I came across a very interesting and powerful editorial that summarized many issues dealing with the worldwide problem of allergy.

Allergy is a major health problem-clearly not in everyone and not in the majority of the population. Worldwide allergy affects 10-30% of people. As far as a single chronic clinical condition, that is a significant number. Also, the prevalence has increased.

The impact of an allergy can be life-threatening (acute severe episodes) or chronic (daily symptoms). The allergic condition does have a major socioeconomic burden and allergy also has the obvious effect on a patient or a family’s quality of life.

Despite advances in research on causes, associations, risk factors, and treatment of allergy there are many inadequacies and unanswered questions. This editorial shares those concerns.

This is a consensus statement from a group of 40 noted researchers and clinicians from four continents who met in Switzerland last year. The banner for the meeting was simply ‘Allergy and Allergic Diseases: Barriers to Cure’.

Allergic conditions deal with many broad areas of medicine. Allergy affects a wide range of organ systems; eyes, respiratory tract, gastrointestinal tract, and skin. The conditions vary in severity and their course.

Listed are the concerns and needs (these come from the experts and are my summations of their summation);

• The cause(s) for the increase in allergy prevalence is unknown. Environmental considerations    include; air quality, diet, climate, UV radiation, direct skin contact, and psycho-social interactions.
• A specific environment may protect or put someone at risk if they have the genetic predisposition towards allergy.
• Interactions between bacteria, pollutants, and the immune system are marginally understood.
• There is inadequate understanding of those natural mechanisms that lead to acute vs. chronic suffering with allergy or resolution of allergy.
• There needs to be a better classification system for severity/types of allergy.
• New therapies need to work on the pathways that lead to an allergic response.
• Better translational research is needed (taking what is learned in the laboratory to the bedside).
• Better tools are needed to analyze the information or data regarding allergy.
• There needs to be a plan for prevention of allergy.
• We need better tools for diagnosis and prediction of a response to treatment.

The article also noted the gap between what we know about allergy and the application of that knowledge to those who struggle with allergy.

• There is a shortage of well-trained allergists in most countries
• Education and training efforts regarding allergy need to start with the medical students, especially for a condition that affects so many people
• Awareness campaigns are needed for targeted groups such as nurses and school teachers
• There needs to be close cooperation with patient organizations
• Decision makers for developing and approving health policies and administration must be made more aware of the issues and problems of allergic diseases

Reviewer’s note-

It scary what we do not know and it is even scarier that we are not doing much about a few things when we can.

Allergy is a public health problem.

The editorial challenges us to make a change.

This year Dr. Vitalpur and I will be offering clinical teaching about the immune system and allergy in particular to first year medical students.

I have always wondered why allergy is not a required resident rotation – a requirement by the governing board of residencies. The condition affects so many children and is thought to affect so many more. I can easily see the impact of having at least a few weeks of exposure to the specialty in our allergy clinic.

We are most happy to speak at support groups or schools and we have done that many times. I am concerned that we are not asked more frequently to go out in the community.

We get involved with patient organizations and are willing to be involved with more.

It is unfortunate that we are not asked about policy or design. More often we have a reactive role in this regard.

The challenge is before us.

FEL (2-2-2012)

A few things to add. I prefer the use of the term ‘peanut-safe’ in deference to ‘peanut-free’. The terms safe and free may have the same intent, however they may be practiced differently. For example, peanut free would mean that no peanuts would pass through the threshold of the institution- that is the policy, that is the law. Now consider ‘peanut-safe’. When you are peanut-safe, it includes the previous concept and adds the idea of continued vigilance; always checking, always looking, being active about keeping peanuts away from those who may have life-theatening events with exposure.

The other item I would add is that at this time, since I write all the material for allergy at Riley, you would have to check out this website for more information. The www.RileyHospital.org gets you to the children’s hosptial website and how to access the children’s hospital. They are working on topic postings.

Thanks for looking,

Fred Leickly (12-11-2011)

Practical guide to skin prick tests in allergy to aeroallergens

I was alerted to this article by my partner Dr. Vitalpur. It comes from Allergy (European Journal of Allergy and Clinical Immunology) 2011 . The purpose of the article was to provide ‘pocket guidelines’ from a consensus report regarding the use of allergy skin prick tests for inhalant or aeroallergens.

The skin prick test (SPT) is a widely used, major diagnostic tool used for the diagnosis of allergy. The introduction of the article points out the many complexities in performing SPTs and recommends that they should be performed only by trained health professionals.

As for the methods used to create the guide; it was a combined effort from the Global Allergy and Asthma European Network (GA²LEN) and the Allergic Rhinitis and its Impact on Asthma (ARIA) task force. Once the document was created, it was reviewed by the membership of the networks. The authors point out that this is not an evidence-based guideline. It should be looked at as ‘…clear-cut answers to frequently asked questions by practitioners and patients.’ The evidence-based aspect follows the guide-in future reports.

The article is broken down into a series of 21 specific questions:

1. What are the indications for skin tests in clinical practice?
2. Which skin tests are recommended?
3. What role do intradermal tests play?
4. What is the recommended skin prick test technique?
5. Which treatments suppress skin tests?
6. Which diseases affect skin tests?
7. Which allergen extracts to choose?
8. Which allergen extracts should be tested?
9. What area of the body should be chosen and what is the ideal distance between tests?
10. Which negative and positive controls are recommended?
11. Which results are regarded as positive?
12. How do skin tests compare with serum-specific IgE?
13. How to interpret skin test results?
14. Which skin tests are recommended in adolescents and adults?
15. Which skin tests are recommended in the elderly?
16. Which skin tests are recommended in young children?
17. What is the role of skin tests in primary care?
18. How can skin tests be used in developing countries?
19. Are skin tests needed in allergen immunotherapy follow-up?
20. Can skin tests be used in research?
21. What are the future needs?

Each question has a short, concise answer. These are common concerns and questions. I would like to point out a few of them for this review. The link will direct the reader to questions not covered here.

1. What are the indications for skin tests in clinical practice?

Asthma and allergic rhinitis are the indications for aeroallergen testing. The SPTs can be used from infancy to old age. The repeating of SPTs is done to detect new sensitizations in children and when changes in symptoms have occurred. 

2.Which skin tests are recommended?

Prick skin tests have a high degree of correlation with symptoms. There is high specificity (a negative test when you do not have the disease) and sensitivity (when the test is positive when you have the condition) with the skin pricks used for inhalant allergy.

 Table 1 Performance of skin prick tests

1. Use standardized extracts when available (We have grass, house dust mites, and cat as standardized extracts.)
2. Include a positive and a negative control solution (histamine is the positive control)
3. Perform tests on normal skin (not on skin affected by severe eczema or urticaria)
4. Evaluate the patient for dermatographism (Means skin writing- pressure to the skin will cause a hive, this is a common reason for someone to allergic to everything including the negative control.)
5. Determine and record medications taken by the patient and the time of the last dose
6. Record the reactions after 15 minutes
7. Measure the longest wheal diameter

Skin prick testing may cause systemic reactions

The common errors in skin testing are listed in table 2

• Tests are placed too close together and overlapping reactions cannot be separated visually.
• Induction of bleeding, leading possibly to false-positive results.
• Insufficient penetration of the skin by the puncture instrument, leading to false-negative results. This occurs more with plastic devices.
• Spreading allergen solutions during the test or when the solution is wiped away.

 3. What role do intradermal tests play?

Intradermal skin tests (when a needle is used to inject the extract- almost like a TB test) are not useful for allergy diagnosis with inhalant allergens. The clinical value is unknown in patients who only have positive intradermal tests. They are less safe to perform. There are practices where this is the only type of test done or they are performed when the SPTs are negative. We use this type of test ONLY in the ‘Bee Clinic’- the protocol for pursuing stinging insect allergy utilizes the intradermal test.

4. Which treatments suppress skin tests?

Drugs can suppress skin tests.

 Antihistamines- have a significant impact on skin test results. They should be avoided for 7 days

Imipramine- anti-depressants, sometimes used for bed wetting- can affect skin test results for 21 days

Steroid ointments and creams- minimal if any effect on skin testing

UltraViolet light – used to treat skin condition, can effect skin test results for up to 4 weeks

Table 3 Inhibitory effect of various treatments on skin prick tests show other agents that may impact skin test results.

5. Which diseases affect skin tests?

Patients with widespread eczema or hives cannot be tested in areas of affected skin. Neurological disorders and infectious diseases (e.g. leprosy) can lead to false-negative results.

6. Which allergen extracts to choose?

The quality of the allergen extract is of key importance as variations in the quality and/or potency of commercially available extracts exists, in particular for animal mites, animal dander, and molds, but even pollens. Use standardized extracts if available.  

7. Which allergen extracts should be tested?

This varies per region. This answer was relevant to Europe. I comment on this at the end of the review.

 8. What area of the body should be chosen and what is the ideal distance between tests?

Usually, the skin tests are performed on the forearms depending on the age of the patient. The distance between tests should be 2 cm. We have used the child’s back for testing. There is a larger surface area to work with. If needed, more items could be evaluated using the larger space. It is also an area which would not be frequently treated with a topical steroid.

 9. Which results are regarded as positive?

The wheal and erythema have been used to assess the positivity of the skin test. However, only the wheal is needed. The largest size of the wheal is considered to be sufficient. Wheal diameters equal to or larger than 3 mm are considered positive in SPTs.  

Redness alone is not a significant response. There needs to be a wheal (swollen area) of proper size to be called significant. In our clinic, the physician who ordered the test reads them and decides on the significance. All too often, slight red marks are interpreted as positives.

 10. How do skin tests compare with serum-specific IgE?

Serum-specific IgE, SPTs and allergen challenge do not have the same biological and clinical relevance and are not interchangeable. Low levels of serum-specific IgE are less often associated with symptoms than higher levels, but they do not exclude allergic symptoms particularly in very young children.

Note- the paper did not use the term RAST. The proper term is serum-specific IgE- that blood test for allergy. I thought that the answer to this question was not as complete as it should have been.

 11. Are skin tests needed in allergen immunotherapy follow-up?

Skin test reactivity decreases with allergen-specific immunotherapy to inhalant allergens, but skin tests cannot be used to assess the efficacy of immunotherapy in practice. Moreover, skin tests cannot be used to decide the cessation of immunotherapy.

Reviewer’s Comments-From the original 21 questions, I chose 11 that tend to be more frequently brought up in our practice. Many of the questions that I omitted dealt with issues unique to Europe or to the adult population.

In a nutshell the skin prick tests for aeroallergens (inhalant allergens) are:

• Indicated for respiratory tract symptoms
• Can be done in very young children
• Should be done with the proper extracts and application technique
• Can be done if a few medications are out of the child’s system
• There may be a problem finding clear skin to do them on a child who has eczema or hives
• May be done on the arms,
• Are considered positive if the wheal (swollen area) is of proper size (redness alone does not qualify)
• Should not be used to monitor an allergy shot program.

This was a very neat, concise, and well done synopsis of how things are done in Europe. An additional tidbit was the answer to the question- Which allergens should be tested? The quick answer is that it depends on the allergen exposure for the area and that a common, standardized battery of tests should be recommended for Europe. The list was short;

• Pollens- Birch, Cypress, Grass (one species or a mix), Mugwort, Olive (or Ash), Parietaria, Plane, and Ragweed
• Mites- two species
• Animals- Cat and Dog
• Mold- Alternaria and Cladosporium (Aspergillus extract is not available in all countries).
• Insects- Cockroach

That panel for respiratory tract allergens would contain only 15 aeroallergens plus the two controls- 17 skin tests done to assess allergen sensitization.

A reference was also made to the National Health and Nutrition Examination Survey (NHANES) performed in the United States (2005) – 10 allergens were used.

FEL

11-30-2011

Usually when I review an article I go directly to that part of the introduction that deals with the purpose of the study. However, the background information provided in the introduction I thought was very helpful in understanding food allergy, noting the concerns regarding food allergy, and sharing how experts in the field of food allergy handle it (especially as they see a significant number of food allergic children in their referral center).

Identified problems with food allergy;

1.  Availability of serum IgE tests for foods
2.  Use of allergy tests to direct avoidance diets
3.  Consequences of avoidance diets
   • Poor weight gain
   •  Malnutrition
4.  Idea that food allergy is the exclusive cause of atopic dermatitis
5.  Food allergy focus leads to neglect of skin care

The allergy test result, whether by skin prick test or by serum IgE (formerly known as RAST) antibody levels, predict the chance of having a reaction with exposure to that food (they also demonstrate the presence of IgE directed against that food). These probabilities have been established for just a few foods; cow’s milk, hen’s egg, fish, peanut, and tree nuts. For all the other foods the levels that predict the chance of the child having a positive reaction have not been established.

Another significant issue that clouds the picture is that both allergic skin testing and serum specific IgE levels obtained from a blood test frequently detect sensitization that is not associated with any symptoms when the food is ingested. The false positive rate- when the test is positive and the story is that there were no problems with ingestion – is 50%! The gold standard for a food allergy is the double-blind placebo-controlled challenge. In other words, the best indicator is the history- what happens when the food is ingested.

The Purpose of the Study- was to raise awareness about the overreliance on serum immunoglobulin results as the primary indicator for establishing a food elimination diet in children (with atopic dermatitis).

Methods-This was a retrospective chart review of children who were seen for atopic dermatitis and food allergy. The number evaluated was 125.

Results

The median age of the children was 4 years. Most of had atopic dermatitis (96%). The severity of the atopic dermatitis varied- 30% were mild, 24% were moderate, and 42% were severe.

There were 364 oral food challenges performed on foods that were avoided at the time of the evaluation. That is almost 3 food challenges per child. Most of these challenges were negative- 325/364 (89%). Of note that during these food challenges, if there was a reaction, it occurred within a 2-hour observation period. Also, there were no documented flares of the skin condition.

Those 364 food challenges occurred in three different groups of children; 111 in whom foods were avoided due to a positive allergy test, 122 in whom a food was avoided due to a previous reaction to a food, and the last grouping was 131 children in whom a food was avoided for other reasons (not a history of a reaction or a positive allergy test). This last group included those who avoided a food because of lack of prior exposure, another family member with an allergy to that food, parental fear, refusal to eat the food, worsening of atopic dermatitis was uncertain with exposure, being too young for the food, and uncertain reasons.

In the group who avoided a food due to a positive allergy test (n=44 children) – with wheat being an exception (at 77% negative), 80% or more of the food challenges were negative. When there was a positive food challenge, the foods involved included egg, banana, peanut, soy, and wheat.

There were 122 food challenges done in a group of children (n=67 children) who had a history of a reaction to the food. When peanut and oats are excluded, more than 75% of the food challenges were negative. The positive food challenges were to; egg, chicken, milk, oat, peanut, soy, pea, wheat, beans, and pork & beans. This group of children had an array of food reactions by history; anaphylaxis (5%), gastrointestinal reactions (17%), lower respiratory tract reactions (8%), upper respiratory tract reactions (10%), and skin reactions (76%).

In the last group, those who avoided a food for other reasons, (n=131) more than 90% of the challenges were negative. There were 11 positive food challenges. The positive foods included egg, fruits (strawberry), meats (beef, chicken), milk, shellfish (shrimp), soy, barley, and Alimentum.

The levels of specific IgE antibody to the food were used to divide those who were challenged versus those who were not challenged. The following table shows the serum IgE level, the offering of a food challenge, and the result of the food challenge. When the serum IgE levels were elevated, no challenges were offered. For these three foods everyone who was below the critical cut-off point passed the food challenge. The decision levels for doing a food challenge were as follows- egg:< 2years of age -2 kU/L and >2 years of age 7 kU/l, Milk:< 2 years of age -5 kU/L and > 2 years of age a5 kU/l, peanut: 14 kU/L.

84-93% of foods that were avoided for a variety of reasons were returned to the child’s diet after a successful food challenge.

Conclusions- the authors concluded that in the absence of a history of anaphylaxis, the primary reliance on serum food-specific IgE testing to establish the need for a food elimination diet is not sufficient, especially within the population of children with atopic dermatitis. Oral food challenges are indicated to confirm the presence of a food allergy.

Many of the children seen were on overly restrictive diets that were inclusive of foods they never had exposure to or foods that were eaten without a problem. This restriction was based on food blood test results. The successful food challenge demonstrated that specific food restriction was not necessary in most instances. A food challenge discerns sensitization from true allergy.

The authors point out that it is important to optimize skin care and clearing to accurately sort out the impact of a food on the condition. It is also stated that there is a significant overreliance on allergy test results in making the diagnosis of food allergy especially in the children with atopic dermatitis. Allergy test results, if not supported by a food challenge, can lead to unnecessary food restrictions. To quote the authors, ‘misinterpretation of food allergy immunoassays, for which there is no correlation between the level and the probability of reacting to a food, is leading       unnecessary dietary restrictions that could result in nutritional deficiencies.’

Reviewer’s Comments- After my first read of the article, I felt that this was a very strongly worded statement against the indiscriminate use of serum IgE testing.  After numerous reads, that opinion of the article has not changed. This work is a strong statement against serum IgE testing for allergy.

It is important to point out that the vast majority of children who were in the study had atopic dermatitis (aka eczema). This clinical condition is notorious for having many false positive food allergy tests. During the 1980’ there were many studies that linked food allergy with atopic dermatitis. During my fellowship at Duke we watched children with severe atopic dermatitis react during the double-blind placebo-controlled food challenges. These studies led to the observation that there were 6 foods commonly associated with the condition; egg, milk, wheat, soy, peanut, and fish. Subsequently, many children with a range of presentations of atopic dermatitis have undergone allergy testing both by the skin prick method and by serum testing.  That has led to the concerns presented in this article.

The current ‘state of the art’ noted in the NHLBI Guidelines for the Diagnosis and Management of Food Allergy  suggests that food allergy considerations should include egg and any other food that the family feels is causative to the skin condition.

The authors point out that the availability of immunoassay food allergy panels to identify possible food allergy has added to the ongoing potential for misinterpretation of the results.

We also have that issue that continuously plagues us- sensitization vs. allergy. The laboratory test tells us that IgE is being made. The significance of that IgE has to be determined by the clinician. Taking a history is one way to begin establishing significance. The food challenge would be the bottom line for establishing relevance and significance of a positive IgE test for a food.

There are many messages within this study. The concerns regarding restrictive diets and avidly pursing food allergy diagnostics can lead to;

1. Failure to thrive due to food restrictions
2. Parental perceptions about unclear messages about which foods must be avoided
3. Attempts to treat atopic dermatitis by diet alone and not proper skin care
4. Pressure from parents to get these blood tests for food allergy
5. Incomplete understanding about the class designations
6. Applying the well-established food specific IgE values to foods that have not been rigorously evaluated

These concerns are seen with parents, primary caretakers, and yes, even allergists.

 When an allergy test for a food is positive yet the food is eaten without any clinical reaction, the test was a false positive. We should not let the laboratory result dictate the care of the child. Specific food allergy testing can be done for the food of interest. Select the test based on the story that supports it.

I think the role of the allergist in the near future will be to clear many of these positive tests. Here at Riley hospital we have an extensive experience in doing food challenges. Most of the time we perform a food challenge to demonstrate that a food allergy has been outgrown. We offer them in a controlled clinical environment. Everything is in place to take care of a reaction. In the near future I am sure we will be doing more food challenges to demonstrate the irrelevance of positive allergy test results.

The serum tests for IgE to food have helped with the decision to offer a food challenge for some foods. I look to the serum tests for food to decide the chance of a reaction and whether or not an oral food challenge should be scheduled. It is always perplexing to have a child present who has had a panel performed. All too often we struggle with results deemed high due to the ‘H’ notation after the specific concentration. We struggle with positive results from foods that the child has never ingested. We very frequently struggle with results on foods that the child has eaten with impunity and never had a problem. The food challenge helps to sort the well from the worried well.

Many times I have witnessed the joy of having the yoke (not yolk) of a food allergy removed by doing the food challenge.

FEL

The July issue of Pediatrics has an article entitled, ‘The Prevalence, Severity, and Distribution of Childhood Food Allergy in the United States’ by R S Gupta, E E Springston, M R Warrier, B Smith, R Kumar, J Pongracic, and J L Holl. The bottom line from this work is that the prevalence and severity of food allergy is greater than previous reports would indicate and this was a fairly large nationwide survey designed to address the question of prevalence. The authors also conclude that disparities exist with the clinical diagnosis of the condition.

Purpose of the paper- to determine the prevalence, severity, and distribution of food allergy in children.

Methods-The authors created a survey that was population-based and cross-sectional. It was administered to a representative sample of the United States population between June 2009 and February 2010. This survey was carefully developed and evaluated prior to its use. It was not a previously used, standardized tool.

Recruiting and survey administration was performed by a survey research company. Internet access was required to participate.

Completion of 40,000 surveys would give the study significant power (0.9) at a significance level of 0.5 to detect overall and allergen-specific food allergy prevalence (between 1-9%) and prevalence variability from 1-7% in groups as small as 1% of the sample.

Outcome Measures

The primary outcomes were food allergy prevalence and severity.

Food allergy was defined as a report of a confirmed or a convincing story of an allergy.

A convincing food allergy was based on at least one of the following;

1. Anaphylaxis- defined as a severe reaction that could lead to death
2. Angioedema (swelling) of the lips, eyes, or face
3. Other Angioedema
4. Coughing
5. Other oropharnygeal symptoms
6. Eczema
7. Flushing
8. Hives
9. Low blood pressure
10. Pruritis (itching)
11. Trouble breathing
12. Vomiting
13. Wheezing

A confirmed food allergy had the above criteria and included a report of a physician-diagnosis with serum-specific IgE, skin prick test results, or the result of an oral food challenge.

The severity of a food reaction was based on the nature of the symptoms;

Mild-moderate food allergy symptoms were limited to;

1. Angioedema of the lips, eyes, or face
2. Other angioedema
3. Coughing
4. Other oropharyngeal symptoms
5. Eczema
6. Flushing
7. Hives
8. Pruritis
9. Vomiting

Severe food allergy symptoms were;

1. Any report of anaphylaxis
2. Low blood pressure
3. Trouble breathing
4. Wheezing
5. Vomiting and angioedema, and coughing in combination

Results

The final sample size was 38,480 children.

The prevalence of food allergy in children was 8%. Multiple food allergies were reported in 2.4% (approximately 1/3 children of those with food allergy had more than one food to report).

Allergen prevalence was as follows;

Peanut- 767/3339 (23% of the reports) 52% had severe reactions, 48% had mild-moderate reactions

Milk- 702/3339 (21% of the reports) 31% had severe reactions, 69% had mild-moderate reactions

Shellfish- 509/3339 (15% of the reports) 47% had severe reactions, 53% had mild-moderate reactions

There was an age variation reported (the highest percentage reporting a specific food allergy);

Peanut- 30% in the 3-5 years of age group

Milk- 32% in the 0-2 years of age group

Shellfish- 24% in the > 14 year old age group

Tree nuts- 15% in the 11-13 year old age group

Egg – 16% in the 0-2 year old age group

Fish (fin) – 7% in the >14 year old age group

Strawberry- 8% in the 0-2 year old age group

Wheat- 8% in the 11-13 year old age group

Soy- 7% in the 11-13 year old age group

Severity of the Food Reactions

The prevalence of a severe reaction to a food was 3.1% of the surveyed population. This translates to 38.7% of the food allergy population. These severe reactions were reported more frequently in the children who had peanut or tree nut allergy. From the note above- 52% of the peanut and 53% of the tree nut allergic group had severe reactions.

When it happens to you or your child- it is 100%. The reassurance factor- just over 1/3 have serious reactions, most do not. Serious reactions are seen just over half the time with peanuts and tree nuts.

Food Allergy Associations- Odd/Risk Factors

The odds of having a food allergy were-

1. Higher in Asian and black children as compared to white children.
2. Higher in all age groups compared to children aged 0-2 years.
3. Higher in geographic areas outside the Midwest.
4. Lower with household incomes <$50,000.
5. Gender did not make a difference
6. Higher for a confirmed food allergy compared to a convincing food allergy history in those children with multiple food allergies.
7. Lower for confirmed food allergy in Asian, black, and Hispanic as compared to white children.
8. Lower for confirmed food allergy in households with incomes <$50,000.
9. Higher for a severe reaction among children in all age groups compared to children 0-2 years of age,  boys compared to girls, and those with compared to those without multiple food allergies.

Conclusions

Eight percent of children have food allergy with 38.7% having a severe reaction and 30.4% having multiple food allergies.

The disparity regarding food allergy diagnosis was seen with race, age, and income.

Reviewer’s Comments

Prevalence refers to the proportion of individuals with the clinical condition in a population at a specific moment in time. It provides an estimate of the risk or probability that an individual will have the condition. This would be the number of cases divided by the total population at a given moment.

When looking over the information there are a few points that need to be stressed. First was the sample truly representative?

The study was not performed on the entire pediatric population of the United States. The population was recruited from 6100 participants through a Web-enabled panel and an additional 33,900 came from on online sample of households with children; they all had access to the internet. This specific population is reported to be representative of U.S. households with children. So the first concern has been answered. However, a question arises as to selection bias. Do families who have children with food allergy have more computer access? Did the lack of computer (internet access) lead to non-selection for the study?

The second point was the definition of a food allergy. This was by the family’s report of a reaction or a confirmed food allergy. This was not a medical record review nor was this a bone-fide food challenge. The authors do point out that another bias; recall bias may be at work.

This was the largest study conducted looking at food allergy prevalence- a uniqueness to the work.

The article points out a number of helpful ‘between the lines’ points. About half of the children with a peanut allergy had a severe reaction. You can have mild-moderate reactions to peanut. The same relationship was seen with shellfish allergy.

The authors used multiple logistic regression models to establish odds. This statistical tool looks at the degree of association between having the condition after adjusting for factors that may be confounding. When the odds equal 1, then there is no increased/decreased relationship. When confidence interval include the number one, then there is no strong statistical difference. There seems to be a tendency for disparity, however I would be cautious due to the stated confidence intervals. The disparities that look clear are

Race- Asian, Black for having food allergy

Less confirmed vs. convincing cases with Asians

Age-compared to two year olds, more food allergy in all other ages

Age- compared to two year olds, more severe food allergy in all other age groups

Income- household income lower than $50,000 was protective for having food allergy, for having fewer confirmed vs. convincing histories, and having less severe food allergy. (In these instances the odds was less than one)

Geographic regions- compared to the Midwest, there was more food allergy in the Northeast, South, and West.

As for summarizing discrepancies in a few sentences- if the child was Asian or Black there was a higher chance of having food allergy, and less of a chance that it was confirmed if the child was Asian. Children over the age of two years have more reported food allergies and they tend to be more severe in the older age groups. If your family made less than $50,000, there was less of a chance that there would be a food allergy (poverty protects?). Lastly, there is less food allergy in the Midwest that in other regions of the country.

I enjoyed reading and reviewing this article. As with many good studies it stimulates more questions.

Respectfully submitted,
FEL

My recollection is that an allergist by the last name of Rome was the speaker. Since this was well before the days of the internet, I was unable to verify Dr. Rome. I would like to reference the author of the ‘Golden Rules of Pediatric Allergy’ and try to get a fix as to when these were written. My guess is that this is from the  1960’s. These ‘rules’ are almost 50 years old.

I love history. If you know your history you know where you come from and that helps when you set your sites on where you need to go. Allergy enjoys a history as well. So, where did these come from? Was there evidence to support these contentions?

Some of these statements have gone by the wayside- many have been disproven over time (that is what evidence-based medicine will do), some have never been proven to be true, some may be dangerous given our current knowledge, and some still remain true to this day- especially rule #33.

Some of these rules are still being practiced, prescribed and proscribed. You could almost tell when a physician was trained when some of these re-surface. I had rule #45 present recently.

This will be a dynamic document. My plan is to look into each rule, try to determine why it became a rule. Then see what we have in the 21^st century to support or refute it.

So, I will need support on this project. Please feel free to help with comments and hopefully references.

Also note that I retyped the ‘rules’ and was exact in my work. What follows is verbatim, including any and all grammatical and spelling errors. Please click the link to access the ‘Golden Rules of Pediatric Allergy’.

FEL

I also suffer with eye allergy problems- allergic conjunctivitis. Grass pollen causes my eyes to itch, water, redden, and swell. My usual response is to rub the eyes and I know that rubbing just makes things worse. The oil, dirt, and grime from the hands will also cause the same symptoms as an allergen. The eye will respond with itch, tearing, redness, and swelling in response to an allergen, an infection, and an irritant.

At the most recent American Academy of Allergy, Asthma, and Immunology (AAAAI) meeting in March, I attended a session – The Diagnosis and Treatment of Ocular Allergy: A Practice Parameter Overview. This was an excellent session. There were three presentations;

• Classification and Epidemiology by Sergio Bonini, MD
• Pathogenesis and Diagnosis of Ocular Allergy by Andrea Leonardi, MD
• Treatment of Ocular Allergy by Leonard Bielory, MD

Classification and Epidemiology

                There are a number of types of allergic conjunctivitis;

• Intermittent or seasonal allergic conjunctivitis -usually seen with nasal symptoms
• Persistent or perennial allergic conjunctivitis-also seen usually with nasal symptoms
• Vernal keratoconjuncitivits-can occur alone or with asthma especially in young boys
• Atopic keratoconjunctivitis-seen with atopic dermatitis
• Contact lens conjunctivitis

Pathogenesis and Diagnosis of Ocular Allergy

                Seasonal allergic conjunctivitis is due to pollen. Trees tend to favor the spring. Grass pollen will begin towards late spring and early summer. Weed pollen would be in summer to late fall or until two killing frosts.

                Perennial allergic conjunctivitis would be due to house dust mites or to multiple allergens.

                The key symptom of the allergic eye is itch. If there is no itch, it is not due to allergy.

                Vernal keratoconjunctivitis is a more severe presentation and is seen mostly in children. In this variation of ocular allergy, there is intense itching, photophobia, a foreign body sensation in the eye, redness, and mucus secretion. The cornea can be involved. Interestingly, only 50% will show clear allergic sensitization with this condition.

 Making the diagnosis

                Get a good history

                No itch = no allergy

                The diagnosis of the seasonal form is clinical

                Vernal and atopic keratoconjunctivitis have unique features/signs

                If the skin of the eyelid is involved, consider a contact allergy

                Consider drug-induced conjunctivitis

                Air pollution may be a cause of eye allergy in those who live in the city

Treatment of Ocular Allergy

                The Allergic Conjunctivitis Practice Parameters (2010-under review) provide a stepwise approach.

                Acute Ocular Allergy

                Primary Treatment

• Avoidance- >30% improvement in symptoms
• Cold compresses- effective for mild to moderate symptoms
• Preservative-free tears- soothing, try refrigeration to improve effect, cheap, comfortable, safe, use as needed
• Contact lenses- act as a bandage/barrier, 67% improvement

                Secondary Treatment- Topicals

• Antihistamines- help with itch
• Antihistamines + Decongestants- help with itch and redness
• Multiple Action Agents- perennial use
• Mast Cell Stabilizing Agents- to prevent

               Tertiary Treatment

• Oral antihistamines
• Topical Steroids
• Multiple Action Agents
• Immunotherapy

Failure of conventional anti-allergy therapy treatment may require a consultation with an ophthalmologist

Pharmacologic Treatment (trade names appear in parentheses)

Topical agents

                Antihistamines

                                Levocabastine (Lecostin)

                                Azelastine (Optivar)

                                Pheniramine  (Opcon A, Naphcon A)

                Decongestants – These are available over-the-counter.

                                Naphazoline (Clear Eyes)

                                Oxymetazoline

                                Tetrahydrozoline (Visine)

                Multiple Action Antihistamines

                                Azelastine (Optivar)

                                Emedastine (Emadine)

                                Epinastine (Elestat)

                                Ketotifen (Acular or Zaditor-OTC)

                                Levocabastine (Levostin)

                                Olopatadine (Patanol)

                Mast Cell Stabilizers

                                Cromolyn (Crolom, Opticrom)

                                Lodoxamide (Alomide)

                                Nedocromil (Alocril)                    

                                Pemirolast (Alamast)

                Non-Steroidal Anti-Inflammatory Agents

                                Ketorolac (Acular)

                Corticosteroids

                                Loteprednol (Alrex)

                                Rimexolone (Vexol)

                                Fluorometholone (Allergan)

                                Prednisolone

                                Dexamethasone

Oral Agents

                Antihistamines

                                Ceterizine (Zyrtec)

                                Desloratidine (Clarinex)

                                Fexofenidine (Allegra)

                                Loratidine (Claritin)

                                Diphenydramine (Benadryl)

                                Chorpheniramine (Chlortrimeton)

                                Brompheniramine

                                Clemastine (Tavist)

                Decongestants

                                Pseudoephedrine (Sudafed) OTC

Nasal    

                Corticosteroid

                                Fluticasone (Flonase)

                                Mometasone (Nasonex)

                Antihistamine

                                Azelastine (Optivar)

This listing was taken from  Bielory et al, Treating the Ocular Component of Allergic Rhinoconjuncitivitis: Treatment Options for Ocular Allergy

 Other things to consider

• Take a shower and wash the hair prior to going to bed to help get the pollen out of the hair and skin
• Keep the windows closed at night
• Do not dry laundry outside
• Try not to use a fan that directly blows on the child, try to pull hot air out
• Be very careful on those windy days

Summation

                Ocular allergy is a real problem with children. Of all the approaches to treatment I would advice first the practice of avoidance. If possible get away from the environment that brought on the symptoms. Next, keep the hands out of the eyes, this is the most common way a child deals with the problem of itchy eyes, but this only makes things worse. Third, an eye flush should be tried. Keep in mind some of the easy things you can do at home- chill the eye drops, cool compresses help too.

                There are a wide variety of medications for the eye and they offer different degrees of help. I am always hesitant about the ocular steroids and I try to get an ophthalmologist involved.

FEL

FOOD ALLERGY

Of course the biggest event in 2010 was the publication of the National Institute of Allergy and Infectious Diseases (NIAID) sponsored ‘Guidelines for the diagnosis and management of food allergy in the United States’. Previous postings on this site go into more detail on those guidelines. The review states that these guidelines should provide tremendous guidance for improved diagnosis and management of food allergy. I think we as allergists may be very busy in the next few years making sure that food allergy was the correct diagnosis. Allergists will be performing more food challenges to test the relevance of test results.

Food Allergy Epidemiology and Risk Factors

For the United States the prevalence of specific food allergy was (percent of the population);

•                 Peanut- 0.8%
•                 Tree Nut- 0.6%
•                 Sesame seed- 0.1%

These were from telephone surveys and are self-reports.

Food allergy in children has increased (self-reported survey data);

                      Food                                             Year

                                            1997                       2002                       2008

                Tree nuts             0.6%                      1.2%                      2.1%

                Peanut                 0.4%                      0.8%                      1.4%

Rates of clinical food allergy risk (National Health and Nutrition Examination Survey 2005-2006)

•                 Food                      Rate
•                 Milk                       0.4%
•                 Egg                         0.2%
•                 Peanut                 1.3%
•                 Shrimp                  1.0%

In this study, children 1-5 years of age, clinical allergy to milk, egg, and peanut was 1.8% for each.

It needs to be pointed out that this information was from surveys and/or from specific IgE levels. They were not the results of a food challenge. So there is the possibility that this represents sensitization only and may be an over-estimate.

Risk factors for food allergy

                Food allergy may be due to deficiency in vitamin D.

Vitamin D has been a most popular topic over the past year. The standards for daily intake of vitamin D are changing; we may need more of this vitamin in our diets. Relative vitamin D deficiency has been reported in a number of clinical conditions.

                Prolonged avoidance of certain foods to infants at risk of developing food allergy has been the standard advice, however two studies were published that shake this concept, at least for milk and egg allergy. When milk exposure was delayed beyond the 15^th day of life, the odds ratio for milk allergy was 19.3. (Odds ratios are the odds that an event will occur compared to the odds that it will not occur). The OR gives an idea of how strongly a variable is associated with an outcome. In this example the odds of milk allergy was 19.3 times more likely to have milk allergy.

When egg was introduced at 4-6 months of life compared to introduction beyond the first year of life, the odds ratio was 3.4 for allergy to egg with late introduction (after age 1 year). The comment was made that oral exposure may promote tolerance and that excessive delays in introducing food allergens may be counterproductive and may allow sensitization to occur via intermittent exposure to the food and possible environmental exposure.

                A study from the Consortium of Food Allergy Research reported that mother’s ingestion of peanut during pregnancy had a positive dose-response association with the infant having increase peanut specific IgE antibodies to peanut. The more peanuts the mother ate, the higher the peanut- specific antibody levels. The reviewers point out that this is sensitization (the blood test only). The children are being followed to see if true peanut allergy appears over time.

Food Allergy Treatment

                Now what about those food labels for allergens. Specifically, when it says may contain an allergen or when there are no warning labels at all on the product. The review commented on a study in which 401 foods were evaluated for egg, milk, and peanut. The foods either had no indication that it contained one of these foods or the label stated that the food may contain an allergen.  Overall, just over 5% of the products that had an advisory label had detectable protein and almost 2% of the food products with no label were contaminated with the food. Food allergen levels were low, but this could still be an exposure risk.

                Avoidance has been the mainstay of food allergy treatment, however that may be changing. A study on peanut oral immunotherapy was published in 2010. There were 23 children who participated in the study. If a peanut has 300 mg of protein, in this study 1 child tolerated 6 peanuts (2000 mg), 5 tolerated 3 peanuts (1000 mg), and 8 had a peanut and a half (500 mg). So 14 of the 23 tolerated peanut- they did not have a serious reaction up to their limit of tolerance.

                A very important editorial appeared in the JACI about peanut oral immunotherapy. The editorial stated that this procedure is not ready for clinical use at this time. There are still concerns about safety, efficacy, and a number of other practical issues. Be excited about the prospects, but be patient as well.

ANAPHYLAXIS

                An updated practice parameter appeared this year on this topic. The highlights stressed the importance of a medical history, the early use of epinephrine, and prevention strategies.

                A very detailed epidemiologic study from England revealed the following;

•                                 Anaphylaxis is more common in those with asthma
•                                 Anaphylaxis is more common in women
•                                 Drug and food reactions were the most common causes

ATOPIC DERMATITIS

                Mechanisms of barrier dysfunction

                                The presence of an abnormal skin barrier is a major feature of this condition. A protein called filaggrin may have abnormal function. Filaggrin defects can lead to the absorption of allergens or enhance the colonization of the skin with bacteria leading to chronic inflammatory changes in the skin.

                Management and Natural History

                                The initial step is to make the correct diagnosis.  Hyper-IgE syndrome can look and act like atopic dermatitis.

                                Treatment includes skin barrier repair, allergen avoidance, infection control, and the use of anti-inflammatory agents. Keeping the skin well hydrated and preventing skin water loss is important. Betamethasone was great at decreasing symptoms but did cause thinning of the skin. The topical steroids are of help in gaining control followed by topical calcineruin inhibitors for long-term therapy.

                                Using probiotics to treat atopic dermatitis is a very controversial area. A study from Europe suggested that formula supplementation with a very specific prebiotic helped to reduce the occurrence of atopic dermatitis in ‘low-atopy-risk infants’.

URTICARIA and ANGIOEDEMA

                Anti-histamines are the first line treatments for urticaria. Higher doses of an anti-histamine may be required for symptom relief. In one report, levocetirizine (Xyzal) or desloratidine (Clarinex) were increased by 5 mg a week to a maximum dose of 20 mg or 20 mg of the other agent was used if there was no relief of symptoms. This increase of the dose did relief symptoms with 75% responding. The authors of this anti-histamine study suggested up to a 4-fold increase may be needed for symptom control and this can be achieved without safety issues.

                Another study looked at cyclosporine at low-dose as an option.

                In pursuit of a cause for chronic urticaria, low vitamin D levels may be causative and supplementing with vitamin D may help.

This was a nice review that summarized 113 articles that appeared in the JACI in 2010.

FEL

How often has this question been asked? Better yet, how often are infants and young children subjected to extensive/ expensive testing and related therapies based on the idea that they are struggling with nasal allergy? This is a common concern and a common diagnosis. I am not sure it is always the correct diagnosis.

A diagnosis should lead to a treatment program. The consequences of (mis)diagnosing nasal allergy in infants may include an altered diet, removal of pets, medications (and the struggles of administering them), and even immunotherapy (a real issue in children less than 5 years of age, may even be contraindicated, and there are no studies regarding safety or efficacy of allergen immunotherapy in this age group). The medical literature has precious few published studies on this problem of infants having nasal allergy. Recently a study has appeared in the literature that takes a hard look at this problem.

So, can infants have nasal allergy (allergic rhinitis- AR) and if they can (and do) what are risk factors associated with the condition? Note that in the study the authors are calling the condition ‘Allergic Rhinitis-like’ .

In the February 2011 issue of  Allergy  (Allergy 2011; 66: 214–221) Herr and colleagues have the following article, ‘Does allergic rhinitis exist in infancy? Findings from the PARIS birth cohort‘. This article has a few things that excite me; allergy, allergy in young children, and epidemiology (from all the extra schooling for my Masters of Public Health). Here is my review of that article.

Purpose of the Study

The purpose of the paper was to look at the prevalence of AR-like symptoms and to study potential risk factors for atopy in a population of infants. The study was performed in Paris, France.

How they did it (Methods)

Participating children/families were part of the PARIS birth-cohort. All participants responded to a standardized questionnaire. Laboratory studies included tests for markers of allergy. The allergens that were evaluated included house dust mite (limited to the species common in Europe), pets, grass pollen, weed pollen, tree pollen, and mold spores. The foods that were tested included egg, milk, peanut, mustard, fish, wheat, soy, hazelnut, sesame seed, shrimp, beef, and kiwi.

What they found (Results)

The entire cohort numbered 4,177 children. From that number, 1,850 were analyzed for this study. The children were evaluated at 18 months of age.

AR-like symptoms occurred in 169/1850 (9%). AR-like symptoms were nasal congestion, nasal discharge, and sneezing.

There was no significant difference between the AR-like group (169) when compared to the non-AR children (1,681) for the following;

•                 Male sex  (no sex predisposition)
•                 Socioeconomic status (household income)
•                 Number of siblings         
•                 Tobacco smoke exposure
•                 Breast feeding
•                 Parental history of asthma or eczema
•                 Total IgE level
•                 Food allergen sensitization
•                 Having only one marker of atopy

The one maker of atopy was one of the following; elevated blood eosinophil count, a total IgE > 45 U/ml (this is determined by a blood test), or sensitization to inhalant allergens only (eosinophils are cells that are associated with allergic reactions). So these factors did not sort out the group with vs. the group without AR-like symptoms. They were not risk factors.

The factors that were significantly different between the groups were;

•                 A parent’s history of nasal allergy
•                 Increased eosinophils in the blood (> 470/mm³)
•                 Inhalant allergen sensitivity (any positive)
•                 House dust mite sensitivity (Dermatophagoides pteronyssinus)
•                 Sensitization only to inhalant allergens
•                 Having >2 of the markers of allergy

This information was entered into a mathematical model which provided an odds-ratio for the risk factors. The factors that increased the odds-ratios were;

•                 Mother having allergic rhinitis (OR =1.54)
•                 Both parents having allergic rhinitis ( OR = 2.09) (Dad’s history adds a little more risk)
•                 Elevated blood eosinophil counts (OR = 1.54)
•                 Inhalant allergen sensitization (OR = 2.21)
•                 Sensitization to house dust mite (D.p.) (OR = 2.91)
•                 >2 markers of allergy      (OR  = 2.16)

(Reviewers note-an Odds-Ratio is the odds of developing the condition when the factor is present divided by the odds of that factor in those who do not have the condition. If the Odds-Ratio is 1.0 there is identity and there is no difference at all. If the OR is negative, there may be a protective effect. If the OR is significantly greater than 1.0 then there is a greater chance of having AR-like symptoms with that risk factor.)

Conclusions (Authors’)

The prevalence of AR-like symptoms was 9.1% by age 18 months in this population of French children. The significant associations for having AR-like symptoms were having both parents with nasal allergy or the child having a marker of atopic disease. Allergic rhinitis can occur as soon as the first year of life.

There is a strong genetic component- there is a twofold increased risk of AR if both parents have AR. This was not seen if the parent had asthma or eczema.

The authors concluded that the total blood IgE level was of borderline significance.

One of the major findings was the association of AR-like symptoms with sensitization to the house dust mite. There was no association found with food sensitization. Pollen, mold, or pet sensitization was not a factor (reference is made to the need for at least two seasons of exposure prior to sensitization to pollen).

The authors point out that one of the strengths of this study is the objective measure of atopy in a very large sample of children <2 years of age.

One of the limitations is the <50% participation rate by the PARIS cohort.

Reviewer’s Comments

I struggled somewhat with cohort studies, relative risks, case-controlled studies and odds-ratios and how they are used. I concluded that this was a cohort for which case-controlled analyses were used. I had to dig up my epidemiology books as I went over the tables/results. Cohort studies and case-control studies lend themselves to different epidemiologic evaluations.

As with many studies, the conclusions are relative to the population which was studied. This is from Europe, the findings may not be valid here. However, the uniqueness of the study is the use of a large population of young children. We have not seen studies of this intensity in a young pediatric population.

Also consider the condition was AR-like. AR-like included symptoms seen in nasal allergy- congestion, discharge, and sneezing. As a long time sufferer from grass pollen triggered AR, I have sneezing fits, runny nose, itchy nose, congestion, as well as the ocular symptoms of red, watery, and very itchy eyes. These respond to an antihistamine. It would have been interesting to know if antihistamines were ever used and what the response was to this standard form of treatment. That may have helped solidify the diagnosis.

As I look at the significant levels of association for risk factors and odds-ratios I see the following risk factors of value when considering nasal allergy in a child with AR-like symptoms-

•                 The presence of nasal allergy in both parents
•                 An elevated blood eosinophil count (if a blood draw is needed)
•                 Evidence of sensitization to the house dust mite

Those things that this study that I found not associated (based on statistical test results)

•                 Total IgE
•                 Allergy tests to foods, pollens, molds, and pets at this age.

So about 10% of children at 18 months of age who have nasal allergy-like symptoms. If allergy is at work in these children then you would have both parents with nasal allergy and/or evidence of sensitization to a house dust mite and/or an elevation of their blood eosinophil count.

Perhaps information like this with help sort out which young children may have allergy accounting for their nasal symptoms and it may help in limiting items for allergy testing.

The other issue comes from forward thinking the problem. Infants usually sleep on plastic encased mattresses, at least here in the USA. So can house dust mites live in such a mattress. Stuffed animals are a huge reservoir of house dust mites. The admittance of a stuffed animal to a baby’s crib may be time dependent with very young children not having such a thing in there sleeping environment due to safety concerns. So did the house dust mite sensitive population have exposure and if so, when in their lives.

As with many good studies, this one gets you to thinking and gets you to ask more questions.

FEL

 My first draft of this was longer than the summary! I needed to trim my commentary so what follows are the new ideas, the controversial issues, and perhaps some of the iconoclastic issues- clearly there needs to be changes in how food allergy is approached. Many of our thoughts and recommendations desperately need updating and change.

As with more recent guidelines, this is an evidence-based report that provides recommendations when there is strong evidence to support an action and makes suggestions when the expert panel recommendations are somewhat weak based on the evidence available.

The evolution of the scientific evidence used is of note; 12,300 titles of articles were screened, 1,200 of these were reviewed,  900 articles were abstracted, and 348 articles helped form the final guidelines. What that means is that a significant amount of work went into this document. (This is an important point- Is the advice given regarding food allergy coming from one’s training, experiences in clinical practice, or through the application of findings from investigation and publication of those findings in peer-reviewed journals?)

Here are some of the highlights- a summary of the summary. Items in bold italics are what I think are the key components. I have included only material that relates to children in this review. (My opinion/commentary appears in parenthesis.)

Definitions

                Food allergy is an adverse health effect due to a specific immune response that occurs reproducibly on exposure to that food.

                A food allergen is a component or ingredient of a food that is recognized by allergen-specific immune cells and elicit a specific immunologic reaction with characteristic symptoms.

                Sensitization  occurs when there are IgE antibodies to the food, but no symptoms with exposure. Sensitization alone is not enough to declare a food allergy. Food allergy requires sensitization and symptoms with exposure.

                Reactions to foods can occur without involving any immune mechanisms. These are food intolerances.

Natural history of food allergy in children

            Most will eventually tolerate milk, egg, soy, and wheat. The timeline to tolerance depends on the food. High specific IgE levels at the time of diagnosis (blood test results) are associated with not outgrowing the allergy.

                Decreasing levels of specific IgE to foods has been associated with the ability to tolerate the food.

                (We see the specific IgE or blood test for food allergy as a predictor of the natural history of a food allergy. A specific blood level of IgE antibody to a particular food helps predict the risk of a reaction. The blood test is used to decide on doing a food challenge.)

Risk factors for developing food allergy in children

            A family history of atopy and having atopic dermatitis are risk factors for sensitization to foods (positive tests) and food allergy (positive tests and symptoms with exposure). (A child with atopic dermatitis and with a sibling or a parent with atopy is at risk for developing a food allergy.)

Risk factors for the severity of an allergic reaction to foods

            Allergic reaction severity is due to many things, however the severity of a reaction cannot be predicted by the severity of a previous reaction . The severity of a reaction cannot be predicted by the amount of specific IgE nor by the size of an allergy skin test. (So it would be inappropriate to say that a child is severely allergic based on the size of a skin test or by the level of a blood test. The severity is what happened with the exposure.)

                Severe reactions occur more often when the co-morbid condition of asthma is present. (Another very good reason for a child with asthma and food allergy to be managed by an allergist,)

Diagnosing a food allergy- The medical history and physical examination

            A detailed history helps decide if it is an allergic reaction and the type of allergic reaction. It is also used to identify the culprit/suspect food.

 (You have to talk to people when you are an allergist. The conversation dictates the nature of the tests. All too often we have a child who has had tests done and no story to support the testing.)

Methods to Identify the causative food- Allergy testing

            Skin prick tests are recommended to help identify foods that may cause an IgE-mediated food reaction. The skin prick test alone is not considered diagnostic of a food allergy.

            Intradermal skin testing (using a needle and injecting the material within the skin) should not be used to diagnose a food allergy.

            Specific IgE (blood tests) for food allergy are recommended to help identify foods that may cause an IgE-mediated food reaction.  Specific IgE tests used alone, are not diagnostic of a food allergy.

            Food allergy patch testing should not be used in the routine evaluation of non-contact food allergy. (Some foods can cause a contact dermatitis for which patch testing can help with the diagnosis.)

Food elimination diets

            Eliminating one or a few specific foods may be useful in diagnosing a food allergy. This may be especially useful in identifying foods responsible for non-IgE- mediated reactions. The blood tests and the skin prick tests are used for IgE antibody detection. Foods can cause problems through other mechanisms. Unfortunately, there are no diagnostic materials for these other reactions. For conditions such as FPIES, Heiner Syndrome, and eosinophilic esophagitis an elimination diet may help.

Oral food challenges

                A food challenge is recommended for diagnosing a food allergy. When a food challenge causes symptoms and those symptoms correspond to history of food reactions, and there is evidence of sensitization from allergy testing, then at this point a diagnosis of a food allergy can be made.

Nonstandardized and unproven procedures

            The expert panel listed 12 tests that have been used to diagnose IgE-mediated food allergy. Of note that Allergen specific-IgG4 is on this list.

The diagnosis of non-IgE-mediated immunologic adverse reactions to food

            The report suggests that skin testing, blood testing, and patch testing may be considered in identifying foods associated with eosinophilic esophagitis, but these tests alone are not sufficient to make the diagnosis of a food allergy. The role of these tests has not been established in other eosinophilic gastrointestinal disorders.

The diagnosis of IgE-mediated contact urticaria (hives)

                The medical history and supportive allergy tests help make the diagnosis. There are two forms of contact hives due to foods. Reactions due to IgE can be localized or systemic (involving other parts of the body and other organ systems). In the non-IgE-mediated form of contact hives, systemic symptoms are rarely seen.

                (This is a common concern in children. Food generally is not intended to be worn on the skin. If contact causes a hive and there is specific IgE demonstrated by allergy testing, then there is a risk of a systemic reaction. If the allergy tests [(blood or skin prick tests] are negative, then the risk of a systemic reaction is low.)

Management of non-acute allergic reactions and prevention of food allergy

            Individuals with documented IgE-mediated food allergy should avoid the food. Avoidance of the food is the recommendation for non-IgE-mediated reactions to food.

                Individuals with proven food allergy and who also have atopic dermatitis, asthma, or eosinophilic esophagitis should avoid their specific allergen(s).

                For individuals without proven food allergy, the guidelines does not recommend avoiding potentially allergenic foods for managing atopic dermatitis, asthma, or eosinophilic esophagitis.

When to re-evaluate

            This will depend on the specific food involved, the age of the child, and the interval medical history.

Pharmacologic prevention of food allergy

                No medications are recommended to prevent food allergy.

Immunotherapy for food allergy

            These guidelines do not recommend allergen-specific immunotherapy to treat IgE-mediated food allergy.

Management of individuals at risk for food allergy

            An ‘at risk’ patient are those who have a biologic parent or sibling with a history of or with current nasal allergy, asthma, atopic dermatitis, or food allergy (Mother, father, brother or sister with these conditions places a child at risk. Grandparents, uncles, aunts, and cousins are of interest but do not put the child at increased risk. ) Those at risk for food allergy- do not limit exposure to dust mites, pollen, or pet dander for the ‘at risk patient (child)’-

                Do not limit exposure to food that may be cross-reactive with the 8 major food allergens (United States relevant population); milk, egg, peanut, tree nuts, soy, wheat, fish, and crustaceans.

                There is insufficient evidence to recommend food allergy testing prior to introducing highly allergenic foods (for example milk, egg, and peanut) in children who are at high risk. There may be some value in doing an oral food challenge in those who have certain risk factors; sibling with a peanut allergy or evidence of another underlying food allergy. The example here was finding positive tests to tree nuts when the history was only positive for peanut.

                The widespread use of allergy skin tests or blood tests are not recommended due to their poor predictive value. “These tests would lead to many clinically irrelevant results and unnecessary dietary restrictions, especially if unconfirmed by oral food challenges”.

                These guidelines suggests that the general population of children not be tested for food allergy to highly allergenic foods prior to their introduction into the diet.

Testing infants and children with persistent atopic dermatitis

            Children less than 5 years of age with moderate to severe atopic dermatitis should be considered for a food allergy evaluation for milk, egg, peanut, wheat, and soy if at least one of the following criteria is met;

                1. The child has persistent  atopic dermatitis in spite of optimizing management and topical therapy.

                2. The child has a reliable history of an immediate reaction after ingesting a specific food.

(This is a major change from the usual clinical approach to the child with atopic dermatitis. Pursue very specific foods only and only in moderate to severe disease who despite appropriate treatment and adherence to the treatment program is not improving.)

Prevention of food allergy

            No recommendation for restricting the maternal diet during pregnancy or lactation.

                Exclusive breast-feeding until 4-6 months unless breast-feeding is medically contraindicated.

                No use of soy in lieu of cow’s milk formula.

                Hydrolyzed infant formula vs. cow’s milk formula may prevent food allergy.

                No need to delay solid food beyond 4-6 months of age. Potentially allergenic foods may be given at this time as well.

It would appear that this summary of a summary is almost as long as the original document. I have made emphasized a few points and issues regarding food allergy that we see commonly hear about in our practice.

These are guidelines and not the law. They evolved from an extensive review of the literature and are evidence-based so there is experience and peer-reviewed scrutiny of the information used. These are recommendations and suggestions to guide us in diagnosing and managing food allergy.

I do foresee us doing more food challenges based on these recommendations. An early posting shared some of our experiences with doing food challenges.

Also, according to the NIAID link, in early 2011 a ‘lay’ version of the guidelines will be available.

Fred Leickly