Category Archives: Food allergy

Finally!

More standardization gives more legitimacy to children with food allergies; hopefully, less bullying.  Kudos to Mike Stobbe from Tulsa World who wrote this. 

Here's what can happen with food allergy!
Here’s what can happen with food allergy!

http://www.tulsaworld.com/scene/food/feds-post-food-allergy-guidelines-for-schools/article_72009af5-fb0a-5aac-ade7-ff8ae23e8191.html

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How To Stay Informed

Thanks for following along with the diagnosis and treatment of eosinophilic esophagitis (EoE)–a condition that during my fellowship training in allergy wasn’t even recognized as a cause of abdominal pain. 

Treatment options for EoE are currently:

  • Corticosteroids–both oral and inhaled
  • Dietary avoidance of known allergic triggers, including but not limited to foods 
  • Use of PPIs such as Nexium & Protonix
  •  Treatment principles focus on reducing symptoms and eosinophil counts while, importantly, protecting and preserving quality of life.
  • Maintaining diet and nutrition which is harder than it looks! Don’t forget that restoring growth parameters are also essential for adults as well as in children.
Tastes Great, but NOT less filling!

As with all diseases, treatment is updated constantly, and new recommendations emerge.   As with many inflammatory conditions, steroids work great, but are NOT less filling.  Side effects from steroids are many and any time an alternative is successful, you’re better off.  Remember, topical steroids are fine, it’s the oral systemic absorption of steroids that contributes to the side effect profile.  

 Due to the long-term side effects associated with high dose corticosteroids and a tendency for relapse after discontinuation, this therapy is not first-line outside of using short bursts and tapers for severe symptoms needing urgent relief (eg, critical dysphagia, stricture, dehydration and acute weight loss.

Topical Corticosteroids

Topical corticosteroid are used in EoE through 1 of 2 routes:

  • “Gulping” the expressed actuations of an inhaled device; or
  • Expressing the contents of a nebulizer respule into a cup, forming a thickened slurry by mixing it with sucralose/maltodextrose (Splenda®), and water.

Use in this manner provides “local” or tailored coating of esophageal tissue, at lower doses (220 μg-1 mg per dose). Faubion and colleagues demonstrated that 880 μg/day of swallowed fluticasone propionate or beclomethasone diproprionate resulted in symptomatic improvement in 4/4 pediatric patients Noel and group at the Cincinnati Children’s Medical Center, noted that non-atopic patients had a better response rate to the topical steroid than the atopic patients.  A randomized, controlled trial by Konikoff and colleagues confirmed similar findings independent of pre-treatment eosinophil numbers. 

Oral viscous budesonide (OVB) is quickly becoming the preferred therapy to fluticasone. The technique of swallowing a liquid dose may be more effective and efficient than “gulping” a hydrofluroalkane gaseous suspension. Additionally, OVB has comparable efficacy. One study found an 80% decrease in a symptom scoring index and regression of cell counts to less than 7 Eos/HPF; after 3 months of therapy there was decreased fibrosis/remodeling from baseline.

Dosing for fluticasone ranges from 220 to 880 μg per day, and for budesonide, from 0.5 to 2 mg per day; both doses are similar to those used in asthma. With either agent, patients are instructed to not eat or drink for 30 minutes after administration. Complications from topical treatment include oral/esophageal candidiasis.  In a 3-year case series studying recurrence, approximately 90% of adults relapsed at a mean of 8 months post discontinuation of 6 weeks of therapy. Just like asthma, when you stop using the controller medication, symptoms will come back.  No study of optimal dose or duration of therapy has been performed, but most adult providers recommend a 6-week course while pediatric providers suggest a 12-week course.  No long-term safety data exist pertaining to bone or adrenal effects from such small but more readily bioavailable dosing methods used in EoE.

Acid Suppression

Technically, EoE should not be diagnosed until response to PPI therapy has been determined, according to the 2007 and 2011 consensus guidelines. A certain subset of patients will have PPI-responsive esophageal eosinophilia.  Typically, dosing is either 10-40 mg omeprazole or 15-30 mg lansoprazole per dose for 2-3 months. High-dose PPI therapy may distinguish GERD from EoE.

Immunomodulating Therapy

Immunomodulating therapies may offer some promise. The best studied therapy is anti-IL-5. In mice, anti-IL-5 decreases blood and tissue eosinophils, and decreases eotaxin-3 levels. Garret and fellow researchers studied anti-IL-5 in 4 patients with hypereosinophilic syndrome. Symptoms and eosinophilia resolved, and in 1 patient who also had EoE, dysphagia and esophageal eosinophils decreased. Stein and colleagues, in an open-label phase I study of anti-IL-5, noted that blood eosinophilia was reduced but not correlated to decreased levels of IL-5, eotaxin-3, or esophageal eosinophilia.   Similarly, there was no significant difference between groups in symptom improvement. Studies of other agents, such as anti-IgE or anti-TNF (infliximab), failed to demonstrate any symptomatic or esophageal histologic improvement. Presently, anti-IL-3 is under investigation in a phase 1 trial, but no data are available pertaining to its safety or efficacy.

Dilation

Dilation relieves critical esophageal narrowing and related symptoms, but will not alter the underlying pathophysiology. Its benefit is maximized for dysphagia and impaction from ring/stricture or other critical narrowing. Several studies have demonstrated the efficacy of dilation, though it is balanced by risks including perforation, deep mucosal tears, pain, linear renting, and bacteremia. Relief is also likely to be transient, because 75%-50% of patients who receive this therapy have recurrence at 2-20 months and need additional dilation.

Dietary Management

A 6-week trial of 10 patients conducted by Kellyand colleagues in 1995 demonstrated the role of an exclusively elemental diet.  At the conclusion of the study, 8/10 had complete histologic and symptomatic resolution and the other 2 subjects showed drastic improvement, demonstrating an elemental diet as a potential treatment. As with steroid therapy, however, upon discontinuation, all patients relapsed. A larger study of elemental diet therapy in 51 patients was conducted by Markowitz and colleagues.  The researchers noted symptomatic response by 8 days and normalization in biopsy by 1 month in 49 of the patients studied. Liacouras and colleagues followed 389 patients with EoE over 10 years, 160 whom were treated with elemental diet and noted a 97% response rate to the diet and biopsy counts that were comparatively lower than 75 patients on swallowed fluticasone. Though exceptionally effective, elemental therapy is limited in that a patient’s only source of nutrition is a very specific hypoallergenic formula. This may not be appropriate for adolescents or adults. Some cases require placement of gastrostomy tube to assist with feeding.

An alternative approach is a tailored/guided diet that avoids only an individual’s known food sensitizations based on skin prick and/or patch testing. Spergel and colleagues described 120 patients placed on a guided elimination diet based on allergen testing.  After 6-8 weeks, 112 had near complete tissue resolution, though 39 relapsed upon reintroducing eliminated foods. In this cohort, 77% had at least 1 positive prick skin test, and 85% had 1 positive atopy patch test. Prick skin tests were most commonly positive to milk, egg, soy, and peanut. The foods that were most commonly positive to atopy patch test were corn, soy, wheat, and milk. Most patients were sensitized to multiple foods, and dietary nonresponders had more sensitizations than responders. Positive predictive value and negative predictive value for 13 commonly positive foods in EoE were published in a previous post.

Follow-up of patients with EoE should be frequent, at least 4 times per year, with consideration for repeat endoscopy at those intervals as well. Repeat endoscopy is the only way to monitor disease progress, because symptoms do not always correlate with disease progression. One pediatric study found that an initial cell count of 6 or greater was predictive of a repeat positive biopsy.

 At each follow-up visit, diet should be reviewed, diet/medication compliance assessed, and consideration given for additional food testing if symptoms or histology are not improving. As noted previously, there are no studies that have evaluated adequate or optimal duration of treatment for either dietary avoidance or topical steroid duration. Very little formal guidance is available to determine key long term predictors of disease resolution, the optimal interval for repeat biopsy, and the effect of these factors on the development of long term sequelae.

Complications from EoE include:

  • Strictures,
  • Schatzki ring
  • Esophageal trachealization and stretching,
  • Esophageal furrowing and narrowing, microabscesses, webbing,
  • Food impaction, persistent/progressive dysphagia, and lamina propria fibrosis.

Esophageal remodeling in EoE occurs as a result of subepithelial fibrosis and is reported in 15%-40% of affected adults. Predictors that influence the likelihood of developing fibrosis are presently unknown. To date, there is no identified association with progression to malignancy directly from the presence of EoE. Some have observed a potential link between celiac disease and EoE, which may share some common gene upregulations with EoE, but this association is not well understood.

The natural history of food allergy/sensitization within EoE has not been well-described. Lastly, while preliminary work and observation indicates that quality of life can be affected significantly, little formal study of EoE quality of life exists. This particular area of research is very important to continue to define, as the quality of life issues that affected families face are distinct from those of the general food allergy community.

From the Journal of Allergy & Clinical Immunology (In Practice)

 Informational video on eosinophilic conditions

A FOOD ALLERGY CURE MAY EXIST AFTER ALL

It’s good to hear from a patient perspective on treatment for food allergy. You can be “desensitized” to food, but it takes time and you can have reactions. At this time, current research is underway for food allergy, but questions we don’t know include how long does the benefit last?

It’s good to hear from a patient perspective on treatment for food allergy. You can be “desensitized” to food, but it takes time and you can have reactions. At this time, current research is underway for food allergy, but questions we don’t know include how long does the benefit last?

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Oral food challenge to peanut

Food allergy is a very common and even popular disease to have.  This results in some predictable patient behavior such as:

1.       I have allergy based on a blood test only, and I tolerate this food all the time.  This may not be allergy at all, but simply a condition called “asymptomatic hypersensitivity”.  Relax, some foods you can eat without allergy symptoms even though a blood or skin test is positive. 

2.       It is fashionable nowadays to have gluten sensitivity.  Many patients will perform gluten challenges at home to see if bread or starches make abdominal cramping, skin rashes, or even concentration problems improve or worsen with the offending food.  This practice becomes a problem if you are concerned with anaphylaxis (difficulty breathing, low blood pressure) to foods such as peanut, milk, or eggs to name a few.  It’s one thing to experience more abdominal bloating after a gluten challenge and a much more dangerous situation to lose consciousness after ingesting peanut. 

3.       I’m grateful to be a member of the American Academy of Allergy, Asthma, and Immunology (AAAAI) in part because they help me as an allergist to stay current of all the thousands of recommendations published every year on my specialty.   One such service is “Ask the Expert” forum and I’d like to share a recent post with you about food challenges.

Here’s the take-home message and the full answer is available if you click on the link below:

1.       Food anaphylaxis can be related to the total amount of food ingested.  In other words, don’t assume that tolerating a very small amount of peanut will guarantee that you can tolerate peanuts ad lib!  Food challenges are performed under close supervision in order to determine HOW sensitive you are. 

2.       Oral desensitization to foods is still in the research stage and the experts on treating food allergy do not recommend this procedure be performed outside of a research protocol.  It only takes one bad outcome to taint any progress made with treatment of food anaphylaxis.

Anyway, it’s lunchtime, and talking about food does make me hungry!

Oral food challenge to peanut.

Pork-Cat connection

Pork-cat syndrome a rare (but real!) allergy

By Cari Nierenberg

Allergic to cats? Then beware of pigs — or at least, the meat that comes from these sty-dwelling swine. A small number of people who are sensitive to felines may also get allergic reactions to eating pork.  Continue reading Pork-Cat connection

What’s New in Celiac Disease

 Has enough been said about the symptoms of Celiac Disease?  Better yet, does everyone have celiac disease?  If you can’t prove that you have gluten intolerance (another name for celiac disease), you might consider this collection of case studies.  And tell them I sent you!

Diagnosing Celiac Disease by Video Capsule Endoscopy (VCE) When Esophogastroduodenoscopy (EGD) and Biopsy is Unable to Provide a Diagnosis

Matthew S Chang, Moshe Rubin, Suzanne K Lewis, Peter H Green  BMC Gastroenterol. 2012;12(90) (Nov 01,2012)

Video capsule endoscopy (VCE) is mainly used to evaluate patients with celiac disease in whom their course after diagnosis has been unfavorable and the diagnosis of adenocarcinoma, lymphoma or refractory celiac disease is entertained, but it has been suggested that VCE could replace esophagogastroduodenoscopy (EGD) and biopsy under certain circumstances.
Methods: We report a single center case series of 8 patients with suspected celiac disease who were diagnosed by VCE.
Results: EGD and biopsy had been performed in 4 patients resulting in a negative biopsy, declined by 2, and contraindicated in 2 due to hemophilia and von Willebrand disease. In all patients, mucosal changes of scalloping, mucosal mosaicism and reduced folds were seen in either the duodenum or jejunum on VCE. Follow-up in 7 patients demonstrated improvement in either their serological abnormalities or their presenting clinical features on a gluten-free diet.
Conclusions:Our case series demonstrates that VCE and the visualization of the characteristic mucosal changes of villous atrophy may replace biopsy as the mode of diagnosis when EGD is either declined or contraindicated, or when duodenal biopsies are negative and there remains a high index of suspicion. Further study is needed to clarify the role and cost of diagnosing celiac disease with VCE.

Here’s my comments on this series:

1. New technology, although expensive, can really change the way we diagnose and treat disease.  This method (VCE) would bypass the need for endoscopy….what that means is no sedation and a less extensive bowel prep. 

2.  As with any new technology, results have to be confirmed in larger studies and by other research groups.  I’ll be waiting to hear about more published work.

3.  If it becomes easier to diagnose celiac disease, perhaps we can limit the number of patients who think they are intolerant to gluten but have never taken the time or money to find out conclusively. 

What do you think?  Would a video camera that you have to swallow make you more likely to find out if you really have celiac disease?

 

 

Are We Beating a Dead Horse?

Ok, another study about the dangers of food allergy (yesterday in USA Today).  You would think the occurrence of food allergy to KNOWN allergens (peanut & milk) would decrease given all the attention given to accidental ingestion.  Evidently, this is not the case.  Explanations?  Maybe we’re afraid of giving epinephrine.  In my personal experience, giving epinephrine is analogous to “waving the white flag.”  It doesn’t have to be nor should it be when treating children with suspected food allergy.  As I tell my nurses, “give the epi, then call the doctor!” 

http://www.usatoday.com/news/health/story/2012-06-25/kids-food-allergies/55797696/1

How to Cure Milk Allergy!

Milk allergy may cause life-threatening anaphylaxis in children & adults.  Wouldn’t it be nice if milk allergy could be “cured?” 

The adverse immune reactions to cow’s milk proteins can range from immediate, potentially life-threatening reactions to chronic disorders. Cow’s milk allergy (CMA) is the most common food allergy in infants and young children, affecting 2–3% of general population.  That’s a lot of kids! Most studies have shown the prognosis for developing tolerance to cow’s milk to be good, with the majority outgrowing their allergy by age 3 years. 

Because no treatments are available to cure or provide long-term remission from food allergy, allergen-specific treatments and strategies that attempt to alter the allergic response to specific food allergens are expected. The approach that attracts a significant interest in the scientific community, as well as the public and media, is oral immunotherapy (OIT).

To begin treatment for food allergy, your doctor should do the following:

  • IgE must be demonstrated to the food in question.  That means skin testing or blood tests.
  • Who wants to be cured?  That’s what desensitization accomplishes.  If you gradually increase the amount of offending food (milk powder for instance), sensitive patients will no longer react to an accidental ingestion.  Pretty cool…but wait, that’s not all!
  • Permanent tolerance, as illustrated, means are you protected from ingestion of milk when you haven’t had exposure for say 2 months?  Because it’s not known how to predict whether patients develop tolerance, this procedure of OIT is not recommended for clinical use at this time. 

Almost all children receiving oral desensitization (OIT) experienced allergic symptoms during the protocol that primarily involved urticaria and angioedema. That’s mild and treatable.

Table 1. Oral food desensitization for IgE-mediated cow’s milk allergy

Study Patients (N) Success rate Comments
Staden et al. [15], CM and egg CM 14; egg 11; control group 20; age 0.6–12.9 years 9/35 (36%) permanent tolerance; 3/25 (12%) tolerance with regular intake (desensitization); 4/25 (16%) achieved partial tolerance The first randomized clinical trial of OIT. The rate of spontaneous food allergy resolution in the control group (7/29, 35%) was similar to the treatment group.
Longo et al. [16], CM CM 60; 30 active group; 30 control group; age 5–17 years 11/30 (37%) tolerated 150 ml f CM; 13/30 (53%) tolerated 5–150 ml The first study including children with previous anaphylaxis to cow’s milk; 3 children 10% discontinued the study because of severe systemic reaction. 17/30 children of active group reported side-effects at home.
Skripak et al. [17], CM CM 20; active to placebo; ratio 2 : 1; age 6–21 years 12 (92%) of active group reached the dose 5140mg of CM (range 2540–8140 mg); no change in the placebo group The first double-blinded, placebo-controlled clinical trial for OIT; the median frequency of side-effect was 35% in the active group compared with 1% of the placebo group.
Pajno et al. [19•], CM CM 30; active to placebo; ratio 1 : 1; age 4–13 years 10 (76%) of active group tolerated 200 ml CM; no change in the placebo group The first blinded trial with the weekly up-dosing regimen carried out in 18 weeks. Two children (15%) of active group discontinued the trial because of systemic reaction.

Legend for the above table:  CM, cow’s milk; OIT, oral immunotherapy.

Desensitization state can be achieved by approximately 36–92% of the children treated with specific immunotherapy; the rate of permanent tolerance is unknown.

An alternative route of allergen delivery is through an epicutaneous patch (EPIT). CMA was confirmed by an oral food challenge at baseline. Children received three 48-h applications (1mg of skimmed milk powder or 1mg of glucose as placebo) through a skin patch each week for 3 months. EPIT-treated children had a trend toward an increased threshold dose in the follow-up oral milk challenge. There was no change in the placebo group. The most common side-effects were local pruritus and eczema at the site of EPIT application.

The possibility of the appearance of adverse events or reactions during OIT is quite frequent. Side-effects have been reported by patients in all trials.

Severe systemic side-effects have been reported with either rush schedule or weekly up-dosing regimen.  The frequency of serious events and the severity of reactions are greatest on the initial days and least on the days following desensitization when high doses of cow’s milk intake are reached by patients.

Mild reactions such as abdominal pain, throat pruritus, gritty eyes, watery eyes, transient erythema and sneezing usually do not require stopping desensitization. On the contrary, when rhinitis, dyspnea, asthma, generalized urticaria and hypotension occur as a single symptom or in combination, OIT should be postponed or stopped.

A life-threatening asthma reaction caused by desensitization to milk was described by Nieto et al.  Adverse events are largely unpredictable, and they can occur during home dosing. Several systemic reactions have occurred at previously tolerated doses in the setting of exercise,viral illness and suboptimally controlled asthma.

Of note, these reactions had been well controlled by antihistamines, steroids or epinephrine. Because desensitization( s) place patients at risk for systemic reactions, it is not appropriate to implement OIT in clinical practice settings at this time. Therefore, OIT can be performed for research purposes or as ‘avant-garde’ and modern therapy for IgE-mediated food allergy in specialized pediatric centers.

  • Patriarca G, Nucera E, Roncallo C,et al. Oral desensitizing treatment in food allergy: clinical and immunological results. Aliment Pharmacol Ther 2003; 17:459–465.
  • Nieto A, Fernandez-Silveira L, Mazon A, Caballero L. Life-threatening asthma reaction caused by desensitization to milk. Allergy 2010; 65:1342–1343.