A message was forwarded to me about a news broadcast from Chicago that highlighted a tool that can be used to help with asthma diagnosis and management. The FDA has recently approved this according to the message. This tool is the measurement of exhaled nitric oxide (eNO). In allergic asthma  airway inflammation involves numerous inflammatory cells especially eosinophils. These inflammatory cells have a marker for their involvement and activation called nitric oxide. We are able to measure this by-product of airway inflammation in the breath. I also received another link on this measure of airway inflammation. In this second newsbroadcast Dr. Wolfe, an allergist, does a nice job in explaining this test, this measure, and allergic asthma.

This is not a new procedure. At Riley Hospital our group has been using this measurement in the care of children with asthma. It is nice to see that the concept of eNO is catching on and its value is appreciated.

I feel that a measure of eNO offers a significant amount of information regarding the role of allergy and the level of control patients with asthma have. I use eNO measures frequently in my Allergy/Asthma practice.

FEL

Saints celebrate a Super Bowl win

I just returned from New Orleans where I attended the American Academy of Allergy, Asthma, and Immunology (AAAAI) annual meeting. It was very hard for an Indianapolis Colts fan to venture into the city that beat my team in the most recent Super Bowl. They still celebrate that victory – deservedly so. It’s just that everywhere you go you see ‘Who dat’ Saints stuff. 

At this meeting I had two major agendas; to update my understanding of the conditions I see and care for in my profession and to begin the process of recruiting our third full-time allergist for Riley Hospital. When I got to Riley in 1994, I was the first staff allergist there in 22 years. The allergy service has been up and running. We (Dr. Vitalpur and I) are looking to expand and we need to expand.  We interviewed a few current fellows in training and we look forward to their visits with us. It is exciting to interact with physicians currently in their training programs. These are young people eager and ready to embark on their career choice of patient care, teaching, and research in the field of allergy/clinical immunology. This is an exciting time for the allergy program at Riley. 

In a later posting I plan to include more material on food allergy. I have been invited to give an update from the meeting (food allergy topics only) at a food allergy support group this Tuesday (March 16) in Greenwood, In.  My thought is to have the group hear my presentation first then publish it on the web. The early preview of the update is for the support group. 

Food Allergy 

More on this later however, the meeting had many talks on the concept of ‘tolerance’. The is the condition by which despite a specific IgE (blood test/skin test) to a food that food has been ingested and continues to be ingested without any clinical symptoms. 

Now here is the clinical scenario that we need to think carefully about. Trail mix (made of peanut and tree nuts and other stuff) is ingested and an allergic reaction occurs. The child is treated in the office and the advice is to not eat peanuts or tree nuts. Blood is drawn and the specific IgE is positive to a number of tree nuts and to peanut. The history of food exposure before the reaction indicated that roasted peanut products are eaten every day by this child. Tree nut exposure has occurred in the past but very irregularly. So which food caused the reaction? Peanut which was a daily part of the child’s diet (you have exposure, constant ingestion, and an positive allergy test) or a tree nut (you have exposure, rare re-exposure, and a positive allergy test).  In this case, despite a positive IgE to peanut, the child was ‘tolerant’ to peanut. The history indicated that there was frequent exposure to peanut. The problem is that by avoiding peanut, tolerance may be lost and re-introduction of peanut may cause clinical symptoms. 

Food sensitization in children may be due to environmental exposures to the food (vs. ingestion). 

The Future of Inhalant Immunotherapy 

Currently we have subcutaneous (SQ) allergen immunotherapy (IT)- allergy shots, injections. This form of therapy has been well established for 100 years. It is somewhat crude/unrefined and reactions can occur. The advances in this field include; 

1.  Sublingual immunotherapy (SLIT)- not approved in this country 

2.  Peptide immunotherapy (PIT) 

3.  Allergen fusion proteins 

4.  Allergens attached to viruses 

Anaphylaxis 

Fatal allergic reactions may not always have skin manifestations. Low blood pressure was seen in 80% and 60% had respiratory effects. Skin reactions occurred in 60%. All too often there is a delay in recognizing anaphylaxis when skin reactions are absent. Not everyone experiencing an anaphylactic reaction will have a skin reaction. 

Asthma 

I was involved as a principle investigator in the first phase of the National Cooperative Inner-City Asthma Study (NCICAS). I attended a session on inner-city asthma given by Herman Mitchell. Dr. Mitchell has been involved with this issue for many years. He shared a number of observations that spanned almost two decades of investigation. 

            Asthma is not just one disease. It is many diseases. It is complex and multi-causal. There are many factors that interact that determine its development and its exacerbations. This would be true for all populations with asthma. 

            The inner-city asthma studies emphasized the importance of sensitization (having a positive allergy test) and exposure (measuring the allergen in the environment). 

            House dust mites were found more often and in greater amounts in detached, low-rise housing and less in high rise apartments. In evaluating a child with asthma, we need to know what type of building they live in. 

            High humidity in the home is a factor. 

            Air pollution poses a conundrum. Overall air pollution levels have decreased, yet asthma prevalence has increased. Could this be a protective effect? Approximately 25% of children currently live in environments that exceed the standards for safe air. Things to consider in the child’s environment include how far away they live from a main road. 

            Asthma is a weighty problem. Inner-city asthma studies have shown 29% of the children with asthma are obese and 56% are over the 85%tile for weight. Between 85-90% of the child’s time is spent indoors where it would be difficult for active play/exercise. Safety concerns of the inner-city environment contributes to this problem. 

Human Genome Studies 

            This is a very hot topic. Most of it is research based however one of the anticipated outcomes would be to look at someone’s genetic profile and be able to predict susceptibility, expression, and severity of asthma and allergic diseases. We may be able to predict the kind of asthma someone will have and design very specific programs to prevent/treat. 

Asthma Treatment- Inhaled Corticosteroids 

            Not everyone responds to inhaled corticosteroids (ICS) given for asthma. Up to 50% of those on ICS may not respond. There are no biomarkers that we can use to determine in which patients a ICS will work; we depend on a clinical response. 

            The question is how long do you wait until it is determined that the ICS has made no difference? 

            This presentation posed many probing asthma management questions. It is important to set goals/outcomes when starting a program and to bring the patient back in a reasonable period of time to see if those goals/outcomes have been achieved. We also have to make sure that there was adherence to the therapeutic program (it is hard to tell if something was a failure/success if it was not used). In this situations it may be of benefit to start at a higher than anticipated dose looking for any response. 

Allergy Blood Testing 

            There are three companies that offer the blood tests for IgE and the results they provide are not equal. You cannot compare one with the other. 

            The future microarray technology will help us sort out relevant allergens. Skin testing and blood tests for allergy use very crude protein extracts that may have different and numerous proteins. The results obtained may be due to cross-reactivity with other substances or even binding to proteins that cause no clinical reactivity. 

            Of importance- the blood test result, the concentration of IgE antibody (kU/L) provides predictive power for a reaction it does not tell us anything about the severity of a reaction. 

            Do not use the term RAST- it is outdated, it refers to a technology no longer used. 

Urticaria- Hives 

            This is one of the most frustrating clinical conditions that we see. Parents, patients, and healthcare providers want the answer for the hives. I think the frustration of not knowing will continue. Idiopathic is the medical term used to describe something for which no cause has been determined. In some contexts it means the healthcare provider is the ‘idiot’ because they were unable to figure it out. 

            More than 80% of the time, chronic (more than 2 months) hives is idiopathic. The evaluation needs to consider the role of aspirin and other non-steroidal anti-inflammatory medications. Physical reasons for hives also need to be considered (light, pressure, water, heat, cold, or vibration). 

            The list of agents used to treat hives was described as ‘weird’. Frequently, a typical (H1) antihistamine has added to it an H2 antihistamine (commonly used to treat excess stomach acid). There are a variety of combinations used, however the definitive study that showed a positive effect was the used of hydroxyzine and cimetidine. The mechanism of action was the impact of the cimetidine on the liver metabolism of the hydroxyzine- cimetidine allowed the hydroxyzine to be around longer. 

            A somewhat new therapy for hives was the immunosuppressive agent cyclosporine. Adding a second H1 antihistamine may help. 

These are some of the highlights from the meeting. More specifically these comments come from the notes taken that I could read. 

Check-in next week – I plan to post my notes on the majority of food allergy topics after my presentation on March 16, 2010. 

FEL 

This young lady’s mother had with her an article that escaped my attention. The article was written by known experts in the field of Allergy (the lead author was Anna Nowak-Wegrzyn with Hugh Sampson, Robert Wood, and Scott Sicherer as contributing authors). The paper was a nice review of FPIES and a study of 14 special children. I think that any allergist who sees young children should review this paper. These young children can present with signs that are possibly consistent with anaphylaxis.

 The article was published in the journal Pediatrics in 2003. It is a review of 14 children who presented over a five year period at the Mount Sinai Pediatric Allergy and Immunology Clinic (New York, NY) and to the Allergy Clinic at Johns Hopkins Children’s Center (Baltimore, MD). The reactions that these children experience include severe diarrhea and vomiting which can lead to dehydration and shock. This is a clinical diagnosis; there are no specific laboratory tests that make the diagnosis. A food challenge can confirm the diagnosis.

Milk and soy have been the most commonly implicated foods causing FPIES. This article shows that other foods specifically solid foods have been shown to be associated with this syndrome; rice, oat, barley, peas, string beans, squash, sweet potato, chicken, and turkey. These children underwent food challenges to show the cause-effect relationship between the exposure and the symptoms. There were many combinations of foods causing the problem; cow’s milk alone, soy milk alone, both cow and soy milk, a single solid food, and more than one grain. The group was compared to children who were only milk/soy sensitive.

                The profile of the Solid Food FPIES population was as follows;

• Age at onset of the reaction:    5.5 months (range 3-7 months)
• Age at resolution:                      24 months (range 14-44 months)

                The Milk/Soy FPIES profile was the following;

• Age at onset of the reaction:   1.0 months (range 2 days to 12 months)
• Age at resolution:                      28 months (range 14-21 y)

This was the first published study of FPIES triggered by solid food. Oat was the most common food causing solid-food FPIES. The study also showed that breast-feeding may have a protective role in preventing/delaying the development of FPIES. The diagnosis of solid-food FPIES was not made until after two reactions. It was also noted that these reactions were severe. The delay in diagnosis was attributed to a number of possible factors; low incidence of the disorder, a presentation that looks like septic shock, and the belief that solid foods such as grains, vegetables, and poultry are of low allergenic potential. It was also noted that the time course of the reaction may delay making the correct diagnosis. The daily feeding of milk – cows and soy, leads to chronic problems. The re-introduction of the milk causes symptoms two hours after the exposure.  As mentioned previously another problem is the lack of any test (other than avoidance and a food challenge) to confirm the diagnosis.

Another point that was made was that almost half of the children in this series had multiple food sensitivities. Children who were already on a casein hydrolysate formula had a median of four solid-foods that they were sensitive to.

No infant developed FPIES with exclusive breast feeding in this series.  The authors pointed out that they were unaware of any reports of FPIES during breast feeding with absolutely no direct oral feeding of an offending food. No infant developed FPIES to milk/soy after age 1 years and the oldest child who had the solid-food FPIES was 7 months old. There were no ‘predictors’ of which child with milk/soy FPIES would go on to develop solid-food FPIES.

The Bottom Line-

The reaction of vomiting/diarrhea possibly leading to shock can be consistent with an IgE-mediated reaction and these are perhaps more common than FPIES. Such a reaction would lead to an allergy evaluation which will be negative if the diagnosis is FPIES. However, the infant is still at risk for a severe reaction with re-exposure.

Board certified allergists are credentialed in the care of allergic conditions in both pediatrics and internal medicine. Some of us went into allergy after completing training in pediatrics and others were trained in internal medicine. FPIES would not have been a clinical entity seen during internal medicine training. It may have been seen/talked about for a pediatric oriented allergist. FPIES favors infants. My point to all this is that although very rare, we need to keep this type of presentation in mind when seeing young infants with scary episodes of vomiting leading to shock with solid-food exposure. Their evaluation will show no evidence of allergic sensitization. We can help by teasing out the history of exposures and clinical course. We can offer recommendations for avoidance of the common foods that have triggered solid food-induced FPIES. This profile of young infants reacting in such a violent way needs to be considered in the evaluation especially if they have had issues with cow’s milk or soy milk.

This young lady made an impression on me. Her story was very scary. She caused me to go back to the literature and review what is known about her presentation.

Fred Leickly

We have seen many children who were evaluated for food allergy and/or who were brought by parents to be evaluated for food allergy because of redness to the cheeks that is observed after eating.

What I haven’t heard about is a syndrome called ‘Frey’s Syndrome’. 

In the January edition of Postgraduate Medicine there is a case report, pictures, and a review of this syndrome which frequently precipitates an allergy evaluation. The problem is not due to allergy. It is an allergy-pretender.

Frey’s syndrome is also called the auriculotemporal nerve syndrome.  It involves redness over the cheeks after eating or drinking. The cause is abnormal nerve regeneration which can happen with forceps delivery or after parotid-gland surgery.  The actual incidence of the syndrome is unknown and it is by this report rare in children. Sucking on a lemon brings out the facial flushing. The use of starch/iodine brings sweating which is seen more in the adult.

The facial flushing with eating, gustatory flushing, may mimic food allergy and lead to unnecessary testing and the consequence of restrictive diets.

The clinical course is benign in children. The authors point out that it is important to recognize it so unnecessary evaluations are avoided.

The treatment is explanation and reassurance.

If you can see the paper, there  pictures of this flushing. The reaction looks distinctly delineated. It follows the distribution of the nerve.  The young lady would experience the flushing after eating sweets, citrus fruit, grapes, tomato sauce, fruit-flavored ice cream, and spicy foods. She had no history of any trauma to the area of the auriculotemporal nerve. There were no other symptoms besides this flushing. There was no personal history of allergy. Her teachers thought that this was a food allergy issue. In the clinic, the flush was seen one minute after eating a citrus-flavored sweet.

 I had not heard of Frey’s syndrome before, but I have seen a good number of red-cheeked children who had no other signs/symptoms of a food allergy. In this case, the types of food that elicited the problem, the timing of the flush in relation to eating, and the specific distribution help with the diagnosis of Frey’s syndrome.

We will start stocking sweet citrus-flavored candies for test purposes only. I am soliciting suggestions. So far I think Skiddles may work. If you can think of a candy that is has more of the citrus bite, let me know.

My thanks to the authors N Hussain, M Dhanarass, and W Whithouse for this article (Postgraduate Medicine Journal January 2010 Vol 86 N0 1011 page 62.)

Fred Leickly

Last week I was interviewed by a reporter from the Wall Street Journal. The topic was food allergy. The reporter came across this website and thought that I be a good resource for her article. We had a delightful talk that went on for 45 minutes. Questions were asked about the increase in food allergy; is it real or is it possibly due to the over use of diagnostics (allergy testing).

Needless to say I was excited about the prospect of being quoted in the Journal.

My hopes were dashed. The reporter had to cutback on material. My name did not appear in the article. The article was very well done and did quote a number of outstanding leaders in the field of food allergy (Drs. Hugh Sampson and Robert Wood).

I do encourage you to read the article written by Melinda Beck.

FEL

N. Nicolaou, M Poorafshar, C Murray,  A Simpson, H Winell, G Kerry, A Woodcock, S Ahlstadt, and A Custovic.  Journal of Allergy and Clinical Immunology(JACI) 2010;125:191-7.

This article appeared in the most recent JACI. Almost as soon as I read the article, I began to put together this review (I am excited about the approach and ideas in this work). This paper states very clearly the problem of positive allergy tests for peanut (sensitization) and demonstrating clinical relevance- that is allergy to peanut. It addresses this problem using a new test for determining sensitization, component-resolved diagnostics.

Background:

          A few very important facts are noted about peanuts;

            1. Peanut is a nutritious and inexpensive food

            2. Peanut is one of the most common food allergies

            3. The prevalence of peanut allergy is increasing

            4. Peanut allergy is usually life-long

            5. Peanut avoidance is the current management of this allergy

            6. Accidental peanut exposure is common

            7. Peanut exposure in the allergic child can be life-threatening

Peanut allergy diagnosis issues:

            1. An accurate diagnosis is very important- sensitized or truly allergic?

            2. The gold standard for the diagnosis of peanut allergy is the

               ‘double-blind placebo-controlled food challenge (DBPCFC)

            3. DBPCFC are costly, time consuming, and dangerous

            4. The diagnosis is made with a suggestive history of what happens after exposure,

                supported by a skin prick test or by the determination of specific IgE in the blood

            5. These tests detect the presence of antibody (sensitization)

            6. Positive allergy tests does not equate to the presence of allergic symptoms after exposure-

                known as clinical allergy

            7. Current tests –both skin prick tests (SPT) and specific IgE tests (sIgE-blood) use crude peanut

                 extracts and contain a mix of the allergic proteins and non-allergic proteins that may

               cross-react with other allergens.

            8. Bottom line- peanut sensitization may not equal peanut allergy

Solving this problem:

            1. A new blood test to detect antibody production by the child to the important proteins in peanut that cause

                allergic symptoms has been developed

            2. This is called component-resolved diagnostics (CRD) – developed by Phadia

            3. This may be a more accurate tool to assess food allergy (vs. sensitization)

The purpose of the paper was to look at the CRD to correctly identify children with peanut allergy.

Methods:

A birth cohort of children enrolled in the Manchester Asthma and Allergy Study (Manchester, England) was evaluated. Information on exposure and reactivity to peanut was collected.  Peanut sensitization was measured by skin prick testing and by Phadia specific IgE.

There were 110 children (cohort contained 1085) who were sensitized and were asked to undergo a more extensive evaluation of their reactivity to peanut. This included more extensive history, skin testing, specific IgE, a DBPCFC, and the CRD.

The definition of peanut allergy included two very specific sets of criteria.

                        1. Sensitization and a positive oral challenge or

                        2. A convincing history and specific peanut IgE >15 kU/L and/ or a skin prick test that was greater than

                           an 8 mm wheal (this group did not have an oral challenge).

Results:

The cohort included 1085 children, 1029 were evaluated at age 8 years. There were 17 (1.6%) who had a history of peanut allergy.

Skin-testing was performed in 919 of the children with 47 (5.1%) having a positive SPT. Sensitization to grass pollen was noted in 59.6% of the children.

Blood studies were performed on 582 children with 71 (12.2%) having a detectable level of specific IgE to peanut. Grass sensitization was found in 67 (94.4%).

Overall, of the 933 children who had either a SPT or sIgE 110 or 11.8% were considered to be sensitized to peanut.

From this group of 110, 108 agreed to participate in the program. Seventeen did not consent to a food challenge. From the remaining 91 children, 12 had convincing histories and SPT/sIgE criteria to fit the definition of peanut allergy. Food challenges were performed in 79.

In the 79 oral food challenges to peanut, 66 had no symptoms with the exposure. Of the 13 who developed symptoms, 7 had two or more signs/symptoms and were declared peanut allergic. The breakdown on these number was- 66 were peanut tolerant and 19 were had peanut allergy (12 not challenged plus the 7 with a positive challenge).

The proportion of children with peanut allergy among those sensitized was 22.4%.

Peanut allergic and peanut tolerant children were compared.

            1. Asthma, eczema, and food allergies were more common in the peanut allergy group.

            2. Allergic rhinitis was more common in the peanut tolerant group.

            3. Peanut tolerant children had lower peanut sIgE and higher grass sIgE.

The CRD results differentiated the peanut allergic from the peanut tolerant group. The peanut allergic group had higher values to the major peanut proteins Ara h 1-3. The peanut tolerant group had higher reaction values to grass components. The response to the peanut protein Ara h 2 was the best discriminator.

A model was developed to discriminate between children with peanut allergy and peanut sensitization. The model misclassified only 2 (6.9%) with peanut allergy and 4 (7.7%) peanut tolerant children.

Conclusions:

The majority of children who have peanut sensitization based on SPT or sIgE do not have peanut allergy. The CRD may help the diagnosis of peanut allergy.

Reviewers Comments:

This is exciting work. In the practice of allergy we struggle with positive tests and their clinical relevance. The authors very clearly point out the differences between sensitization and allergy. The test makes no one allergic. The test only tells us that specific IgE is being made. The history and/or a food challenge help define that clinical relevance in making the diagnosis of food allergy.

Phadia has developed a very specific assay which will help in making the diagnosis of peanut allergy. I am excited about the prospects for CRD. Phadia’s science is at the cutting edge of food allergy and I look forward to using this assay for the large number of children we see in our practice with a positive test for peanut antibody. I have always had the greatest respect for Phadia’s science; it is the marketing part that I have issues with (topic of a few of my posts).

The authors point out the strengths of this study. They performed a very extensive evaluation and used the DBPCFC for verification.

The small number of children reported is a recognized weakness. The authors encourage replication of their work.

The study looked at 8 year old children. I wonder about why that age and from the paper my guess is that this was the most recent year of evaluation on their cohort. This birth cohort attended the clinic at ages 1, 3, 5, and 8 years. In our clinic we use age 5 as our cut-off for peanut challenges. At this age, most children are able to communicate with us regarding the subtle aspects of allergic reactions.

Look at the rate of positive tests for peanut. The testing of a population of children revealed that almost 12% will have a positive test for peanut.

The last paragraph in the paper goes as follows; “The majority of children within the general population with positive skin test or measurable serum IgE to peanut do not have clinical peanut allergy.

So how has this year shaped-up?

There are 36 posts-what appears on the home page (reviews, stories, comments) and there are 11 pages. Of course the home page will grow as hot topics in the world of allergy appear. I still need to create pages dealing with more of the clinical conditions we see in the allergy clinic- look for anaphylaxis, allergic rhinitis, recurrent infection, drug allergy, and stinging insect allergy. I also want to post a page on ‘non-allergy’ .

The site has an analytical program attached that keeps tract of a visit to the site. Over the past year ‘Leickly Stories’ has had 3,500 visits from 69 countries. Two-thirds of those visits are new.

I also want to thank my 4 subscribers- apparently there are four people who receive a notice that this site has an update to share. To become a subcriber just click on that curly logo in the upper right corner of the home page. It is an RSS feed for the site.

Hopefully, I can start collecting allergy experiences from children/families that I see in my practice to share with others. The world of allergy can be scary. For those who are new to it, hearing how others have dealt with the problems helps establish a confidence and comfort level. It also lets people and children know that they are not alone in this struggle.

Fred Leickly

Key Points

•  Food allergies can be classified as IgE-mediated, non-IgE-mediated, or mixed.
•  The diagnosis is made from a complete history and performing directed testing.
•  Despite new developments in treatment, for now it is only avoidance.

Purpose of the article

               The purpose of this article is to review the current state of knowledge regarding the mechanisms, the diagnosis, and the treatment of food allergy and eosinophilic esophagitis.

Background

               Food allergy affects 6-8% of children and 3-4% of adults. The prevalence of food allergy is increasing.

               Any food can cause a reaction. There are a few foods that account for most reactions; cow’s milk, soy, wheat, eggs, peanuts, tree nuts, fish, and shellfish.

               Most food allergy presents in the first few years of life.

               Almost 80% of children resolve allergies to milk, egg, wheat, and soy. Far fewer resolve tree nut allergy (about 9%) and peanut allergy (20%). Allergies to fish and shell fish tend to persist into the adult years.

               A major risk factor for the development of food allergy is a family history of allergy. The presence of allergy in the parents, not extended family member is the risk factor.

Becoming allergic or tolerant

               Food allergy may be more prevalent in children due to; an immature gut barrier, low IgA levels in the gut, lower stomach acid levels (high pH), and low levels of digestive enzymes. There are also immune mechanisms in play that suppress an immune response that can lead to developing a food allergy. Normally, the immune system works to achieve food tolerance. Alterations to the immune system checks this drive towards tolerance and can lead to sensitization and food allergy.

Factors that contribute to food allergy

• The dose of the food
• The structure of the food
• Processing of the food
• The route of the initial exposure
• The gut flora (bacteria in the gut)
• The acidity of the stomach
• Genes

High doses and low doses of food can lead to tolerance (no allergy), but how this happens varies to the food. Food allergens that are soluble (dissolve) are less sensitizing.  Dry-roasted peanuts are more allergenic than raw or boiled peanuts (less soluble).

Gut flora refers to bacteria in the gastrointestinal system. Current research with germ-free mice suggests that they are prone to develop more food allergy or fail to develop food tolerance. The use of antibiotics in these germ free mice leads to the development of sensitization to food and subsequent food allergy. The acidity of the gut may be too high not allowing for proper digestion of food. The use of antacids increases the risk of developing food allergy.

Types of Immune Responses to Food

• Metabolic- lactose intolerance
• Pharmacologic- chemicals/contaminants
• Bacterial- food poisoning
• Psychological- food aversion
• Immunologic- allergy (IgE, non-IgE, mixed)

The Diagnosis of IgE-mediated Food Allergy

               The most important aspect in making the diagnosis is the history- NOT THE LABORATORY RESULT!

               Food allergy is not subtle. The appropriate questioning will tease out the exposures.

• What are the potential food culprits?
• How much was eaten?
• What was the timing between exposure and symptoms?
• What were the symptoms- are they consistent with an IgE-mediated reaction?
• Any related factors- exercise, alcohol, medication use

               The symptoms of an IgE-mediated reaction (predictable by allergy testing) will generally occur soon after the exposure, but may be delayed for a few hours.

               The symptoms of a non-IgE-mediated reaction will occur several hours to days later.

               The ‘gold standard’ for the diagnosis of a food allergy is the double-blind, placebo-controlled food challenge.

Allergy Testing- Commercially available skin prick tests are a rapid and sensitive way to screen for food allergy. Negative allergy skin prick tests have more than a 95% negative predictive value- when I show that the skin test is negative to a food, I have a 95% chance of being correct and 5% chance of being wrong with this study.

               The positive test indicates the presence of IgE antibody against the food and SUGGESTS a clinical food allergy.  The specificity of the test is 50% making a positive result more difficult to interpret than the negative skin test result. This is why we need to be careful in selecting allergy tests.

               The size of the skin test response does not necessarily correlate with the potential severity of a reaction- You cannot say a child is very allergic based on the size of their test. You can say that they make a significant amount of antibody.

Allergy Testing- Immunoassays

               DO NOT USE THE WORD ‘RAST’ ANY MORE. The tests no longer use radioactive materials. They are tests for specific IgE.

               These blood tests for allergy are generally less sensitive, more expensive, and the results are not immediately available.

               Threshold values for food specific-IgE have been established for a few foods. When the value exceeds the critical cutoff value, there is an increased risk of a reaction. Only a few foods have these critical cutoff values established.

               Note that an undetectable specific IgE by an immunoassay has a low negative predictive value. Reactions can occur in 10-25% of patients who have undetectable specific IgE to a food.

Managing  Food Allergy

• Current management involves the following. Anything else is experimental.
• Avoidance
• Education
• Medical alert jewelry
• Medications for reactions- epinephrine, diphenhydramine

Experimental treatments

• Humanized monoclonal anti-IgE- use limited in food allergy
• Oral Immunotherapy- recent work suggests this may induce tolerance

The Oral Immunotherapy must be considered investigational- more studies are needed to address the effect and the safety of this form of treatment.

The Role of Food Allergy in Eosinophilic Esophagitis (EE)

This is a clinical condition that has increased in frequency. Symptoms include; difficulty feeding, failure to thrive, vomiting, epigastric/chest pain, dysphagia, and food impaction.

The diagnostic criteria are;          

• Clinical symptoms
• >15 eosinophils per high powered field on biopsy
• No response to a proton-pump inhibitor for 1-2 months or a normal pH probe study
• Exclusion of other causes

The cause of this condition is not completely understood. Atopy (tendency towards allergy) has been implicated as a factor with >50% of EE patients having an atopic condition. Most patients improve with either dietary restrictions or elemental diets, so food sensitization appears to play a role.

A review of responses to dietary manipulation revealed the percent of patients who had symptom improvement/resolution from 96-100% in four studies that used an elemental diet and 57-94% improvement/resolution with restricted or 6- food elimination diets. A study with only wheat or rye avoidance demonstrated only 17% with improvement/resolution.

How to identify potential food triggers of EE

               Potential food triggers have been hard to identify in EE.

               A recent consensus report did not recommend in vitro food allergy testing (specific IgE) due to a lack of positive or negative predictive values for food-specific IgE level testing in EE. Furthermore, the absence of IgE does not eliminate a food as a potential trigger. Non-IgE mechanisms may play a role.

               With skin prick testing, 2/3 patients with EE had positive reactions to at least one food such as cow’s milk, egg, soy, wheat, and peanut, but also to rye, beef, and bean.

               Atopy patch testing may show some usefulness in identifying foods that may elicit a non-IgE response.  Currently these types of tests are not validated and have only been evaluated in a very small number of studies (these are all from the same research group). There are no standardized materials, methods of application, or interpretation of results. Also, importantly there has been no study that has included a control (non-sick) population to validate atopy patch testing.

Reviewers comments- This was a fun article to read and review for you. Two huge areas, food allergy and eosinophilic esophagitis were condensed in a very scholarly fashion. This is a contemporary review that included many references. It eagerly and cautiously points out strengths and weaknesses of what is going on in diagnostics for food allergy problems. I applaud the points made about blood tests for allergy especially the limitations for their use in EE. There is interest in patch tests for food reactions, however the major proponents of its utility tend to be from only one group that publishes on the topic. The patch testing for foods does need validation in the proper population.

For those of you who are interested in food allergy, you should look at this article.

FEL

As with all of these courses I learned from a group of wonderful speakers and there are a few things I will add to my practice. Here are a few things to share.

First- I was under the impression that warmth would be associated with places that had the word “Mexico” associated with it. Santa Fe was colder than back home here in Indiana! There was snow as well. Surprise! Despite the weather it is a most beautiful place.

Second- the people are very warm and friendly. Here is an example-my hat has many pins from a variety of states, countries, and places that I have visited. I was with my wife and our friends having the obligatory ice cream after a dinner with a rather spicy salsa. A gentleman came up and gave me a pin that commemorates the celebration of 400 years of Santa Fe, New Mexico. He loved the hat and thought that the pin would be a welcome contribution. I offered to pay for the pin but was denied. The gentleman was the president of the Santa Fe 400 year committee and he assured me that he had a plentiful supply of those pins. I didn’t catch your name- thanks yet again.

Places and things visited- Santa Fe 400 (left lower).

Third- The speakers for this program were all top-notch.

• Dr. Veda Ackerman- Pulmonary- James Whitcomb Riley Hospital for Children, Indiana
• Dr. Meg Fisher- Infectious Diseases- Children’s Hospital at Monmouth Medical Center, New Jersey
• Dr. Ivor Hill- Gastroenterology- Wake Forest University School of Medicine, North Carolina
• Dr. Todd Mahr- Allergy & Immunology- University of Wisconsin Medical School,  LaCross, Wisconsin
• Dr. Anthony Mancini- Dermatology- Northwestern University Feinberg School of Medicine, Chicago, Illinois
• Dr. David Schonfeld- Developmental/Behavioral Pediatrics- Cincinnati Children’s Hospital Medical Center, Ohio

Fourth- Here are just a few excerpts from the program;

Pediatric Pulmonology I work with Dr. Ackerman. In fact it was at an AAP course that I first met her and she was instrumental in recruiting me to Riley Hospital. Over the years I have heard her talk on many subjects for a wide variety of audiences.

Cough suppressants have no real role in children. There are no studies to support the safety and efficacy of these agents in children. Cough suppression in children may be hazardous and contraindicated.

Infectious Disease Very few bacteria lung infections cause wheezing except for mycoplasma infections. Most of the wheezing from infection is due to respiratory viral infections.

Most viral respiratory tract infections have a gradual onset of symptoms. The exception is influenza which hits hard and fast.

Fever may be helpful- the influenza virus will not survive/replicate in a host with elevated temperature. Treating the fever may help the virus to continue to replicate which can prolong the illness and prolong the spreading of the virus. Viral shedding may be prolonged with antipyretics (acetaminophen, ibuprofen).

Gastroenterology Celiac disease is a common concern. Confirm the diagnosis before treating. Constipation is not due to a food allergy in children. In dealing with constipation, the child controls the sphincter- this makes yelling at the child quite useless as a therapy.

Allergy Air filters for house dust mite avoidance do not work due to the nature of dust mite allergens. However a HEPA filter on a vacuum cleaner helps filter the exhaust. Carpeting on concrete (finished basements) helps house dust mites grow.

Food allergens are proteins/glycoproteins they are not fats or carbohydrates (sugars).

The peanut allergy child/family needs to be aware that peanut is sometimes made to look like or substitute for tree nuts. Faux almonds in baked goods may be peanuts. READ THE LABEL AND IF YOU DON’T KNOW, THEN DON’T EAT IT.

Dermatology I could not resist asking the definition of eczema, atopic dermatitis (AD), allergic atopic dermatitis, and non-allergic dermatitis. The answer restored my faith in this area: you should work with eczema and atopic dermatitis and forget the other two terms. Thank you Dr. Mancini!

One of the shared conditions with allergy is ‘atopic dermatitis’.  The presentation debunked myths associated with this condition.

These myths were-

•             Topical steroids are unsafe and should be avoided.
•             Antihistamines don’t really help.
•             Staph Aureus is an innocent bystander
•             Food Allergy is a common culprit

The debunking

•             Topical steroids are the mainstay of treatment.
•             Antihistamines help with itch and help with sedation.
•             Treating staph infections of the skin help with healing.
•             While 30-60% have a positive test for a food, only 10-30% have worsening of the condition due to a food exposure.

The role of allergy is recognized, but it is only part of a much larger scenario. Foods seem to be part of the problem in the more moderate to severe cases. Full and strict avoidance of a food in many cases does not modify the course of the disease. All too often parents blindly eliminate foods which can lead to dietary and nutritional deprivation. Co-management of AD by dermatology and allergy is vital.

Aeroallergen issues were a concern in the teenager with AD.

Developmental/Behavioral Pediatrics The specialties of D/B and allergy rarely mix except in CME programs like this one. Behavioral issues are not secondary to allergy. Given this, we don’t have many if any consults from the specialty.

Dr. Schonfeld’s lectures were; Supporting children in times of crisis, Connecting with patients and families to conduct a behavioral/mental health interview, and How children come to understand illness and how we can learn to explain it better.

These were very interesting topics and Dr. Schonfeld did fantastic job. I am sure he is wonderful with his patients.

I have always tried to engage the child in my evaluations. After all, the child is the patient. In our practices we need to be sure the child is involved to some extent (depending on age/maturation). There should be no secrets about their condition. The child can better deal with what is going on if they understand it. Our job is to facilitate that understanding and the processing of the information. Adherence to therapy should be improved with comprehension. We should also understand that we should not try to do all this in one visit.

Dr. Schonfeld pointed out that ‘health education’ is rarely taught in medical school. In my situation, I learned about health education in my MPH curriculum. A quote that I will always keep in mind is “You don’t need to be an expert in pediatrics to explain illness to children-you need to be an expert in children.

This was a great conference and it was made great by an outstanding faculty. If you have a chance hear any of these pediatric specialists speak, do not hesitate in listening to what they have to say. If you have a chance to see them for the care of a child, then I am assured that you are in very capable hands.  

Fred Leickly