Highlights from the 2009 Allergy Meeting
I recently attended the 2009 annual meeting of the American Academy of Allergy, Asthma, and Immunology(AAAAI) in Washington, DC. There were five days of extraordinary educational activities (March 13-17, 2009). I thought that while I could still read my notes I would share with you a few things I observed, heard, and learned in the ever evolving world of allergy.¬†I plan to adopt many of these changes in¬†my practice.
The meeting’s¬†agenda covered a wide variety of clinical conditions. It would have been impossible to attend every session. I chose sessions on the allergic environment, eczema, immunotherapy, food allergy, re-certification, headaches, and asthma. There are a number of ideas that are evolving and a number of things currently done in allergy/asthma care that¬†need to change. Each and every one of these topics is truly worthy of more extensive review. I would be happy to use this blog to delve into topics in more detail (per request).
Atopic Dermatitis (aka Eczema)
I still need to be convinced regarding what to call this condition. Dr. Jeff Travers (chief of Dermatology at the IU School of Medicine) and I go back and forth on this topic. During the meeting I heard the concept of extrinsic and intrinsic atopic dermatitis. Extrinsic means from the outside and intrinsic from the inside. These terms have also been used for years to describe two presentations of asthma: extrinsic¬†asthma due to allergy, and intrinsic asthma when no allergy is found.¬†The word atopic¬†means 1) the tendency to come from families with allergy, 2) to make the antibody seen with allergy (IgE, which would be elevated) and 3)¬†to have positive allergy tests. Thus,¬†Intrinsic AtopicDermatitis¬†means no allergy demonstrated (intrinsic) in a condition associated with allergic sensitization (atopic). This blending of terms leads to confusion–why not stick with the simpler term of eczema?
I¬†learned¬†about¬†the use of silver impregnated clothing to decrease the amount of bacteria on the skin. Skin bacteria can cause flaring of atopic dermatitis.
A number of ¬†genes associated with atopic dermatitis have been discovered. These discoveries¬†should increase our understanding on how this condition starts and hopefully how we can manage it better.
There was¬†information on allergens that contain enzymes called proteases and how these protease containing allergens¬†aggravate the skin.
Probiotics have been used to treat allergic conditions especially conditions related to food allergy. A review of studies on probiotics have not¬†shown them to be¬†effective in preventing¬†or treating atopic dermatitis.
I listened to¬†debates about being proactive in skin care therapy vs. being reactive. Proactive would be trying to prevent and reactive being treating only when there is a problem. This idea was particularly interesting. Atopic Dermatitis Guidelines and package inserts for a variety of medications used for atopic dermatitis treatment stress short courses of use,¬†the reactive approach. The proactive debater posed the problem of a chronic disease that will have episodic flaring. The abnormality of the skin is¬†there all the time requiring the need for medication to be used perhaps twice a week to avoid flares (those times when the skin is more itchy, more inflamed, and more broken down). Pediatrics deals extensively with disease prevention. My pediatric perspectives are preventative- proactive. All too often we (as patients) tend to be crisis-oriented or reactive to chronic conditions. I am obviously on the proactive side of this argument.
Therapies emphasized moisture and more moisture. Keep these kids wet! This is clearly a major step that is contrary to previous approaches that recommended the avoidance of¬†frequent soaking/bathing.¬†The avoidance of baths is clearly one of those¬†long established principles¬†of atopic skin care that has fallen by the wayside in contemporary skin care.
Foods are an issue in atopic dermatitis. The protease containing allergens such as molds, pets, and mites may have a role in triggering flares.
In Boston a program that has had success includes insuring compliance with the medications (taking them as prescribed), addressing the parents concerns about medication side-effects (helps with compliance), decreasing the itch, and increasing sleep. These are all essential elements to help with control of the condition.
Of note, we need to re-think the role of a specific therapy and make adjustments. Antihistamines are frequently used in atopic dermatitis. In allergic rhinitis and in hives, these products help control itch. However, in atopic dermatitis, the antihistamines have little effect on itch. The role of the anti-histamine is to sedate. Most of the scratching happens at night. A sedating antihistamine used at night works best.
There were a number of new ideas regarding asthma. Look for vitamin D to have a possible role in treatment.
Current recommendations from evidenced-based asthma guidelines point out a difference between adults and children and the use of the long-acting bronchodilators in the two populations. These agents are called long-acting broncho-dilators (LABAs). In children, we should increase the dose of the inhaled corticosteroid before adding a LABA. This recommendation appears in two major asthma guidelines with type A evidence used to support the recommendation. This type of evidence (A) means that there are a substantial number of studies that support this statement.
Asthma may be related to bacterial colonization at birth and to the occurrence of the common cold virus later in life. Evidence was also presented regarding the observation from large population studies that the process of airway inflammation starts well before actual symptoms. We heard about diet, viruses, stress, ozone, and endotoxin having a role in the development of asthma. The gene or genes for asthma need to be present. These genes¬†then need to be activated or expressed for the child to show the signs and symptoms of disease. Bacterial colonization and a variety viruses may have a role in activating the genes.
This was a great session. The audience heard from an ENT surgeon, an allergist, and a neurologist regarding their approach to headaches. The consensus was that migraine is the biggest player in these situations. The connection of allergy to headache has always been a concern. However, headache is not a manifestation of allergy. There are many studies that have looked at this. People with headaches can have positive allergy tests but does that make the allergen the cause of the headache? Think about other conditions or associations. Could there be an allergic cause for an appendicitis?
I heard of the concept of ‘allergic appendicitis’ during this presentation. It was very odd to hear about this in a headache session, but a valid point was made. This concept¬†of the¬†allergic appendix was compared to allergic headaches. Follow along; data from a national health survey from 1994 indicated that 50% of the population reported that they had allergy. So if someone who had problems with the appendix was allergy tested, the chances are very high that allergy would be found. This however does not make the inflammation of the appendix due to allergy. You can find a significant number of positive allergy tests, be sure of why the tests are being ordered. Think migraine more often¬†as a reason for headache. Allergy is not a major reason for headaches.
The biggest news from the meeting was the work done by Wes Burks at Duke on peanut allergy. This is exciting and long awaited for those who have peanut allergy and for the families who have someone with peanut allergy. Immunotherapy for peanut trials have allowed the equivalent of about 12 peanuts to be eaten without any problems/reactions. This would certainly take the fear from accidental exposure to peanut especially from tabletops at school cafeterias. I have to check my note again, but I had written down the treatment would be a suppository(?).
There was a very popular abstract (a quick presentation of work in progress prior to it being published in a journal) on food allergy and the over- use of panels for food allergy (pet peeve). A New York Times article a few months ago reported that food allergies were being over diagnosed. Dr. Sears at National Jewish Hospital in Denver, Colorado reported on over one hundred children seen at their center who had food allergy as determined by blood test panels. The average number of food allergies reported were six. After undergoing food challenges the number decreased to only 2 foods. 88% of the foods this group of children were told to avoid based on RA ST panels were added back into the diet. Using a food challenge, no one with meat ‘allergy’ had a positive food challenge (where meat caused a problem), 88% of the grain ‘allergic’ children were negative on challenge, and 83% of the fruit and vegetable group were also negative after a food challenge. Bottom line- the use of these panels is giving falsely positive information and leading to a misdiagnosis of food allergy.
I learned that I should no longer use the word RAST. The term is outdated and refers to a technology not used. The blood tests for allergens should no longer have a 0-6 grading scale and should only be reported in what is actually measured kU/l of serum. The test measures a concentration of a specific antibody in the blood. The relationship of that concentration to clinical activity needs to be determined by the clinician. I predict that the interpretation of the blood test results may be a huge issue.
A new in vitro or blood test for specific IgE in the blood is called an ISAC chip. This technology will help with cross-reacting proteins. We see the problem of cross-reactivity with multiple positive allergy tests to legumes (peanut, soy, beans, and peas). I think this will be a very worthwhile test in allergy.
There are three blood tests out there for detecting specific IgE. These are the Immunolite, ImmunoCap, and Hytec. Each of these measure something different. They measure a different population of IgE antibodies and may not be comparable. Caution was advised regarding the blood tests for specific IgE. The physician should know the method used, the validity of the assay, the performance of the laboratory in doing the assay, and realize that no test for allergy is infallible.
Each and every one of these topics could stand alone for more detail and interpretation and I would be most happy to elaborate in more detail. Let me know if you would like more information by adding a comment. If there continues to be an increase in the use of specific IgE panels (as advocated¬†by those who market these tests) we will be doing significantly more food challenges in our office. Usually we are doing food challenges for those who may have outgrown a food allergy. We certainly can offer a food challenge for a child who has been told that food allergy exists based on blood test results. One of my tasks upon my return to the office is to look at our track record of doing food challenges. I hope to report on our successes and failures for our food challenge experience with milk, egg, soy,wheat, and of course peanut.