New NEA blog post on allergy tests for eczema

I just wrote a new post on the NEA blog, about food allergy tests for eczema. I interviewed Jon Hanifin, a professor at Oregon Health Sciences University and one of the giants in the field of eczema research and practice. (Eczema is commonly diagnosed using the "Hanifin and Rajka" criteria.) Read the post if you are wondering how useful allergy tests are for food triggers of eczema.

The last few weeks my family has been under a lot of stress because my five-year-old son just started kindergarten. He has been unhappy about moving to a new school--where he's in a class of 28 (his preschool had 14 kids) and about 500 students attend total. He cries when we drop him off, when we mention school, and at night when he protests that he doesn't want to go. Plus there's homework--four pages a day, for a kindergartner! and Dad's Club and PTA. So you can understand why my posts have been a bit sparse. The pace will pick up again, I'm sure.

Voov makes it to three--and eczema, food reactions continue

Looks like my daughter, Voov, is stuck with eczema for life. She recently turned three and had her annual checkup. The pediatrician told us what we already knew, which is that children whose eczema persists past the age of two usually carry it into adulthood.

But at least her affliction isn't severe. It's not nearly as bad as what I've dealt with myself and what I see discussed on forums and in the National Eczema Association newsletter.

We're also still waiting to see what will happen with her asthma. She takes medication twice a day through an inhaler, but only because when she gets sick, as she is now, she wheezes. She hasn't had an asthma attack.

Food allergies/reactions are another issue. God, she's been eating the same stuff for years. Let me see: chicken, turkey, soy. Rice and oatmeal. Carrots, peas, sweet potato, corn. Apple, pear, banana. That's it! How boring. We've also given her tomato, potato, orange, green beans, and pork, and she refuses to eat any of them, although she doesn't have a reaction.

Two weeks ago, my wife, Hidden B, gave her cow's milk instead of soy milk by mistake, and Voov announced she felt ill and then threw up all over the kitchen floor.

Bummer.

I like to cook, and I keep hoping that someday I'll be able to make one meal for the whole family. At the moment I cook food for Voov and then food for everyone else. We have to tell her over and over again that she can't eat what we and other people eat, because she's special. I wonder how long that fiction will hold up.

The weird thing is that she's hardly ever had an eczema flareup that we could connect to a food we've tried. Voov seems to have allergies or intolerances that aren't directly connected to eczema.

In a few weeks she's going to have a skin prick allergy test for all the same things she was tested for two years ago. We're hoping we'll find that she's grown out of some of her allergies. I myself would like to just give her foods and see whether she reacts, but Hidden B has overruled me. Probably wise, if Voov's reaction to milk is any indication.

Lymph node immunotherapy may be simpler, safer

A new, improved method of immunotherapy is emerging: injection of modified allergen, directly to the lymph node--which promises to prevent allergy to specific triggers with only a few treatments and minimal risk.

A group of Swiss, German, and Swedish scientists reports in the latest issue of the Journal of Allergy and Clinical Immunology that they reduced nasal tolerance of cat dander, a major trigger for atopic allergy, by a factor of 74 in a group of 20 subjects, using only three injections over two months. That means it took 74 times as much dander to cause the same amount of allergic reaction--the scientists used the flow of liquid from the nose as their measure--in a treated person as in a subject given placebo.

[This article featured in JACI's Journal Club.]

Immunotherapy for specific allergens currently requires 30 to 80 injections over three to five years and includes a risk of anaphylactic reaction. It is not popular. The new method, if confirmed, looks much more practical.

The researchers, Gabriela Senti of University Hospital Zurich and colleagues, were basically repeating an earlier, successful study that they had done with grass pollen. (I consider cat allergy avoidable but grass pollen is a big deal--you can't get away from it, unless you're in Antarctica.)

But the new study came with a twist--the researchers modified the cat dander allergen with two molecular changes. The first added a short chain of amino acids that helped the allergen enter the cell membrane--essentially, the membrane of B and T cells, since it was injected into the lymph nodes. This seems to have prevented other white blood cells, such as macrophages and mast cells, from encountering the allergen and provoking inflammation.

The second modification ensured that the allergen didn't get immediately destroyed inside the cells, but instead got chopped up and presented on the surface of antigen-presenting cells, which are a key element of the antibody arm of the immune system. Thus, by a process I don't really understand, your immune system becomes "tolerant" to that allergen.

Treatment with the modified cat allergen did not increase IgE antibody levels, or induce any "adverse events" in the treated group, which, it has to be said, numbered only 12. It's possible that in a larger test group some problems might reveal themselves.

If an environmental allergy is a big problem for your eczema, and you can stand nurses injecting things into your lymph nodes, this looks like good news. I don't know how long it might be until the FDA approves this treatment in the US though.

Jon Hanifin: Barrier defects come first in eczema; allergies follow

Atopic dermatitis is a disease that arises primarily because of a breakdown in the barrier properties of the skin, and allergic reactions typical of AD are a consequence of this breakdown, Jon Hanifin told an audience last week at the annual meeting of the American Academy of Dermatology, held in San Diego.

Hanifin is one of the US's leading dermatologists, and practices at Oregon Health and Science University in Portland. He was kind enough to send me the Powerpoint of his talk, which I wanted to read because I figured from its title ("AD Pathogenesis: What's New") that it would give me a good picture of the field.

His talk was encyclopedic and technical and I'm not going to attempt to cover the whole thing. But it did make clear to me that the standard model for how eczema arises and develops is in a state of flux.

For a long time, it was thought that allergy was the dominant factor in eczema. But a key paper in 2006 linked higher risk of developing eczema and asthma to mutations in the gene coding for the protein filaggrin. Filaggrin is a long protein, consisting of a string of subunits, that has an important structural role in skin cells, especially in the uppermost layer (the stratum corneum), and also gets broken down at the surface into something called "natural moisturizing factor." From that first paper came a flood of research into filaggrin, which has helped paint a fuller picture.

One thing that jumped out at me from Hanifin's talk was that the relationship between filaggrin mutation and eczema is not simple. The severity of eczema depends on where mutations are within the protein; it's possible to have more than one mutation, which greatly increases the likelihood that you'll get eczema.

Hanifin cautions that filaggrin is not the only genetic culprit in the origins of eczema. Mutations in certain other proteins can compromise the skin barrier.

If filaggrin is messed up, your skin barrier will be too--it'll be leaky--and this means that your body gets exposed early on to a wide variety of antigens that it otherwise wouldn't be. Recently I wrote about the "hygiene hypothesis," which posits that it's good for kids to get exposed to germs because that helps prevent allergies later on, but it seems that it's not good to get exposed to too many germs, because that leads to allergies later on. There's a Goldilocks-just-right amount of germs that your immune system needs to encounter to develop properly. Hanifin laid out the current thinking, which goes as follows:

• Defects in skin cell proteins let in irritants, microbes, allergens
• This causes skin cells to release a signaling molecule called "TSLP"
• TSLP stimulates white blood cells to develop an immune system dominated by type 2 helper T cells (which act via antibodies and inflammation, rather than by macrophages that eat pathogens)
• Th2 cells induce production of IgE antibodies, and then you have classic allergies linked to eczema.

It's just a logical progression. Allergy caused by skin defects seems generally to make more sense to clinicians and researchers these days than skin defects caused by allergy.

Now, is it possible to have atopic dermatitis without abnormal IgE/Th2? Hanifin replied by email:

Yes, roughly 20% of AD patients have typical eczema without any Th2/IgE abnormalities or asthma, etc. ( I call that "pure AD" but allergists tend to call it "intrinsic.") It's been known for years and is the reason we've always doubted that allergy was causative for the skin disease--IgE is clearly involved with hay fever, food allergy and some cases of asthma that usually accompany AD.

Hanifin lays a lot of stress on the precise definition of food allergy, which is specifically defined as an adverse health effect, rather than an adverse immune response. (He refers you, and me, to the NIAID Food Allergy Guidelines.) A positive IgE test for a food doesn't necessarily mean you're allergic. You have to get ill after eating something to be truly allergic to it. Hanifin clarifies:

Not necessarily ill, but usually rapid onset of hives, maybe nausea, cough--sometimes anaphylaxis...The tests are often imprecise and not everyone with high specific IgE levels reacts to that food. Whether they have become tolerant or never were allergic can only be speculated.

My guess is that Hanifin and other dermatologists are increasingly under siege from overinformed patients such as myself who have garnered information from the internet and are now demanding that their doctors conduct allergy tests to nail down the one or two things they're convinced must be causing their eczema. In his email, he comments that there are currently "enormous financial incentives associated with the belief of allergy causation of AD." Patients, and the insurance system, are paying a lot of money for test results that aren't useful.

What I'd like to see an explanation of is why most children grow out of eczema. What is it that's happening to their skin barrier and immune systems as they mature over the ages of 3-8 or so that is freeing them from the disease? Maybe, if we knew, we could capture and intensify that process and apply it to at-risk children and adults who have remained affected.

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?

An ill-advised comment on peanuts

Upon arriving home this evening I was not only welcomed by Hidden B (torrid spousal kiss), Voov (loud acclamation from high chair), and Shmoop (whiny complaint from the floor, where he was lounging, practising to be a teenager) but also, on the kitchen table, this quarter's issue of The Advocate, the NEA's house publication.

The Advocate is best savored at leisure, like a fine malt whisky, so I'll save my review for future posts. Today I want to mention that the annual meeting of the American College of Allergy, Asthma, and Immunology is still ongoing in Phoenix. It was at this meeting that, on Saturday afternoon, Donald Leung and three other immunology heavyweights engaged in the knock down, drag out brawl known as the Great Atopic Dermatitis Raft Debate. The four presenters each argued that their pet cell types (keratinocytes, T cells, etc.) play the most important role in eczema. Man, I'd like to know what they said, but the event wasn't webcast. I did find out, however, that the proceedings of the entire conference were videorecorded and are available on DVD-ROM-- for me, at the low low price of $340.

Maybe there's some way to get just the session I'm interested in, but it'd probably take more effort than I can spare. (I was also informed that audio recordings might be cheaper... but who's going to pay a hundred dollars for a podcast when these scientists are probably leaning heavily on Powerpoint diagrams?)

* * *

The ACAAI meeting has been in the news, because the president of the whole shebang has gone on the record saying that people take peanut allergies too seriously. I'm sorry, but this immediately discredits his expertise. I know that latex and peanut allergies can be life-threatening; and their incidence is increasing. It doesn't matter if the incidence is low (~0.5%)-- in a school of, say, 1000, that means you have five kids who could potentially die if one of their classmates (it is clinically proven that 100% of kids are capable of being idiots) thought it might be funny to see what happens if Johnny takes a bite out of the wrong sandwich.

I know someone who died of an asthma attack; I also know someone whose wife nearly died from a latex allergy. I'm no expert, but I think peanuts probably pose the same caliber of problem.

This is one area in which America's "sue first, ask questions later" culture will work for the good of society. I can't imagine a school principal revoking a peanut ban because Dr. Bahna said so. Fewer peanut bans may get enacted, though.

For the record, I loves me some Snickers, and I eat PB&J every single day. But I'd quit on the spot if someone's life was endangered.

* * *

A blog post worth checking out: in which a UK citizen of east Indian descent talks about her teenage experience with eczema. For me, too, eczema came on with a vengeance not long after I got interested in the opposite sex. I didn't develop big boobs to compensate, as she did-- but, on reflection, that's probably a good thing.

Maybe your kid CAN eat more foods

I'm back from my weekend trip to New Haven for the science writers' conference. A smashing idea, getting about 500 of us in the same place and giving us drink tickets. The hubbub of eager networking (freelance writers have to network nonstop if they want to eat) at times almost drowned out the science-themed standup comedians and a cappella groups.

My trip was a success not only professionally, but because twice in the space of two days I got up at 4:30 am, endured the stress of making a flight, sat for 7 hours in the dry, recirculated, funky air of a Boeing 737, ate at McDonald's (Hartford airport is no food paradise), and downed my share of beer and wine-- and here I am at the end of it with dry skin, yes, but no eczema to speak of. Score!

I'm going to continue the food allergy thread today. There's a recent study out of National Jewish Health Center in Denver that found that many children with eczema are unnecessarily leaving foods out of their diets, for fear of food allergies that don't exist. The main issue the authors are making is that the proof of most food allergies is in the eating. Blood test results for IgE allergies are not believable unless they show you are positive for cow's milk, hen egg, fish, peanut, or tree nuts.

If a test shows your kid IS allergic to one of those five things, you definitely shouldn't eat it. But David Fleischer and colleagues (including Donald Leung, leader of the Atopic Dermatitis Research Network, who appears to be the heavyweight author) took 125 children who had been on restrictive diets based on IgE tests, and, in a controlled fashion, let the kids eat food that they had previously avoided. The result: "Depending on the reason for food avoidance, 84 to 93 percent of foods being avoided were restored to their diets."

This matters because your young child needs a balanced diet to develop properly, and also because substitute foods (goat milk, almond butter) are expensive.

I find the study personally interesting because Voov (18 month daughter) has been on an extremely restricted diet for many months. Skin prick tests showed allergies to a number of things and the allergist recommended, at first, some ridiculous diet--seriously, like "she can only eat sweet potato, broccoli, and chicken." Completely unreasonable, and after Hidden B protested, and we got advice from a nutritionist, the allergist relented a bit and permitted these items:

• zucchini
• broccoli
• asparagus
• sweet potato
• pears
• bananas
• chicken
• turkey
• rice
• soy

That is what Voov has been eating for at least six months, over and over. (She's also breastfed.) We're allowed to pour canola oil over her food so that she gets some omega-3 oils for her brain. She's a happy enough kid, but still has eczema flares, and she has to be getting pretty tired of this food by now. I know that I'm getting bored of making it, when it's my turn to boil the zucchini.

Fleischer et al. don't say whether skin prick tests are as useless as most IgE blood tests. But I sure would like to expand Voov's diet, so she can experience some new tastes. Wouldn't it be great if she could just eat the same things we do!

Mr. Peanut need not apply

Eczema Mom recently posted about her experience being on a plane with her kid, who's been diagnosed with severe peanut allergy-- some guy opened a bag of peanuts in the row ahead of them, and the smell drifted back, and she could do nothing but wait and see whether her kid would have a reaction. (On a plane! What are you going to do if he DOES have a reaction?)

Peanuts-- I love to eat peanut butter, and Snickers, but I'm learning that a lot of people have severe allergies to them. In fact, Voov was diagnosed with a peanut reaction on her skin prick test-- Hidden B will know all the details. Hidden B is breastfeeding Voov (who's been on solid food for a while now, being 18 months old) and has had to avoid peanut butter herself. I get in trouble for eating the sunflower and almond butter-- which somehow seem more exotic and tasty than my peanut butter.

Peanuts are in the news at the moment. There's a study out in the Journal of Allergy and Clinical Immunology by a group at the Mount Sinai School of Medicine in NYC, indicating that pregnant women ought not to eat peanuts if they can help it. The specifics-- seems only to apply to kids who are suspected of being allergic to milk or eggs, or have eczema and allergies to milk or eggs. (An odd study group, that-- but I can't see the details because my institution doesn't have access to the paper itself.)

Kids with eczema really have it tough-- the itch, the rash, the food reactions, and then they're at higher risk of developing a life-threatening peanut allergy. Life's a bitch.

I had a short email today from a reader, Jon, letting me know that his partner, who's had eczema for a long time, had recently seen a dramatic improvement after cutting out dairy products. That's awesome and I encourage anyone who has eczema and who has never tried an elimination diet to do the same thing. Cut out, one at a time and for two weeks or more, milk, soy, peanuts, wheat, and eggs. (And fish, if you eat it regularly-- Hidden B hates fish, so I never cook it.)

Here's my personal take: I draw a distinction between food ALLERGIES and food (or drink) that causes REACTIONS. I might have a food allergy; I don't know for sure. But I do know I have reactions to alcohol and hot peppers, which both dilate the blood vessels in the skin. I get itchy after drinking booze or eating a hot curry in the same way I do after I exercise. I'm guessing the heat or blood flow somehow stimulates itch nerve fibers. And then, I also have reactions (oh, so vicious) to aged cheese like real Parmesan, and to preserved foods that are high in histamine. These just have to be triggering inflammation systemically.

Does this mean I never have a drink, or enjoy a fine double Gloucester? Hell no. You have to live. But I often regret it the day afterward.