Daughter is allergic to sesame, horses. Horses!?

Unfortunately medicine is still far from the Star Trek tricorder stage, at which you can just wave your iPhone over someone and tell what they’re allergic to, but the next best thing is specific IgE testing. We got my daughter V’s results back today. I found the process and fascinating and the outcome illuminating.

IgE are the antibodies responsible for allergy. The IgE results we got consisted of an antibody quantity in units/ml (whatever “units” are), plus a “class” (from 0 to VI) which indicates the degree of allergy. Class can range from “negative” to “extremely high positive.”

Now, I need to talk to an allergist to figure out what is meant by “class”. It seems to be a value that a clinician makes a guess at based on the IgE measurement and the patient’s medical history and, possibly, the allergen in question. From what I can tell the class reported can vary depending on the assay and the person doing the estimating.

The results:

V  is apparently moderately allergic to peanut (3.7 U/ml, class III) and almond (2.5 U/ml, class II) so tree nuts are still out.

She’s allergic to milk (8.3 U/ml, class III), which we know all too well, since only last week I gave her milk by accident and she spent the next half hour barfing on the kitchen floor.

Quite a surprise to find out was that her highest antibody level is to sesame (14.7 U/ml, class III). I once gave her sesame sticks once and she vomited. I gave her a sesame bagel and she said her stomach hurt. But she’s been happily eating pressed sheets of nori (seaweed) that apparently contain sesame oil. Anyway, from now on: no sesame!

And here’s the funny thing. Along with her brother, she gets horse-riding lessons every two weeks. She comes back from them all blotchy in the face. We thought it might be from grass pollen, but on a whim my wife had her tested for allergy to “horse dander.” And she tested positive (3.4 U/ml, class II)!

But no allergy to rye grass pollen.

Allergic to horses. Who knew. Well, that ought to be an easy one to avoid. And it’ll give me a great excuse when she starts demanding a pony for her birthday.

Allergy testing reminds me how little I know about medicine

Yesterday my daughter V went in for what has become a yearly ritual: her specific IgE blood test. She bravely went in after listening to the previous patient scream for 20 minutes. She yelped when she was stuck, but gritted it out while the nurse drew four vials of blood.

Four vials seems like a lot. My wife, who is a veterinarian, says she only takes one vial to test dogs for multiple allergens.

The process reminds me how little I know about medicine in practice.

IgE is a type of antibody, a Y-shaped molecule with sticky ends that recognizes allergens and triggers inflammation. Kaiser Permanente, our HMO, uses the ELISA test to measure IgE levels, instead of RAST, which has been abandoned since 2010 because it involves using radioactive material.

The first result came back as “IgE, QN    368    Standard range 0 - 75    U/mL”

"U" is for "unit." How many antibodies in a unit? I have no idea. The internet is no help here. 368 U/ml, from what I can tell, is her measure of total IgE, all the antibodies of this type she has circulating in her blood.

So that means V's IgE is five times the maximum normal limit. That’s typical for someone with atopy.

We’re still waiting for the specific results. I wouldn’t put it past Kaiser to waste at least one vial doing the wrong test, and then tell us we need to come in and give more blood.

Last year, among other things, V tested positive for IgE against milk, with 7.8 U/mL. I find it remarkable that her titer of antibodies to milk is 10% of the maximum number of antibodies that a “normal” person should have against everything.

V has eczema and mild asthma. Positive IgE tests are no guarantee of allergy, but we know she’s allergic to milk, since she vomits every time we give it to her. (Our son has no allergies and my wife and I have accidentally switched the kids’ glasses at lunch. Oops.)

She also has consistently tested positive for peanut and walnut allergy (and beef!), though there are as yet no incidents where she’s eaten some and had a reaction. We’re just trying to keep tabs on her allergies as she grows up, hoping, of course, that they will go away—but also fearing that she could develop a life-threatening allergy.

It's World Allergy Week. Is anything happening?

April 8-14 is World Allergy Week.

What is World Allergy Week? It appears not to be much more than a name, although the organizers held phone conferences Monday and today. Google News doesn’t list any items for World Allergy Week; nor does the website for the Asthma and Allergy Foundation of America.

Here’s the official press release.

WAW is a creation of the World Allergy Organization, a loose federation of 93 national allergy societies.

This year’s WAW is focused on food allergies and sensitivities. Food sensitivities (and allergies) can trigger eczema for many people—and allergies to pollen and pets are also a major problem.

I was alerted to WAW by Elopy Sibanda, a professor of clinical immunology and allergy at the College of Health Sciences in Harare, Zimbabwe. I value Sibanda’s perspective because his work makes it clear that allergy can affect people around the globe and is not something that can be automatically blamed on modern science and medicine.

Come to think of it, that may be the point of World Allergy Week.

I asked Sibanda a number of questions by email. Let’s hope he responds.

Eczema Q&A with Zimbabwean immunologist Elopy Sibanda

When developing countries appear in news stories about eczema, they mostly serve as contrast with industrialized countries, where allergic disease is on the rise. We also tend to hear only from scientists in the US, the UK, Europe, and Japan. That is why I was fascinated to read a recent story about eczema in The Herald, a government newspaper published in Harare, Zimbabwe.

The story focuses on the physical and social costs of eczema that we are so familiar with. It quotes Odwell Gwengo, founder of the Eczema Association of Zimbabwe Trust:

"Judging by the numerous cases attended to, eczema is common in our communities than we had anticipated."

Which makes you think that perhaps Western scientists have not got a complete handle on the statistics of allergic disease in the developing world. This is understandable, when HIV/AIDS, malaria, Ebola, cholera, etc., claim priority. 

The story also quoted Dr. Elopy Sibanda, a professor of clinical immunology and allergy at the University of Zimbabwe. I wrote to Dr. Sibanda with a few questions--I am well aware of my own first-wold slant--and he graciously responded to the cold call. Here's the Q&A:

Spanish Key: In the USA and elsewhere there is a perception that our societies are too clean--this is the "hygiene hypothesis"-- and that infants are not exposed to enough microbes in their early years, so that their immune systems tend toward an allergic response, and we develop eczema and asthma as a result. What is your perspective on the hygiene hypothesis?

Elopy Sibanda: I am familiar with the hygiene hypothesis but I am unsure about the extent to which it applies to our population. In immunological parlance this boils down to a Th1 to Th2 lymphocyte shift. We have seen no evidence of such a shift. The hypothesis is not an adequate explanation for the  the increase in allergic diseases. [SK comment: I'd guess in the end we will find that antibiotic overuse is to blame.]

Spanish Key: There is also a small, but vocal, anti-vaccine movement that claims that the relatively large number of vaccines given to children predisposes them to develop allergic diseases and even autism. As a result quite a few people, some of whom I have met personally, do not vaccinate their children. What is your perspective on this phenomenon?

Elopy Sibanda: There are pockets of religious sects that are against the immunization of children for various reasons. Immunization rates in Zimbabwe are quite high. I have not seen any convincing evidence of immunization influencing allergic trends. The anti-vaccine advocates just have to provide us with the evidence. [SK comment: I would love to see Dr. Sibanda in conversation with a Marin County anti-vaccine advocate.]

Spanish Key: I have read that eczema may be an evolutionary development to protect the body against helminthic worms. What is your opinion?

Elopy Sibanda: My experience is that  people with eczema are at no lesser risk of helminthic infections than those without. If it was developed for that purpose it is failing in its role. [SK comment: very interesting. I wonder why eczema has persisted in our DNA despite being so debilitating in some cases, if it does not have some hidden benefit. But then look at all the other hereditary diseases we are passing along to our children--diabetes, Tay-Sachs, Huntington's, multiple sclerosis, etc.]

Spanish Key: What do you think are the most important therapies that African children and adults with eczema lack?

Elopy Sibanda: Before we can address the issue of therapies, the challenge we face is patient education and disease awareness. Once the people understand the disease, they will begin to appreciate the interventions and establish treatment options and priorities. Like everywhere in the world medical interventions aim to stop the itch (anti-histamines), reduce the dryness (mosturisers and ointments) and prevent infection. [SK comment: very similar to the NEA's outlook here in the US. Although antihistamines generally not considered useful for treating itch of chronic eczema, as I have discussed in earlier blog posts.]

I am grateful to Dr Sibanda for replying and I hope to add other voices to this blog to build a truly global perspective on eczema.

Contact dermatitis, delayed allergies, and eczema

Contact dermatitis is a more important and complex factor than I thought for patients with atopic dermatitis, I learned from reading a presentation given by Dr. Luz Fonacier at the annual meeting of the American College of Allergy, Asthma and Immunology, held this year in Anaheim, CA. (I was not present at the meeting.)

Fonacier is head of the allergy section of the Division of Rheumatology, Allergy & Immunology at Winthrop University Hospital in Mineola, NY. Her talk, titled “Food Allergy and Atopic Dermatitis: Generating a Common Approach with the Dermatologist,” covered many well-known techniques to diagnose food allergy. She also devoted a large section to a controversial test: the atopy patch test.

What stood out for me was the role of contact dermatitis in atopic dermatitis. According to Fonacier, contact dermatitis, a specific type of allergic reaction to substances such as certain metals and fragrances, affects roughly two-thirds of young (infant to teenage) patients with chronic eczema. Rash and inflammation from contact dermatitis can intensify AD and change the long-term course of the disease, presumably for the worse--by exposing you to more allergens and pathogens.

While contact dermatitis often affects the hands, arms, and face, a systemic exposure to an allergen to which a person has a contact allergy can affect skin over the entire body. Metals, fragrances, and other substances that cause contact dermatitis are often present in foods. When a person eats a food containing a substance to which he or she has a contact allergy, it can manifest as a body-wide skin inflammation.

So how is this different from “classic” food allergy?

The differences lie in the timing and pathway of the reaction. “Type I” allergens such as wheat, soy, milk, and the usual culprits provoke a specific type of allergy, initiated by IgE-class antibodies, that appears over 30 minutes to two hours.

“Type IV” allergens—and I am not even sure I am using the correct term for these substances—cause a “delayed-type hypersensitivity” reaction driven by T cells that manifests hours or days later.

Nickel. You probably don't want to eat this stuff.
But it's in your cutlery and tofu.

Fonacier lists several allergens in food that can cause systemic contact dermatitis: the most common are nickel sulfate and something called “balsam of Peru,” a natural resin that contains a mixture of oils and chemicals and is used in many processed products.

Nickel is overwhelmingly found in soy and a small number of other foods, according to Fonacier’s slides. (That means that you can have a type IV allergy to soy but not necessarily test positive on a skin prick test or IgE assay.) Balsam of Peru, in contrast, is found in a wide variety of foods. Check out slide 15 of the presentation—see spices, citrus, tomatoes? I have no idea how balsam of Peru ends up in citrus peel or tomatoes; maybe it's an agriculture or food industry thing [update: Fonacier says that tomatoes contain chemicals similar to those in balsam of Peru].

Now, how to diagnose contact dermatitis? Patch testing, in which a nurse applies an array of patches containing potential allergens to a patient’s back. About two days later, an allergist looks for inflamed spots, and the corresponding patches indicate which items you should avoid.

Balsam of Peru. Appearing soon in toothpaste near you.
(And spices, and citrus, and tomatoes, and fragrances...)

Fonacier does explain patch testing in her slides, probably because it’s so obvious to an allergist. Instead, she devotes a large section of the presentation to the “atopy patch test,” or APT, which is a patch test in which the allergens are dairy, wheat, soy, and so on--those commonly assessed for type I allergies by skin prick tests and specific IgE measurements. But an APT tests for type IV hypersensitivity reactions, the delayed ones.

The advantages of the APT are that it apparently can predict type IV allergies to cow’s milk, egg, and wheat pretty well. The disadvantages are that it takes a long time and the person observing the results has to be well-trained. According to one slide, an NIAID expert panel recommends that the APT not be routinely used in the clinic because it is not as reliable as oral food challenges.

So when does Fonacier recommend using the APT? If a patient has a history of severe and persistent AD, and skin prick and IgE tests have been done, and no trigger has been identified—or if there are multiple instances of IgE reactions that have no apparent connection to AD—then it's time to try the APT.

Bizarre flareup goin' on

It’s rare that my own skin deviates from its usual dryness and sporadic eczema flares. But right now, if I look at things from a detached perspective, things are interesting.

By any measure my skin’s been terrible since I left for vacation with the family. The return trip, which involved a 17-hour moisturizer-free delay in Newark, did me no favors. My scalp is a disaster. And since I got back I have had two weird episodes where my face and torso have gotten all puffy, tight, and red.

Last weekend we spent Saturday night on my kids’ preschool campout. I woke up Sunday with a red face and a weird crusty oozing above both eyelids.

Maybe I brought this on by standing next to the campfire. Maybe it's a reaction to pollen. All I know is that I had to grit my teeth and get through the morning until I could have a shower and moisturize at home. I took an Allegra. I felt pretty shitty.

I even thought I was going to miss work on Monday. But Monday morning my skin had calmed down enough for me to go in.

Then, after I went swimming on Wednesday, a co-worker asked if anything was wrong. “Your face is all red,” she said. It was starting up again. Even my wife, who is quite the diplomat, was looking at me strangely in the evening.

So today I had an appointment with the doctor. He doesn’t know what’s going on, and I don’t think he even expects to find out, but he mumbled something about oedemic urticaria and gave me a shot of prednisone in the butt. Also at some point soon I need to go in for a blood test to see if I have a “complement deficiency"—something wrong with a particular arm of my immune system. But, as with most aspects of eczema, I expect it will remain a mystery.

Diversity of food eaten in first year linked to less eczema afterward

Feeding your child a variety of foods, especially yogurt, in the first year of life appears to reduce the chances he or she will develop eczema later on, a group of European scientists reported recently in the Journal of Allergy and Clinical Immunology.

The group, led by Caroline Roduit of Children's Hospital at the University of Zurich, had considerable overlap with the researchers who reported two years ago that the mother's exposure to farm animals before birth reduced the incidence of eczema. Both studies were based on data from the Protection against Allergy--Study in Rural Environments (PASTURE) project.

The authors say that, in the existing scientific literature, there is no consistent evidence that avoiding food allergens during pregnancy or infancy prevents allergies later. Because they conducted this study, it would seem they believe the opposite: that exposing kids to allergens could lead to tolerance and therefore fewer allergies. And eczema often has an allergic component, although it's sometimes difficult to classify the precise type of reaction that a patient has to a food.

The authors considered data from 1041 children, seeking to correlate the variety of foods fed eaten with whether the children developed eczema (not whether they developed food allergies). They reported an inverse correlation: the more foods eaten, the less eczema in the children. Here's Figure 2, the key graphic.

Looks to me like the first two foods make the most difference. After that, the curve is essentially flat.

Four interesting features stand out in the paper:

1) the authors observe that it is very hard to study the connection between food and eczema before a child is one year old, because if a child has symptoms of eczema early, or if one or both of the parents has allergies, the child tends to be given very few foods in addition to breast milk. So a naive researcher might immediately conclude that giving a kid only one or two foods leads to eczema. To be rigorous, the authors restricted their study to children who developed eczema after the first year.

2) yogurt, according to this data, is a special case. If a child eats yogurt, and very few other foods, it appears to reduce the odds of developing eczema to 40% of what they were to begin with. That may be because the yogurt bacteria somehow provide a probiotic effect in the gut.

3) the six major food groups that the authors consider as independent are vegetables and fruits; cereals; meat; bread; yogurt; and cake. (Cake is a separate food group in Europe?) I find this odd, given that bread and cake are made from cereals and the three groups must contain very similar allergens.

4) Europeans apparently give their children very few soy-based foods. North Americans must have been influenced by Asian cuisine and include tofu and soy sauce in their diets more than they used to. Or maybe it just looks that way because I live in the Pacific Rim.

I wouldn't make any radical changes to my kids' diet based on this paper, but you can't do any harm feeding them yogurt.

Blood tests for food allergies/sensitivities that may cause eczema

Just out in the Canadian Medical Association Journal: a primer, presumably for doctors [media summary] on how to handle patients who arrive in the doctor's office clutching printouts of blood tests taken to find what foods might be causing trouble for them.

I'd imagine this happens all the time. I don't blame patients at all. Who cares most about your health? You do. Do you think your medical providers, whatever system you use, are doing as well as they could for you? Probably not. So if you've got a chronic condition that seems to be related to what food you eat, you get a blood test done to try to find the culprit(s).

There's more than one problem with this, however. Most patients don't understand the difference between food allergy, reaction, and sensitivity. The primer's author, Elana Lavine, briefly explains:

Food allergy is an adverse health effect arising from a specific immune response that occurs reproducibly on exposure to a given food. Nonimmunologic adverse reactions to food are termed food intolerance and include conditions such as lactase deficiency, dietary protein–induced enterocolitis syndromes and eosinophilic gastrointestinal disease. Food sensitivity is a nonspecific term that can include any symptom perceived to be related to food and thus may be subject to a wide range of usage and interpretation.

Eczema patients (in my understanding), are usually subject to the first and third categories. We probably have IgE antibody-based allergies to one or more foods (in addition to pollen and pet dander). And our skin inflammation is exacerbated by anything that causes increased blood flow at the surface, such as spices, alcohol, and histamines from fermented or aged foods such as Parmesan.

Lavine says that many patients get blood tests based on measuring levels of IgG --a separate class of antibodies from IgE. But, she says,

neither total IgG nor IgG4 [a subclass] levels correlate with food allergy as shown on double-blind placebo controlled food challenges.

IgG4 floating around in our systems may just mean that we have been exposed to a food and become able to tolerate it.

I did a quick web search and found a company called ALCAT that claims to test for food sensitivity using their proprietary technology, which measures how white blood cells change size when exposed to antigen. I'd have to consult an expert but I have trouble believing that results from such a test would truly reflect how your body is reacting--or not--to foods.

So what can you do to determine whether food is causing your eczema to flare up? Lavine says

Making the diagnosis of a specific food allergy may include the following: a full medical history, physical examination, skin prick testing, carefully selected food-specific IgE levels and oral food challenges to suspected food allergens in some instances.

There's no easy answer. To nail an allergy, you need the whole shebang. Avoiding a food entirely and seeing whether your eczema improves is a good start. The trick is, in my experience, to eat as few processed foods as possible so you can get control of the ingredients. Beware: even something as simple as soy sauce may contain wheat, for example.

[added later] I realized that I didn't address the topic of IgE tests. I don't think that a consumer (in the US) can get this test done without a referral from a doctor. The last time I asked an allergist about getting tested for IgE (the technology available at the time was RAST), he told me that "they" didn't do RAST on atopic patients because the circulating level of IgE was so high that it inevitably saturated the measurement no matter what they tested for. However, a quick Google search reveals that Quest Diagnostics now touts the ImmunoCAP blood test as a way to determine IgE allergy. Has anyone tried ImmunoCAP?