We all want to be realllllly healthy and it makes sense that what we eat is a place to start. Right? Well not so fast. Jenny (isn’t her real name to protect the innocent) went to her health club to lose some weight and get into shape. Jenny had always struggled with being overweight and was even laughed at in grade school because she was plump. (not funny if you’re one of those kids) Continue reading The Problem with Foods–foods that make me want to throw up
It’s nice to have resources like this when you (the kids) need the resources!
Originally posted on gutsandgrowth:
From my colleague, Jeff Lewis: “The camp is called Camp Weekaneatit, it is July 13 to July 18, overnight camp, strictly gluten-free so the kids can eat what they want without having to worry. Its part of Camp Twin Lakes – an organization that hosts tons of medical camps. We have kids from all over – as far away as California the last two years. Scholarships are available.”
Anyone who tries to follow a strict gluten-free diet knows how difficult it can be to take a trip outside the home. This camp lets kids enjoy camp without the worry about the next meal or snack. Spread the word!
Originally posted on 123MyMD:
Seafood allergy is a major problem because as it worsens in someone’s life, the seafood allergy, actually, can become a problem that can be even life-threatening. Now, initially, people who have problems with seafood, actually, suffer difficulties which are more like stomach irritation, diarrhea, vomiting. But as the seafood allergy worsens, and as the symptoms start to get worse, what invariable happens is people start to have hives and even anaphylactic reactions.
We always appreciate your comments and suggestions. For more information, please go to http://www.123MyMD.com.
Food allergy is a constant source of anxiety to parents of children who could in fact die or suffer a severe reaction to foods. Believe it or not, the government has done a nice job with information pertaining to public safety, in this case, food allergy in schools. In case you think I’m kidding about the severity of food allergy, the YouTube link below should change your mind. The second link from the CDC is the “official word” on food allergy in schools.
Always be careful when you didn’t make the food!
Originally posted on WhyRiskIt? Teen Allergy Blog:
With allergies, comes decision-making; should I eat this, should I go there, should I risk it? You need to remember to always do what is right for you! You know what situations may be dangerous for you and need to do what is best for your health and safety.
With the holidays quickly approaching, potlucks are upon us. Trusting other people with food allergies can often be a tricky thing to do. Last year I had a negative experience with a school potluck that is making me reconsider my decision to attend this year. Everyone was informed of the allergens that were not to be brought to the potluck, but people forgot and they were present. I was not comfortable eating any of the food and left the room, as there was food on most surfaces.
It was upsetting as I had been looking forward to the Christmas party and…
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This question comes up in my office almost everyday….should I do skin testing or blood work? As you can see from the response of national experts, it depends. There is NO test that can boast 100% accuracy to predict whether or not you will react to a food. In fact, the gold standard if you will, is still the oral food challenge. Here is some food for thought (really, do you have to pun)
- Clinical history is very important in determining food allergy. If you can eat a food without difficulty breathing, rash, or hives, you are most likely not allergic. You may have a positive test, but that only means you’ve had previous exposure to the food.
- I will often obtain both skin testing and ImmunoCap (blood work) to clarify the presence of IgE-mediated allergy. If both tests are negative, you may have an adverse reaction to a food, not the severe life-threatening anaphylaxis. Very important distinction!
- If in doubt, a food challenge is always a procedure to consider. Here’s why.
- Sometimes the food in question just isn’t worth the trouble to challenge. No one says you have to eat strawberries!
- If you challenge peanuts for example, in the doctor’s office and experience anaphylaxis, better there than at home. Epinephrine is more readily available and in many cases, IV access and full resuscitation is available within minutes of your reaction.
- This is another reason why a single test or treating allergy without experience is not a good idea. Read the link below and tell me just how complicated things can become!
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.
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 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.
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 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 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.
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:
- 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.
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?
Originally posted on food allergy empowerment:
I had great hope for Oral Immunotherapy to solve the emerging epidemic of Food Allergies until I started reading the research articles. This therapy isn’t a cure. It is dangerous and difficult to go through and difficult to maintain. It is similar to a pirate of the eighteenth century building up their tolerance to a poison by consuming small doses of it over time.
I believe, that we need to be looking for a cure some place else; let’s look to the cause.
How can an emerging epidemic be considered 70% genetic? How can a parent or grandparent’s smoking habit be a possible cause for a child’s food allergy, even when the child was never exposed to the smoke? Epigenitcs.
Our epigemone is the condition and regulation under which our genome functions. Through proteins and methylation groups, these conditions and regulations can be passed down to future generations.
In other words, If the genome (our DNA) is the piano, then the epigenome is the piano…
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