Update on Early Peanut Introduction and Prevention of Allergy

Consensus Communication on Early Peanut Introduction and the Prevention of Peanut Allergy in High-Risk Infants

On behalf of American Academy of Asthma Allergy and Immunology, American Academy of Pediatrics, American College of Allergy, Asthma & Immunology, Australasian Society of Clinical Immunology and Allergy, Canadian Society of Allergy & Clinical Immunology, European Academy of Allergy and Clinical Immunology, the Israel Association of Allergy and Clinical Immunology, the Japanese Society for Allergology, Society for Pediatric Research, and the World Allergy Organization

Introduction and Rationale

Peanut allergy is an increasingly troubling global health problem, which affects between 1-3% of children in many westernized countries. Although multiple methods of measurement have been used and specific estimates differ, there appears to be a sudden increase in the number of cases in the past 10 – 15 year period, suggesting that the prevalence may have tripled in some countries, such as the USA. Extrapolating the currently estimated prevalence, this translates to nearly 100,000 new cases annually (in the USA and UK), affecting some 1 in 50 primary school-aged children in the USA, Canada, UK, and Australia. A similar rise in incidence is now being noted in developing countries such as Ghana.1-6

The purpose of this brief communication is to highlight emerging evidence to existing guidelines regarding potential benefits of supporting early, rather than delayed, peanut introduction during the period of complementary food introduction in infants. The recent study, entitled “Randomized Trial of Peanut Consumption in Infants at Risk for Peanut Allergy (Learning Early About Peanut – LEAP Trial),” demonstrated a successful 11% – 25% absolute reduction in the risk of developing peanut allergy in high-risk infants (and a relative risk reduction of up to 80%) if peanut was introduced between 4 and 11 months of age. In light of the significance of these findings, this document serves to better inform the decision-making process for healthcare providers regarding such potential benefits of early peanut introduction. More formal guidelines regarding early-life, complementary feeding practices and the risk of allergy development will follow in the next year from NIAID-sponsored Working Group and EAACI, and thus this document should be considered as interim guidance.

Summary of New Evidence

In the LEAP trial, 640 high-risk UK infants (See Textbox 1) between the ages of 4 to 11 months were randomized to consume peanut products at least three times a week (6 g of peanut protein; equivalent to 24 peanuts or 6 teaspoons of peanut butter per week) or to completely avoid peanut products for the first five years of life. This included 542 infants found to have negative skin prick tests (SPT) to peanut at study entry, and 98 infants with SPT wheal diameters to peanut between 1 to 4 mm (minimally SPT positive) at study entry. An additional 76 children were excluded from study entry prior to randomization based on SPT > 5mm, which was assumed to have a very high likelihood of reacting to a peanut challenge. In an Intention-To-Treat (ITT) analysis, 17.2% in the peanut avoidance group compared to 3.2% in the peanut consumption group developed food challenge-proven peanut allergy by age 5 years, corresponding to a 14% absolute risk reduction, a number needed to treat (NNT, e.g. number of persons needed to be treated for one to receive benefit) of 7.1, and a relative risk reduction of 80%.7

When examined in further detail, the isolated beneficial effects for both the primary and secondary prevention of peanut allergy translated to a NNT = 8.5 within the SPT negative and NNT = 4 within the minimally SPT positive infants. Secondary analyses also showed similar levels of prevention in White, Black and Asian (Indian and Pakistani) children. Overall, the risk of early introduction in this group was low– 7 of the 319 children randomized to the consumption group reacted to peanut at the baseline food challenge suggesting that peanut food challenges and introduction, even in minimally SPT positive infants, is safe and
feasible. Six children in the consumption group developed peanut allergy during the study indicating that peanut allergy can still develop despite attempts at primary and secondary prevention. Finally, the LEAP trial only included high-risk infants with a minimal or negative SPT to peanut, and therefore does not address a strategy for those without these risk factors for developing peanut allergy.7

How Does The LEAP Trial Affect Present Guidance for Early Complementary Feeding Practices?

Existing guidelines pertaining to the early introduction of complementary foods have indicated that the introduction of highly allergenic foods, such as peanut, need not be delayed past 4 or 6 months of life. However, they do not actively recommend introduction of peanut between 4 – 6 months of age in high-risk infants, and some of these guidelines specify that those infants considered at risk for the development of allergic disease are strongly recommended to first consult an expert.8-14

The LEAP data provide Level 1 evidence that the practice of early peanut introduction is safe and effective in selected high-risk infants. This study is the first prospective, randomized trial of early peanut intervention, and informs provider decision-making regarding high-risk infants, including those already with a positive peanut SPT but not yet clinically reactive, to receive the benefits noted in the LEAP study, which may reduce the risk of developing peanut allergy up to 80%.

Of note, since children with lesser risk factors for peanut allergy were excluded from enrollment in LEAP, there are no prospective, randomized data investigating the benefit or risk of early peanut introduction in the general to low-risk populations. However, multiple guidelines have not recommended delaying allergen introduction in these populations. On this basis, this communication is limited to helping integrate the findings learned in the LEAP trial to other similar high-risk children in more diverse settings internationally.

Interim Guidance Regarding Early Peanut Introduction

Based on data generated in the LEAP trial and existing guidelines, the following interim guidance is suggested to assist the clinical decision-making of healthcare providers:

There is now scientific evidence (Level 1 evidence from a randomized controlled trial) that healthcare providers should recommend introducing peanut-containing products into the diet of “high-risk” infants early on in life (between 4 – 11 months of age) in countries where peanut allergy is prevalent, since delaying the introduction of peanut may be associated with an increased risk of developing peanut allergy.
Infants with early-onset atopic disease, such as severe eczema, or egg allergy in the first 4-6 months of life (see Text Box 1 for example LEAP criteria), may benefit from evaluation by an allergist or physician trained in management of allergic diseases in this age group to diagnose any food allergy and assist in implementing these suggestions regarding the appropriateness of early peanut introduction. Evaluation of such patients may consist of performing peanut skin testing and/or in- office observed peanut ingestion, as deemed appropriate following discussion with the family. The clinician may perform an observed peanut challenge for those with evidence of a positive peanut skin test to determine if they are clinically reactive before initiating at-home peanut introduction. Both such strategies were used in the LEAP study protocol.
Adherence in the LEAP trial was excellent (92%) with infants randomized to consume peanut ingesting a median of 7.7 g peanut protein (interquartile range: 6.7 – 8.8 g)/week during the first 2 years of the trial compared to a median of 0 g in the avoidance group (see Text Box 2 for examples of peanut-containing foods utilized in the LEAP trial). While the outcome of the LEAP regimen was
excellent, the study does not address use of alternative doses of peanut protein, minimal length of treatment necessary to induce the tolerogenic effect, or potential risks of premature discontinuation or sporadic feeding of peanut.

Rationale for evaluating and applying this policy to a high-risk population

The LEAP study demonstrates that early peanut introduction can be successfully carried-out in a high-risk population (such as the population defined in the LEAP trial). However, without intervention by healthcare providers, there is the potential that such high-risk infants will remain at risk for delayed introduction of solids and allergenic foods into their diet because of the widespread belief that such foods may exacerbate eczema.

Future more extensive guidelines will be forthcoming from the NIAID Working Group and EAACI Guidelines Group with their multidisciplinary stakeholders. These groups will consider all the available data and determine whether there is sufficient evidence to apply prevention strategies to the general population. However, engagement of the primary care, allergy and dermatology communities to rapidly implement these findings and change the culture of early feeding practices is essential, and the forthcoming NIAID Working Group’s and EAACI Guidelines Group’s documents will better clarify a best-practices approach.

Acknowledgements:

Primary Contributors: (AAAAI) David Fleischer, MD; (AAP) Scott Sicherer, MD; (ACAAI) Matthew Greenhawt, MD; (ASCIA) Dianne Campbell, MB BS FRACP PhD; (CSACI) Edmond Chan, MD;
(EAACI) Antonella Muraro, MD, PhD & Susanne Halken, MD; (ISACI) Yitzhak Katz, MD; (JSA) Motohiro Ebisawa, MD, PhD; (SPD) Lawrence Eichenfield, MD; (WAO) and Hugh Sampson, MD.

LEAP Study Team: Gideon Lack, MD, (WAO); George duToit, MD; and Graham Roberts, MD (EAACI); and Tee Bahnson, PhD, (Rho, Inc).

Secondary Contributors: (AAAAI) Jonathan Hourihane, MD, Jonathan Spergel & Michael Young, MD; (ACAAI) Amal As’aad, MD; (ASCIA) Katrina Allen, BMedSc MB BS FRACP PhD & Susan Prescott, BMedSc MB BS FRACP PhD; (CSACI) Sandeep Kapur, MD; (JSA) Hirohisa Saito, MD, PhD; (EAACI) Ioana Agache, MD, Cezmi Akdis, MD, PhD, Hasan Arshad, MD, Kirsten Beyer, MD, Anthony Dubois, MD, Philippe Eigenmann, MD, Monserrat Fernandez-Rivas, MD, Kate Grimshaw, Karin Hoffman –Sommergruber, PhD, Arne Host, MD, Susanne Lau MD, Liam Mahoney, MD, Clare Mills, PhD, Nikos Papadopoulos, MD; (ISACI) Nancy Agmon- Levin, MD, and Aharon Kessel , MD; (SPD) Richard Antaya, MD, Beth Drolet, MD; (WAO) Lanny Rosenwasser, MD.

References

1. Nwaru BI, Hickstein L, Panesar SS, et al. The epidemiology of food allergy in Europe: a systematic review and meta-analysis. Allergy 2014;69:62-75.
2. Osborne NJ, Koplin JJ, Martin PE, Gurrin LC, Lowe AJ, Matheson MC, et al. Prevalence of challenge- proven IgE-mediated food allergy using population-based sampling and predetermined challenge criteria in infants. J Allergy Clin Immunol. 2011;127:668-76.

3. Venter C, Hasan Arshad S, Grundy J, et al. Time trends in the prevalence of peanut allergy: three cohorts of children from the same geographical location in the UK. Allergy 2010;65:103-8.
4. Sicherer SH, Muñoz-Furlong A, Godbold JH, Sampson HA. US prevalence of self-reported peanut, tree nut, and sesame allergy: 11-year follow-up. J Allergy Clin Immunol 2010;125:1322-6.

5. Soller L, Ben-Shoshan M, Harrington DW, Fragapane J, Joseph L, St Pierre Y, et al. Overall prevalence of self-reported food allergy in Canada. J Allergy Clin Immunol. 2012;130:986-8.
6. Amoah AS, Obeng BB, Larbi IA, Versteeg SA, Aryeetey Y, Akkerdaas JH, et al. Peanut-specific IgE antibodies in asymptomatic Ghanaian children possibly caused by carbohydrate determinant cross- reactivity. J Allergy Clin Immunol 2013;132: 639-47.
7. DuToit G, Roberts G, Sayre PH, Bahnson HT, Radulovic S, Santos AF et al. Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med 2015; 372:803-813

8. Greer FR, Sicherer SH, Burks AW; Effects of early nutritional interventions on the development of atopic disease in infants and children: the role of maternal dietary restriction, breastfeeding, timing of introduction of complementary foods, and hydrolyzed formulas. Pediatrics 2008: 121: 183-91
9. Muraro A, Halken S, Arshad SH, Beyer K, Dubois AE, Du Toit G, et al. EAACI food allergy and anaphylaxis guidelines. Primary prevention of food allergy. Allergy 2014; 69: 590-601

10. de Silva D, Geromi M, Halken S, Host A, Panesar SS, Muraro A, et al. Primary prevention of food allergy in children and adults: systematic review. Allergy 2014; 69: 581-9
11. Fleischer DM, Spergel JM, Assa’ad AH, Pongracic JA. Primary prevention of allergic diseases through nutritional interventions; J Allergy Clin immunol Pract 2013; 1: 29-36.

12. Chan ES, Cummings C; Canadian Paediatric Society, Community Paediatrics Committee and Allergy Section. Dietary exposures and allergy prevention in high-risk infants: A joint statement with the Canadian Society of Allergy and Clinical Immunology. Paediatr Child Health. 2013;18:545-54
13. Agostoni C, Decsi T, Fewtrell M, Goulet O, Kolacek S, Koletzko B, Et al. Complementary feeding: a commentary by the ESPGHAN committee on nutrition. J Pediatr Gastroenterol Nutr 2008; 46: 99-110

14. Australasian Society of Clinical Immunology and Allergy (ASCIA). [Internet] ASCIA Infant Feeding Advice: Available from URL: http://www.allergy.org.au/images/stories/aer/infobulletins/2010pdf/ASCIA_Infant_Feeding_Advice_2010. pdf. (Accessed April 2, 2015)

Text Box 1: Enrollment Criteria Used in the LEAP Study
Infants considered at “high risk” as defined by the LEAP study criteria:

Egg allergy: Children with either –

1)  a SPT wheal diameter ≥6 mm from exposure to raw hen’s egg white and no history of

previous egg tolerance,

or
2)  a SPT wheal diameter ≥3 mm from exposure to pasteurized hen’s egg white and allergic

symptoms related to exposure to hen’s egg.
Severe eczema: An eczematous rash that –

1)  requires the application of topical creams and/or ointments containing corticosteroids or calcineurin inhibitors, and if the participant is <6 months of age, lasted for at least 12 out of 30 days on two occasions, or if >6 months of age, lasted for at least 12 out of 30 days on two occasions in the last 6 months,

or
2)  is currently or was previously graded ≥ 40 using the modified SCORAD evaluation
Example of method of skin prick testing: used in the LEAP study

• Skin prick test to peanut extract done in the presence of a negative control and a positive histamine control.
• Skin prick testing should be performed in duplicate and the maximum wheal diameter of the two skin prick tests should be calculated and rounded up to the greatest whole millimeter

Of note, in the LEAP trial, the use of IgE measurement to peanut resulted in considerably higher rates of sensitization compared to skin testing, which could lead to numerous unnecessary oral peanut challenges.

Text Box 2: Examples of Peanut-containing Foods Utilized in the LEAP Trial

Smooth peanut butter (2 teaspoons) mixed with milk or with mashed or pureed fruit
*Bamba® snack (Osem; ~2/3’s of 1 oz. (25 g) bag; 21 sticks of Bamba®)

– for young infants (<7 months), softened with 20 – 30 ml water or milk and mixed with milk or with mashed or pureed fruit or vegetables
Peanut soup
Finely ground peanuts mixed into other foods such as yoghurt
(*Other foods more customary to particular nations/cultures may be substituted)

Whole peanut is not recommended for introduction as this is a choking hazard in children under the age of 4.

Asthma and Peanut Allergy

A recent abstract promoted at the American Thoracic Society meeting on the topic of children with asthma being prone to peanut sensitization. The authors suggest children who do have asthma are more likely to be sensitive to peanuts and therefore kids with asthma should be tested for peanut allergy.

This abstract was received with a lot of controversy. If there is no clinical history of peanut allergy in a child that has asthma, no there is no indication to test for peanut allergy, but environmental testing may be helpful. There is no evidence in diagnosing peanut allergy helps treat asthma. Chronic asthma is not a manifestation of peanut allergy or peanut sensitization.

The diagnosis of food allergy results in symptoms of cough, wheezing, hives, swelling, vomiting etc. Without a history of this, food testing is not indicated. These reactions usually occur within 2 hours after ingesting a food, and usually it occurs much sooner. Besides peanuts, the most common food allergies are tree nuts, shellfish, fish, wheat, milk, soy and eggs.

Chronic and poorly uncontrolled asthma is not a result of a hidden food (peanut) allergy. There is no reason to do food allergy testing in these patients unless the clinical history indicates it as above. But asthmatic children who have asthma could benefit from inhalant (environmental testing). i.e. pollen, animal dander, dust mites.

Food allergy testing from a blood test or a skin test is insufficient to diagnose a food allergy. Many patients on food testing show up positive to a food and there is no clinical history after eating the food in question. Positive food testing results should always be interpreted with a clinical history. If a patient has no history of any allergic reactions after eating a certain food, then allergy testing for that food is not necessary.

While children who have food allergy have a higher risk of asthma, and children who have asthma have a higher risk of food allergies, food allergy testing every asthmatic child is not indicated. What is more worthwhile is environmental allergy testing. Many children with asthma are triggered by allergens in the environmental such as trees, grass, weeds, dust mite, molds, dogs and cats. Knowing which inhalant allergens a child is allergic to can help manage asthma.

So in conclusion if your child has asthma it is not necessary to do allergy tests for foods (especially peanut), but allergy testing for inhalant allergens is actually more beneficial. Your local allergy doctor or allergist can perform allergy testing in the office for you.

ORIGINAL TEXT AVAILABLE AT http://allergylosangeles.com

Antibiotics and food allergy induction

The hygiene hypothesis is the most common theory for increased food allergy. It begins with a lack of  early childhood exposure to infections. Without proper stimuli the immune system does not receive necessary education. When presented with food proteins, the normal response (tolerance) is replaced by hypersensitivity.

A recent article, in the early edition of Proceedings of the National Academy of Science*, adds further support for a revised hygiene hypothesis, with emphasis on symbiotic microorganisms living in the gastrointestinal tract. The authors identified a common bacteria found in the gut (aka probiotic) that may prevent development of food allergy, specifically peanut. Much research is needed but here is another potential pathway to a cure for peanut allergy.

clostridia

 

 

* Commensal bacteria protect against food allergen sensitization; Stefka et al.

Allergic reactions without answers

Chronic hives are a common problem in the general population and in my practice. Children and adults can suffer daily itching and hives for months or years without explanation. However, symptoms often resolve spontaneously and most importantly, the risk of a severe reaction is very low.

On the other hand, there is a separate condition called idiopathic anaphylaxis. People with this condition will have more severe allergic reactions; symptoms may include hives and swelling but there may also be upper airway obstruction, wheezing, shortness of breath, decreased blood pressure or fainting.

If a patient presents to the office after having a severe reaction, my primary goal is to identify what caused the reaction. Subsequent avoidance can prevent future problems. The most common (known) causes include foods, medications and stings. Unfortunately, a thorough history and physical exam may night identify a cause (or even a suspect). This situation occurs in 30-60% of adults and up to 10% of children. Risk factors include female gender and reported penicillin allergy.

Here are some possible explanations for idiopathic anaphylaxis:

  • Hidden food allergens. Expanding testing to include a large food panel may help to identify the cause. Unfortunately studies have shown little success, finding a cause in only 7% of cases. Other studies have ruled out food preservatives as causes of idiopathic anaphylaxis, including sulfites, MSG and aspartame.
  • Female hormones.
  • Immune abnormalities.
  • Increased sensitivity to histamine.
  • Autoimmune disease.
  • Delayed allergy to beef, pork or lamb. An allergic reaction to the oligosaccharide alpha-gal. Transmitted by the Lone Star tick.
  • Conditions which mimic anaphylaxis: somatoform disorder, scromboidosis (poisoning form “spoiled” fish).

Here are some tests that may be done:

  • Skin (or blood) testing to foods and/or medications.
  • Serum anti-alpha-gal IgE.
  • Tryptase level. Prostaglandin D2.
  • Urinary histamine metabolites.
  • Genetic analysis.

Here are possible treatments:

  • Anti-histamines.
  • Oral Steroids.
  • Oral albuterol.

 

Food allergy resources

A new diagnosis of food allergy is life-changing. The questions are endless.

I am putting together a new section on the website for parents and patients with food allergy, new and old. I will include links, recipes, diet sheets and school forms.

If you have a valuable resource that you would like to share, please let me know.

Check it out.

Update: Oralair approved for grass pollen allergy

The FDA has approved the first product for oral immunotherapy! 

Oralair is a tablet containing five grass allergens; Sweet Vernal, Orchard, Perennial Rye, Timothy and Kentucky Blue Grass. It is manufactured by Stallergenes, a French pharmaceutical company. It will be marketed and sold in the United States by Greer Laboratories.

Allergy immunotherapy is the most effective treatment for environmental (and possibly food) allergies. It is all natural, containing only the allergens you are allergic to, and the only treatment that prevents disease. Immunotherapy can be given as a shot, drop or tablet.

It is no surprise that our first [glossary slug=’sublingual’]sublingual[/glossary] option is coming out of Europe. For many years, allergists in Europe have chosen the sublingual route rahter than subcutaneous (shots). There are other differences in the way allergies are treated here and abroad. Most sublingual products contain only one allergen. For example, grass pollen. However, up to 40% of patients have allergy to more than one substance. Allergists in the United States attempt to treat as many of the patient’s allergies as they can, administering a mix of several allergens in shot form. For example, grass pollen plus dust mites. Here is a more complete discussion, see this article (Allergy Tablet Approval Warrants Caution for Some).

It is not clear which method is better, one allergen or many. Probably there is no one right answer that would apply to everyone. The same is true in the debate, shots vs. drops/tablets. Shots are more effective but drops/tablets are more convenient. In the end, the approval of ORALAIR provides an additional treatment option for allergy specialists and their patients. If more patients get treatment then we all benefit.

UPDATE (2): TOO LATE FOR 2013

For best results, Oralair should be started 2 months prior to the grass pollen season. In the northeast, May and June are the months with peak grass pollen levels. If Oralair is available this May then it would be too late for 2013.

PRESS RELEASE (excerpts):

– Grass allergy is the most common seasonal allergy in the United States and most people are allergic to more than one type of grass. ORALAIR contains a mix of five grass pollens: Sweet Vernal, Orchard, Perennial Rye, Timothy, and Kentucky Blue Grass. The five grass pollens contained in ORALAIR represent those to which most patients in the U.S. are exposed.

– ORALAIR is indicated as immunotherapy for the treatment of grass pollen-induced allergic rhinitis with or without conjunctivitis confirmed by positive skin test or in vitro testing for pollen-specific IgE antibodies for any of the five grass species contained in this product. ORALAIR is approved for use in persons 10 through 65 years of age.

– ORALAIR is a tablet that dissolves under the tongue. The first dose is taken in the doctor’s office under medical supervision, and subsequent doses are administered once a day by the patient or the patient’s caregiver. ORALAIR treatment should be started four months before the expected onset of each grass pollen season and continued throughout the season. Allergy symptoms are reduced beginning with the first grass pollen season.

– ORALAIR was originally approved in Europe in 2008 and is currently authorized in 31 countries around the world, including most European countries, Canada, Australia, and Russia for the treatment of grass pollen allergy. In Canada, ORALAIR was launched in 2012, making it the first allergy immunotherapy tablet to be registered and marketed in North America. Worldwide post-marketing experience with ORALAIR includes more than 20 million doses given to more than 110,000 patients.

– ORALAIR has been approved based on results from an extensive clinical development program. ORALAIR has been studied in double-blind, placebo-controlled trials, in both Europe and the United States in over 2,500 adults and children. The results of these trials demonstrated that pre-seasonal and co-seasonal treatment reduces patients’ allergy symptoms and their need for symptom-relieving medication. In the clinical development program, the most common adverse reactions for ORALAIR (reported in >=5% of patients) were oral pruritus, throat irritation, ear pruritus, mouth edema, tongue pruritus, cough, and oropharyngeal pain.

Stress & Allergy

It is clear to those suffering, allergies cause stress. Constant runny nose, decreased quality of sleep, missed days at school and work are among the many reasons why. A new study from Ohio State University* flips this conclusion on its head and asks; can stress cause allergies?

Our bodies immune system is not limited to the nose. It involves organs and cells throughout the body. The inflammatory chemicals produced during an allergic reaction can have wide ranging effects. Likewise, the endocrine system will respond to stress by increasing (or decreasing) hormone levels throughout the body. These two systems do not live in isolation.

In this study, subjects were asked to complete daily diaries. They recorded allergy symptoms, mood and stress levels using a secure website. The data showed that patients with higher stress scores experienced more allergy flares. Also, there was a similar relationship between negative mood and rhinitis symptoms. For most patients, the effect was spread out over time, a stressful day did not occur together with a bad allergy day. However, for a few more sensitive subjects there was a pattern of increased allergy symptoms on stressful days.

The authors conclude that allergic individuals with persistent emotional stress have more frequent allergy symptoms. They recommend stress reduction techneques, such as meditation for the treatment of allergy symptoms. However, it should be noted, this study does not prove cause and effect. There is no evidence that the stress causes the allergy as opposed to the allergy causing the stress. Either way, stress-reduction is a good thing.

 

* Patterson A, Yildiz V, Klatt M, Malarkey W. Perceived stress predicts allergy flares. Ann Allergy Asthma Immunol 112 (2014) 317-321.

What is Eosinophilic Esophagitis?

Eosinophilic esophagitis (EoE) is an inflammatory condition affecting the esophagus (the tube that connects the throat with the stomach). The esophagus contains too high a number of eosinophils, an allergic white blood cell. This causes several gastrointestinal symptoms, including difficulty swallowing, nausea,vomiting and reflux.

Diagnosis: To confirm the diagnosis requires an upper endoscopy and biopsy. Unfortunately, no less invasive procedures are available to diagnose or monitor EoE.

The Role of Allergies: The majority of individuals with EoE have family histories of allergies and symptoms of one or more allergic disorders such as asthma, nasal allergies, atopic dermatitis or food allergy. Food allergy is a major cause of EoE in children, and a less probable factor in adult EoE. Environmental allergies such as dust mites, animals, pollens and molds may also play a role.

Treatment of EE:
– Diet. Avoidance of common allergens (milk, egg, soy, wheat, nuts and fish) may eliminate the symptoms and underlying inflammation of EoE. Atopy patch testing may help to guide food choices.

– Medications. Steroids are effective at shutting down inflammation and eosinophil production. Local delivery helps to lessen side effects. This is achieved by swallowing those steroids indicated for asthma (either a fluticasone inhaler or budesonide for the nebulizer machine).

The initial diagnosis of EoE can be overwhelming. Working closely with your healthcare team is the best way to assure you are receiving proper care. Additionally, families often benefit from participation in support groups, such as the American Partnership for Eosinophilic Disorders (APFED) at www.apfed.org.

Xolair approved for chronic hives

The FDA has approved omalizumab (Xolair) for the treatment of chronic hives. This is the first medication with a specific indication for [glossary slug=’chronic-idiopathic-urticaria’ /] (CIU). There are many patients with CIU that remain symptomatic, covered in hives and itchy despite multiple medications. The addition of Xolair may help these patients get their symptoms under control.

The good:

– Current treatment options are limited and often ineffective.

– Convenience. Xolair is given as an injection on a monthly basis. Current medication regimens may include up to 20 pills per day.

The bad:

– Xolair is expensive and will require pre-approval.

– Several clinical studies have demonstrated a high degree of safety. However, there are concerns that Xolair use may increase the risk of cardiac events and severe allergic reactions.

The ugly:

– Xolair, like other available medications, suppresses the hives but does not fix the underlying problem. Optimally, a cause can be identified and corrected or avoided.

 

Allergy shots, a new source of savings

dollar_icon

dollar_iconAllergies are common and costly. Total costs are in the billions. An increasing proportion of this number is being shifted to the patient, in the form of higher copays and deductibles. The price of health care is now a real part of our health care conversation.

When choosing the most appropriate allergy treatment, doctors and patients should consider efficacy, side effects and cost. The most common treatment options for allergy patients are:

1. Avoidance

2. Medications

3. Immunotherapy (also know as allergy shots)

It is well established that allergy shots provide the most relief but are they worth the cost? A recent study* used an advanced computer model to address this question.  They considered these factors most important in making a decision:

  • patient age
  • life expectancy
  • number of months per year medications are required
  • cost of medications
  • number of allergies
  • duration of immunotherapy (3 vs 5 years)

A virtual allergy patient was put through economic analysis. He was doing well using an intra-nasal steroid, the gold standard in treatment. Unfortunately, nasal sprays do not alter the course of the disease, symptoms recur shortly after they are discontinued. There is no endpoint for the patient.  On the other hand, immunotherapy can induce long term tolerance after only 3-5 years of therapy. This means that the benefits will continue long after your shots are finished. Despite this advantage, allergy shots are usually reserved for patients who fail medical therapy. Economically, younger patients would be better off with 3-5 years of shots, not a lifetime of nasal steroids.

cost_chart

 

 

 

 

 

 

 

 

The attached figure demonstrates a large area where immunotherapy is more cost effective than medical therapy. It must be noted, this figure only represents those patients that are doing well on nasal sprays.  For patients who continue to have symptoms despite medications, the decision would be shifted heavily in favor of allergy shots.

 

* Kennedy J, Robinson D, Christophel J, Borish L, Payne S. Decision-making analysis for allergen immunotherapy versus nasal steroids in the treatment of nasal steroid‐responsive allergic rhinitis. American Journal of Rhinology & Allergy.  2014; 28(1) 59-64.