Fish oil supplementation during pregnancy may lower asthma risk

fish oil

Preventing allergy is a priority for both physicians and parents. There have been many studies attempting to lessen the risk of both food and environmental allergies.

Here are a few examples of possible interventions to decrease the risk of allergy;

  • Frequent application of emollients (moisturizers) from birth.
  • Breast feeding, hypoallergenic formulas, early introduction of foods.
  • Probiotics.
  • Avoiding pets OR adding more pets.

A study, started in 1990 and recently completed and accepted for publication, looked at fish oil supplementation in pregnancy*. Over 500 pregnant mothers were given supplements containing fish oil, olive oil or no oil. The hypothesis was that maternal supplementation with long chain n-3 polyunsaturated fatty acids (PUFAs) may have immunological effects on the developing fetus and decrease allergies and asthma. The children were evaluated when they reached 18 years of age.

RESULTS:

The probability of having had asthma medication prescribed was significantly reduced in the fish oil group compared to the olive oil group (HR=0.54, 95% CI: 0.32-0.90, p=0.02). The probability of having had allergic rhinitis medication prescribed was also reduced in the fish oil group compared to the olive oil group (HR=0.70, 95% CI: 0.47-1.05, p=0.09), but the difference was not statistically significant. Self-reported information collected at age 18-19 years supported these findings.

CONCLUSION:

Maternal supplementation with fish oil may have prophylactic potential for long-term prevention of offspring asthma.

REFERENCE:

Hansen S, Strøm M, Maslova E, Dahl R, Hoffmann HJ, Rytter D, Bech BH, Henriksen TB, Granström C, Halldorsson TI, Chavarro JE, Linneberg A, Olsen SF, Fish oil supplementation during pregnancy and allergic respiratory disease in the adult offspring, Journal of Allergy and Clinical Immunology (2016), doi: 10.1016/j.jaci.2016.02.042.

Hypoallergenic dog or marketing myth?

Dog allergies are very common, up to 20% of the population are affected. This has not limited the popularity and enjoyment of having a dog at home. The ASPCA estimates that 37-47% of all households in the United States have a dog. Patients with dog allergies may have upper respiratory symptoms (sneezing, runny nose, itchy eyes), lower respiratory symptoms (cough, wheezing) or even skin symptoms (itching, rash). An allergist can confirm dog allergy as the cause of these symptoms.

What’s next? What are the options? Removing the dog from the home is an option, but not very pleasing for the owners or their dogs. There are medications that can lessen symptoms. However, patients are looking for  other ideas. Suggestions have included, frequent washing, frequent vacuuming, putting air filters in the house and buying a “hypoallergenic dog.”

What is a “hypoallergnic dog?”  The substance produced by a dog, causing an allergy is an allergen. The word hypoallergenic means less likely to cause allergy. This implies that the dog would produce less allergen. As of today, there have been six identified dog allergens, named Can f 1, 2, 3, 4, 5 and 6. These proteins are found in hair, skin, dander (skin flakes), saliva and urine. Each allergen can be found in each type, or breed of dog. Can f 1 and 5 are considered major allergens, causing allergy in a large percentage of patients. However, patients can be allergic to any single allergen or any combination as well. Interestingly, Can f 5 is found only in male dog urine, suggesting that some patients may be allergic to male dogs only.

These proteins come off the dog and are found throughout the home. For example in carpets, couches and pillows. They can also be found in places without a dog. For example, in a classroom or on an airplane.

A Google search will recommend, if you have allergies buy a hypoallergenic dog. Dogs that do not shed or with wiry hair.

So is there such thing as a hypoallergenic dog? A dog breed that produces less allergen than other breeds? Is there anyone certifying or testing breeds to show that there are real benefits?

Here are a few studies that may answer these questions:

TITLE: Dog factor differences in Can f 1 allergen production. Allergy 2005.

CONCLUSIONS:

  • Allergen levels (Can f 1) were highest for Poodles (17) and Yorkshire Terriers (16) and lowest for the Labrador retriever (2).
  • Males produced less allergen than females.
  • There was no difference according to hair length or hormonal status.
  • Skin seborrhea caused higher allergen levels.

TITLE: Can f1 levels in hair and homes of different dog breeds: Lack of evidence to describe any dog breed as hypoallergenic. JACI 2012.

CONCLUSIONS: Allergen levels in hair and coat samples were higher in breeds considered hypoallergenic. Although there was a lot of variability between dogs of each breed. The amount of allergen in dust samples was similar for hypoallergenic and other breeds. Although certain dog breeds are described and marketed as being “hypoallergenic”, no evidence was found that these breeds are less allergenic.

TITLE: Dog allergen levels in homes with hypoallergenic compared with nonhypoallergenic dogs. American Journal of Rhinology & Allergy 2011.

CONCLUSIONS: Clinicians should advise patients that they cannot rely on breeds deemed to be “hypoallergnic” to in fact disperse less allergen in their environment.

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The evidence is pretty clear, at this time there is no “hypoallergenic” dog breed. Some dogs may produce more allergen than other dogs. Some people may be more allergic to one dog than other dogs. There is no consistency for which breed is best. Here are some tips for patients with dog allergy. Unfortunately, they are based more on common sense then scientific evidence.

Here is some more practical, but no better proven advice, for patients with dog allergies :

  • Choose a small dog. They will shed less dander.
  • Keep the dog out of the bedroom and other rooms in which you spend a lot of time.
  • Keep the dog out of the house. Remember, dogs may bring pollen or other allergens inside with them.
  • Bathe your dog weekly.
  • Remove carpet or other places dog dander may reside.
  • Get a cat.
  • MOST IMPORTANTLY: see an Allergist.

 

Nonceliac Wheat Sensitivity is associated with Autoimmune Disease

There is much interest in wheat sensitivity in people without celiac disease, many of these patients have been labeled with nonceliac wheat sensitivity. Little is known about any risks associated with nonceliac wheat sensitivity. A recent study published in the journal of Gastroenterology evaluated autoimmune diseases in patients with nonceliac wheat sensitivity and investigated whether they carry the autoimmune antibody (ANA).

The study looked at patients who were given the diagnosis of nonceliac wheat sensitivity, celiac disease and control subjects. The ANA (autoimmune antibody) was measured in 3 groups. The authors concluded from the study that significantly higher proportions of patients with nonceliac wheat sensitivity or celiac disease have autoimmune disorders with positive ANA’s. This data provides physicians with an awareness that patients with nonceliac wheat sensitivity might have an increased risk of autoimmune diseases.

Nonceliac wheat sensitivity remains a not well defined clinical condition. In fact there are some doubts about whether it is a real diagnosis. This study showed a higher frequency of autoimmune diseases, in particular thyroiditis, psoriasis and type 1 diabetes mellitus were reported.

Allergists see many patients who are concerned regarding gluten allergy, many patients may in fact have nonceliac wheat sensitivity. This is relatively new diagnosis that there is not much information about. These are patients who do not have celiac disease or wheat allergy, but do have problems with eating gluten and/or wheat. Although allergy testing may be negative for these patients, this study shows that patients with nonceliac wheat sensitivity may have some autoimmune issues. There is still a lot to learn about nonceliac wheat sensitivity and as more studies come out we will learn more about it.

Celiac disease has been in the news a lot recently http://allergylosangeles.com/allergy-blog/gluten-free-in-the-news/

As always speak to your doctor about any concerns that you have regarding gluten or wheat.

Generic Nasonex Now Available

Generic Nasonex will soon be available for allergy sufferers. Apotex, is a generic pharmaceutical company, based in Florida, has successfully gotten FDA approval of the generic Nasonex (mometasone furoate).

Generic Nasonex will still need a prescription. This is different than over the counter nasal steroid sprays that are available without a prescription from your doctor. There are currently 3 over the counter nasal steroid sprays available. Flonase, Nasocort and Rhinocort.

Flonase will go Over the Counter (OTC)

Nasocort is now Over the Counter (OTC)

Rhinocort OTC is now available

Many insurance companies are not covering any prescription nasal steroid sprays because others are available over the counter as we mentioned earlier. Although some patients seem to respond better to one more than another. Recently newer types of nasal steroid sprays have come on the market, Qnasl and Zetonna. These are nasal aerosol sprays that are not in a liquid form, so patients do not get the post nasal drip symptoms.

Generic Nasonex likely won’t be as cost prohibitive as the branded version of Nasonex, making it more affordable for patients. Nasonex is the only nasal steroid spray that has an indication for nasal polyps.

Seasonal and perennial allergic rhinitis is a major problem in the United States. Many allergy sufferers are allergic to allergens such as tree pollen, grass pollen, weed pollen, dust mites, cat dander, dog dander and molds. First line treatment for nasal congestion symptoms are nasal steroid sprays such as Nasonex. Generic Nasonex will be very helpful to many patients who did not insurance coverage for the branded version Nasonex, although it remains to be seen if insurance carriers will cover generic Nasonex or they still may say the patient will have to try over the counter versions of nasal steroid sprays such as Flonase, Nasocort or Rhinocort.

Sanofi US Issues Voluntary Nationwide Recall of ALL Auvi‑Q® Due to Potential Inaccurate Dosage Delivery

Sanofi US Issues Voluntary Nationwide Recall of ALL Auvi‑Q®
Due to Potential Inaccurate Dosage Delivery

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Due to high volume of calls being received on the Auvi‑Q customer service phone line, callers may periodically receive a message that the line is down. We appreciate your patience and please call back.

Sanofi US is voluntarily recalling ALL Auvi‑Q® (epinephrine injection, USP). The recall involves ALL Auvi‑Q currently on the market and includes both the 0.15 mg and 0.3 mg strengths. The Lot numbers include every consecutive lot number beginning with 2081278 through 3037230. The products have been found to potentially have inaccurate dosage delivery.

If a patient experiencing a serious allergic reaction (i.e., anaphylaxis) did not receive the intended dose, there could be significant health consequences, including death because anaphylaxis is a potentially life‑threatening condition. As of October 26, 2015, Sanofi has received 26 reports of suspected device malfunctions in the US and Canada. None of these device malfunction reports have been confirmed. In these reports, patients have described symptoms of the underlying hypersensitivity reaction. No fatal outcomes have been reported among these cases.

Auvi‑Q (epinephrine injection, USP) is used to treat life‑threatening allergic reactions (anaphylaxis) in people who are at risk for or have a history of these reactions. Auvi‑Q is packaged with two active devices and one trainer device in a corrugate box. Auvi‑Q was distributed throughout the United States via wholesalers, pharmacies and hospitals. All Auvi‑Q is being recalled.

Sanofi US is notifying its distributors and customers who include doctors, pharmacies, wholesalers and other customers in the supply chain by letter, fax, email and phone calls and is arranging for return and reimbursement of all recalled products.

Customers with questions regarding this recall can go to www.Auvi‑Q.com and call 1‑877‑319‑8963 or 1‑866‑726‑6340 Monday through Friday 8 a.m. to 8 p.m. ET for information about how to return their Auvi‑Q devices. Sanofi US will provide reimbursement for out of pocket costs incurred for the purchase of new epinephrine auto‑injectors with proof of purchase.

Customers should immediately contact their healthcare provider (HCP) for a prescription for an alternate epinephrine auto‑injector. In the event of a life‑threatening allergic reaction (anaphylaxis), patients should only use their Auvi‑Q device if another epinephrine auto‑injector is not available, and then call 911 or local medical emergency services. Customers should contact their physician or HCP if they have experienced any problems that may be related to taking or using this drug product.

Any adverse events or quality problems experienced with the use of this product should be reported either to Sanofi or to the FDA’s MedWatch Program.

To report an adverse event to Sanofi US: call 1‑800‑666‑1630, Option 2.
To report an adverse event to the FDA Med Watch Program: by fax 1‑800‑FDA‑0178, by mail at MedWatch, FDA, 5600 Fishers Lane, Rockville, MD 20852‑9787 or on the MedWatch website at www.fda.gov/medwatch/report.htm
This recall is being conducted with the knowledge of the U.S. Food and Drug Administration.

Sanofi US is committed to patient safety and the quality of Auvi‑Q, and will continue to work closely with customers and regulatory authorities to resolve this issue in a timely manner.

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.