What is an allergy in physiological terms

Of the 16 subjects (12 women, 4 men; age 25 — 50 years), 9 were Phadiatop-positive and 7 were Phadiatop-negative. The median and range of body mass index (, — v. , — ) and percentage body fat (%, — % v. %, — %) did not differ significantly between Phadiatop-positive and negative groups. Baseline testing of vital signs was within the normal range, and subjects did not present with evidence of medical conditions that could own placed their health at risk. Table 1 presents the results of the Phadiatop assay and peak sIgE concentrations.

The criteria for post-race RTS were met by 12 (75%) subjects, of whom 7 (58%) were Phadiatop-positive and 5 (42%) were Phadiatop-negative.

The median (IQR) pre- and post-race RTS index scores of the Phadiatop groups did not differ significantly (p>) (Fig. 1).

Fig. 2 presents the median (IQR) sIgE concentrations of the subjects (adjusted for PV). There was a non-significant (p=) rise in the sIgE concentrations of the entire group over the course of testing, with highest concentrations recorded in 75% of subjects at the 24PR time period. There was a highly significant (p<) difference between the sIgE concentrations of the Phadiatop-positive and negative groups.

Concentrations of sIgE reached clinical significance (peak sIgE > IU/ml) in 5 (42%) of the 12 RTS-positive subjects (4 Phadiatop-positive and RTS-positive subjects and 1 Phadiatop-negative and RTS-positive subject).

There was no significant exercise-induced elevation in PV-adjusted concentrations of either basophils or eosinophils over time (p>), and the difference between Phadiatop-positive and negative groups in terms of eosinophil or basophil response to 3 days of exercise was not significant (p>).


Discussion

The incidence of post-exercise RTS in endurance runners in this study (n=12, 75%) was higher than that in most other reported studies,1 possibly owing to the inclusion of subjects with a prior history of allergy; in most previous studies, allergy was seen as a confounding factor in determining the incidence of URTI and was therefore excluded.

Interestingly, in this field trial, subjects with systemic evidence of RTS associated with an allergic reaction accounted for 42% (n=5) of the 12 cases with post-exercise RTS.

However, as seen by the lack of significance between post-race RTS incidence in Phadiatop-positive and negative groups (Fig. 1), the incidence of post-race RTS symptoms was not defined by the Phadiatop test.

Our primary finding was that, of the 7 Phadiatop-positive subjects who developed post-race RTS, only 4 (58%) displayed clinically elevated sIgE concentrations above the cut-off point for allergy (sIgE > IU/ml). The mildly elevated eosinophil concentrations often seen in allergic responses13 were not evident in the Phadiatop-positive group (p>).

Although specific sIgE antibody testing (SPT) provides evidence of sensitisation to an allergen, an allergic disease response only develops once the individual is exposed to that specific allergen; therefore, although the Phadiatop test may provide satisfactory accuracy in identifying predisposition to allergic responsiveness to airborne allergens, on its own it may not predict the development of allergic disease in trail runners.

Owing to the fixed selection of allergens, it is theoretically possible to miss subjects who are sensitised to less common inhalant allergens (such as local flora or fauna), as was the case in one of our subjects.

The predictive validity of the Phadiatop assay for the incidence of exercise-induced RTS of allergic origin in the trail runners must therefore be questioned.

Acknowledgements. Ms Heidi Mocke and the Wildlands Conservation Believe are thanked for permitting the collection of these data at the Three Cranes Challenge multi-day trail run and for providing the research team with accommodation in the &#x;race village&#x; located in the Bushwillow Campsite.

Dr Rentia Dennisen, Professor Andrew Mckune, Mr Navin Singh and Mr Ronnie Naicker are thanked for their support with the field-side collection of data reported in this article. Mr Asokaran Rajh is thanked for his assistance with the graphic artwork.

References

1. Peters EM, Bateman ED. Ultramarathon running and upper respiratory tract infections. S Afr Med J ; [PMID: ]

1. Peters EM, Bateman ED. Ultramarathon running and upper respiratory tract infections. S Afr Med J ; [PMID: ]

2.

Walsh NP, Gleeson M, Shephard RJ, et al. Position statement. Part 1: Immune function and exercise. Exerc Immunol Rev ; [PMID: ]

2. Walsh NP, Gleeson M, Shephard RJ, et al. Position statement. Part 1: Immune function and exercise. Exerc Immunol Rev ; [PMID: ]

3. Schwellnus M, Lichaba M, Derman W. Respiratory tract symptoms in endurance athletes &#x; a review of causes and consequences. Current Allergy & Clinical Immunology ;3(2)

3. Schwellnus M, Lichaba M, Derman W. Respiratory tract symptoms in endurance athletes &#x; a review of causes and consequences.

Current Allergy & Clinical Immunology ;3(2)

4. Spence L, Brown WJ, Pyne DB, et al. Incidence, etiology, and symptomatology of upper respiratory illness in elite athletes. Med Sci Sports Exerc ;39(4) [] [PMID: ]

4. Spence L, Brown WJ, Pyne DB, et al. Incidence, etiology, and symptomatology of upper respiratory illness in elite athletes. Med Sci Sports Exerc ;39(4) [] [PMID: ]

5. Cox AJ, Gleeson M, Pyne DB, Callister R, Hopkins WG, Fricker PA. Clinical and laboratory evaluation of upper respiratory symptoms in elite athletes. Clin J Sport Med ;18(5) [] [PMID: ]

5. Cox AJ, Gleeson M, Pyne DB, Callister R, Hopkins WG, Fricker PA.

Clinical and laboratory evaluation of upper respiratory symptoms in elite athletes. Clin J Sport Med ;18(5) [] [PMID: ]

6. Reid VL, Gleeson M, Williams N, Clancy RL. Clinical investigation of athletes with persistent fatigue and/or recurrent infections. Br J Sports Med ; [PMID: ]

6. Reid VL, Gleeson M, Williams N, Clancy RL. Clinical investigation of athletes with persistent fatigue and/or recurrent infections. Br J Sports Med ; [PMID: ]

7.

Anderson SD, Kippelen P. Airway injury as a mechanism for exercise-induced bronchoconstriction in elite athletes. J Allergy Clin Immunol ;(2) [] [PMID: ]

7.

What is an allergy in physiological terms

Anderson SD, Kippelen P. Airway injury as a mechanism for exercise-induced bronchoconstriction in elite athletes. J Allergy Clin Immunol ;(2) [] [PMID: ]

8. Bermon S. Airway inflammation and upper respiratory tract infection in athletes: is there a link? Exerc Immunol Rev ; [PMID: ]

8. Bermon S. Airway inflammation and upper respiratory tract infection in athletes: is there a link? Exerc Immunol Rev ; [PMID: ]

9.

What is an allergy in physiological terms

Peters E M. Postrace upper respiratory tract &#x;infections&#x; in ultramarathoners &#x; infection, allergy or inflammation? South African Journal of Sports Medicine ;16(1)

9. Peters E M. Postrace upper respiratory tract &#x;infections&#x; in ultramarathoners &#x; infection, allergy or inflammation? South African Journal of Sports Medicine ;16(1)

Thomas S, Wolfarth B, Wittmer C, Nowak D, Radon K, GA2LEN-Olympic StudyTeam. Self-reported asthma and allergies in top athletes compared to the general population: results of the German part of the GA2LEN-Olympic Study, Allergy, Asthma & Clinical Immunology ; [] [PMID: ]

Thomas S, Wolfarth B, Wittmer C, Nowak D, Radon K, GA2LEN-Olympic StudyTeam.

Self-reported asthma and allergies in top athletes compared to the general population: results of the German part of the GA2LEN-Olympic Study, Allergy, Asthma & Clinical Immunology ; [] [PMID: ]

Bonini S, Bonini M, Bousquet J, et al. Rhinitis and asthma in athletes: an ARIA document in collaboration with GA2LEN. Allergy ;61(6) [] [PMID: ]

Bonini S, Bonini M, Bousquet J, et al. Rhinitis and asthma in athletes: an ARIA document in collaboration with GA2LEN.

Allergy ;61(6) [] [PMID: ]

Vidal C, Gude F, Boquete O, et al. Evaluation of the Phadiatop test in the diagnosis of allergic sensitization in a general adult population. J Investig Allergol Clin Immunol ;15(2) [PMID: ]

Vidal C, Gude F, Boquete O, et al. Evaluation of the Phadiatop test in the diagnosis of allergic sensitization in a general adult population. J Investig Allergol Clin Immunol ;15(2) [PMID: ]

Morris A. Atopy, anamnesis and allergy testing. InnovAiT ;2(3) []

Morris A.

Atopy, anamnesis and allergy testing. InnovAiT ;2(3) []

Garcia-Marcos L, Sanchez-Solis M, Martinez-Torres AE, Lucas Moreno JM, Hernando Sastre V. Phadiatop compared to skin-prick test as a tool for diagnosing atopy in epidemiological studies in schoolchildren. Pediatr Allergy Immunol ; [] [PMID: ]

Garcia-Marcos L, Sanchez-Solis M, Martinez-Torres AE, Lucas Moreno JM, Hernando Sastre V. Phadiatop compared to skin-prick test as a tool for diagnosing atopy in epidemiological studies in schoolchildren.

Pediatr Allergy Immunol ; [] [PMID: ]

Dill DB, Costill DL. Calculation of percentage changes in volumes of blood, plasma and red cells in dehydration. J Appl Physiol ; 37(2) [PMID: ]

Dill DB, Costill DL. Calculation of percentage changes in volumes of blood, plasma and red cells in dehydration. J Appl Physiol ; 37(2) [PMID: ]

Accepted 9 February

Table 1.

Phadiatop assay results and peak race-induced sIgE concentrations of the 16 subjects

Phadiatop-positive

(n=9)

Phadiatop-negative

(n=7)

Subject

Phadiatop result*

(sIgE conc.) (IU/ml)

Peak sIgE conc.

(IU/ml)&#x; (time-point)

Subject

Phadiatop result*

(sIgE conc.) (IU/ml)

Peak sIgE conc.

(IU/ml)&#x; (time-point)

1

(24PR)

5

(24PR)

2

(24PR)

6

(72PR)

3

(24PR)

10

(24PR)

4

(24PR)

12

(24PR)

7

(24PR)

14

(24PR)

8

(72PR)

15

(24PR)

9

(24PR)

16

(24PR)

11

(24PR)

13

(S1pre)

Median

&#x;

&#x;

Median

Fig.

1. Median (IQR) pre- (left) and post-race (right) entire RTS index scores of Phadiatop-positive* (n=9) and negative (n=7) groups. (*sIgE concentration > IU/ml in Phadiatop assay)

Fig. 2. Median (IQR) of absolute sIgE* concentrations&#x; of Phadiatop-positive and negative groups, at 8 stages during and after a 3-day 95 km trail run. (*Adjusted for plasma volume; &#x;Reference range 0 — IU/ml)

Anaphylaxis: Synopsis

Updated: April,
Updated: September,
Originally Posted: July

Richard F.

Lockey, MD
Professor of Medicine, Pediatrics and Public Health
Director of the Division of Allergy and Immunology
Joy McCann Culverhouse Chair of Allergy and Immunology
University of South Florida College of Medicine and the James A. Haley Veterans' Hospital
Tampa, Florida, USA

This disease summary is provided for informational purposes for physicians only.

Epidemiology

B = Breathing

Assess adequacy of ventilation and provide the patient with sufficient oxygen to maintain adequate mentation and an oxygen saturation of at least 91% as sure by pulse oximetry. Treat bronchospasm as necessary. Equipment for endotracheal intubation should be available for immediate use in event of respiratory failure and is indicated for poor mentation, respiratory failure, or stridor not responding immediately to supplemental oxygen and epinephrine.

B = Benadryl (diphenhydramine)

Antihistamines are not useful for the initial management of anaphylaxis but may be helpful once the patient stabilizes.

Diphenhydramine may be istered intravenously, intramuscularly or orally. Cimetidine offers the theoretical benefit of reducing both histamine-induced cardiac arrhythmias, which are mediated via H2 receptors, and anaphylaxis-associated vasodilation, mediated by H1 and H2 receptors.

What is an allergy in physiological terms

Cimetidine, up to mg every 6 to 8 hours, may be istered orally or slowly I.V. Doses must be adjusted for children.

Insect venom anaphylaxis

Studies from Australia, France, Switzerland and the USA propose incidences of systemic reactions to Hymenoptera stings ranging from % to 4% of the population. In the USA, at least 40 allergic deaths happen each year as a result of Hymenoptera stings.

Emergency Treatment of Anaphylaxis

Antibiotics and Other Drugs

PENICILLIN, CEPHALOSPORIN, AND SULPHONAMIDE ANTIBIOTICS

Penicillin is the most common cause of anaphylaxis, for whatever reason, not just drug-induced cases.

Penicillin and other antibiotics are haptens, molecules that are too little to elicit immune responses but which may bind to serum proteins and produce IgE antibodies. Serious reactions to penicillin happen about twice as frequently following intramuscular or intravenous istration versus oral istration, but oral penicillin istration may also induce anaphylaxis. Neither atopy, nor a genetic history of allergic rhinitis, asthma or eczema, is a risk factor for the development of penicillin allergy.

MUSCLE RELAXANTS

Muscle relaxants, for example, suxamethonium, alcuronium, vecuronium, pancuronium and atracurium, which are widely used in general anesthesia, account for % of every allergic reactions occurring during general anesthesia.

Reactions are caused by an immediate IgE-mediated hypersensitivity reaction.

Exercise

Exercise alone can cause anaphylaxis as can food-induced anaphylaxis, Exercise-induced anaphylaxis can happen during the pollinating season of plants to which the individual is allergic.

Food-induced anaphylaxis

The prevalence of food-induced anaphylaxis varies with the dietary habits of a region. A United States survey reported an annual occurrence of cases per , person years. By extrapolating this data to the entire population of the USA, this suggests approximately 29, food-anaphylactic episodes each year, resulting in approximately 2, hospitalizations and deaths.

Similar findings own been reported in the United Kingdom and France. Food allergy is reported to cause over one-half of every severe anaphylactic episodes in Italian children treated in emergency departments and for one-third to one-half of anaphylaxis cases treated in emergency departments in North America, Europe and Australia. It is thought to be less common in non-Westernized countries. A study in Denmark reported a prevalence of cases of food anaphylaxis per , inhabitants per year with a fatality rate of approximately 5%.

Risk factors for food anaphylaxis include asthma and previous allergic reactions to the causative food.

Latex

Latex is a milky sap produced by the rubber tree Hevea brasiliensis.

What is an allergy in physiological terms

Latex-related allergic reactions can complicate medical procedures, for example, internal examinations, surgery, and catheterization. Medical and dental staff may develop occupational allergy through use of latex gloves.

Aspirin, Ibuprofen, Indomethacin and other Non-steroidal Anti-inflammatory Agents (NSAIDs)

IgE antibodies against aspirin and other NSAIDs own not been identified. Affected individuals tolerate choline or sodium salicylates, substances closely structurally related to aspirin but diverse in that they lack the acetyl group.

Idiopathic Causes

A = Adrenalin = epinephrine

Epinephrine is the drug of choice for anaphylaxis.

It stimulates both the beta-and alpha-adrenergic receptors and inhibits further mediator release from mast cells and basophils. Animal and human data indicate that platelet activating factor (PAF) mediates life-threatening manifestations of anaphylaxis. The early use of epinephrine in vitro inhibits the release of PAF in a time-dependent manner, giving support to the use of this medication with the first signs and symptoms of anaphylaxis. The usual dosage of epinephrine for adults is mg of a w/v solution given intramuscularly, preferably in the anterolateral thigh, every minutes or as necessary. The dose for children is mg/kg to a maximum of mg intramuscularly, preferably in the anterolateral thigh, every minutes as necessary.

Lower doses, e.g., mg to mg istered intramuscularly, preferably in the anterolateral thigh, as necessary, are generally adequate to treat mild anaphylaxis, often associated with skin testing or allergen immunotherapy. Epinephrine should be given early in the course of the reaction and the dose titrated to the clinical response. For severe hypotension, 1 cc of a , w/v dilution of epinephrine given slowly intravenously is indicated. The patient's response determines the rate of infusion.

Whole Blood, Serum, Plasma, Fractionated Serum Products, Immunoglobulins, Dextran

Anaphylactic responses own been observed after the istration of whole blood or its products, including serum, plasma, fractionated serum products and immunoglobulins.

One of the mechanisms responsible for these reactions is the formation of antigen-antibody reactions on the red blood cell surface or from immune complexes resulting in the activation of complement. The athletic by-products generated by complement activation (anaphylatoxins C3a, C4a and C5a) cause mast cell (and basophil) degranulation, mediator release and generation, and anaphylaxis. In addition, complement products may directly induce vascular permeability and contract smooth muscle.

Cytotoxic reactions can also cause anaphylaxis, via complement activation. Antibodies (IgG and IgM) against red blood cells, as occurs in a mismatched blood transfusion reaction, activate complement.

This reaction causes agglutination and lysis of red blood cells and perturbation of mast cells resulting in anaphylaxis.

Modulators of Arachidonic Acid Metabolism

Catamenial Anaphylaxis

Catamenial anaphylaxis is a syndrome of hypersensitivity induced by endogenous progesterone secretion. Patients may exhibit a cyclic pattern of attacks during the premenstrual part of the cycle.

Muscle relaxants

Anaphylaxis to muscle relaxants occurs in approximately 1 in 4, of general anesthesia, with fatalities occurring in 6% of these cases.

Risk factors are female sex (80% of cases). Atopy is not a risk factor; previous drug allergy may be a risk factor. In patients with a history of anaphylaxis, skin tests to diverse muscle relaxants may be helpful. If the test result is positive, the muscle relaxant should not be used. A negative result provides evidence that the muscle relaxant can probably be istered safely.

Insects

Hymenoptera venoms (bee, wasp, yellow-jacket, hornet, fire ant) contain enzymes such as phospholipases and hyaluronidases and other proteins which can elicit an IgE antibody response.

Radiocontrast Media, Low-molecular Weight Chemicals

Mast cells may degranulate when exposed to low-molecular-weight chemicals.

Hyperosmolar iodinated contrast media may cause mast cell degranulation by activation of the complement and coagulation systems. These reactions can also happen, but much less commonly, with the newer contrast media agents.

Food-associated, exercise-induced anaphylaxis

This is more common in females, and over 60% of cases happen in individuals less than 30 years of age. Patients sometimes own a history of reacting to the food when younger and generally own positive skin tests to the food that provokes their anaphylaxis.

Miscellaneous

Examples of miscellaneous agents which cause anaphylaxis are insulin, seminal proteins, and horse-derived antitoxins, the latter of which are used to neutralize venom in snake bites.

Individuals who own IgA deficiency may become sensitized to the IgA provided in blood products. Those selective IgA deficient subjects ( of the general population) can develop anaphylaxis when given blood products, because of their anti-IgA antibodies (probably IgE-anti-IgA).

Elective Medical Procedures

Allergen immunotherapy

Cytoxic and Immune Complicated – Complement-Mediated Reactions

Anaphylaxis caused by radio-contrast media

Mild adverse reactions are experienced by approximately 5% of subjects receiving radio-contrast media.

U.S. figures propose that severe systemic reactions happen in exposures with death in ,, exposures.

Penicillin-induced anaphylaxis

One percent to 5% of courses of penicillin therapy are complicated by systemic hypersensitivity reactions. Point two percent is associated with anaphylactic shock, and mortality occurs in % of the cases. If a patient has a strongly positive skin test or circulating IgE antibody to penicillin, there is a % risk of an anaphylactic reaction upon subsequent challenge. In patients with a case history suggestive of penicillin allergy and negative skin tests, the risk of anaphylaxis is extremely low.

Atopy and mold sensitivity are not risk factors for the development of penicillin allergy.

A = Airway

Ensure and establish a patent airway, if necessary, by repositioning the head and neck, endotracheal intubation or emergency cricothyroidotomy. Put the patient in a supine position and elevate the lower extremities. Patients in severe respiratory distress may be more comfortable in the sitting position.

C = Corticosteroids

Corticosteroids do not benefit acute anaphylaxis but may prevent relapse or protracted anaphylaxis. Hydrocortisone ( to mg) or its equivalent can be istered every 6 to 8 hours for the first 24 hours.

Doses must be adjusted for children.

Definition of Anaphylaxis

Anaphylaxis is an acute, potentially life-threatening hypersensitivity reaction, involving the release of mediators from mast cells, basophils and recruited inflammatory cells. Anaphylaxis is defined by a number of signs and symptoms, alone or in combination, which happen within minutes, or up to a few hours, after exposure to a provoking agent. It can be mild, moderate to severe, or severe.

Most cases are mild but any anaphylaxis has the potential to become life-threatening.

Anaphylaxis develops rapidly, generally reaching peak severity within 5 to 30 minutes, and may, rarely, final for several days.

Classification

The term anaphylaxis is often reserved to describe immunological, especially IgE-mediated reactions. A second term, non-allergic anaphylaxis, describes clinically identical reactions that are not immunologically mediated. The clinical diagnosis and management are, however, identical.

Prevention of Anaphylaxis

Agents causing anaphylaxis should be identified when possible and avoided.

Patients should be instructed how to minimize exposure.

Beta-adrenergic antagonists, including those used to treat glaucoma, may exacerbate anaphylaxis and should be avoided, where possible. Angiotensin-converting enzyme (ACE) inhibitors may also increase susceptibility to anaphylaxis, particularly with insect venom-induced anaphylaxis.

Epinephrine is the drug of choice to treat anaphylaxis. Individuals at high risk for anaphylaxis should be issued epinephrine syringes for self-istration and instructed in their use.

Intramuscular injection into the anterolateral thigh is recommended since it results in immediate elevation of plasma concentrations and has immediate physiological effects. Subcutaneous injection results in delayed epinephrine absorption. Patients must be alerted to the clinical signs of impending anaphylaxis and the need to carry epinephrine syringes at every times and to use it at the earliest onset of symptoms. Unused syringes should be replaced when they reach their use-by/expiration date, as epinephrine content and bioavailability of the drug decreases in proportion to the number of months past the expiration date.

Pre-treatment with glucocorticosteroids and H1 and H2 antihistamines is recommended to prevent or reduce the severity of a reaction where it is medically necessary to ister an agent known to cause anaphylaxis, for example, radio-contrast media.

Other significant patient instructions include:

a) Personalized written anaphylaxis emergency action plan
b) Medical Identification (e.g., bracelet, wallet card)
c) Medical record electronic flag or chart sticker, and emphasis on the importance of follow-up investigations by an allergy/immunology specialist

Symptoms and Signs of Anaphylaxis

The initial manifestation of anaphylaxis may be loss of consciousness.

Patients often describe "a sense of doom." In this instance, the symptoms and signs of anaphylaxis are isolated to one organ system, but since anaphylaxis is a systemic event, in the vast majority of subjects two or more systems are involved.

Gastro-intestinal: Abdominal pain, hyperperistalsis with faecal urgency or incontinence, nausea, vomiting, diarrhea.

Oral: Pruritus of lips, tongue and palate, edema of lips and tongue.

Respiratory: Upper airway obstruction from angioedema of the tongue, oropharynx or larynx; bronchospasm, chest tightness, cough, wheezing; rhinitis, sneezing, congestion, rhinorrhea.

Cutaneous: Diffuse erythema, flushing, urticaria, pruritus, angioedema.

Cardiovascular: Faintness, hypotension, arrhythmias, hypovolemic shock, syncope, chest pain.

Ocular: Periorbital edema, erythema, conjunctival erythema, tearing.

Genito-urinary: Uterine cramps, urinary urgency or incontinence.

Severe initial symptoms develop rapidly, reaching peak severity within minutes.

There may occasionally be a quiescent period of 1–8 hours before the development of a second reaction (a biphasic response). Protracted anaphylaxis may happen, with symptoms persisting for days. Death may happen within minutes but rarely has been reported to happen days to weeks after the initial anaphylactic event.

Differential Diagnosis

The differential diagnosis for anaphylaxis includes:

  1. pulmonary embolism
  2. myocardial infarction
  3. foreign body aspiration
  4. hypoglycemia
  5. cholinergic urticaria
  6. respiratory difficulty or circulatory collapse, including vasovagal reactions
  7. seizures
  8. cold urticaria
  9. epiglottitis
  10. overdose of medication
  11. pheochromocytoma
  12. globus hystericus
  13. hereditary angioedema
  14. carcinoid syndrome
  15. status asthmaticus
  16. sulfite or monosodium glutamate ingestion

Upper airway obstruction, bronchospasm, abdominal cramps, pruritus, urticaria and angioedema are absent in vasovagal reactions.

Pallor, syncope, diaphoresis and nausea generally indicate a vaso-vagal reaction but may happen in either condition.

If a reaction occurs during a medical procedure, it is significant to consider a possible reaction to latex or medication used for or during anesthesia.

Causes of Anaphylaxis

Sulfiting Agents

Narcotics

Narcotics are mast cell activators capable of causing elevated plasma histamine levels and non-allergic anaphylaxis. They are most commonly observed by anesthesiologists.

IgE-Mediated Reactions

Foods

In theory, any food glycoprotein is capable of causing an anaphylactic reaction.

Foods most frequently implicated in anaphylaxis are:

  1. Tree nuts (walnut, hazel nut/filbert, cashew, pistachio nut, Brazil nut, pine nut, almond)
  2. Shellfish (shrimp, crab, lobster, oyster, scallops)
  3. Fish
  4. Chicken eggs
  5. Seeds (cotton seed, sesame, mustard)
  6. Peanut (a legume)
  7. Milk (cow, goat)
  8. Fruits, vegetables

Food sensitivity can be so severe that a systemic allergic reaction can happen to particle inhalation, such as the odors of cooked fish or the opening of a package of peanuts.

A severe allergy to pollen, for example, ragweed, grass or tree pollen, can indicate that an individual may be susceptible to anaphylaxis or to the oral allergy syndrome (pollen/food syndrome) (manifested primarily by severe oropharyngeal itching, with or without facial angioedema) caused by eating certain plant-derived foods.

This is due to homologous allergens found between pollens and foods. The main allergen of every grasses is profilin, which is a pan-allergen, found in numerous plants, pollens and fruits, and grass-sensitive individuals can sometimes react to numerous plant-derived foods.

Typical aero-allergen food cross-reactivities are:

  1. Birch pollen: apple, raw potato, carrot, celery and hazelnut
  2. Mugwort pollen: celery, apple, peanut and kiwifruit
  3. Ragweed pollen: melons (watermelon, cantaloupe, honeydew) and banana
  4. Latex: banana, avocado, kiwifruit, chestnut and papaya

Food-associated, exercise-induced anaphylaxis may happen when individuals exercise within hours after ingesting a specific food.

The individual is, however, capable to exercise without symptoms, as endless as the incriminated food is not consumed before exercise. The patient is likewise capable to ingest the incriminated food with impunity as endless as no exercise occurs for several hours after eating the food.

C = Circulation

Minimize or eliminate continued exposure to causative agent by discontinuing the infusion, as with radio-contrast media, or by placing a venous tourniquet proximal to the site of the injection or insect sting. Assess adequacy of perfusion by taking the pulse rate, blood pressure, mentation and capillary refill time. Establish I.V. access with large bore ( to gauge) catheter and ister an isotonic solution such as normal saline.

A second I.V. may be established as necessary. If a vasopressor, such as dopamine becomes necessary, the patient requires immediate transfer to an intensive care setting.

The same ABC mnemonic can be used for the pharmacologic management of anaphylaxis:

Sodium and Potassium Sulfites, Bisulfites, Metabisulfites, and Gaseous Sulfur Dioxides

These preservatives are added to foods and drinks to prevent discoloration and are also used as preservatives in some medications. Sulfites are converted in the acid environment of the stomach to SO2 and H2SO3, which are then inhaled.

They can produce asthma and non-allergic hypersensitivity reactions in susceptible individuals.

Non-immunologic Mast Cell Activators

Idiopathic Anaphylaxis

Flushing, tachycardia, angioedema, upper airway obstruction, urticaria and other signs and symptoms of anaphylaxis can happen without a recognizable cause. Diagnosis is based primarily on the history and an exhaustive search for causative factors. Serum tryptase and urinary histamine levels may be useful, in specific, to law out mastocytosis.

Management

Allergy / immunology specialists frolic a uniquely significant role to confirm the etiology of anaphylaxis, prepare the patient for self istration of epinephrine, educate the patient and/or family about allergen avoidance, and law out any underlying condition, such as mastocytosis, which can predispose a patient to develop anaphylaxis.

Referral to an allergist / immunologist is indicated for patients with this disease.

After informed consent, subjects will be randomly assigned to ILIT group or placebo group in double-blind manner. In both group, causal allergen or placebo will be injected into inguinal lymph node through guidance by ultrasonography three times with 4-week interval. In ILIT group, initial dose of allergen will be 1,fold diluted solution from maximal concentration of allergen extract for subcutaneous immunotherapy (Tyrosine S, Allergy Therapeutic, West Sussex, UK) in volume of ml.

If skin is highly reactive in skin prick test, the initial dose will be fold dilution from maximal concentration where diameter of wheal is less than that of histamine. After the first dose, allergen concentration will be escalated 3-fold at second dose, and fold at third dose if there are no (or mild) local or systemic hypersensitivity reaction. The allergen concentration will not change at second or third dose if there is moderate local or systemic reaction. The allergen concentration will decrease by 10 or fold from previous concentration or further injection will be held if there is severe local or systemic reaction after sufficient explanation and discussion with subjects.

The investigators will assess allergic rhinitis symptom score before and 4, 12 months after the initial treatment.

Rhinoconjunctivitis Quality of Life Questionnaire (RQLQ) and Sino-Nasal Outcome Test (SNOT) will be used. Visual analogue scale (VAS) of symptoms including rhinorrhea, sneezing, nasal obstruction, postnasal drip, eye/nose/ear/palate itching, dyspnea, wheezing, chest discomfort as well as urticaria, angioedema, and itching on exposed skin during exposure to causal allergen in daily life will be also evaluated. Skin prick test (SPT), intradermal test (IDT), blood sampling for serum entire immunoglobulin E (IgE), allergen-specific IgE, and allergen-specific immunoglobulin G4 (IgG4), nasal lavage for Th1, Th2, and Treg cytokines, and nasal provocation test (NPT) with Df and/or Dp allergen (in subjects whose AR symptoms are provoked by Df and/or Dp) will be also performed before and 4, 12 months after the initial treatment.

In addition, the investigators evaluated the change of subjects’ recognition of causal allergens, their avoidance, and AIT during this study. Using VAS, subjects were requested to score the rate of agreement with "Allergen provokes allergic symptoms in daily life", "Allergen avoidance can reduce allergic symptoms", "Allergen-specific Immunotherapy (AIT) can reduce allergic symptoms", "I can pay 50, Korean Won (KRW)/month for allergen avoidance", "I can pay , KRW/month for allergen avoidance", "I can pay , KRW/month for allergen avoidance", "I can pay , KRW for each injection of ILIT", "I can pay , KRW for each injection of ILIT", "I can pay , KRW for each injection of ILIT" before and after SPT/IDT, after NPT, 4 months and 1 year after ILIT.

Adverse events will be recorded and graded according to Muller classification and Ring and Meissner classification.

Twenty-five patients living in a tick-endemic region of Sydney, New South Wales developed red meat allergy after experiencing large local reactions to tick bites.

This represents a potentially novel cross-reaction between an arthropod and a food protein.

Clinical records

Between  and , 25 patients (seven men, 18 women; mean age [range],  [21–63] years) presented to our allergy practice in Sydney, New South Wales with a history of an allergic reaction to red meat.

All 25 patients reported a clinical reaction (one or more of: urticaria, angioedema, respiratory distress, syncope) after ingesting red meat. Ten of the 25 patients (40%) reported a delayed onset of symptoms, as defined by manifestations occurring more than 4 hours after ingestion.

Seventeen of the 25 patients (68%) had severe reactions, characterised by cardiorespiratory involvement (one or more of: tongue swelling, throat constriction, shortness of breath, wheeze). Beef was the most commonly implicated red meat, followed by lamb, pork and game; 11 individuals reported reactions to more than one type of red meat.

All patients lived in the northern beaches region of Sydney, which is endemically infested with several tick species.

Twenty-four of the 25 patients gave a history of large local reactions to tick bites, defined as the rapid or delayed onset of a painful, pruritic lesion greater than 50 mm in diameter that persisted for at least 1 week.1 They every stated that the organism responsible for their local reaction was a hard-bodied tick, based on the presence of an armoured shell (scutulum). They also provided an estimate of the tick’s size, which ranged from 3 to 10 mm, and recalled the shape as resembling that of a human fingernail.

No patient reported a history of large local or generalised reactions to other bites or stings, such as those from honeybees, wasps or mosquitoes. The remaining patient did not report any reactions, despite having incurred multiple tick bites. In every but one case, tick exposure preceded the development of the meat allergy by 1 to 6 months. One patient’s onset of meat allergy preceded the tick bite by 6 months.

Patients’ IgE-mediated responses to red meat were confirmed by skin-prick test and/or fluoroenzyme immunoassay (ImmunoCAP, Phadia, Uppsala, Sweden). Every patients had a positive result for at least one type of red meat; 22/25 (88%) had a positive reaction to more than one type (Box 1).

There was no correlation between the wheal size on skin-prick testing or the quantity of specific IgE detected by fluoroenzyme immunoassay and either the severity of the response to red meat ingestion or the size of the local reaction to the tick bite.

The records of 29 patients (10 men, 19 women; mean age [range],  [17–71] years) with confirmed IgE-mediated responses to foods other than red meat, attending the same practice and residing in the same region, were examined as a retrospective control. The control group comprised patients with reactions to a spectrum of foods, most commonly seafood, peanut, tree nut and soybean.

Every 29 patients had reported a history of tick bites without subsequent reaction.

These findings propose that, in our patient population, the overwhelming majority of cases of the relatively rare condition of red meat allergy were preceded by sensitisation to tick bites.

Discussion

Based on our experience of 25 patients, we propose a novel association between tick bite reactions and red meat allergy. We speculate that individuals are sensitised to tick salivary proteins that are cross-reactive with proteins found in various red meats.

Cross-reactivity between milk and beef,2 and between animal epithelia and meat,3,4 has been previously described, suggesting mechanisms of secondary sensitisation to meat.

The association with reactions to tick salivary proteins may represent another such example. Anaphylactic and large local reactions to tick bites are IgE-mediated responses to tick salivary proteins.1

We infer that the species of hard-bodied tick most likely to be responsible for these local reactions is Ixodes holocyclus, commonly known as the paralysis tick (Box 2). I. holocyclus is not only the major species of tick found in the northern beaches region of Sydney that affects humans, but is also the species responsible for hypersensitivity reactions in humans.5 However, a skin-prick solution comprising paralysis tick antigens has not been standardised, and an in-house preparation carries a risk not only of anaphylaxis, but also of introduction of tick-borne disease; hence, there is currently no dependable, safe method of detecting IgE antibodies against I.

What is an allergy in physiological terms

holocyclus.

It is intriguing that none of our patients who developed red meat allergy had an anaphylactic reaction to tick bite. It is possible that diverse allergens are involved in IgE-mediated local reactions and anaphylaxis, and that the allergens involved in local reactions are also found in red meat proteins, or, alternatively, that the inoculated allergens are processed differently in diverse individuals. There may be poorer inactivation of allergens by mast cells at the local site in some individuals, resulting in a more prolonged immunological stimulus.6

Bovine serum albumin has been identified as a major allergen responsible for a number of cases of meat allergy.7 More recently, IgE antibody to galactose-α-1,3-galactose has been identified as a cause of anaphylaxis and delayed immune reactions to red meat.8 This molecule is also present in recombinant mouse-derived monoclonal antibodies, such as cetuximab, and a number of invertebrates, such as amoebae and worms.9 It remains to be sure whether such homologous allergens exist in tick saliva.

An alternative explanation is simply that the transfer of animal allergens by the tick occurs in genetically predisposed individuals. Bandicoots, possums and dogs, rather than cattle, are recipients of bites from the I. holocyclus species of tick, and it is therefore possible that there are allergens with a high level of homology found within bandicoot, possum and various ingestible red meat proteins. Also, the possibility of cutaneous exposure as a route of sensitisation to food allergens has been postulated as a mechanism for the development of peanut allergy

To determine the true prevalence of this cross-reactivity, a prospective study could examine consecutive patients who are bitten by ticks (with and without adverse reactions) for the subsequent development of red meat allergy.

A standardised in-vitro assay for specific IgE against tick salivary allergens would need to be developed and incorporated into each participant’s evaluation. Further studies are required to characterise these allergens with immunoblotting and inhibition studies.

1 Skin-prick test and fluoroenzyme immunoassay results for patients with clinical reactions to red meat

Patient

Skin-prick test


Fluoroenzyme immunoassay


Beef

Pork

Lamb

Game*

Beef

Pork

Mutton


1

+

+

nd

+

+

2

+

nd

nd

nd

nd

nd

nd

3

nd

nd

nd

nd

+

+

+

4

+

+

nd

+

+

+

5

+

nd

nd

nd

nd

nd

nd

6

+

+

nd

+

nd

nd

nd

7

nd

+

nd

nd

nd

nd

nd

8

nd

nd

+

nd

+

nd

+

9

+

+

+

+

nd

nd

nd

10

+

+

+

nd

nd

nd

nd

11

+

+

+

nd

nd

nd

nd

12

+

+

+

nd

nd

nd

nd

13

+

+

+

nd

nd

nd

nd

14

nd

nd

nd

nd

+

+

+

15

+

+

+

+

+

+

+

16

+

+

nd

nd

nd

nd

17

+

+

nd

+

nd

nd

nd

18

nd

nd

nd

nd

+

+

nd

19

+

+

+

nd

20

+

+

nd

21

+

+

+

nd

nd

nd

nd

22

+

nd

+

nd

nd

nd

nd

23

+

+

+

nd

nd

24

+

+

nd

nd

nd

nd

25

nd

+

nd

+

+

+

+

2 Developmental stages of Ixodes holocyclus


Methods

This longitudinal study was part of a larger study examining physiological responses during the Three Cranes Challenge (a 3-day 95 km trail run) in Karkloof, KwaZulu-Natal on 25 — 27 February Local institutional ethical approval was obtained, and a sample of 22 volunteers signed informed consent forms.

After routine baseline testing on the afternoon before the race, venous blood samples were collected at a entire of 8 time points, before and after each day&#x;s stage (S1pre, S1post, S2pre, S2post, S3pre and S3post), 24 hours post-race (24PR) and 72 hours post-race (72PR).

RTS data were collected over a day period, from 14 days prior to the race until the 14th day after the race. Of the 22 subjects, 16 completed the race and complied with every the study requirements. Two subjects were excluded as a result of failure to finish the race, and a further 4 did not finish post-race testing.

Athletes were asked to record the daily incidence and severity of RTS before, during and after the race using a graded 1 — 3-point scoring system.

Symptoms monitored included cough, runny nose, sneezing, blocked nose, sore throat, headache, fever, tight chest and itchy eyes. A entire RTS index score was sure using the sum of severity scores and the length of time that the symptom(s) persisted.

To determine which subjects qualified for post-exercise RTS, any subject presenting with a single RTS lasting <2 days or any nonspecific symptom (e.g. headache, itchy eyes) not accompanied by RTS lasting >1 day, was excluded. A peak post-stage or post-race serum IgE (sIgE) concentration under the clinically significant range ( IU/ml) excluded the possibility of the RTS being of allergic origin.

Full blood counts, pre-race Phadiatop status and sIgE concentrations were sure by Ampath Laboratories, Howick, KwaZulu-Natal, using an automated UniCAP system.

In the Phadiatop assay, concentrations > IU/ml represented a positive response, irrespective of range

Exercise-induced changes in plasma volume (PV) over this 3-day event were sure from pre- and post-exercise haematocrit and haemoglobin concentrations Post-exercise sIgE levels and concentration-dependent leucocyte counts were adjusted for percentage exercise-induced change in PV.

After confirmation of the absence of normality of the data, they were logarithmically transformed. A generalised linear model was applied to the median (range) sIgE and differential leucocyte concentration data from multiple subjects over multiple time points and between Phadiatop-positive and negative groups.

The Mann-Whitney U-test was used to compare the RTS data pre- and post-race and between Phadiatop-positive and negative groups. Data are presented as the median (interquartile range (IQR)) in box-and-whisker plots in Figs 1 and 2. Significance was set at p=



Brief Biography

Thomas Eiwegger earned his doctoral degree at the Medical University of Vienna, Austria, where he also completed his paediatric training. He did his post doctoral training in the Swiss Institute of Asthma and Allergy in the group of Cezmi Akdis from to and after returned to the Medical University of Vienna where he trained in paediatric allergy and respiratory medicine.

Before moving to Sickkids, Eiwegger was Principal Investigator and Associate Professor at the Department of Paediatrics and Adolescent Medicine, Medical University of Vienna, Austria.

Research Interests

Developing and facilitating new concepts in the treatment of food allergy

Eiwegger’s main interests are mechanisms of IgE-mediated allergy. He will focus in specific on a better understanding of the mechanisms of tolerance development to food allergens and markers thereof. Eiwegger will define new treatment approaches by delineating the sequence of events that take put in children that lose their food allergy.

Publications

Saidova A, Hershkop AM, Ponce M, Eiwegger T.

Allergen-Specific T Cells in IgE-Mediated Food Allergy. Arch Immunol Ther Exp (Warsz) in press.

Gona-Hopler M, Pfaller B, Argeny J, Kanolzer S, Gruber S, Schmidthaler K, et al. Aspergillus fumigatus-specific immunoglobulin levels in BALF of CF patients. ERJ Open Res ; 3.

Diesner SC, Lukas J, Stifter E, Raimann A, Nachbaur E, Eiwegger T, Renner S, Geleff S, Emminger W, Szépfalusi Z.

What is an allergy in physiological terms

Bilateral infiltrative dacryoadenitis and granulomatous pneumonia in an year ancient boy: a case report. Klin Padiatr ;

Diesner SC, Bergmayr C, Pfitzner B, Assmann V, Krishnamurthy D, Starkl P, Endesfelder D, Rothballer M, Welzl G, Rattei T, Eiwegger T, Szépfalusi Z, Fehrenbach H, Jensen-Jarolim E, Hartmann A, Pali-Schöll I, Untersmayr E, A distinct microbiota composition is associated with protection from food allergy in an oral mouse immunization model. Clin Immunol. Dec; doi:

Akdis M, Aab A, Altunbulakli C, Azkur K, Costa RA, Crameri R, Duan S, Eiwegger T, Eljaszewicz A, Ferstl R, Frei R, Garbani M, Globinska A, Hess L, Huitema C, Kubo T, Komlosi Z, Konieczna P, Kovacs N, Kucuksezer UC, Meyer N, Morita H, Olzhausen J, O’Mahony L, Pezer M, Prati M, Rebane A, Rhyner C, Rinaldi A, Sokolowska M, Stanic B, Sugita K, Treis A, van de Veen W, Wanke K, Wawrzyniak M, Wawrzyniak P, Wirz OF, Zakzuk JS, Akdis CA: Interleukins (from IL-1 to IL), interferons, transforming growth factor beta, and TNF-alpha: Receptors, functions, and roles in diseases.

J Allergy Clin Immunol ;

Broekman HCH, Eiwegger T, Upton J, Bogh KL. IgE – The Main Player of Food Allergy. Drug Discovery Today: Disease Models – October DOI: /

Hansen CS, Hansen CS, Dufva M, Bøgh KL, Sullivan E, Patel J, Eiwegger T, Szépfalusi Z, Nielsen M, Christiansen A, Linear epitope mapping of peanut allergens demonstrates individualized and persistent antibody binding patterns, Journal of Allergy and Clinical Immunology (), doi: /

Ponce M, Diesner SC, Szepfalusi Z, Eiwegger T, Markers of tolerance development to food allergens.

Oct;71(10) doi: /all

Angelina A, Sirvent S, Palladino C, Vereda A, Cuesta-Herranz J, Eiwegger T, Rodriguez R, Breitendeder H, Villalba M, Palomares O. The Lipid-interaction capacity of Sin a 2 and Ara h 1, major mustard and peanut allegens of the cupin superfamily, endorses allergenicity. Allergy. Mar 17 doi /all (epub ahead of print).

O’Mahony L, Akdis CA, Eiwegger T. Innate mechanisms can predict successful allergy immunotherapy.

J Allergy Clin Immunol. Feb, (2)

Christiansen A, Kringelum JV, Hansen CS, Bogh KL, Sullivan E, Patel J, Rigby NM, Eiwegger T, Szepfalusi Z, de Masi F, Nielsen M, Lund O, Dufva M. High-throughput sequencing enhanced phage display enables the identification of patient-specific epitope motifs in serum. Sci Rep ; 5:

Soyka MB, Holzmann D, Basinski TM, Wawrzyniak M, Bannert C, Bürgler S, Akkoc T, Treis A, Rückert B, Akdis M, Akdis CA, Eiwegger T.

The induction of IL in the sinus epithelium and its influence on T-helper cell responses. PlosOne ; e

Boyman O, Kaegi S, Akdis S, Bavbek S, Bossios A, Chatzipetrou A, Eiwegger T, Firinu D, Harr T, Knol E, Matucci A, Palomares O, Schmidt-Weber C, Simon HU, Steiner UC, Vultaggio A, Akdis CA and Spertini F. EAACI IG Biologicals task force paper on the use of biologic agents in allergic disorders. Allergy ; 70(7):

Upton J, Eiwegger T. How Endless Should We Go. Int Arch Allergy Immunol. ;(3) doi: / Epub Jan

Ackerbauer D, Bublin M, Radauer C, Varga EM, Hafner C, Ebner C, Szépfalusi Z, Fröschl R, Hoffmann-Sommergruber K, Eiwegger T, Breiteneder H.

Component-resolved IgE profiles in Austrian patients with suspected peanut allergy. Int Arch Allergy Immunol ;

Szepfalusi Z, Bannert C, Ronceray L, Mayer E, Hassler M, Wissmann E, Dehlink E, Gruber S, Graf A, Lupinek C, Valenta R, Eiwegger T, Urbanek R. Preventive sublingual immunotherapy in preschool children: first evidence for safety and pro-tolerogenic effects. Pediatr Allergy Immunol ;

Martin-Fontecha M, Eiwegger T, Jartti T, Rueda-Zubiaurre A, Tiringer K, Stepanow J, Puhakka T, Ruckert B, Ortega-Gutierrez S, Lopez-Rodriguez ML, Akdis M, Akdis CA, Palomares O.

The expression of cannabinoid receptor 1 is significantly increased in atopic patients. J Allergy Clin Immunol ; e

Bublin M, Eiwegger T, Breiteneder H. Do lipids influence the allergic sensitization process? J Allergy Clin Immunol

Bogh KL, Nielsen H, Eiwegger T, Madsen CB, Mills EN, Rigby NM, Szepfalusi Z, Roggen EL. IgE versus IgG4 epitopes of the peanut allergen Ara h 1 in patients with severe allergy. Mol Immunol ;

Tiringer K, Treis A, Kanolzer S, Witt C, Chanim B, Gruber S, Schmidthaler K, Renner S, Dehlink E, Nachbaur E, Frischer T, Klepetko W, Akdis CA, Szepfalusi Z, Eiwegger T. Differential expression of IL and HMGB1 in the lungs of stable cystic fibrosis patients.

Eur Respir J. Sep;44(3) doi/

Tiringer K, Treis A, Fucik P, Gona M, Gruber S, Renner S, Dehlink E, Nachbaur E, Horak F, Jaksch P, Doring G, Crameri R, Jung A, Rochat MK, Hormann M, Spittler A, Klepetko W, Akdis CA, Szepfalusi Z, Frischer T, Eiwegger T. A Th and Th2-skewed cytokine profile in cystic fibrosis lungs represents a potential risk factor for pseudomonas aeruginosa infection. Am J Respir Crit Care Med ;

Prelog M, Schonlaub J, Jeller V, Almanzar G, Hofner K, Gruber S, Eiwegger T, Wurzner R. Reduced varicella-zoster-virus (VZV)-specific lymphocytes and IgG antibody avidity in solid organ transplant recipients.

Vaccine ;

Diesner SC, Gruber S, Dehlink E, Muhlebner A, Eiwegger T, Szepfalusi Z. Somnolence upon allergen provocation in a kid with hen’s egg allergy. Klin Padiatr
Soyka MB, Wawrzyniak P, Eiwegger T, Holzmann D, Treis A, Wanke K, Kast JI, Akdis CA. Faulty epithelial barrier in chronic rhinosinusitis: The regulation of tight junctions by ifn-gamma and IL J Allergy Clin Immunol ; e

Soyka MB, Treis A, Eiwegger T, Menz G, Zhang S, Holzmann D, Akdis CA, Meyer N. Regulation and expression of il in chronic rhinosinusitis.

Allergy ;

Meyer N, Christoph J, Makrinioti H, Indermitte P, Rhyner C, Soyka M, Eiwegger T, Chalubinski M, Wanke K, Fujita H, Wawrzyniak P, Burgler S, Zhang S, Akdis M, Menz G, Akdis C. Inhibition of angiogenesis by il Possible role in asthma. J Allergy Clin Immunol ; e

Mayer E, Bannert C, Gruber S, Klunker S, Spittler A, Akdis CA, Szepfalusi Z, Eiwegger T. Cord blood derived cd4+ cd25(high) t cells become functional regulatory t cells upon antigen encounter. PLoS One ;7:e

Gruber S, Eiwegger T, Nachbaur E, Tiringer K, Aigner C, Jaksch P, Keplinger M, Klepetko W, Lang G, Taghavi S, Graf A, Eichler I, Frischer T, Szepfalusi Z.

Lung transplantation in children and young adults: A year single-centre experience. Eur Respir J ;

Eiwegger T, Gruber S, Szepfalusi Z, Akdis CA. Novel developments in the mechanisms of immune tolerance to allergens. Hum Vaccin Immunother ;

Bogh KL, Nielsen H, Madsen CB, Mills EN, Rigby N, Eiwegger T, Szepfalusi Z, Roggen EL. Ige epitopes of intact and digested ara h 1: A comparative study in humans and rats. Mol Immunol ;

Phadiatop testing in assessing predisposition to respiratory tract symptoms of allergic origin in athletes

Anton H de Waard, Edith M Peters

Objectives.

To validate the use of the Phadiatop test as a predictor of allergy-associated respiratory tract symptoms (RTS) in trail runners.

Methods. The incidence of self-reported RTS was documented in 16 runners for 31 days and related to the Phadiatop status and circulating markers of allergic responses (changes in concentrations of serum IgE (sIgE), differential leucocyte counts) at 8 time points before, during and after a 3-day 95 km trail run.

Results. Twelve (75%) athletes, of whom 7 (58%) were Phadiatop-positive, presented with post-race RTS. A peak sIgE concentration > IU/ml accompanied RTS in only 4 (57%) of the symptomatic Phadiatop-positive subjects.

There was no significant difference between the eosinophil and basophil concentrations of the positive and negative groups (p>). One Phadiatop-negative subject presented with RTS as well as a peak sIgE concentration > IU/ml.

Conclusion. The Phadiatop assay does not accurately predict the development of post-exercise RTS of allergic origin in trail runners.

S Afr Med J ;(5)

Division of Human Physiology, School of Laboratory Medicine and Medical Sciences, College of Health Sciences, University of KwaZulu-Natal, Durban

Anton H de Waard, M Tech Hom

Edith M Peters, MSc (Med), PhD

Corresponding author: E M Peters ([email protected])

Since the early s there has been concern about the high incidence of upper respiratory tract infections (URTIs) among athletes during periods of intensive exercise training and exhaustive endurance events.1,2 This results in interrupted training schedules and impaired performance in competitive events.

Exercise immunologists own sought methods to identify the cause of these symptoms, which own now been extended to include the lower respiratory tract.3

Of post-exercise respiratory tract symptoms (RTS), 30 — 40% of cases are the result of infection, a further 30% are due to inflammation, and the final 30% are from unknown causes.2,4 Numerous theories own been proposed to account for the occurrence of non-infective post-exercise RTS, including the development of hyper-reactive airways,7 runaway inflammatory responses,8 reactivation of latent viral infection6 and allergic reactions.3,9

It has been documented that athletes experience higher rates of allergic disease than the general population10 and that the cited incidence of allergy among Olympic athletes is increasing Exercise-induced symptoms of infection of the respiratory tract can mimic an allergic reaction,3 and exercise induces a TH2-dominant immunological shift;2 therefore, it may up-regulate an allergic response in those already sensitised.9 Increased exposure of athletes to irritants and allergens may contribute to this.3,11

Although the skin prick test (SPT) is generally accepted as the standard method for detecting IgE-related allergic sensitisation,12 its limitations include a lowered response in the elderly, greater difficulty in grading the response in dark-skinned persons, its contra-indication in pregnancy, the quality and selection of allergens, and the theoretical risk of anaphylaxis

Specific IgE antibody testing is accepted as an alternative to the SPT Combination tests such as the Phadiatop assay (Pharmacia & Upjohn Diagnostics, Uppsala, Sweden) simultaneously test for IgE to a mixture of allergens causing common inhalant allergies.

Allergens included in the Phadiatop assay are Artemisia, dust mites (Dermatophagoidespteronyssinus and e), mixed moulds (Penicillium, Cladosporium, Aspergillus and Alternaria), pet dander (cat and dog), mixed grasses (Parietaria, Lolium, Phleum and Cynodon), and mixed trees (Acer, Betula, Olea, Salix, Pinus, Ulmus, Quercus, Eucalyptus, Acacia and Melaleuca) This assay has been found satisfactory for the diagnosis of IgE allergic sensitisation in the general population, with a sensitivity of % and a specificity of % compared with the SPT

Our objectives were to: (i) investigate the validity of the Phadiatop test as a predictor of allergy-associated RTS in athletes competing in a 3-day 95 km trail run, (ii) document the incidence of RTS before, during and after the event, and (iii) relate these incidences to the concentrations of serum IgE, leucocyte sub-classes and Phadiatop status of the athletes throughout and after the event.


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