Interesting Items from the AAAAI Meeting- 2013

The American Academy of Allergy, Asthma, and Immunology had their Annual Meeting in San Antonio in late February, 2013. As is the habit of this author I would like to share a number of items that I found interesting, thought provoking, and potentially practice changing. The meeting started on Friday and ended on Tuesday. There were too many offerings to report on all of them. My retyped notes span 23 pages.

Allergy Testing-Extracts, Blood Tests, and Allergens (Robert Hamilton)

There are about 200 allergens available to look at with specific IgE, clearly more things cause allergy. For allergen immunotherapy- allergy shots, there are 19 standardized extracts. A standardized extract allows easly migration from one allergist to another if the patient is on immunotherapy with one of these standardized extracts. There are 1269 allergen extracts out there that have not been standardized and 566 allergen extracts that are being used without any literature to support their use. Unless studies appear to support their use, they will no longer be available.

Allergen component testing is the new wave of diagnostics. This gets down to the specific protein that is responsible for symptoms. This technology may help explain cross-reactivity between allergens. Some of the proteins that a patient reacts to on testing may not be associated with significant reactions.

New issues with allergy diagostics includes dealing with the lower range of detection- previously the blood tests could not measure below 0.35 kU/L. Now levels of 0.1 kU/l can be dected. We are not sure what the range 0.1 to0.35 kU/L means and if it is useful. There is also a need to establish blood test levels that predict reactions.

A point re-itereated many times- the patient’s history drives the selection of diagnostic tests.

Accelerated Immunotherapy Schedules  (David Kahn)

The bottom line here;

  • Convenient- Yes
  • Just as safe- No

Types

  • Rush Immunotherapy- first reported on in 1930 (RIT)
  • Cluster Immunotherapy (CIT)
  • Conventional Immunotherapy (IT)

Rush

  • The accelerated program goes to a target dose that is less than maintenance
  • After the rush, the build-up to maintenance continues per a wide array of schedules
  • Systemic reactions are dose- related

Cluster

  • Maintenance achieved in 4-8 weeks
  • Systemic reactions vary considerably
  • More reactions seen in the United States literature
  • Delayed reactions occur

Summary

  • A pateint who is a candidate for IT is also a candidate for RIT/CIT
  • CIT and RIT are alternatives to IT
  • CIT reactions in the US are higher with the aqueous extract  than with the European depot extract
  • RIT reaction rates are higher than seen with IT
  • Premedication may help decrease reactions
  • The offering of CIT and RIT sets apart the allergist from the quasi-allergist

The Development of the Immune Response in Children living in the Inner-City (James Gern)

More wheezing was observed in children who were colonized in the neonatal period with Streptococcus, Moraxella,

and H. Influneza.

Changing Concepts of Food Allergy in the Past Three Decades- (Hugh Sampson)

This was a fascinating review of food allergy. It is easy to perhaps note at which time a healtcare provider trained based on their shared knowledge base regarding food allergy. This also points out the evolution of thought and practice as science has pushed this frontier forward.

  • Thirty years ago- food reactions were anectodal reports, for the most part ignored by serious clinicians.
  • Food allergy has evolved into a science that generates hundreds of publications per year in high-impact journals
  • The increased interest parallels the increased prevalence- 0.2% to 10% of children
  • Severe reactions were rare to foods, they are now the leading cause of anaphylaxis seen in the emergency department
  • There has been a 3.5 fold ( a fold is 100) increase in hospital admissions for food-related disorders.
  • The ‘epidemic’ for unknown reasons is confined to industrialized nations.
  • The new interest is the microbiome- susceptibility to food allergy may be related to gut bacteria
  • The foods causing the major reactions have not changed , but peanut and tree nut are more prevalent.
  • The tools used then and now are the same, but more refined. We started with a history and skin testing then added the food challenge. That old blood test called RAST was used by a few allergists due to poor specificity. Currently the quantitative value of food specific IgE and skin prick tests have been demonstrated. We are now working with food components that elicit responses. The gold standard remains as the food challenge.
  • Food allergy management has not changed much-Avoidance and Support Groups.
  • Strict avoidance was advocated, however due to poor labeling/lack of information the allergens were frequently unknowningly ingested. Currently the thought is that the aggressive strict avoidance may have interferred with the development of tolerance.
  • Oral immunotherapy for food was first reported on in 1910. Thirty years ago this was not done, but over the past 10 years this approach has shown promise. WARNING- the studies show promise, however we need more evidence regarding safety and long-term efficacy before this can go primetime.
  • Thirty years ago avoidance during the last trimester of pregnancy,  lactation, and withholding major allergens from susceptible newborns- milk for one year, egg for two years, and peanut until age 3 was the guidance. Now it has been concluded that there was insufficient information to make these recommendations. Recent work suggests that early introduction of these foods may actually prevent the development of allergy.

Dr. Sampson went on to list 12 questions that still need to be answered regarding food allergy;

  1. Why is this seen in the western world and why is it increasing?
  2. Why do some patients have significant levels of food-specific IgE and yet not react to the food?
  3. What accounts for a one time mild reaction followed by a near-fatal reaction?
  4. Why does the serum tryptase (a measure of mast cell release) not rise with food reactions?
  5. Why are some foods so allergenic (peanut, fish, shellfish) and others rarely so (corn)?
  6. What are the mechanisms for food tolerance?
  7. What is the best way to treat and perhaps cure food allergy?
  8. What are the mechanisms responsible for non-IgE mediated food allergy (eosinophilic esophagitis)?
  9. What is the best way to prevent food allergy?
  10. How does exercise, NSAID, and alcohol associated anaphylaxis happen?
  11. What biomarkers will better predict clinical reactivity in IgE and non-IgE mediated food allergy?
  12. What genetic and epigenetic factors are involved with the development of food allergy?

We have come a long way  in 30 years- we still have further to go.

Early Dietary Exposures to Food Allergens (Mona Kidon)

The late introduction of highly allergenic foods was recommended by the AAP in 1995. We see more allergy in the northern states vs. the southern states. Could this be due to a combination of bad genes and not enough Vitamin D?

Oral vs.Sublingual Immunotherapy for Food Allergy (Wes Burks)

This was a report by Wes Burks, MD- it is to be noted that there are not many children in these studies. In the peanut oral immunotherapy trial there are 25 children ages 5-7 years. In the peanut sublingual immunotherapy trial (SLIT) there are 40 patients- most are adults and adolescents. The usual dose of peanut that would cause a reaction is 100 mg. Those on SLIT could tolerate up to 1700 mg. So far, these studies do not tell us about the duration of peanut tolerance. In the 5-6 year olds in the studies, the specific IgE was about 100 and did not change during the program. The IgG4 to peanut increased.

Other Food Allergy Related Points

  • 10% of food reactions are life-threatening
  • The old dogma was that strict avoidance will prevent food allergy.
  • Strict avoidance was hard in the past due to mis-labeling and contamination
  • Early exposure to these highly allergenic foods acutally leads to less allergy.
  • A significant skin test response is a wheal >3 mm over the response of the negative control
  • When the wheal is >8 mm greater than the negative control- the food challenge was positive

The Pancake Syndrome

Anaphylaxis would occur immediately after eating foods contaminated with wheat flour. The contamination was with mites- mostly storage mites that cross-react with house dust mites. Most of the time it is with pancake mix. There are 135 case reports in the literature. The risk factors for such a reaction are previous allergic disease, house dust mite sensitization, NSAID hypersensitivity, the ingestion of pancakes or other meals with wheat flour, and that flour contaning more than 1 mg of mite allergen- >500 mites per gram of flour.

Taking the Myth-stery out of Mold (James Anderson and Peter Pityn)

There is a significant amount of misunderstanding, misinformation, mystery, and mythology about exposure to mold and mold products. The two major culprits for this are the media and the internet. In the seminar, a number of points were made;

  • Regarding ‘Mold Certificaton’- who does it? What are the credentials?
  • That musty aroma- may not be mold- consider cockroach, cat, dog,
  • Increased humidity can lead to more respiratory tract problems- an association, not a cause/effect
  • Guidelines do exist
  • The AAP had a statement regarding not raising a child in the presence of visible mold, that has been retracted
  • There is no proof that mycotoxins cause health problems in the home
  • The ‘3’ benchmark used- if the concentration is 3x that of the outdoor world = a problem, is not true

Merchants of Mold- an impressive industry;

  • Mold testing
  • Mold inspection
  • Mold remediation
  • Mold litigation
  • Mold inspection-equipment and supplies
  • Mold home tests
  • IAQ (indoor air quality) equipment and supplies
  • Mold remdiation, equipment, and supplies

Mold Schools

  • Mold certification
  • Mold training
  • Mold inspection
  • Mold remediation
  • Mold testing
  • Mold career planning
  • Mold marketing

An internet search for symptoms related to black mold (adding key words like health, black toxic mold, the lungs, toxins, toddlers) reveals the following conditions; allergy, asthma, allergic bronchopulmonary aspergillosis, hay fever, cancer, fever, malaise, difficulty concentrating, farmers lung, fatigue, tonsillitis, bloody nose, arthritic aches, headaches, coughing, crawly skin, depression, dizziness, congestion, seizures, loss of balance, memory loss, hearing loss, eyesight loss, nausea, restlessness, runny nose, sinus congestion, skin rashes, sneeezing, difficulty breathing, irritability, upper respiratory tract distress, toxic headache, death, and flu-like symptoms.

The health effects from mold are allergy, toxicity, and infection. Molds cause problems when the patient inhales bioaerosols, ingests the product, or has skin contact.

There are a number of diseases associated with mold

  • Allergic rhinitis
  • Allergic asthma
  • Allergic bronchopulmonary aspergillosis (ABPA)
  • Infection
  • Toxicity
  • Hypersensitivity pneumonitis
  • Fungal sinusitis
  • Irritant responses
  • Dermatitis
  • Organic dust toxic syndrome

Where do you find mold- 99% of mold exposures are outdoors.

Mycotoxins- these are metabolites or by-products from the life cycle of a mold. They are of high molecular weight (heavy products) and of low volatility. One mold can produce multiple mycotoxins and many molds can produce the same mycotoxin. Mycotoxins are not always produced by molds. The most common mold productin mycotoxins are;

  •  Aspergillium-Alfatoxin
  • Stachybotrys
  • Memnoniella
  • Fusarium
  • Trichoderma
  • Alternaria

Current scientific evidence does not support the proposition that human health has been adversely affected by inhaled mycotoxins in the home, school, or office environment. In a typical mold-contaminated office or home, it is virtually impossible to inhale sufficient mycotoxin to cause an adverese effect. The presence of a mold in a building does not automatically equate to either the product of a mycotoxin or exposure to a building occupant.

MVOCs- volatile organic compounds-

Can be responsible for the musty odor, but these products are not toxic. In regards to the irritant effects- this can occur, however the levels obtained in most buildings are so low that they would not be expected to cause irritative effects in people.

The session concluded with the statement ‘There is no real Mystery about Mold, however Mold Mythology will persist.

A reference is made to a Centers for Disease Control (CDC) document-

  • Molds are found in virtually every environment and can be detected indoors and outdoors all year round.
  • Some people are sensitive to mold
  • Current evidence indicates that allergy is the type of disease most often associated with mold
  • Standards for judging what is an acceptable, tolerable, or normal quantity of mold have not been established
  • Consult a general health provider who may refer you to an allergist, an infectious disease specialist, or a pulmonologist.

The Role of Filaggrin Mutations in Human Disease and Allergic Sensitization- Alan Irvine

Filaggrin is a protein in the skin that hangs on to water. When the genes for this protein are missing- severe atopic dermatitis is seen. When only one of the two genes is missing, there may be mild or no disease.

With severe atopic dermatitis 48% are missing one or both genes.

The odds ratio (OR) for asthma when one gene is missing is 1.5, but that is only in the patient with atopic dermatitis.

Interestingly- with atopic dermatitis the OR for peanut allergy is 3.3.

A decrease in the number of filaggrin genes is associated with atopic dermatitis and with peanut sensitization. There is more topical sensitization than oral sensitization.

A cat changes things- dramatically. To have a filaggrin mutation and to have a cat is a bad combination. Having a cat and having a filaggrin defect is associated with the occurence of atopic dermatitis.

Note that there is more allergy present when there is a filaggrin mutation. More asthma is seen in this population.

Prevention of Food Allergy: Is it possible? (Susan Prescott)

Food allergy is the second wave of the allergy epidemic. The first was asthma. There has been a 5-fold rise in food allergy in preschool children over the past 10 years. Most affected are the pre-school population.

  • 1/5 will have a positive skin prick test (SPT)
  • 50% of those with a positive SPT will have a positive food challenge
  • 1/10 will have a relevant IgE mediated food allergy

Other points made

  • Children with Asian heritage are more susceptible
  • Food allergy is more common, seen earlier in life, is more severe, and with less resolution
  • The early and regular exposure to foods leads to tolerance
  • The delay in food exposure increases the risk of sensitization
  • Fish oil to prevent food allergy- 9% withf food allergy in the treatment group vs. 13% in the placebo group
  • Probiotics-20 studies-7% with food allergy on probiotics vs. 12% on placebo

Practice Pearls from the session on Pediatric Dilemnas: Allergy and Beyond

Immune evaluations-Evaluating Antibody Responses

  • A 1.3 mcg response to a pneumococcal serotype is considered protective
  • When doing a pre/post evaluation- look for responses to the protective level
  • Be wary of repeating immunizations- if done too soon you may geta decreased response- wait a year
  • Do not depend on2-4 fold changes in the values

Idiopathic Anaphylaxis

  • Pork-Cat syndrome- a cat allergy child reacts to pork.
  • This is due to cross-reactivity.
  • In this situation, the reaction can occur 30 minutes to 2 hours after the meal.
  • There may be a relationship with exercise, cooking temperatures, and the amount ingested to cause anaphylaxis

Where do the current asthma guidelines need ‘tweeking’?

  • Guidelines are not mandatory, binding, nor enforced
  • Guidelines need to evolve for the co-morbid conditions; obesity, GERD, and Rhinosinusitis
  • Obesity- s/p bariatric surgery better ACG and AQLQ
  • GERD- do not use PPIs routinely with poorly controlled asthma
  • Inhaled Corticosteroids (ICS) in children with mild asthma

For children with mild asthma

  • Should not be treated with rescue albuterol alone
  • The most effective treatment to prevent exacerbations is the daily use of ICS
  • Rescue use of ICS with albuterol might be an effective step-down strategy for children with well-controlled mild asthma
  • This approach may decrease ICS side-effects

 

Incorporating newer pharmacologic agents into existing asthma guidelines (William Busse)

  • LAMAs
  • Intermittant vs. continuous ICS for mild asthma
  • Thermoplasty
  • Step-down- first to go are the LABAs
  • Antibiotics
  • ICS and LABAs for maintenance and resuce
  • Anti-IgE
  • Anti-IL4
  • Personalized vs. Stratified treatment- one does does not fit all

The AAAAI meeting gives me a chance to see what is on the cutting edge of allergy care. Meetings like this help keep me up to date. We we discover helps drive discussions about changes in the practice and how to better take care of our allergic children. The more exciting topics were the oral immunotherapy presentations for food allergy and the evolution of the idea of early food exposure to prevent food allergy.

FEL (3-16-2013)

 

 

 

 

 

 

 

 

 

 

 

 

 

March 16, 2013 · fleickly · No Comments
Tags:  · Posted in: AAAAI Meeting Higlights, Allergies, Allergy in Children

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