I swear that I have not been cultivating ragweed. It grows naturally and loves fields, upturned sole, the sides of the road and developing land. Some of our Giant Ragweed plants are more that 9 feet tall! It is a bumper crop this year.

Giant ragweed has a very typical leave and those large anthers (?) from which that yellow pollen falls and becomes airborn. The species is called  ambrosia- for those allergic to ragwee, truly not a drink of the gods but a real source of respiratory and ocular misery.

Short ragweed is the most problematic for allergic individuals. The specific proteins in each species does vary, but they do share a number of allergenic proteins.

                                                 Short Ragweed                                                   Ragweed pollen

Does improvement management of atopic dermatitis influence the appearance of respiratory allergic diseases? A follow-up study. Clinical and Molecular Allergy 2010 8:8 Published June 30, 2010. Authors- G Ricci, A Patrizi, A Giannetti, A Dondi, B Bendandi, and M Masi.

Background and purpose of the study

Atopic dermatitis (AD) is one of the most common skin conditions that affect children. AD is characterized by dry, itchy, rough, and flaky skin. Between 70-80% of children who have AD have an elevation of the antibody associated with allergy- IgE and antibodies to foods/inhalants.  Many children outgrow this condition and in some it persists into their adulthood. In some children AD is the first step along the allergic march; going on to have asthma and allergic rhinitis. Depending upon who you ask or quote, 25-80% go on to have asthma. That is a huge range. The authors of this study published a 10 year follow-up study in 2006 looking at this issue. They showed that the AD disappeared in 60%, 34% developed asthma, and 58% developed nasal allergy. So some, not all finish the allergic march with a better chance of having nasal allergy and about a 1/3 chance of developing asthma. This begs the question as to whether or not anything can be done about it.

This current study looked at the effect of clinical management on the subsequent development of other allergic conditions and they used more standardized and contemporary measures of the conditions in asking what are the risk factors in children who have AD that may predict the development of other allergic conditions.

This is a study from Italy. It was a retrospective analysis; children who had AD between 9-16 months of age were contacted for participation. They had to have been seen in the clinic between 1993-2002.

Methodology

The assessment included;

1. Diagnosis of AD based on Hanifin and Rajka criteria (well established for this condition)

2. AD was evaluated by the SCORAD index at the first visit ( a measure of disease severity)

The clinical management program involved;

1. Environmental management- house dust mite avoidance, high-filtration vacuum cleaning,

2. Skin care- emollients, topical corticosteroids, calcineurin inhibitors, oral steroids, immunosuppressants, biologicals, antibiotics, antihistamines, and leukotriene inhibitors

Allergy Assessment;

1. Skin prick tests (SPT), total IgE  and specific IgE tests- milk, egg, soybean, wheat, peanut, nut, codfish, apple, grass pollen, house dust mite, cat dander, and dog dander. A positive was any value >0.35 for the blood test and a wheal response on the SPT.

Telephone interviews

Results

Telephone interviews were conducted with the families of 176 children. Their ages ranged from 6-12 years. The average age at the time of the first evaluation was about 1 year.

One hundred of the 176 (57%) showed a sensitization by SPT to at least one of the foods/inhalants.

One hundred and three of the 176 (58.5%) had an elevation at least one specific IgE blood test.

After an average of 7.5 years 84 (48%) still had AD- it disappeared in 52%. In the group of children who still had AD, 44% had a single site involved (mostly on a limb) and 18% had multiple locations of AD.

When AD disappeared on the average, the child was 3.25 years old.

In this group of children, respiratory allergy conditions appeared in 66/176 (37.5%).The specific respiratory ailments were; 36 (20.5%) developed only nasal allergy, 18 (10%) developed only asthma, and 12 (7%) developed both.

The nasal allergy appeared at 4.8 years of age. The mean age of appearance of asthma was 3.33 years. Asthma tended to precede the development of the nasal allergy.

A mathematical model, logistic regression, was used to predict the occurrence of asthma. A child who developed nasal allergy or was positive to at least one inhalant (serum specific IgE >0.35) at the time of the first evaluation had a greater risk to develop asthma (odds ratio was 4.219).

Conclusions (authors’)

The results of this study were compared to their earlier study in which disease-specific management was not evaluated. In the current study, the use of integrated management of AD did not seem to influence the natural course of AD. However, the early diagnosis and improved management at specialty centers decreased the percentage of children who went on to develop respiratory allergic disease. The presence of early allergic sensitization at age 1 year may predict the development of respiratory allergy.

                                Percentage of Children with Allergic Conditions – Comparing the two studies

                                1981-1989 study                                                                               1993-2002 study

Resolved AD             60.5%                                                                                                  52%^*

Asthma                     34.1%                                                                                                  17%

Nasal Allergy            57.6%                                                                                                  27%

* not significantly different

In the present study at age 8 years (mean age of the children) 15% already had asthma. In the previous study, 29% had asthma by age 8 years. The management program accounted for a reduction in the appearance of asthma in this group. Similarly, the percentage with nasal allergy fell from about 35% to 17%. This could be due to better management of the AD.

This study used quantitative evaluations with determinations of specific IgE sensitivities and the use of improved clinical tools for assessing AD (SCORAD index, environmental prevention, integrated management) that helped with the early diagnosis, appropriate therapy, and monitoring of children with AD. This may have been  helpful in decreasing the numbers who go on to have respiratory allergy.

Reviewer’s comments

I was surprised at the wide range of children who go on from Atopic Dermatitis to Asthma to Allergic Rhinitis. More definitive epidemiologic work is needed to have a more precise estimate. I hear all too often from other allergists that it is an absolute fact; if the child has AD they will have…..This group of investigators had previously  looked at this evolution to other allergic conditions in the 1980s. This earlier study served as a nice comparison group for the current study.

Back in the80′s the tools and criteria differed. The current study tries to standardize the diagnosis of the allergic conditions. The entire group of children were evaluated with the same tools for AD severity and for respiratory allergy.

This study looks at the impact of early evaluation and the impact of management programs on the occurrence of detouring children who may have been on that allergic march. The first detour was asthma and the second change of course was allergic rhinitis.

Evaluation and management seems to re-direct some of these children away from respiratory allergy. it is not known if these conditions appear later in life. That will be a paper for review perhaps 10 years from now.

 The foods that were important were eggs and milk. A specific IgE level was >2.0KU/L to milk or egg was found to be predictive of sensitization to inhalants in late infancy.

Other considerations are that this is a group of children from Italy- the genetics may differ and certainly the environment differs. Such a study needs to done on our population of children to see if the results can be replicated.

As noted by the authors, demographic information was lacking making it a bit more difficult to describe and characterize the population.

Do we need to be more aggressive with our AD children? When should all these evaluations be performed. In this study many of the children had progressed and were very severe at the time they presented to the specialty clinic. The study did not look at how long treatment should be tried before embarking on a more Allergy/Dermatology Specialty oriented evaluation.

I like the selection of allergy tests here. Nut and apple were a surprise for a first evaluation for specific IgE to food at age 1 year. We did not see shrimp or scallops as a choice here.  Also, the evaluation for the inhalants was looking at sensitization- has the child begun to make antibodies towards these items? The study used these as associations and not necessarily as cause/effect items.

I think we need to re-think about the number of children who march from AD to other allergic conditions. It never was 100% – here is it about a third of children who do this. A take home message here is to consider being more aggressive with our evaluations, monitor more frequently, and carefully in hopes of halting that march from AD to Asthma to Allergic Rininits.

FEL

During a career you hear many words of wisdom from your mentors who are with you seeing children in the office and from meetings, curbside conversations/consultations, and from the literature. The adage that allergic children get sick easier, more frequently, and have more severe illnesses has been out there for many years. There are a number of theories for this contention. Children with allergy tend to remedy their itchy nose with internal manipulation, otherwise known as nose-picking. The finger serves as the vector for direct inoculation of viral particles onto the respiratory tract. Also, a number of years ago a publication reported that allergic noses actually had more receptors for the cold virus than non-allergic noses.

The May issue of the  Journal of Allergy, Asthma, and Immunology (Volume 125 No 5.) has an article by Jaime Olenec, ‘Weekly monitoring of children with asthma for infections and illness during common cold seasons’ concluded that atopic (showing IgE antibodies) children with asthma do have more frequent and more severe asthma exacerbations due to the common cold. The bottom line for me is the impact that the specialty of allergy and the determination of sensitization to allergens can make on children with asthma. The study did not address allergen control measure effects on frequency/severity of asthma symptoms.

My review of the study-

The group who did this is excellent and has a long established research track record and publication record regarding the role of viruses and allergy in pediatric asthma.

The journal in which this was published is peer-reviewed and a top-notch allergy journal. Also of note is that the manuscript was submitted in September, 2010 and was accepted for publication four months later.

The support for the work was from the National Institutes of Health.

The purpose of the study was to look at the impact of viral infections and allergic sensitization on the loss of asthma control during the peak ‘cold’ season.

The study involved 58 children between the ages of 6-8 years who were known to have asthma. These children were followed for three years. Skin testing and specific IgE testing was performed on all. Nasal samples were collected and analyzed for human rhinovirus infection. Diary cards were kept for symptoms. Cold and asthma symptom scores were collected along with peak flow value recordings and notations of the frequency albuterol (rescue inhaler) usage.

There were 42 children who had at least one season of complete data. The average age was 6.5 years and there were 30 boys and 12 girls. In this group 50% had one or more positive skin prick test for an allergen. Of note is that 69% had one or more positive blood tests for an allergen. Additional baseline information included; daily asthma controller medications used by 88%, and oral corticosteroids were used by 57% in the past year. Fifty five percent of the mothers and 40% of the fathers had allergy.

The number of viral illnesses per season was higher in the allergen sensitized group; 47% more virus-associated illness per season. During documented viral infections (viral cultures were frequently performed), the non-atopic children commonly reported no or mild cold symptoms. In the sensitized (atopic) children symptoms tended to be more moderate or severe. Also, almost half of the viral infections in the sensitized children caused moderate or severe asthma symptoms.

The author’s conclusions were that respiratory tract illnesses (asthma symptoms) due to viruses were more severe and were more frequent in children who are atopic.

These were children with asthma who had a positive allergy test. The terms sensitized and atopy were used to describe the group. Asthma frequency and asthma severity was increased in those who have made at least one IgE antibody to something.

This was a small study which was done in only one site. Larger studies in a variety of populations need to be done to confirm these observations.

This work re-affirms my practice of being aggressive with my allergic asthmatic children when the first signs of a cold occur. I advocate stepping-up the treatment program and continuing it for up to 14 days. One of the charts shows that the average duration of cold symptoms was 8.1 +/- 5.6 days and the average duration of asthma symptoms was 7.2 +/- 7.8 days in those who had a documented rhinovirus infection. For me this fits nicely with what I advise- on the average cold symptoms may begin the day prior to asthma symptoms and at the extremes of the range, asthma symptoms may last 14 days in some children.

FEL

When I was at Henry Ford Hospital, Dennis Ownby, MD analyzed the house dust material that was used in the immunotherapy program. Of note is that there was more cat allergen in the house dust mix than what was available in the cat preparation that was available at the time. This house dust extract came from homes. I learned that dust is a mixture of many things.

During my fellowship we went on a field trip across the state of North Carolina to Greer labs. The house dust used for allergen diagnostics and for treatment sets came from collections from a large number of homes. The house dust extract had cat, dog, house dust mite fecal material, roach, other insects, food, mold, and IgA from human spittle.

The June issue of the journal Pediatrics had a quip from the editor emeritus, Jerold F. Lucey, MD regarding the ‘Dirt on Dust’. Dust is a big deal in allergy so this interested me. The note starts with the statement that simple house dust may not be as simple as all that. His source was a text box by Andrew Grant which was part of a more elaborate article by Michael Tennesen in the May 2010 issue of Discover magazine.

Mr. Grant reports that we are responsible for our own house dust. A scientific analysis of house dust reveals that it contains fibers from clothing, crumbs from food, and human dander. Hopefully, so far this is not too disgusting.

House dust has the remnants of other living creatures- plants, bacteria, mold, fungi, decaying insect carcasses, and fecal droppings from house dust mite (yes that is poop!). Had enough? It gets worse.

Our open windows and our shoes bring in the chemical villains. A study by the US Geological Survey from January, 2010 reported on numerous harmful chemicals discovered in house dust. Included in the samples were polycyclic aromatic hydrocarbons. This is used to coat parking lots. DDT, a pesticide banned 40 years ago was detected in house dust samples. Reference was made to another study in which arsenic and lead contaminated soil was found in house dust samples. The lesson here is that we track it in to our home on our shoes.

Clearly, dust is not so simple. It is a hodgepodge of items- biological and chemical. Some can elicit an allergic response; some can cause illness in other ways.

This has caused me to wonder about dust. My wonderment has lead to a few questions;

• If the house dust has all this stuff from our shoes, I wonder what is lurking on the mat at the front door?
• Are there enough food particles in house dust to trigger an allergic reaction in someone sensitive to food?
• What is the composite listing of what is in house dust? Endotoxins would be on that list.
• What is the seasonal variation in house dust composition?
• How do various methods of cleaning change what is in house dust? Now that we have been scared, what can we do about it?
• Are certain types of homes more conducive to certain dust components.

Good studies and information always beget more questions. I am now removing my workday shoes prior to walking into my home!

Fred Leickly

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 

Authors: Amy Branum and Susan Lukacs

Reference: Pediatrics Volume 124 (6) December 2009

This title caught my eye. The impression in clinical practice is that more and more children have food allergy. This article looks at the prevalence of food allergy in children. I wanted to get this review posted this week. I am off to Santa Fe to moderate an AAP Practical Pediatrics Course. This AAP meeting is similar to the one I reported on earlier on this home page (Rhode Island). This meeting has an excellent cast of presenters. I plan to take notes and post a few updates upon my return.

Purpose of the article: To describe trends in the prevalence of food allergy and food allergy-related health care utilization in children in the United States.

Methods (how was this study conducted?): Data from a number of national health surveys were reviewed.

• Food allergy prevalence was evaluated in children 0-17 years of age from surveys conducted over the years 1997-2007. The question asked about food allergy was “During the past 12 months has the child had any kind of food or digestive allergy?”
• Blood tests for IgE antibodies to foods were taken from the National Health and Nutrition Examination Survey (NHANES) 2005-2006. Specific IgE antibodies to peanut, egg, and milk were measured using the Pharmacia ImmunoCap 1000 System. Specific IgE to shrimp was measured only in children over the age of 6 years. The range of specific IgE values was 0.35 to 1000 kU/L.
• Information regarding food allergy-related visits to physician offices and hospital facilities was taken from two additional surveys.
• The results were analyzed using rather sophisticated statistical tools that included weighing the data for the analysis of trends.

Results (what the study found):

• The prevalence of reports of food allergy in children has increased from 3.3% in 1997 to 3.9% in 2007.
• Peanut IgE antibodies were found in 9.3%, egg IgE antibodies were found in 6.7%, milk IgE antibodies in 12.2%, and shrimp specific IgE was found in 5.2% of children.
• Ambulatory care visits for food allergies tripled between 1993 and 2006. Between the years 2003 and 2006 there were 317,000 visits/years to emergency departments and outpatient offices. Hospitalizations with a recorded diagnosis related to food allergy increased from 2600 to 9500 discharges/year.

Conclusions:

                These national surveys show that food allergy prevalence and/or food allergy awareness has increased in recent years.

Commentary:

                The authors point out a number of limitations in the study, however the major contribution here is reporting on what these surveys reveal about the parent’s report regarding food allergy. Food allergy may be rising however it is possible that the results may be due to increased food allergy awareness which is also a very good thing. This is a report of prevalence and does not go into the possible reasons for the increases.

                It is important to note that this was a survey. A simple question was asked. These were not absolutely proven cases of food allergy. The question included digestive allergy which has the potential to include a number of clinical conditions that are more common and may or may not be allergy; lactose intolerance, eosinophilic esophagitis, and celiac disease for example. This was a report on what a parent thought about food allergy in their child.

                The report has a few ‘between the lines’ issues as well. The conclusion is that food allergy and digestive tract allergy has a prevalence of 3.9%. The study also included a survey in which a blood test for allergy was performed. Using the blood test the prevalence of peanut, egg, milk, and shrimp ‘allergy’ exceeds the overall food allergy prevalence. The authors do point out this difference and are very careful about what is allergy and what sensitization to food is.  “Although serum IgE measurements cannot be used alone to determine the prevalence of food-specific allergies or to predict reactions to certain foods, they give an indication of increased atopy and risk for allergic reactions to food.” I define allergy and atopy on my allergy testing page.

                We also need to be a bit careful on the hospital data. The information on health care utilization included children who had a diagnosis of a food allergy. This did not necessarily mean that they were in the health care facility for a food allergy issue. There is a tendency in coding encounters to include as many codes as possible and to include codes that will help with health care utilization reimbursements.

                The statistical analyses on papers like this always fascinate me. During my MPH training I had a number of biostatistics courses. The weighing of the data is frequently done and when it is done, differences can be found. Sometimes it is interesting to see what the results were before any weighing. I have also wondered what went into the ‘weighing’ of the data. What elements of the data were assigned a ‘weight’ to make them work into the analysis?

                This was a nicely done paper and does answer some questions however as many quality studies also do it has us asking many more questions about food allergy in children.

Fred Leickly

I should be receiving my copy of the journal soon. I am concerned about how food allergy will be defined in the paper: will the diagnosis of food allergy be based on a history of exposure confirmed with appropriate allergy testing or will this be based on only laboratory results and no history?

As soon as I have this in hand I will post a commentary.

Fred Leickly

There are two excellent sources to look to for advice. The Academy of Pediatrics (AAP) has issued a policy statement  regarding influenza vaccination. Both the TIV and LAIV (the injection and the nasal spray) “should not be given to children who have a history of hypersensitivity, including anaphylaxis to egg, to any previous influenza vaccine or to any of the vaccine components”.

The Centers for Disease Control state that the TIV is “contraindicated when there is anaphylactic hypersensitivity to egg or other components of the vaccine unless the recipient has been desensitized” (taken from the CDC Statement). For the LAIV, the statement is a little different and reflects the AAP statement; “the LAIV is contraindicated in persons with a history of hypersensitivity, including anaphylaxis, to any of the components of LAIV or to eggs”.

In our specialty clinic at Riley Children’s Hospital we offer the TIV (the injection) and not the LAIV (nasal spray). This is because the vast majority of children who we see in both Allergy and Pulmonology have asthma. The intranasal vaccination is not indicated in the child who has asthma.

The CDC statement identifies only anaphylaxis- a serious life threatening reaction to egg as a contraindication to the TIV vaccination. With this guideline, a child with only a positive allergy test (skin prick test or specific IgE blood test), contact hives, diffuse hives, atopic dermatitis, eosinophilic esophagitis, and vomiting could get the immunization without any further discussion.

It is important to point out that both the AAP and the CDC state that it is a history of hypersensitivity to egg. This is an important point to make. It is the history of a reaction that dictates the approach. Allergy tests for foods have a high degree of false positivity. The history of a reaction and a test to verify the IgE (allergy) mechanism is required for the diagnosis of allergy. A test shows sensitization. A positive test alone to egg without any clinical correlates (history) is not the same as a history of an anaphylactic reaction to egg.

So how can we help? We found some guidance from an article by Robert A. Wood ( Pediatrics 122, Number 3, September 2008 e771-e777) . The article dealt with immunizations in general and it has some specifics on the influenza vaccination.

This is a summary of our approach to this problem;

1. Is there a history of an egg or vaccine reaction?

          a. If no, give the immunization

          b. If yes, ask if the reaction was anaphylaxis

          c. If unknown due to no known exposure to egg (see below)

2. If the reaction was anaphylaxis- a desensitization procedure is indicated.

3. If the reaction was not serious, not life threatening to egg

          a. Give the vaccine- watch 60 minutes OR

          b. Give the 10% of the vaccine wait 30 minutes

             then give the remaining 90% of the vaccine

             and watch 60 minutes Or

          c. Do the diagnostics- skin testing for reactivity to the vaccine-

            this includes a few intra-dermal tests all done in our allergy office.

4. If there has been no exposure to egg, but there is a positive allergy test to egg-

    This is one of the more difficult areas. There are a few choices here and they all depend upon the comfort level of the family and the physician-

          a. Give the full vaccine and watch OR

          b. Give 10% of the dose and watch for 30 minutes

            followed by the remaining 90% and

           watch for an additional 60 minutes

            OR

          c. Do the diagnostics in the allergy office (see 3c above)

Clearly the safest route is to do the desensitization. The desensitization takes about 3 hours and involves a number of injections (around five). However, there are a number of other approaches to look at. The use of these alternatives needs to consider the comfort level of the family and the primary caretaker in giving the vaccination.

Please note that this procedure applies for both the standard influenza vaccination (seasonal) and for the new H1N1 vaccine.

I do recommend getting the influenza vaccinations.

FEL

Your Indiana Joint Asthma Coalition (InJAC)  just put online a Continuing Medical Education (CME) offering on the most recent national asthma guidelines. As the chair of the Health Care Committee of InJAC it was my job to oversee the project. This gave me the opportunity to go over that 400+ document known as the “Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma”. The CME program can be viewed by anyone without registering for the credit. The online program is a slide set on the various sections of the guidelines. Each reviewer summarized the essential points and provided notes for each slide in the presentation. A shorter Summary report of the Asthma Guidelines (EPR-3) is also available.  This is the 3rd such report. The first came in 1991. Number two was 1997. There was a publication that dealt with 5 specific hot topics from the guidelines in 2002. In 2007 the most recent EPR was published.

As I reviewed the EPR-3 I noted how often allergy/atopy appears in the document. Consider a few of the following statements;

1. Atopy, the genetic predisposition for the development of immunoglobulin E (IgE)-mediated response to common aeroallergens, is the strongest identifiable predisposing factor for developing asthma (Key Point- page 11).
2. The onset of asthma for most patients begins early in life with the pattern of disease persistence determined by early, recognizable risk factors including atopic disease, recurrent wheezing, and a parental history of asthma (Key Point- page 12).
3. This working definition (of asthma) and its recognition of key features of asthma have been derived from studying how airway changes in asthma relate to the various factors associated with the development of airway inflammation (e.g. allergens, respiratory viruses, and some occupational exposures) and recognition of genetic regulation of these processes (page 14).
4. Sensitization and exposure to house-dust mites and Alternaria (mold) are important factors in the development of asthma in children (page 22).
5. The asthma predictive index…..identifies the following risk factors for developing persistent asthma among children younger than 3 years of age who had four or more episodes of wheezing during the previous year: either (1) one of the following: parental history of asthma, a physician diagnosis of atopic dermatitis, or evidence of sensitization to aeroallergens, or (2) two of the following: evidence of sensitization to foods, > 4 percent peripheral blood eosinophilia, or wheezing apart from colds (page 25).
6. Tests to consider in the differential diagnosis of asthma- allergy testing (page 45).
7. Key Points in the Initial Assessment of Asthma- identify precipitating factors (inhalant allergens…) and identify co-morbid conditions that may aggravate asthma (rhinitis –nasal allergy…) page 47.
8. Referral to an Asthma Specialist for Consultation and Co-management- ….for allergy skin testing (authors note- not RAST or blood specific IgE)…..for consideration of allergen immunotherapy (page 68).

The above excerpts came from section 2 (asthma definition, pathophysiology, pathogenesis, and natural history of asthma) and section 3 part one- Asthma Management- measures of asthma assessment and monitoring. These remaining sections comprise over 300 pages of material. 

The remaining sections of the EPR-3 cover education, environmental control, medications, long-term management, and managing exacerbations of asthma. These sections also include information on the significant role of allergy in asthma. These sections go over specifics on how to manage the allergens.

 Through the allergist’s eyes- Asthma is significantly intertwined with allergy. We should look at it as a manifestation of the allergic condition. It is not allergy and asthma anymore, in many children it is allergy showing itself as asthma! Asthma can be a manifestation of allergy.

FEL