Leickly Stories

I have many patients and families who have significant concerns about peanut allergy. I have been at Riley for 15 years, and during that time I have seen a significant rise in peanut allergy. Once upon a time I would see a new peanut patient about once a week. Now it is closer to a daily occurrence. I have had a couple of my kids (patients) featured in the newspapers regarding peanut allergy and one of them was the Riley (State of Indiana) representative for the Child’s Miracle Network for peanut anaphylaxis. I am always looking for more on peanut allergy and am eager for a way to take the fear out of this situation.

There has been a considerable amount of research going on with peanut allergy. Most recently,  in the February 2009 edition of one of the premier journals of allergy, the Journal of Allergy and Clinical Immunology, there was an article from the United Kingdom that looked at peanut consumption in a household as a risk factor for the development of peanut allergy. The article was accompanied by an editorial from a dear friend of mine who is one of the lead figures in this quest for answers about peanut allergy, Dr. Wes Burks- chief of allergy at Duke University (actually, Dr. Burks and I trained together at Duke back in the day).

The article concludes that high levels of exposure to peanut in infancy promote sensitization. Low levels of exposure in the environment may be protective. There was no effect of mother’s consumption of peanuts during pregnancy or lactation. The findings supported the idea that sensitization (making an IgE antibody) to peanut occurs through the child’s environment.

Dr. Burks’ editorial urges caution regarding some of the recommendations and conclusions. The editorial also talks about an article yet to be published, including some real world differences in the peanut cultures of the populations in the study.  In the current study, a questionnaire was used to address maternal exposures/consumption of peanut. Dr. Burks points out that there can be problems with recall information used for a questionnaire. The article suggested that avoiding peanuts lessens tolerance and increases the risk of allergy through possible skin exposure to peanut. Dr. Burks issues caution regarding advice about early feeding to prevent food allergy. The theory has not had enough support to make this part of our clinical practice.

The ideas in the article are interesting, exciting, and provocative.

I also had a few ideas on the article. In my professional career I have had great mentors, and one in particular: Dr. Charles Hoppel. I met Dr. Hoppel as a graduate student in pharmacology at Case Western Reserve University. From him I learned how to look at an article with a very critical eye. Here goes my perspective on the article ‘Household peanut consumption as a risk factor for the development of peanut allergy‘.

First, the journal is what we call top tier, highly peer-reviewed. Second, the group has a track record in the area of interest. Third, the work was supported by a government grant. These are all good things.

The purpose of the article was to ‘investigate the relevant routes of exposure to peanut that lead to peanut allergy’.

Now how did they do this or what were their methods? The study was a questionnaire-based case-controlled study of children less than four years of age. There were three groups; children with peanut allergy, children at high risk to develop peanut allergy, and a low-risk control group. The questionnaire was completed by parents before they knew that the child had peanut allergy. There were 133 with peanut allergy, 160 high-risk controls, and 150 low risk controls. If peanut allergy was suspected, the child was excluded from the study. Most of the peanut allergic children had eczema. A case (peanut allergic child) had a positive skin test, a positive blood test, or a positive food challenge. The high-risk to develop peanut allergy were children with egg allergy (about 20-30% may go on to develop peanut allergy).

Detailed questions were asked about peanut consumption by all household members during the child’s first year of life and mother’s peanut habits during pregnancy and during breast feeding. The questions asked about peanut containing foods, frequency of ingestion, and how much was eaten. Household peanut consumption was then calculated.

What did they discover- what were their results?

Eczema was present in 92% of the peanut allergic group and 88% of the high-risk to develop peanut allergy group. Concerning peanut consumption during pregnancy and breastfeeding:

• Peanut allergic cases– mothers ingested 2.4 grams of peanut/week during pregnancy,  0.6 grams/week during breastfeeding
• High risk cases– mothers ingested no peanut products (0)/week during pregnancy, no peanut products (0)/week during breastfeeding
• Low-risk cases– mothers ingested 1.1 grams of peanut/week during pregnancy, 0.9 grams/week during breastfeeding

Household peanut consumption:

• Peanut allergic cases- 18.8 grams/week
• High-risk cases – 1.9 grams/week
• Low-risk cases – 6.9 grams/week

Next the importance of the route of exposure to peanut was evaluated with Odds Ratios and logistic regression. The authors looked at the numbers in the groups who had one of three exposures (environmental, pregnancy, or breastfeeding) in one of three groups (peanut allergy, high-risk to develop peanut allergy, and the normal controls). When the peanut allergy group was compared to the low risk controls, only household peanut exposure was associated with peanut allergy and not consumption of peanuts by the mother during pregnancy/breastfeeding. There were 134 children in which there was no maternal peanut consumption during pregnancy. In this group peanut allergy was more common with increasing household peanut exposure.

The study also looked at the source of the peanut exposure. Most of the household exposure was peanut butter followed by whole peanuts.

 

 

The last analysis dealt with that high-risk group who had known egg allergy. This group had low household peanut exposure and tended to not develop peanut allergy. The question was asked as to why those in this group with rather high household peanut exposure did not develop peanut allergy? The suggestion was made that it was due to well-controlled eczema (skin barrier not broken allowing environmental access) or they were tolerant due to ingestion of peanuts prior to age 12 months.

The authors concluded that high environmental levels of peanut during infancy lead to sensitization with low levels offering protection. There was no effect from maternal consumption during pregnancy/breastfeeding. Sensitization occurs through environmental exposures. Early dietary introduction may be the way to develop peanut tolerance.

My take on this:

• This is a new perspective on the issue.  I appreciate the author’s comments that if sensitization is occurring throughout the environment, then this has public health policy implications.
• I am sure we will be seeing more on this to validate the findings in other populations.

My concerns with the article:

• Perhaps the title should be changed from peanut allergy to peanut sensitization (atopy).
• The subgroup analysis on the possibility of early exposure to peanut products was not the purpose of the paper.
• Questionnaires do have limitations.

Why do I suggest that the title be changed? Allergy means a reaction; therefore, peanut allergy would be a reaction to peanut (according to the definition by the World Allergy Organization). I expected, based on the title, that this would involve children with reactions to peanut. The study actually excluded anyone who had a suspected peanut allergy. The population was predominantly children with eczema, a condition in which positive tests to peanut are found with great frequency without symptoms and without exposure. Eczema (atopic dermatitis) is notorious for false positive tests to foods. The definition of a case was a positive skin test, a blood test over a critical level, or a positive food challenge. I think the proper case definition would include: a positive test for specific IgE (skin or blood) and a positive food challenge. We do not know how many children fulfilled the criteria of test and symptoms with exposure.

The authors did point out that the case criteria was validated in study published in the JACI in 2005. In the 2005 study, patients with a suspected history of peanut reactions were used. This type of patient was excluded from the current study. In the 2005 study, 40 children from a generalized health survey were used, but we are never told how many of that group were without a history of a reaction to peanut. I am not convinced that the extension of case definitions from a symptomatic peanut group are applicable to a group in which a history of peanut reactivity was an exclusion criteria. This should be household peanut exposure and sensitization since we do not know who if any in the group will actually react or did react in the food challenge. Perhaps just looking at that group would be of value.

This is very interesting work and very provocative. Should peanut sensitization become a public health issue? Can we validate these finding in our population?

Respectfully submitted,

Fred Leickly