the first documented patient with strawberry allergy. Fig. 2. Oscar Menderson Schloss (1882– 1952), the first author to describe the ‘scratch test’ and the first documented case of food allergy.
Fig. 3. Prick-to-prick tests with raw apples and vegetables.
Radioallergosorbent Test – Significant Progress in the Diagnosis of Immunoglobulin E-Mediated Food Allergies The discovery of immunoglobulin (Ig) E as a new class of immunoglobulins with reagin activity and the development of sensitive and quantitative in vitro methods like the radioimmunosorbent test for the determination of total serum IgE [27], or the radioallergosorbent test (RAST) for detection of circulating antibodies with IgE specificity [28], without doubt represents a major advancement in allergy diagnosis, including food allergy. By using highly purified cod fish allergen extracts in children with allergic symptoms after fish consumption, 100% concordance be-
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tween history, RAST and skin test was found [29]. The spectrum of available food species for IgE determination was gradually extended; however, it was also recognized that the diagnostic reliability of RAST as a skin test is limited. Positive IgE detection only measures sensitization against the food, but does not prove clinical relevance, indicating the occurrence of allergy symptoms after exposure. In contrast, the lack of detection of serum IgE antibodies against foods by RAST or other modified in vitro techniques, such as the ImmunoCAP FEIA (fluor enzyme immunoassay), cannot exclude a certain kind of food as the cause of the elicitation of symptoms. Many food extracts are poorly standardized. Degradation of allergenic proteins during the extraction process represents a common phenomenon, resulting in too low concentrations of allergens in the final extracts. On the other hand, similar molecular structures in foods and aeroallergens (pollen, house dust mite, latex, etc.) give rise to multiple positive results in skin tests and RASTs due to cross-reacting IgE antibodies [30].
Component-Resolved Diagnostic Techniques A new promising strategy to distinguish crossreactions from genuine co-sensitizations as possible therapeutic consequences can be seen in the use of recombinant allergens which are already available for the ImmunoCAP System (Phadia, Thermo Fisher, Uppsala, Sweden). The component-resolved diagnostics, namely the detection of the specific IgE against molecular marker proteins within foods, is able to distinguish relevant from irrelevant sensitizations [31]. At the same time, allergologic research in
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[17], the leukopenic index [18], drop in basophil leukocytes [19], the platelet drop [20, 21] and – in patients with exclusively gastrointestinal symptoms – complex exposure tests at the small intestine [22]. At the end of the 1950s, Black and Bryan developed a leukocytotoxic test (Bryan’s test) for the detection of allergies against foods and additives based on the microscopic evaluation of activation-induced alterations or autolysis of leukocytes after adding food or food extracts to the blood. This test was not registered for proving allergies in the USA because of unreliability [23, 24]. The ALCAT test (antigen leukocyte cellular antibody test) or leukocyte activation test, which even nowadays is still advertised as a diagnostic method for qualitative determination of food intolerances, is nothing more than a modified Bryan test. Many national and international societies state that this test cannot be used in the diagnosis of food allergy [25, 26].
Double-Blind Placebo-Controlled Food Challenge – The Gold Standard and the Diagnosis of Food Allergy Oral provocation tests are often the last diagnostic opportunity to detect actual food allergy or intolerance. The so-called double-blind placebo-controlled food challenge (DBPCFC) is regarded as the only scientifically accepted detection method of food allergy or intolerance [30]. Even if the DBPCFC is the gold standard of clinical studies, this procedure is rather complex for routine diagnosis and only used in special allergy centers since provocation tests can always implicitly lead to generalized anaphylactic reactions.
Fatal Food Allergies A fatal reaction after a food challenge was published in 1926 [33]: an 18-month-old infant with atopic eczema and three episodes of generalized allergic reaction after the consumption of a few spoons of pease pudding was tested under in-patient conditions at a pediatric hospital during the lunch break when the head nurse gave a carrot/pea mixture to the infant. Immediately after the application the child developed angioedema, cyanosis and shock, and died in spite of intensive emergency treatment. The first case of a spontaneous fatal allergic food reaction was published 25 years ago [34]. A 24-year-old female patient with peanut allergy died after eating a cake. The Canadian pa-
History of Food Allergy
tient had repeatedly eaten and tolerated hazelnut cake with marzipan and almond icing. However, a short time after eating a few bites of the cake she suddenly developed a severe allergic reaction leading to suffocation and death. The forensic autopsy of this extraordinary case revealed that the paste used for the icing of the cake contained ‘arachides’, a name for peanuts that was not known to the English-speaking baker. Fatal or potentially fatal or life-threatening allergic reactions to foods in infants and children are unfortunately no rarity any more, especially in adolescents and young adults. Since the end of the 1990s, a series of fatal cases have been published in the USA, mostly after exposure to hidden food allergens, commonly peanuts, but also other tree nuts, Brazil nut and cashew nut, and also cow’s milk, hen’s egg, fish and crustacea (lobster, crabs) [35–37]. The lay press regularly reports such fatalities [38]. It is estimated that in the USA approximately 120 fatal cases occur each year due to anaphylactic reactions against foods. Hidden allergens, for example peanut allergens in sweets or chocolate, often make avoidance strategies difficult or impossible in spite of improved declaration rules.
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Pollen-Associated Food Allergies and the ‘Oral Allergy Syndrome’ At the end of the 1970s, Scandinavian allergists reported that 30–50% of patients with pollinosis against birch, hazel or alder pollen suffer from untoward symptoms like itch in the lips or the palate after eating raw apples. Similar symptoms were reported after consumption of other fruits, raw carrots or celery [39, 40]. A sensitization was proven by scratch or prick-to-prick tests with fresh materials [15, 16, 40, 41]. The most common symptoms in this oral ‘contact urticaria syndrome’ [42] or ‘oral allergy syndrome’ [43, 44] often start immediately after contact with certain foods, especially apples, raw vegetables, celery, nuts, hazel nuts and almonds. They are not necessarily only itch or swelling of the lips and tongue, or in the cavum oris or the palate, but can also be hoarseness due to discrete laryngeal edema, difficulties in swallowing and dyspnea. Furthermore, sneezing, rhinorrhea, obstruction of the nose ventilation and conjunctivitis can be observed.
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recent decades has identified marker allergens for certain disease conditions, respective of clinical symptoms, for example wheat-dependent exerciseinduced anaphylaxis (WDEIA) with s-IgE against rTri-α-omega-5-gliadin. With the immuno solidphase allergen chip (ISAC), we now have a test system for in vitro diagnosis that allows the analysis of a large number of allergen components in a single step. Using the ISAC technology, many relevant allergy elicitors can be measured in one analysis with a rather small volume of patient serum [32]. Due to the magnitude of the results and relatively high costs, the ISAC test should only be used by allergists or physicians with special knowledge in the field.
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celery is not the urticariogenic substance, because it did not yield any reaction.’ While the first botanic taxonomical associations with Rosaceae (the rose family) and Apiaceae (or Umbelliferae; known as carrot or parsley family) were suspected, it soon became apparent that several allergens, especially Bet v 1 and Bet v 2 (profilin), in birch pollen were responsible for these cross-reactivities [59–61] (fig. 4). The thermostable allergen in mugwort pollen and celery is yet to be identified; however, a lipid-transfer protein is most likely [62].
‘Derivative Allergy’ – A Rare Pathway of Elicitation of Food Allergy The elicitation of food allergy via a mediator in the form of a second person (mother, partner) was described as the phenomenon of ‘derivative allergy’ in 1954 by Erich Fuchs [63]. The first report of a kissinduced oral allergy syndrome described a birch pollen-allergic woman who developed symptoms after kissing her boyfriend, who had eaten an apple. An even more severe reaction occurred in a highly sensitized peanut-allergic man after kissing his girlfriend, who again had eaten a few peanuts 2 h previously [55, 64–68]. In one case it was possible to use the saliva of a man, who had eaten a suspected fruit, to elicit positive skin prick tests in his birch and grass pollen-allergic girlfriend, but only when the saliva was used within 5 min after the consumption of the fruit (e.g. kiwi), probably due to the instability of the birch pollen cross-reactive kiwi allergen [66]. This phenomenon is not at all rare: out of 379 allergic individuals with severe life-threatening reactions to peanuts and tree nuts, 20 (5.3%, 4 males, 16 females) reported to have suffered from a reaction after kissing. The symptoms ranged from oral allergy syndrome, lip swelling, massive angioedema and lid swelling to dyspnea with expiratory wheezing in 4 cases [68]. In most cases the symptoms occurred between less than 1 min and 30 min after the kiss, but occasionally also after some hours (indicating the stability of peanut and tree nut allergens). Recently, the media reported a fatal anaphylaxis in a 15-yearold Canadian girl with severe peanut allergy after kissing a friend who had eaten a peanut butter sand-
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Classical immediate symptoms of gastrointestinal food allergy like gastric cramps, vomitus, nausea, abdominal pain, colic or diarrhea are rare in patients with oral allergy syndrome [13, 45]. Recent investigations using molecular allergens in patients with oral allergy syndrome showed that a sensitization to birch pollen often reflects the thermolabile major antigen Bet v 1 [46, 47]. Birch pollen-associated food allergy has been shown to occur in 40–93% of birch pollen-allergic individuals in various studies. At the beginning of the 1980s, several authors from Finland [45], Sweden [48], Germany [49], Austria [50], France [51, 52] and Switzerland [13, 53] independently reported anaphylactic reactions or shock fragments after the consumption of celery in association with birch, mugwort pollen or spice allergy. The term, ‘celery-mugwort-spice syndrome’ or ‘celery-carrot-mugwort-spice syndrome’ was proposed [53–56]. It was stressed that in these patients the consumption of celery root (celeriac), either boiled, raw or used as a spice in soups, was able to elicit severe reactions in contrast to cases of birch pollen-associated celery allergy, in which only raw celery, and not cooked celery, induced symptoms, mainly oral allergy syndrome. The first publication of a celery allergy comes from Zurich [57] and was proven for the first time using DBPCFC in 2000 [58]. In 1926, Werner Jadassohn and Margarete Zaruski described a young woman who developed urticaria, dyspnea and fever at three different times after eating celery. Other ‘idiosyncrasies’ were unknown, except for a mild hay fever [57]. After application of celery juice to the skin treated with abrasive paper or scratching, wheals with red flares occurred, while the application of the same celery juice to healthy skin did not induce reactions. The allergen was regarded as ‘coctostabile’ since the affect was not diminished after 5 min of boiling. The pellets developed during boiling and dialysis were as effective in the skin test as the supernatants. According to Prausnitz and Küstner the transfer was positive in 18 out of 20 volunteers, including with celery dialysate, while when the serum was heated for over half an hour to 56 ° C the sensitizing properties were lost. The authors postulated that: ‘our antigen most likely is not a protein and probably not a very high molecular substance and that the substance apiol from
Apiaceae (or Umbellifereae) celeriac (celery root) cooked celery spice celery stalk, cooked Solanaceae chili pepper red pepper tomato potato raw
Asteraceae
Mugwort pollen (Asteraceae or Compositae)
artichoke tarragon camomile wormwood
ragweed dandelion sunflower chrysanthemum
2
Piperaceae green pepper black pepper
Cucurbitaceae melon cucumber, pumpkin
Apiaceae (or Umbellifereae) celery root (or celeriac) raw dill aniseed fennel carrot raw lovage coriander parsley cumin
Labiatae basil majoram oregano thyme
Rosaceae Betulaceae hazelnut
Birch pollen (Betulaceae)
apple raw peach raw apricot raw almond
pear raw plum raw cherry raw strawberries raw
Exotic fruits kiwi litchi
Fig. 4. Birch and mugwort pollen-associated food allergy.
History of Food Allergy
Food-Induced/Food-Dependent ExerciseInduced Anaphylaxis In 1979, American authors observed a phenomenon in which an allergic sensitization was elicited in a marathon runner only after the concomitant exposure of physical exercise and food, while exercise alone or consumption of the food alone were each tolerated without reaction [71]. The term ‘food-de-
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wich [69]. Also, a case of food allergy elicited by sexual intercourse was reported as ‘connubial allergy’ [70]. The eliciting allergen was from Brazil nuts which had been eaten by a man prior to intercourse with his girlfriend, who was severely allergic to nuts. Prick tests with sperm were negative before and positive after Brazil nut consumption. Thus, foods eaten by other persons can endanger the life or the quality of life of food-allergic individuals.
2 1
1 Years
0
a
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SPT +
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Start OMD 1:10 250 ml
1
K
50 g Gruyère
SPT ±
SPT – Cheese fondue
Pasta
Stop
**
0 –0.5 0
pendent exercise-induced anaphylaxis’, or FDEIA, was coined in 1983 [72]. FDEIA is quite common today, especially after wheat (WDEIA; see above) [73] and has to be differentiated from exercise-induced anaphylaxis [74] and idiopathic anaphylaxis [75].
Oral Desensitization – Long Controversial, but Now Established On several occasions since the 1980s we have published, initially in the German literature [13, 76– 79] and later in international medical literature [80, 81], the possibility of oral desensitization in food allergy, especially with untreated cow’s milk. Some authors have repeated our results [82–84]. However, the European Academy of Allergy and Clinical Immunology, EAACI, did not accept this technique, since there were no placebo-controlled studies and
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2
SPT ++
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b
Cheese fondue
K
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4
SPT milk –; SPT cheese –
Start OMD 1:100 *1 dl 30 g Gruyère *Pasta
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thus no ‘scientific evidence regarding efficacy’(!). Experts violently rejected this stance [85]. Meanwhile, the method was re-discovered by pediatricians who did not even quote the first articles in the literature [86–89]. In severe allergy oral desensitization with food can be performed, however, under utmost caution: the treatment has to be started with adequate dilutions of the allergen and under emergency conditions. Lack of success may be explained by very low tolerance thresholds on the one hand, or a too rapid increase on the other hand. After reaching the maintenance dose it is important that the tolerated food is consumed every day since even short intervals can break the tolerance. This first phase may be called tolerance induction; the later application over months or years then leads to true desensitization and can be proven in negative test results in skin tests and RAST against milk proteins such as casein (fig. 5). In a series of 16 patients with IgE-mediated
Wüthrich
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Class
3
Class
[skin prick tests (SPT) and specific IgE (RAST) results] under oral desensitization with cow’s milk in 2 patients with severe allergic reactions after intake of a small amount of cheese or hidden diary products. a Case 1, 29-year-old female: SPT with cheese (Gruyère) +++; RAST to milk class 4. Oral milk desensitization (OMD) started with a drop of 1: 100 milk:water dilution, increasing the dose to 250 ml of undiluted milk daily without any interruption. After 2 years the SPT and RAST became negative and the patient could eat a cheese fondue and other dairy products without any problems. * = Dyspnea, eyelid edema. b Case 2, 45-year-old female: SPT with raw cow’s milk ++; RAST to milk class 4. After 6 months under a strict elimination diet, OMD was started with a drop of 1: 10 milk:water dilution, increasing to 250 ml of undiluted milk daily without any interruption. The SPT became negative after 4 years, and the RAST only after 5.5 years, so that the daily intake of 250 ml milk was stopped and the patient could drink milk and eat dairy products. After 6 years, the patient could eat a cheese fondue. ** = Urticaria, cramps; K = ketotifen.
SPT milk –; SPT cheese +++
4
Fig. 5. Clinical and immunological course
cow’s milk allergy, in 50% of cases complete tolerance to cow’s milk and cheese was induced after a 3- to 5-year treatment program [80]. In 4 patients (25%) partial tolerance could be induced; these patients were able to consume at least 1 dl of cow’s milk every day together with some cheese, but not hard cheese. In 4 patients (25%) oral hypersensitization had to be stopped because of repeated allergic
reactions occurring even with low doses and concomitant therapy with antihistamines or ketotifen [80]. Acknowledgement I would like to thank Johannes Ring for the English translation.
2 References
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History of Food Allergy
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Prof. em. Dr. med. Brunello Wüthrich Im Ahorn 18 CH–8125 Zollikerberg (Switzerland) E-Mail bs.wuethrich @ bluewin.ch
