Why House Dust Avoidance is Hard

Another way to title this is ‘Why allergists can be meanies’. How could we even think of shattering such a peaceful, tranquil, and sweet image? I wonder if this is the more commonplace reality of young children and stuffed animals.

A colleague of mine, Dr. Veda Ackerman once told me that an allergist can never give a talk without saying something about house dust mites and/or showing a picture of a house dust mite. She is probably correct on that.

The simple retort is that house dust mites are important allergens. Individuals can be sensitized and allergic to proteins in the fecal pellet of the house dust mites. Yes that is where the allergen is found in feces (also known by a number of other terms not allowed on this site). I recall the look of horror when a patient on oral drops from house dust mites realized the source of the allergen.

In the lore of allergy, it has been said that inch for inch that there are more house dust mites in stuffed animals than any other item manufactured by mankind. Given that fact, when there is sensitization to house dust mites and this is suspected as a reason for allergy symptoms, the most effective therapy is avoidance of the house dust mite. So the recommendation is the removal of the stuffed animals from the child’s environment. There are a few other options; placing the stuffed animal in the freezer over night once a week or dry cleaning the critter. I fear that in this situation, the freezer would be filled to capacity with these friends.

 This picture of my granddaughter clearly shows why advising avoidance of stuffed animals can be a problem. It is often said that more than one stuffed animal in the bed with a house dust mite sensitive/allergic individual is too many.  Fortunately Stella has no allergic conditions. This picture is precious. My daughter labels it as ‘Stella and her friends’.

Stella’s Papa

FEL

This young lady’s mother had with her an article that escaped my attention. The article was written by known experts in the field of Allergy (the lead author was Anna Nowak-Wegrzyn with Hugh Sampson, Robert Wood, and Scott Sicherer as contributing authors). The paper was a nice review of FPIES and a study of 14 special children. I think that any allergist who sees young children should review this paper. These young children can present with signs that are possibly consistent with anaphylaxis.

 The article was published in the journal Pediatrics in 2003. It is a review of 14 children who presented over a five year period at the Mount Sinai Pediatric Allergy and Immunology Clinic (New York, NY) and to the Allergy Clinic at Johns Hopkins Children’s Center (Baltimore, MD). The reactions that these children experience include severe diarrhea and vomiting which can lead to dehydration and shock. This is a clinical diagnosis; there are no specific laboratory tests that make the diagnosis. A food challenge can confirm the diagnosis.

Milk and soy have been the most commonly implicated foods causing FPIES. This article shows that other foods specifically solid foods have been shown to be associated with this syndrome; rice, oat, barley, peas, string beans, squash, sweet potato, chicken, and turkey. These children underwent food challenges to show the cause-effect relationship between the exposure and the symptoms. There were many combinations of foods causing the problem; cow’s milk alone, soy milk alone, both cow and soy milk, a single solid food, and more than one grain. The group was compared to children who were only milk/soy sensitive.

                The profile of the Solid Food FPIES population was as follows;

• Age at onset of the reaction:    5.5 months (range 3-7 months)
• Age at resolution:                      24 months (range 14-44 months)

                The Milk/Soy FPIES profile was the following;

• Age at onset of the reaction:   1.0 months (range 2 days to 12 months)
• Age at resolution:                      28 months (range 14-21 y)

This was the first published study of FPIES triggered by solid food. Oat was the most common food causing solid-food FPIES. The study also showed that breast-feeding may have a protective role in preventing/delaying the development of FPIES. The diagnosis of solid-food FPIES was not made until after two reactions. It was also noted that these reactions were severe. The delay in diagnosis was attributed to a number of possible factors; low incidence of the disorder, a presentation that looks like septic shock, and the belief that solid foods such as grains, vegetables, and poultry are of low allergenic potential. It was also noted that the time course of the reaction may delay making the correct diagnosis. The daily feeding of milk – cows and soy, leads to chronic problems. The re-introduction of the milk causes symptoms two hours after the exposure.  As mentioned previously another problem is the lack of any test (other than avoidance and a food challenge) to confirm the diagnosis.

Another point that was made was that almost half of the children in this series had multiple food sensitivities. Children who were already on a casein hydrolysate formula had a median of four solid-foods that they were sensitive to.

No infant developed FPIES with exclusive breast feeding in this series.  The authors pointed out that they were unaware of any reports of FPIES during breast feeding with absolutely no direct oral feeding of an offending food. No infant developed FPIES to milk/soy after age 1 years and the oldest child who had the solid-food FPIES was 7 months old. There were no ‘predictors’ of which child with milk/soy FPIES would go on to develop solid-food FPIES.

The Bottom Line-

The reaction of vomiting/diarrhea possibly leading to shock can be consistent with an IgE-mediated reaction and these are perhaps more common than FPIES. Such a reaction would lead to an allergy evaluation which will be negative if the diagnosis is FPIES. However, the infant is still at risk for a severe reaction with re-exposure.

Board certified allergists are credentialed in the care of allergic conditions in both pediatrics and internal medicine. Some of us went into allergy after completing training in pediatrics and others were trained in internal medicine. FPIES would not have been a clinical entity seen during internal medicine training. It may have been seen/talked about for a pediatric oriented allergist. FPIES favors infants. My point to all this is that although very rare, we need to keep this type of presentation in mind when seeing young infants with scary episodes of vomiting leading to shock with solid-food exposure. Their evaluation will show no evidence of allergic sensitization. We can help by teasing out the history of exposures and clinical course. We can offer recommendations for avoidance of the common foods that have triggered solid food-induced FPIES. This profile of young infants reacting in such a violent way needs to be considered in the evaluation especially if they have had issues with cow’s milk or soy milk.

This young lady made an impression on me. Her story was very scary. She caused me to go back to the literature and review what is known about her presentation.

Fred Leickly

We have seen many children who were evaluated for food allergy and/or who were brought by parents to be evaluated for food allergy because of redness to the cheeks that is observed after eating.

What I haven’t heard about is a syndrome called ‘Frey’s Syndrome’. 

In the January edition of Postgraduate Medicine there is a case report, pictures, and a review of this syndrome which frequently precipitates an allergy evaluation. The problem is not due to allergy. It is an allergy-pretender.

Frey’s syndrome is also called the auriculotemporal nerve syndrome.  It involves redness over the cheeks after eating or drinking. The cause is abnormal nerve regeneration which can happen with forceps delivery or after parotid-gland surgery.  The actual incidence of the syndrome is unknown and it is by this report rare in children. Sucking on a lemon brings out the facial flushing. The use of starch/iodine brings sweating which is seen more in the adult.

The facial flushing with eating, gustatory flushing, may mimic food allergy and lead to unnecessary testing and the consequence of restrictive diets.

The clinical course is benign in children. The authors point out that it is important to recognize it so unnecessary evaluations are avoided.

The treatment is explanation and reassurance.

If you can see the paper, there  pictures of this flushing. The reaction looks distinctly delineated. It follows the distribution of the nerve.  The young lady would experience the flushing after eating sweets, citrus fruit, grapes, tomato sauce, fruit-flavored ice cream, and spicy foods. She had no history of any trauma to the area of the auriculotemporal nerve. There were no other symptoms besides this flushing. There was no personal history of allergy. Her teachers thought that this was a food allergy issue. In the clinic, the flush was seen one minute after eating a citrus-flavored sweet.

 I had not heard of Frey’s syndrome before, but I have seen a good number of red-cheeked children who had no other signs/symptoms of a food allergy. In this case, the types of food that elicited the problem, the timing of the flush in relation to eating, and the specific distribution help with the diagnosis of Frey’s syndrome.

We will start stocking sweet citrus-flavored candies for test purposes only. I am soliciting suggestions. So far I think Skiddles may work. If you can think of a candy that is has more of the citrus bite, let me know.

My thanks to the authors N Hussain, M Dhanarass, and W Whithouse for this article (Postgraduate Medicine Journal January 2010 Vol 86 N0 1011 page 62.)

Fred Leickly

As with all of these courses I learned from a group of wonderful speakers and there are a few things I will add to my practice. Here are a few things to share.

First- I was under the impression that warmth would be associated with places that had the word “Mexico” associated with it. Santa Fe was colder than back home here in Indiana! There was snow as well. Surprise! Despite the weather it is a most beautiful place.

Second- the people are very warm and friendly. Here is an example-my hat has many pins from a variety of states, countries, and places that I have visited. I was with my wife and our friends having the obligatory ice cream after a dinner with a rather spicy salsa. A gentleman came up and gave me a pin that commemorates the celebration of 400 years of Santa Fe, New Mexico. He loved the hat and thought that the pin would be a welcome contribution. I offered to pay for the pin but was denied. The gentleman was the president of the Santa Fe 400 year committee and he assured me that he had a plentiful supply of those pins. I didn’t catch your name- thanks yet again.

Places and things visited- Santa Fe 400 (left lower).

Third- The speakers for this program were all top-notch.

• Dr. Veda Ackerman- Pulmonary- James Whitcomb Riley Hospital for Children, Indiana
• Dr. Meg Fisher- Infectious Diseases- Children’s Hospital at Monmouth Medical Center, New Jersey
• Dr. Ivor Hill- Gastroenterology- Wake Forest University School of Medicine, North Carolina
• Dr. Todd Mahr- Allergy & Immunology- University of Wisconsin Medical School,  LaCross, Wisconsin
• Dr. Anthony Mancini- Dermatology- Northwestern University Feinberg School of Medicine, Chicago, Illinois
• Dr. David Schonfeld- Developmental/Behavioral Pediatrics- Cincinnati Children’s Hospital Medical Center, Ohio

Fourth- Here are just a few excerpts from the program;

Pediatric Pulmonology I work with Dr. Ackerman. In fact it was at an AAP course that I first met her and she was instrumental in recruiting me to Riley Hospital. Over the years I have heard her talk on many subjects for a wide variety of audiences.

Cough suppressants have no real role in children. There are no studies to support the safety and efficacy of these agents in children. Cough suppression in children may be hazardous and contraindicated.

Infectious Disease Very few bacteria lung infections cause wheezing except for mycoplasma infections. Most of the wheezing from infection is due to respiratory viral infections.

Most viral respiratory tract infections have a gradual onset of symptoms. The exception is influenza which hits hard and fast.

Fever may be helpful- the influenza virus will not survive/replicate in a host with elevated temperature. Treating the fever may help the virus to continue to replicate which can prolong the illness and prolong the spreading of the virus. Viral shedding may be prolonged with antipyretics (acetaminophen, ibuprofen).

Gastroenterology Celiac disease is a common concern. Confirm the diagnosis before treating. Constipation is not due to a food allergy in children. In dealing with constipation, the child controls the sphincter- this makes yelling at the child quite useless as a therapy.

Allergy Air filters for house dust mite avoidance do not work due to the nature of dust mite allergens. However a HEPA filter on a vacuum cleaner helps filter the exhaust. Carpeting on concrete (finished basements) helps house dust mites grow.

Food allergens are proteins/glycoproteins they are not fats or carbohydrates (sugars).

The peanut allergy child/family needs to be aware that peanut is sometimes made to look like or substitute for tree nuts. Faux almonds in baked goods may be peanuts. READ THE LABEL AND IF YOU DON’T KNOW, THEN DON’T EAT IT.

Dermatology I could not resist asking the definition of eczema, atopic dermatitis (AD), allergic atopic dermatitis, and non-allergic dermatitis. The answer restored my faith in this area: you should work with eczema and atopic dermatitis and forget the other two terms. Thank you Dr. Mancini!

One of the shared conditions with allergy is ‘atopic dermatitis’.  The presentation debunked myths associated with this condition.

These myths were-

•             Topical steroids are unsafe and should be avoided.
•             Antihistamines don’t really help.
•             Staph Aureus is an innocent bystander
•             Food Allergy is a common culprit

The debunking

•             Topical steroids are the mainstay of treatment.
•             Antihistamines help with itch and help with sedation.
•             Treating staph infections of the skin help with healing.
•             While 30-60% have a positive test for a food, only 10-30% have worsening of the condition due to a food exposure.

The role of allergy is recognized, but it is only part of a much larger scenario. Foods seem to be part of the problem in the more moderate to severe cases. Full and strict avoidance of a food in many cases does not modify the course of the disease. All too often parents blindly eliminate foods which can lead to dietary and nutritional deprivation. Co-management of AD by dermatology and allergy is vital.

Aeroallergen issues were a concern in the teenager with AD.

Developmental/Behavioral Pediatrics The specialties of D/B and allergy rarely mix except in CME programs like this one. Behavioral issues are not secondary to allergy. Given this, we don’t have many if any consults from the specialty.

Dr. Schonfeld’s lectures were; Supporting children in times of crisis, Connecting with patients and families to conduct a behavioral/mental health interview, and How children come to understand illness and how we can learn to explain it better.

These were very interesting topics and Dr. Schonfeld did fantastic job. I am sure he is wonderful with his patients.

I have always tried to engage the child in my evaluations. After all, the child is the patient. In our practices we need to be sure the child is involved to some extent (depending on age/maturation). There should be no secrets about their condition. The child can better deal with what is going on if they understand it. Our job is to facilitate that understanding and the processing of the information. Adherence to therapy should be improved with comprehension. We should also understand that we should not try to do all this in one visit.

Dr. Schonfeld pointed out that ‘health education’ is rarely taught in medical school. In my situation, I learned about health education in my MPH curriculum. A quote that I will always keep in mind is “You don’t need to be an expert in pediatrics to explain illness to children-you need to be an expert in children.

This was a great conference and it was made great by an outstanding faculty. If you have a chance hear any of these pediatric specialists speak, do not hesitate in listening to what they have to say. If you have a chance to see them for the care of a child, then I am assured that you are in very capable hands.  

Fred Leickly

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

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

Fred Leickly

Looking for a doctor? Look no further. Presenting our selection of Top Doctors, recommended by their peers and leading physicians nationwide.

Indianapolis Monthly Magazine (11/09)

It is quite an honor to be selected as one of the ‘Top-Docs’ by Indianapolis Monthly Magazine. My most sincere thanks go to those physicians who nominated me. This listing of 142 physicians from 47 specialties also included two other members members of the Pediatric Pulmonology, Critical Care and Allergy section at James Whitcomb Riley Hospital for Children; our section chief Dr. Howard Eigen and Dr. Young-Jee Kim. Congratulations to my colleagues.

Thank you!!

Fred Leickly

I write this entry with a tear in my eye. In the Sunday Indianapolis Star I read the following story ‘Alas, the Pontiac- R.I.P..

My 1967 Lemans-May 3, 2009

Mr. Dan McFeely noted on the next line that ‘Aficionados lament General Motors’ decision to end production of the brand now likely to be a hot classic’. The obituary noted that GM life support for Pontiac was pulled on April 27^th, 2009. Pontiac (nee the Oakland Motor Car Company) was born in 1926 in (appropriately) Pontiac, Michigan. Pontiac was the proud parent of GTO, Firebird, Catalina, Grand Prix, Bonneville, the Chief, the Star Chief, Fiero, and my beloved Lemans (just to name a few ).

I  owned a 1967 Pontiac Lemans convertible in 1973. I had that car for six months before it became car number five in a six car sandwich. The car was totaled in April in Cleveland, Ohio. I never had a chance to put the top down and enjoy it. I owned it for six months of which only one month was considered spring (I lived in Cleveland at the time).

In 2001 I thought I had seen a ghost. Appearing on the internet was the exact same car. It was the same color, the same year, the same make, the same everything. It was for sale in Southern California by its second owner who enjoyed driving the car to the beach with his surf board in the back.

Friends of mine looked at the car and I made the purchase. For the past eight years I have an exact copy of my 1967 Lemans (as I remember it from 1973).

I am sure you have all heard of the GTO and perhaps not so much about the Lemans. The Lemans has been called the poor man’s GTO. It has a very similar shape and look. This is my toy.

1967 Pontiac Lemans and home.                                                       

 1967 Lemans – top down and ready to go cruising for burgers.

No 1967 muscle car would be complete without a hula girl on the console. This was courtesy of ‘Old Blue’s’ previous owner.

Fred Leickly

I always scan the articles and a while back I came across a little quip that caught my attention. It made me wonder about the many times I had suggested using a teaspoon measure of medication.

When we prescribe medications we all have the tendency to use the teaspoon/tablespoon measure of delivery. Our assumption is that a teaspoon is five milliliters (mls) and a tablespoon is three teaspoons so that would equate to 15 mls. The question was asked whether or not teaspoons are standardized. I discovered that they clearly are not and the use of teaspoons for dosing could lead to more overdosing as opposed to under dosing.

So the question is, do you use mls or teaspoons?

The article was amazing- It was a clinical tip about the timely death of the ‘teaspoon’ at least for giving medications. The work was done by Alvin N. Eden, MD, and Mohammad Mir, MD Department of Pediatrics, Wyckoff Medical Center Brooklyn, N.Y. and appeared in the November 1, 2008 Contemporary Pediatrics.

The background is that more than 50% of liquid preparations given to children are written as a number of teaspoons. This small research project looked at the volume of 53 teaspoons brought in by physicians, nurses, and the receptionists at a general pediatric practice. Only one of the teaspoons actually measured 5 milliliters. The range was 4.3-12.9 mls! Based on these findings, using the tsp format could result in overdosing by 2.5 times the intended dose.

This made me think about the use of oral steroids for our children who have a flare of their asthma. The medications are 15 mg per 5 mls and the dose would be 2 mg/kg of body weight per day. If a teaspoon that measured 12.9 mls was used, then 38.7 mg were given and not the intended 15 mg!  Steroid side-effects could occur due to the over-exposure via generous teaspoons.

Due to this extreme variability in volume and the chance of an overdose, the milliliter format was suggested as the proper way to administer liquid medications.

Go metric- ask for how many milliliters and use the proper dosing apparatus.

Fred Leickly

The meeting’s agenda covered a wide variety of clinical conditions. It would have been impossible to attend every session. I chose sessions on the allergic environment, eczema, immunotherapy, food allergy, re-certification, headaches, and asthma. There are a number of ideas that are evolving and a number of things currently done in allergy/asthma care that need to change. Each and every one of these topics is truly worthy of more extensive review. I would be happy to use this blog to delve into topics in more detail (per request).

Atopic Dermatitis (aka Eczema)

I still need to be convinced regarding what to call this condition. Dr. Jeff Travers (chief of Dermatology at the IU School of Medicine) and I go back and forth on this topic. During the meeting I heard the concept of extrinsic and intrinsic atopic dermatitis. Extrinsic means from the outside and intrinsic from the inside. These terms have also been used for years to describe two presentations of asthma: extrinsic asthma due to allergy, and intrinsic asthma when no allergy is found. The word atopic means 1) the tendency to come from families with allergy, 2) to make the antibody seen with allergy (IgE, which would be elevated) and 3) to have positive allergy tests. Thus, Intrinsic AtopicDermatitis means no allergy demonstrated (intrinsic) in a condition associated with allergic sensitization (atopic). This blending of terms leads to confusion–why not stick with the simpler term of eczema?

I learned about the use of silver impregnated clothing to decrease the amount of bacteria on the skin. Skin bacteria can cause flaring of atopic dermatitis.

A number of  genes associated with atopic dermatitis have been discovered. These discoveries should increase our understanding on how this condition starts and hopefully how we can manage it better.

There was information on allergens that contain enzymes called proteases and how these protease containing allergens aggravate the skin.

Probiotics have been used to treat allergic conditions especially conditions related to food allergy. A review of studies on probiotics have not shown them to be effective in preventing or treating atopic dermatitis.

I listened to debates about being proactive in skin care therapy vs. being reactive. Proactive would be trying to prevent and reactive being treating only when there is a problem. This idea was particularly interesting. Atopic Dermatitis Guidelines and package inserts for a variety of medications used for atopic dermatitis treatment stress short courses of use, the reactive approach. The proactive debater posed the problem of a chronic disease that will have episodic flaring. The abnormality of the skin is there all the time requiring the need for medication to be used perhaps twice a week to avoid flares (those times when the skin is more itchy, more inflamed, and more broken down). Pediatrics deals extensively with disease prevention. My pediatric perspectives are preventative- proactive. All too often we (as patients) tend to be crisis-oriented or reactive to chronic conditions. I am obviously on the proactive side of this argument.

Therapies emphasized moisture and more moisture. Keep these kids wet! This is clearly a major step that is contrary to previous approaches that recommended the avoidance of frequent soaking/bathing. The avoidance of baths is clearly one of those long established principles of atopic skin care that has fallen by the wayside in contemporary skin care.

Foods are an issue in atopic dermatitis. The protease containing allergens such as molds, pets, and mites may have a role in triggering flares.

In Boston a program that has had success includes insuring compliance with the medications (taking them as prescribed), addressing the parents concerns about medication side-effects (helps with compliance), decreasing the itch, and increasing sleep. These are all essential elements to help with control of the condition.

Of note, we need to re-think the role of a specific therapy and make adjustments. Antihistamines are frequently used in atopic dermatitis. In allergic rhinitis and in hives, these products help control itch. However, in atopic dermatitis, the antihistamines have little effect on itch. The role of the anti-histamine is to sedate. Most of the scratching happens at night. A sedating antihistamine used at night works best.

Asthma

There were a number of new ideas regarding asthma. Look for vitamin D to have a possible role in treatment.

Current recommendations from evidenced-based asthma guidelines point out a difference between adults and children and the use of the long-acting bronchodilators in the two populations. These agents are called long-acting broncho-dilators (LABAs). In children, we should increase the dose of the inhaled corticosteroid before adding a LABA. This recommendation appears in two major asthma guidelines with type A evidence used to support the recommendation. This type of evidence (A) means that there are a substantial number of studies that support this statement.

Asthma may be related to bacterial colonization at birth and to the occurrence of the common cold virus later in life. Evidence was also presented regarding the observation from large population studies that the process of airway inflammation starts well before actual symptoms. We heard about diet, viruses, stress, ozone, and endotoxin having a role in the development of asthma. The gene or genes for asthma need to be present. These genes then need to be activated or expressed for the child to show the signs and symptoms of disease. Bacterial colonization and a variety viruses may have a role in activating the genes.

Headaches

This was a great session. The audience heard from an ENT surgeon, an allergist, and a neurologist regarding their approach to headaches. The consensus was that migraine is the biggest player in these situations. The connection of allergy to headache has always been a concern. However, headache is not a manifestation of allergy. There are many studies that have looked at this. People with headaches can have positive allergy tests but does that make the allergen the cause of the headache? Think about other conditions or associations. Could there be an allergic cause for an appendicitis?

I heard of the concept of ‘allergic appendicitis’ during this presentation. It was very odd to hear about this in a headache session, but a valid point was made. This concept of the allergic appendix was compared to allergic headaches. Follow along; data from a national health survey from 1994 indicated that 50% of the population reported that they had allergy. So if someone who had problems with the appendix was allergy tested, the chances are very high that allergy would be found. This however does not make the inflammation of the appendix due to allergy. You can find a significant number of positive allergy tests, be sure of why the tests are being ordered. Think migraine more often as a reason for headache. Allergy is not a major reason for headaches.

Food Allergy

The biggest news from the meeting was the work done by Wes Burks at Duke on peanut allergy. This is exciting and long awaited for those who have peanut allergy and for the families who have someone with peanut allergy. Immunotherapy for peanut trials have allowed the equivalent of about 12 peanuts to be eaten without any problems/reactions. This would certainly take the fear from accidental exposure to peanut especially from tabletops at school cafeterias. I have to check my note again, but I had written down the treatment would be a suppository(?).

There was a very popular abstract (a quick presentation of work in progress prior to it being published in a journal) on food allergy and the over- use of panels for food allergy (pet peeve). A New York Times article a few months ago reported that food allergies were being over diagnosed. Dr. Sears at National Jewish Hospital in Denver, Colorado reported on over one hundred children seen at their center who had food allergy as determined by blood test panels. The average number of food allergies reported were six. After undergoing food challenges the number decreased to only 2 foods. 88% of the foods this group of children were told to avoid based on RA ST panels were added back into the diet. Using a food challenge, no one with meat ‘allergy’ had a positive food challenge (where meat caused a problem), 88% of the grain ‘allergic’ children were negative on challenge, and 83% of the fruit and vegetable group were also negative after a food challenge. Bottom line- the use of these panels is giving falsely positive information and leading to a misdiagnosis of food allergy.

Allergy Testing

I learned that I should no longer use the word RAST. The term is outdated and refers to a technology not used. The blood tests for allergens should no longer have a 0-6 grading scale and should only be reported in what is actually measured kU/l of serum. The test measures a concentration of a specific antibody in the blood. The relationship of that concentration to clinical activity needs to be determined by the clinician. I predict that the interpretation of the blood test results may be a huge issue.

A new in vitro or blood test for specific IgE in the blood is called an ISAC chip. This technology will help with cross-reacting proteins. We see the problem of cross-reactivity with multiple positive allergy tests to legumes (peanut, soy, beans, and peas). I think this will be a very worthwhile test in allergy.

There are three blood tests out there for detecting specific IgE. These are the Immunolite, ImmunoCap, and Hytec. Each of these measure something different. They measure a different population of IgE antibodies and may not be comparable. Caution was advised regarding the blood tests for specific IgE. The physician should know the method used, the validity of the assay, the performance of the laboratory in doing the assay, and realize that no test for allergy is infallible.

Conclusions

Each and every one of these topics could stand alone for more detail and interpretation and I would be most happy to elaborate in more detail. Let me know if you would like more information by adding a comment. If there continues to be an increase in the use of specific IgE panels (as advocated by those who market these tests) we will be doing significantly more food challenges in our office. Usually we are doing food challenges for those who may have outgrown a food allergy. We certainly can offer a food challenge for a child who has been told that food allergy exists based on blood test results. One of my tasks upon my return to the office is to look at our track record of doing food challenges. I hope to report on our successes and failures for our food challenge experience with milk, egg, soy,wheat, and of course peanut.

Respectfully submitted,

Fred Leickly

Up until a week ago, I had never heard of fenugreek.  On my first day back at Riley to start the 2009 new year, I had a young man, just under 2 years of age who presented with concerns about reactions to legumes. The list of suspects included peas, green beans, black beans, baked beans, and lentils. The mother also shared with me that during breast feeding she used ‘fenugreek’. This product is used to help nursing mothers. In our discussion, the mother brought up the concern that the fenugreek may have contributed to the legume reactions.

I had not heard of ‘fenugreek’ prior to this. I have been involved with allergy long enough to know that any food product ingested by mankind for as long as we have been on the planet has been implicated in an allergic response. I wanted to know more about this ‘fenugreek’.

I consulted my online food ‘Allergy Advisor’ regarding fenugreek and got a wealth of information to get me started. To my surprise later that week the Journal of Allergy and Clinical Immunology (JACI) had an article from a group in Norway regarding fenugreek.

Fenugreek (aka Greek hay, Greek fennel, Bird’s foot, Greek hay-seed) is a legume. It is used as a flavoring in many foods including curry, blends of spice, and even tea. As an herbal medication it has been touted as being helpful in initiating and maintaining milk production. There are references for its use in diabetes and hypertension. Importantly, it is a legume and many legumes share certain proteins and may be cross-reactive in some patients.

The purpose of the JACI article was to evaluate the allergenicity and antigenicity of the proteins in fenugreek. There were 29 patients in the study who had specific IgE antibodies to legumes, peanut, soy, pea, lupin, and fenugreek. These patients ranged from 1 to 53 years of age. High levels of antibody to both peanut and fenugreek were found in most patients and the sensitization to fenugreek was believed to be due to cross-reactivity in those patients with peanut allergy. In this study, the reactivity to the other legumes was weaker. Here the other legumes (specifically peanut) were implicated in causing sensitization to fenugreek. With the young lad that I saw I wondered if there is the possibility that the fenugreek may have worked in the opposite direction – fenugreek exposure causing sensitization to the other legumes.

I was not aware of this association: fenugreek and peanut. In my clinic notes I debated about doing the peanut test since he had no exposure, but since he reacted to a large number of the other legumes I had the skin test placed. His response was positive to peanut.

The world of IgE-mediated reactions to foods is growing significantly. Our diets are changing with significantly more opportunities for ingredients in foods from other lands becoming part of our lives. Herbal supplements may contain a variety of items that could lead to sensitization. It is important to inquire about the use of such products.