What’s medicine and what’s just candy! Read on to find out. My own personal thought is many patients with vocal cord dysfunction (VCD) respond to vocal hydration which can occur while sucking on a cough drop/candy. Maybe we’ve been treating VCD all along with HALLs! Stranger things have happened.
Finally, the voice of consumers is being heard! That is gluten-sensitive patients.
My transcriptionists are not only good at what they do, but when they hear me talk as much as I do, it’s almost family.
I am reading a book called, Don’t Kill the Birthday Girl by Sandra Beasley, and I thought of you.
- It’s a memoir about the author’s life with food allergies, what it was like growing up with allergies, etc. She has a variety of food allergies along with environmental allergies.
- It’s not very long but it seemed like a book parents who have kids with allergies or individuals suffering from allergies in general would really be able to relate to. Good advice Stephanie!
- The author is really honest about what it’s like living with allergies but she’s humorous about it at the same time.
- The one thing that shocked me is that when the author was a teenager she thought about overdosing on Benadryl because she was tired of living with allergies. Don’t kid yourself, the quality of life in patients with allergy isn’t very good….much worse than heart disease or even diabetes.
- I think this book could help people with allergies, so they don’t feel alone. I don’t feel alone but I know I’m the only one in my family with allergies and none of them get what an allergic reaction is really like so I’m really enjoying this book.
Stephanie, thanks for the suggestion and I’m sure many of our readers will also enjoy the book. You’ll have to ask her permission to “friend”, but here’s her link—>profile.php?id=1192230038&sk=photos
Here’s the link from Amazon about further information on the book: Book on Allergies from Amazon
The Evaluation of a Patient With Suspected EoE
Our series is on eosinophilic esophagitis (EoE) and I’ve covered how you present with this condition and a little bit about what the heck this condition really is! The website reference is http://www.medscape.com/viewarticle/754206?src=mp&spon=38
Patients with suspected EoE should be evaluated by both an allergist and a gastroenterologist.
- A careful history should include screening for the presence of reflux/GERD, growth delay, feeding/swallowing difficulty, and a past history of allergic disease.
- Symptoms of interest include history of weight loss or poor weight gain, dysphagia or odynophagia, multiple emergency department visits for impacted food, altered eating habits such as food aversions, overcutting or overchewing one’s food or eating very deliberately and requiring lots of fluids to wash down each bite.
- A family history of similar symptoms or atopy can also be a clue.
- EGD with multilevel biopsy is needed to make the tissue based diagnosis. Careful attention should be paid to gross features when performing the procedure. Dilation may frequently be performed in conjunction with the biopsy.
Allergen testing should be performed only in patients with biopsy proven EoE, because the tests do not have good positive predictive value without established disease. Unfortunately, skin testing can be positive AND negative in biopsy proven EoE, which leads to much confusion from a diagnostic standpoint.
Testing is guided by foods reported to cause symptoms, but should include 13 common foods with established predictive values for EoE. What are those foods? I’m glad you asked. Milk, egg, soy, wheat, corn, beef, chicken, apple, rice, potato, peanut, oat, barley. This means BOTH skin testing and patch tests to the above list. Patch testing is a bit different in that I make a “paste” with the food and place it in a Finn chamber on the back for 48 hours. Keeping it on can be a challenge, but good results.
Inhalants should also be tested given aeroallergy can play a role. Food atopy patch testing assesses for a cellular-mediated mechanism, and should be placed for food items not positive on initial testing, and read at a minimum of 48 hours after placement. Both prick and patch tests have independent positive and negative predictive values, as well as combined values. Foods positive on either test are generally recommended to be removed from the diet. There is no established role for ImmunoCAP® testing or other allergy blood tests in diagnosing EoE.
- So there you have it…find out if EoE is even present before testing for foods.
- Use both skin tests and patch testing to identify suspected foods that will need to be eliminated.
- And in case you’re wondering, here’s what a positive patch test looks like…..
What is the most likely diagnosis? How did you do compared to your colleagues?
|Your Colleagues Responded:|
|Eosinophilic esophagitis||Correct Answer||67%|
|Irritable bowel syndrome||1%|
Eosinophilic Esophagitis: Definition, Epidemiology, and Pathophysiology
Clinical Definition–summary only.
- Eosinophilic esophagitis (EoE) is chronic, inflammatory esophageal clinico-pathological condition. The diagnosis is made following a biopsy confirming ≥ 15 eosinophils(eos)/high-powered field (hpf), at a minimum of at least 2 esophageal levels (eg, distal and proximal) because the process does not uniformly affect one particular area.
- Clinical symptoms indicative of esophageal dysfunction, such as dysphagia, odynophagia, and vomiting are present. Additionally, patients generally also note reflux often presenting as chest pain and regurgitation. These symptoms are not diagnostic in the absence of a positive biopsy.
- Gross features found on esophagogastroduodenoscopy (EGD) may include narrowing, ulcers, or furrowing. Additional histologic features may be seen, such as microabscess formation or fibrosis.
- However, no histologic or gross finding is diagnostic of EoE beyond peak cell count.
The earliest literature reports of EoE date to the late 1970s, as case reports of GERD patients unresponsive to H2-receptor antagonists who were found to have numerous eosinophils on esophageal biopsies. Recent evidence suggests that EoE has likely been present for decades, but was poorly recognized. When I was a resident & fellow in the early 90’s we diagnosed many children with “functional abdominal pain”. Wonder how many of those cases were EoE!
Studies in the mid-1990s demonstrated the role that diet and steroids (both systemic and topical) could play in the disease treatment, which provided evidence that allergy had a relevant role in the pathogenesis and fit the observations that many of these patients were atopic (this means allergic!) Some studies have noted that less treatment-responsive patients tend to have either a personal or family history of atopy. However, up to 25% of all known cases are not associated with atopy.
EoE appears to disproportionally affect non-Hispanic, white, atopic males. The male-to-female ratio is 3:1, and EoE tends to congregate within families, although no true hereditary link has been established. EoE has been reported on every continent to date except Africa, and across all age ranges, although the typical age of onset is the third or fourth decade of life.
Presenting symptoms vary drastically across the ages, and are summarized in the Table.
Table. Presentation of Eosinophilic Esophagitis: Children and Adults
|Children: Appear SICK||Adults: Appear WELL!|
|Failure to thrive (5%-19%)||Dysphagia (29%-100%)|
|Vomiting (5%-38%)||Food impaction (25%-100%)|
|Abdominal pain (5%-68%)||GERD (7%-100%)|
|Diarrhea (1%-24%)||Chest pain (1-58%)|
|GERD (5%-82%)||Mild eosinophilia (5%-50%)|
|Chest pain (17%-20%)||Delay in diagnosis!|
|Food impaction (10%-50%)|
With both age groups, a history of eating slowly, taking small bites, excessive drinking after each bite, and avoidance of textured foods is common and represents compensatory mechanisms.
EoE is an allergic disease, but it’s not that simple. In affected esophageal tissue there is upregulation of interleukin (IL)-4, IL-5, and IL-13 expression. However, both immune globulin E(IgE) and non-IgE (cellular-mediated) mechanisms contribute, as is seen in atopic dermatitis.
This means that sometimes skin testing is helpful and sometimes it is not. Foods to eliminate with negative skin tests comes down to trial and error. IL-5 is the main cytokine responsible for eosinophil maturation, bone marrow development, esophageal remodeling, and signals for eotaxin-3, the most crucial eosinophil chemotaxis factor. IL-5 deficient mice cannot develop EoE, and intratracheal IL-13 induces dose-dependent EoE. In mice, anti-IL-13 blocked development of EoE. IL-13 induces eotaxin-3 production, and may be an independent factor inducing tissue remodeling. IL-13 is central to an emerging hypothesis of epidermal barrier dysfunction as a mediator of EoE and directly downregulates gene transcription of filaggrin and involrucin.
Is there a genetic basis for EoE? Eotaxin-3 SNP’s are present in 14% of cases, and researchers have identified an “EoE Transcriptome” — a unique set of approximately 1% of genes that are overexpressed in EoE. More recently, a genome wide association study identified a disease susceptibility locus at 5q22, and a polymorphism in TSLP (thymic stromal lymphoprotein). So in short, yes, genetics play a role, but more research is needed.
Ok, enough of the basic science stuff. Tomorrow I’ll discuss how to evaluate a patient you suspect has EoE. And how do you spell that again?
So how much can we hear about food allergy? As unfortunate as it is to have a severe food allergy, what bothers patients most is lack of reliable information about their condition and the lack of concern about a potentially fatal reaction. Just look on Facebook to find hundreds of stories about the tragedy of food allergy or anaphylaxis. Here’s an example of the anxiety that results from a child with food allergy—>
If you’re going to treat food allergy, you have to know it’s there–duh. But not so fast….most kids never get the appropriate food challenges to make the diagnosis. Consider this:
- Oral food challenges are the gold standard for diagnosing food allergies in children, but only a small fraction of kids in the United States are getting them.
- At the American College of Allergy, Asthma & Immunology 2011 Annual Scientific Meeting Dr. Gupta reported from her study that oral food challenge was done in just 15.6% of children that really needed the test.
- As a result, it is likely that childhood food allergy is seriously underdiagnosed
“Food allergy guidelines just came out in March of this year from the National Institutes of Health NIAID [National Institute of Allergy and Infectious Diseases] stating that oral food challenge is the proper test to diagnose food allergy, along with medical history and positive skin and blood testing,” Dr. Gupta said.
In Dr Gupta’s study, only 47% had a skin test and 40% had a blood test for food allergy.
“Overall, what this tells us is that food allergy is not being diagnosed optimally and oral food challenges are definitely not being done enough,” she said.
What are your thoughts about food allergy? Have any readers experienced a “misdiagnosis” of food allergy? I’d love to hear from you!
Advances in allergic skin disease, anaphylaxis, and hypersensitivity reactions to foods, drugs, and insects in 2011. J Allergy Clin Immunol 2012;129:76-85
So what’s new in allergy to foods, drugs, and insects? I promise, I won’t bore you with basic science facts useful only for allergy boards, but here’s some facts for you to digest with the new year:
A US study estimates a food allergy emergency department visit every 3 minutes, on average. This is a very remarkable statistic for a condition that was “trivial” during my allergy fellowship training.
Food allergy health care costs are estimated at $500 million in 2007. Ditto the above–now you know why so much research is focused on a permanent cure for food allergy.
Severity of peanut allergy varies regionally, likely based on the source of sensitization (pollen related vs oral). Not only region variation, but also determined by culture. For instance, infants in Israel who are fed peanut early in life have less allergy than their European counterparts that withhold peanut until age 2 or 3.
Vitamin D deficiency is associated with increased risk for food sensitization (peanut). Is there anything that Vitamin D doesn’t do? Cod liver oil, here we come!
- Freezing fresh fruits for prick-prick testing does not result in a significant loss of potency. Who cares? Well, your doctor may want to test you by pricking a fresh fruit (say peaches) and then testing your skin. Don’t worry about how you’re going to get the fruit to the appointment….just freeze it for later.
Clinical studies of peanut oral and sublingual immunotherapy show promise. Why not eat small amounts of peanut and develop tolerance to it? It works and several studies are beginning in 2012 to find out more information about safety and who are the best candidates for this procedure. Want to be involved in this type of study? Call me for details.
Several studies support the use of Xolair™ for not only asthma, but also food allergy: Milk and peanut to name two. This treatment may also be useful for chronic urticaria refractory to antihistamines–>hives.
During a safety study of a food allergy herbal formula based on traditional Chinese medicine, a trend toward modulation of basophil responses was observed. This means some science exists behind the nutritional and herbal medicine “craze.”
New insights into the use of vitamin D, phototherapy, methotrexate, azathioprine, and immunoadsorption in treating severe AD were shown.
Several studies support the notion that egg content of seasonal influenza vaccines is low, that skin testing is not necessary, and that the vaccine can be safely administered to persons with egg allergy!! See my previous post on egg allergy and Flu vaccine.
A Canadian study shows only 55% with diagnosed food allergy had selfinjectable epinephrine. Folks, this is a life-threatening reaction and only 55% had the lifesaving treatment on hand?
A clinical study of children with delayed urticarial and maculopapular rashes shows a low recurrence rate and efficacy of drug rechallenge. If you’re faced with a rash occurring 4-6 hours after taking a medication, you probably won’t react with the second exposure
Is this enough to absorb in one day? Happy New Year!