Allergy & Asthma Disease Management Center: Ask the Expert: Food Allergy

- Food Allergy -

12/13/2005 RE: Peanut oil induction of peanut sensitivity

I recently received a call from a pregnant female who has been prescribed a progestin agent containing peanut oil. She has one son who is peanut allergic. She has asked the question should she avoid the peanut oil containing pregestin agent for fear that this will put her fetus at risk for sensitization. As I was taught, the IgE antobody does not cross the placenta. Is there are risk for this agent increasing the risk for sensitization.? Is there felt to be any food consumed during pregnancy that increases the risk of sensitization of the infant? I am aware that breast feeding can pose a risk.

To respond to your question, I obtained input from Dr. Robert Zeiger of the Kaiser Permanente Medical Group in San Diego. Dr. Zeiger is an expert in food allergy including the effects on the child of foods eaten by the mother during the previous pregnancy (see enclosed abstract of one of Dr. Zeiger's recent publications in this area of study). Also enclosed is an abstract of a report in this area by many food allergy experts, including Dr. Zeiger. Dr. Zeiger's prompt and informative response is enclosed just below.

Dr. Zeiger's comments:

The role of fetal exposure to peanut protein during gestation to the subsequent development or not of peanut sensitization or peanut allergy is unknown. Recommendations of peanut avoidance by mother during pregnancy is not yet based on good evidence and some data is appearing that suggests that it might have no demonstrable effect and in addition successful peanut avoidance has been very difficult to maintain. With respect to peanut oils in progestin within the U.S. one could be confident that the oil is highly refined. Studies have documented that ingestion of refined peanut oil is unlikely to induce symptoms in peanut allergic patients. As such, progestin, if indicated, should not be avoided for the fear of inducing peanut allergy.

J Allergy Clin Immunol. 2005 Jun;115(6):1238-48. Related Articles, Links
The role of breast-feeding in the development of allergies and asthma.
Friedman NJ, Zeiger RS.
Southern California Permanente Medical Group, 7060 Clairemont Mesa Boulevard, San Diego, CA 92111, USA.
Breast-feeding is the preferred method of infant nutrition for numerous reasons. However, its role in the prevention of allergic disease remains controversial. Reasons for this controversy include methodological differences and flaws in the studies performed to date, the immunologic complexity of breast milk itself and, possibly, genetic differences among patients that would affect whether breast-feeding is protective against the development of allergies or is in fact sensitizing. The preponderance of evidence does suggest, however, that there would be much to lose by not recommending breast-feeding. In general, studies reveal that infants fed formulas of intact cow's milk or soy protein compared with breast milk have a higher incidence of atopic dermatitis and wheezing illnesses in early childhood. Consistent with these findings, exclusive breast-feeding should be encouraged for at least 4 to 6 months in infants at both high and low risk of atopy and irrespective of a history of maternal asthma.

Pediatr Allergy Immunol. 2004 Aug;15(4):291-307. Related Articles, Links
Dietary prevention of allergic diseases in infants and small children. Part III: Critical review of published peer-reviewed observational and interventional studies and final recommendations.
Muraro A, Dreborg S, Halken S, Host A, Niggemann B, Aalberse R, Arshad SH, Berg Av A, Carlsen KH, Duschen K, Eigenmann P, Hill D, Jones C, Mellon M, Oldeus G, Oranje A, Pascual C, Prescott S, Sampson
H, Svartengren M, Vandenplas Y, Wahn U, Warner JA, Warner JO, Wickman M, Zeiger RS.
Department of Pediatrics, University of Padua, Padua, Italy.

The role of primary prevention of allergic diseases has been a matter of debate for the last 40 years. In order to shed some light on this issue, a group of experts of the Section of Pediatrics EAACI reviewed critically the existing literature on the subject. An analysis of published peer-reviewed observational and interventional studies was performed following the statements of evidence as defined by WHO. The results of the analysis indicate that breastfeeding is highly recommended for all infants irrespective of atopic heredity. A dietary regimen is unequivocally effective in the prevention of allergic diseases in high-risk children. In these patients breastfeeding combined with avoidance of solid food and cow's milk for at least 4-6 months is the most effective preventive regimen. In the absence of breast milk, formulas with documented reduced allergenicity for at least 4-6 months should be used.

12/1/05 re: Giardia , IgE and allergies

My patient, male, 32, chronic patient of year round rhinitis had IgE 1238 IU and Eosinophil 545 with Giardia cysts in his stool. Rest of the tests were normal. He also suffers from unusual type of so-called brain fatigue during teaching sessions. The fatigue remained so severe that he had to quit his teaching job. Treatment with Effexor(SSRI-anti depressant) has shown some improvement in his mental, unusual fatigue. I treated him with Metronidazole 400 mg, Diloxanide furoate 500mg thrice a day for 13 days, than waited for one month and repeated blood test. This time his IgE is 528 and Eosinophil is 400 showing significant drop for these two. Stool test is negative, so far, for Giardia. But he has not shown any improvement in his year round allergy(rhinitis with occasional eczema) and so called brain fatigue. My questions are:
a) Why reduction in IgE and Eosinophils did not reduce his allergy?
b) Will repeating Metronidazole/Diloxanide furoate result in further reduction of IgE and Eosinophils. Is it worth repeating?
c) Is there any link between Extreme, unusual form of mental fatigue and IgE/Eosinophil? In my opinion there may be because the patient does not have psychological stresses in his life. His unusual brain fatigue seem to be Endogenous rather than exogenous.
d) Can Mastocytosis be suspected in this case?

Although infection with Giardia involves mainly the G-I tract, products released from large number of such parasites in the G-I tract can stimulate both production of IgE and eosinophilia (see enclosed abstract). Therefore, these findings may not be directly related to the presence of typical IgE-mediated allergies. Indeed, there is debate whether there is an increased incidence of respiratory or food allergies in individuals heavily parasitized. Some groups report a somewhat greater anti-food IgE antibody levels (see enclosed abstract) However, studies from east Africa have suggested a lower incidence of allergies and asthma in children with heavy G-I parasitic infestation. A single study (from South America) of which I am aware found that the incidence of allergies/asthma actually increased in children after they were cleansed of parasites by extensive pharmacotherapy. Therefore, to answer your questions:

1) Reduction of the IgE and eosinophil levels may be due to less stimulation by reduced numbers of Giardia after your treatment but not related to allergies to inhalants and/or foods.
2) Further pharmacotherapy for Giardia should depend on the current studies for the frequency of Giardia organisms in the G-I tract, not on the IgE or eosinophil levels.
3) At very high eosinophil levels, one could have central nervous system manifestations, likely due to local toxic effects of the very cationic components of eosinophils such as eosinophil-derived neurotoxin . However, the eosinophil levels in your patient are not that elevated,-not nearly as high as reported in those hypereosinophilia syndrome patients.
4) Systemic mastocytosis (SM) can cause CNS symptoms. Eosinophilia is common in SM but not increased serum IgE levels. A good screening test for SM would be to measure the total tryptase level in the serum. In about 80% of those with SM and systemic symptoms, the serum tryptase level is over 20. Further investigation would involve biopsy of the bone marrow and ant suspicious skin lesions, with special staining (including immunostaining for tryptase, if available) looking for clumps of mast cells.

Arch Med Res. 1994 Summer;25(2):171-7. Related Articles, Links
Evaluation of the immune response in symptomatic and asymptomatic human giardiasis.
Perez O, Lastre M, Bandera F, Diaz M, Domenech I, Fagundo R, Torres D, Finlay C, Campa C, Sierra G.
Finlay Institute, Havana, Cuba.

To better understand the common association of Giardia lamblia infection and allergic reactivity, total and specific IgE values were evaluated and different manifestations of symptomatic and asymptomatic infected human hosts were analyzed. The humoral, cellular, and nonspecific immune responses were evaluated in Cuban adults. Increased total serum IgE levels were significantly higher (p < 0.01) in Giardia patients than in negative controls; cure of giardiasis was characterized by a decrease in IgE levels and some patients regained normal IgE values. The skin test was positive in 91% (103/123) of chronic patients and only in 23% (20/123) of negative controls (p < 0.05). A positive test was seen in patients with antecedents of recent giardiasis (< 4 months). Specific IgE was higher in patients than in control sera, and in the former it decreased with sera dilution. During the follow-up period of cured patients, the proportion of IgE decreased and the opposite occurred in noncured patients. The cellular response evaluated by LIF was positive in 92% (11/12) of carriers and significantly higher (p < 0.05) than in symptomatic patients 8% (1/12); the same occurred with IgG and IgA antibody response; titers mainly of IgA were higher in asymptomatic carriers than in patients; all carriers were negative to the skin test. These results indicate the presence of total and specific IgE responses in humans infected with Giardia, but the response in symptomatic cases (patients) is different from that in asymptomatic cases (carriers).

Ann Allergy Asthma Immunol. 1998 Sep;81(3):261-5.
Association between giardiasis and allergy.
Di Prisco MC, Hagel I, Lynch NR, Jimenez JC, Rojas R, Gil M, Mata E.
Institute of Biomedicine, Central University of Venezuela, Caracas.

BACKGROUND: Previous studies have indicated that there may be an association between infection by the intestinal protozoan Giardia lamblia and the expression of allergic disease.
OBJECT: We evaluated a group of children who attended the Outpatient Clinic of the Children's Hospital in Caracas, Venezuela, a group in which both allergic disease and giardiasis were common.
METHODS: We performed feces examination and measured total and specific serum IgE (immunoglobulin E) in these children.
RESULTS: We found that 70% of the children infected with G. lamblia presented symptoms of allergy, in contrast to 43% of the non-Giardia parasitized group (P <.05). In addition, the G. lamblia parasitized children showed significantly higher levels of total serum IgE (1194 IU/mL) than the non-Giardia group (822 IU/mL) (P <.005). Children infected with G. lamblia showed higher levels of specific serum IgE antibody against food allergens compared both with the non-parasitized group (P <.0001) and children infected with parasites other than Giardia (P<.05). In contrast, IgE responses against the house dust mite Dermatophagoides pteronyssinus were similar in all the groups studied.
CONCLUSIONS: These results reveal a clear relationship between giardiasis and allergy, possibly because infection by this protozoon enhances sensitization towards food antigens, due to increased antigen penetration through damaged intestinal mucosa

11/16/05 re: Allergic reaction cause of episodes

I have a 41 YO male military officer present with tachycardia and elevated blood pressure. Patient arrived in Germany in March 2005 with no previous symptomology. The patient describes mild chest pain or discomfort. The patient has experienced 8-9 episodes where he has developed progressive fatigue and profound malaise in addition to a warm sensation in his chest that will radiate towards his head. After the onset of symptoms during his initial episode, he presented for evaluation to a German hospital where he was noted to be markedly hypertensive (174/112) on presentation in addition to tachycardia. No acute ischemic changes were noted on his ECG. He was admitted for observation, and his symptoms and vitals gradually improved during the period of observation. Additional testing included serial cardiac enzymes which were negative for evidence of ischemia, normal CRP and TSH. An echocardiogram was noted to be normal. His symptoms eventually attributed to a GI etiology, and he was treated with increased doses of rabelprazole. Since that time, he has experienced similar episodes on 8 additional occasions. When evaluated, he has demonstrated significant hypertension and tachycardia without other evidence of ischemia. In retrospect, the patient describes moderate ingestion of wine/beer on all of the occasions within 24 hours of the onset of symptoms, but recall one episode that was not related to Etoh ingestion. On other occasions, he has been able to drink wine or beer without problems. Otherwise, the patient has no prior history of cardiac disease or prior cardiac evaluation. He has been in general good health. Current medications: Lisinopril, Zocor, Rabeprazole, Aciphex. Conducted normal stress test with noted resting tachycardia with accelerated heart rate. CBC/DIFF, Metabolic panel, T4 Free, Thyrotropin, urinalysis, 24 hr urinalysis - all labs normal. Echo - normal. LSL Allergy consult results: SKT pos to mite, pollen, hazelnut, hops. Recommended additional tests and Tx.

I assume that you have raised the question of an allergic reaction cause of the episodes described because several of such episodes followed wine ingestion. Ingestion of non-intoxicating quantities of wine occasionally causes acute reactions which are not truly allergic.

1) In one type of reaction, sulfites present as a preservative in some wine causes acute respiratory symptoms (generally wheezing and/or coughing) due to the sulfur dioxide released by metabolism of the ingested sulfites. Such reactions are more common in those with underlying asthma. Hypertension is very unusual in such reactions.
2) Some wines contain amines which can cause vascular reactions. These are generally limited to individuals taking monoamine oxidase inhibitor therapy so that amines are not catabolized in the usual manner.

I think that both these types of reaction are unlikely as the cause of the symptoms in your patient you described. This does also not sound like an allergic reaction to grape components.The first thought that came to my mind when reading the description you sent was that a pheochromocytoma should be looked for. I did not see any lab studies suggesting such an investigation. Intermittent, pronounced hypertension with tachycardia is commonly seen in pheochromocytoma.

11/8/05 re: Tolerance of pecan pollen allergic to pecan nuts

I have a patient who has positive allergen specific IgE to pecan tree pollen. Will this patient react to pecan nuts if ingested?

I have had no personal experience with pecan pollen allergy since that type of tree is not grown in our geographic area. I could not find any reference to pecan nut tolerance or not in a few reports about pecan pollen allergy I found in a Medline search. Therefore, I obtained input from a colleague in one of the academic hospitals in Israel, a country where pecan trees are common and pecan pollen allergy has been reported. His response is enclosed below. It sounds as if there should be no allergic reaction to pecan nut in your patient. Nevertheless, it may be prudent for the patient to start any pecan nut ingestion with a very small amount and then increase the amount ingested gradually, as tolerated.

We do have patients with pecan pollen allergy. In few clinics they even use immunotherapy with pecan extracts. Those who are sensitive to pecan pollens are not allergic to the nuts. The same applies to olives.

11/4/05 re: Lactic acid ingestion in a milk sensitive person

I had a patient ask about lactic acid which was listed in the ingredient list of a margarine. She is wondering if her child who has a milk allergy needs to avoid lactic acid.

The milk components that cause allergic reactions are proteins (e.g., lactalbumins, casein - see enclosed abstract). Lactic acid is not a protein but a natural, low molecular weight compound released in anerobic metabolism in our bodies. Indeed, excessive lactic acid release in the muscles may be a partial cause of the muscle cramps that occur in some people after sudden vigorous exercise, particular in those not used to such exercise. Therefore, one would not expect an allergic reaction in a milk-sensitive person to lactic acid present as a food component.

Ann Allergy Asthma Immunol. 2002 Dec;89(6 Suppl 1):3-10.
Cow's milk proteins/allergens.
Wal JM.
Laboratoire d'Immuno-Allergie Alimentaire, Service de Pharmacologie et d'Immunologie, INRA-CEA, CEA de Saclay, Gif sur Yvette, France.

OBJECTIVE: The primary objective of this review is to provide updated data on the structure and function of the main cow's milk proteins (CMPs) identified as allergens and on the characterization of their epitopes. DATA SOURCES: The review represents a synthesis of basic literature and most relevant original recent publications on both topics of clinical and epidemiologic aspects of milk allergy and of milk protein's bio- and immunochemistry. STUDY SELECTION: The expert opinion of the author was used to select the relevant data for the review. RESULTS: Most CMPs are potential allergens, even the proteins present at very low concentration. There are both conformational and linear epitopes, widely spread all along the protein molecules. They may be short fragments, located in hydrophobic parts of the molecule which comprise highly conserved sequences responsible for immunoglobulin E cross-reactivity with corresponding milk proteins of other mammals, including human beings. Those sequential epitopes have also been proposed as good markers of persistent allergy to CMPs.
CONCLUSIONS: No specific structure nor function is associated with allergenicity of CMPs. Variability and heterogeneity of the human immunoglobulin E response preclude anticipating the allergenic potential of any CMP or fragment thereof, as well as justify the need for being careful before using peptides for desensitization or proposing any milk protein hydrolysate in a diet for highly allergenic children.

11/3/05 re: Food allergy and move to China

I am an allergist in MD and have looked at many of the FAQs on the AAAAI site, but couldn't find mine. My patient is an 18 month old girl with significant eczema and positive skin and CAP RAST for milk, egg and peanut. She has also been dropping off of her growth curve since age 15 months. I discussed food avoidance and pediatric dietitians with the mom, but the punchline is that the family is moving to China in July, 2006 and her parents are concerned about the food allergies while overseas. There have not been any �anaphylactic' reactions to the foods, but I gave the parents an Epi-pen Jr because the child has �turned red' after eating eggs once.

So, basically the question is simple, but there's a twist. How do you manage something like this in a country like China, where peanuts and sesame are ubiquitous, they don't speak the language and peanut allergy is not as common?

To help respond to your questions, I obtained input from Dr. Scott Sicherer of the Mt Sinai School of Medicine in New York. As you likely know, Dr. Sicherer and his colleagues are leading experts in food allergy-related matters. His detailed response is enclosed below.

Dr. Isenberg-Feig presents an 18 month old who has atopic dermatitis, poor growth and likely allergy to egg, milk and peanut who will be moving to China in 9 months time from the inquiry. While the query ends with a question of management of food allergy in China, I would focus first upon the 9 months opportunity to secure a diagnosis and management plan while simultaneously using this time for making contact in China regarding treatment plans there. Obviously, I do not have details of this child's full history, and I cannot and would not propose a diagnosis or treatment plan via the internet, but I have posed general comments that may or may not be applicable to this child.

When a child is not growing well, has atopic dermatitis (AD) and food allergy, a comprehensive approach is needed to identify the reasons and reverse the rash and growth problems. It is known that children with significant AD and a food allergy frequently have some degree of malabsorption if food allergens remain in the diet. A series of possibilities must simultaneously be addressed. Is the child consuming enough calories (calorie count/diet record review/dietitian consultation)? Is the child using too many calories (severe AD) and needs better skin care/diet alteration to remove unidentified allergens and reduce caloric needs used to replace skin and fight skin infection (topical medications/antibiotics/etc)? Is the child experiencing evident gastrointestinal symptoms (malabsorption/GI consultation)? Are there residual food allergens in the current diet that need to be identified (e.g., egg/milk contamination, etc) and removed (careful diet review/consideration of other possible allergens/elimination/challenge/more testing)? Is there a problem that has not been diagnosed (Celiac/immunodeficiency/etc)? Before going off to China it would be important to have the weight on track by securing the diagnoses, having a treatment plan underway, and a safe diet knowing exactly what foods are or are not safe in the diet. It is possible that a �complete� hypoallergenic formula is needed.

Assuming things are more on track nearing the time for travel, there are many things to have in place that can be approached starting now. In regard to general medical care, ability to obtain safe foods, treat acute reactions, etc., each of these issues should be addressed in advance. It is hard to imagine that the family plans to place themselves in an area and situation where they have absolutely no means of communication at all, no way to talk to people about foods, no way to speak to health care providers, no translation, no access to health care, etc.. (I have patients who live in Asia, have multiple food allergies, and continue to visit with me yearly for specific food allergy evaluations and they are doing well but do have contacts with English-speaking providers in China ). If it were truly the case that they were essentially "stranded" with no means of communication/translation it does not seem like it would be possible to live safely and comfortably (even apart from food allergy). Assuming they can communicate with those around them, various issues of preparation are still needed to ensure a safe environment and continue care.

As you know, allergies to certain foods are likely to resolve, and so repeated assessments will be needed and the family should find a source for this (or plan to return to see you for this re-evaluation). More important in the short run, they need to ensure availability of anaphylaxis care, and being able to discuss the ingredients of foods. Preparation for anaphylaxis can be headed off with prescriptions of self injectable epinephrine, antihistamines, and maybe oral steroids all top have on hand from the US (especially because they are traveling. In regard to acquiring foods, once the diet is known, the general approach would be to obtain simple foods prepared simply. If the child is on a formula, it may be possible to identify a similar one, or ship from the US (well in advance of need). Obviously, some ability to communicate with persons who provide the foods is needed. The Food Allergy & Anaphylaxis Network (FAAN; 800-929-4040; www.foodallergy.org ) has a book about travel with food allergy. Similar to children in the US with multiple food allergies, it may be necessary to make foods fresh and items (restaurants where you cannot communicate about ingredients and issues of cross-contact).

Of course, egg, milk, peanut, seeds and fish are common in the diet in Asia, but so too are they common in the US, in both countries possibly as "hidden" ingredients, and so education about avoidance in various locations and circumstances (airline travel, hotels, restaurants, day care, etc) is imperative for here and abroad, as is a review of anaphylaxis care. The family apparently cannot read any ingredient labels in China, and they may not be accurate; again, fresh simple ingredients prepared simply would be needed (though certainly this is more work). As an aside, though peanut allergy is less common in China, and theories for this observation include less overall allergy in China and use of boiled/fried peanut, if this child has a peanut allergy I would NOT allow them any peanut product in China no matter how they are prepared. I will not attempt to review all of the details of the issues that should be discussed, but numerous materials on these topics are available through FAAN.

10/14/05 re: Thermal stability of bean allergens

I have a patient with anaphylaxis associated with raw beans. Will cooked beans denature the allergenic proteins akin to fresh fruit being cooked?

You did not specify which bean type was involved in your case. I am using soybeans as an example because it is likely the most frequent bean allergen causing clinical reactions and has therefore been studied most extensively. The current evidence is that the major soybean allergens are thermo-stable and would therefore likely persist in most products containing cooked beans. This contrasts with the tree pollinosis-associated thermo-unstable food allergens in the Bet v1 family thought to cause the oral allergy syndrome but infrequently cause systemic reactions (see abstract of a recent review article enclosed below).

Biotechnol Adv. 2005 Sep;23(6):395-9. Related Articles, Links
Plant food allergens--structural and functional aspects of allergenicity.
Breiteneder H, Clare Mills EN.
Department of Pathopysiology, Medical University of Vienna,
AKH-EBO-3Q, Waehringer Guertel 18-20, 1090, Vienna, Austria.

The three dominating plant food allergen groups belong to the prolamin and cupin superfamilies and to the family 10 of pathogenesis-related proteins. The prolamin superfamily comprises allergenic 2S albumins, nonspecific lipid transfer proteins and cereal alpha-amylase/trypsin inhibitors. These allergens have related structures and are stable to thermal processing and proteolysis. The cupin superfamily comprises the allergenic 7S and 11S globulin storage proteins from peanuts, soybean and tree nuts which are heat stable and can form immunogenicity enhancing aggregates. The Bet v 1 family of allergens includes tree pollinosis-associated food allergens with low stability which induce the symptoms of the oral allergy syndrome

10/6/05 re: Prevention of transfer of peanut allergen

I am a pediatric emergency medicine physician. My children's elementary school has a few severely peanut allergic children. As a result, the school has banned all peanut products, and is now requiring all 1st and 2nd grade children to dip their hands in a bucket of warm soapy water between snack/lunch and going out onto the playground, in an effort to be sure no peanut residue will be on playground equipment. The children are not actually washing their hands - they are merely dipping them into a bucket. Since only 2 buckets are prepared for 200 children, I am concerned about the hygiene involved, and the risk of transmitting infectious diseases. Do you know of any scientific evidence to show that dipping your hands into soapy water (and air drying, not wiping them off with a towel) effectively removes peanut allergen? If a child ate some contraband peanuts and did not dip his/her hands, what is the likelihood of sufficient peanut residue to cause an anaphylactic reaction in a severely allergic child being transmitted via playground equipment? Are there any studies that address these issues?

If the school insists on this policy, a group of parent/health professionals planned to suggest individual wipes (although this will be expensive and create a lot of trash each day). I know from the Johns Hopkins study that running water alone or alcohol based antibacterial rubs don't seem to remove allergen.

To respond to your questions, I referred them to Dr. Scott Sicherer of the Mt. Sinai School of Medicine in New York . Dr. Sicherer is one of the leading experts in food allergy in the world, with a particular interest and experience in peanut allergy. His very rapid, detailed and thoughtful response is enclosed below.

The scenario and questions posed by Dr. Young raise a variety of questions about how best to manage food allergy in the school setting. The issue at hand, no pun intended, is about hand cleaning. Dr. Young is aware of a study from Johns Hopkins (J Allergy Clin Immunol. 2004 May;113(5):973-6.) that assessed the presence of peanut allergen in school settings and also evaluated various methods of hand washing and table cleaning in regard to removal of peanut allergen. Indeed, dipping hands in a bucket of water was not tested. Although the study identified a variety of useful means to clean hands purposely contaminated with a teaspoon of peanut butter (e.g., washing with soap and water or commercial wipes worked but water alone or hand sanitizer did not) it should be appreciated that this was a study of adult volunteers, not schoolchildren. Without performing an actual study, it is difficult to comment on the efficiency of dipping hands in a bucket; again, no one has studied the efficiency of hand washing in the usual way for young children. For that matter, we do not know how efficient small children are at cleaning hands by any means. I would share Dr. Young's concern that the untested modality suggested, a dip bucket, would likely pose additional concerns. Aside from the issue of having 200 children dip hands in a bucket leading to spreading bacteria (without towels I can envision children licking the water from their hands!), has the school considered that they already banned peanut and it may be likely that the egg, milk, soy, fish and wheat allergens on the children's hands would now be in the bucket and find their way to children who may have those allergies?

The original question and my counter-example of an allergen-contaminated bucket of water must also be considered in the context of what is needed in a particular school, for a particular child or children. There are many solutions and procedures to providing a safe school environment and some actions may vary depending upon the children's ages and behaviors, type of supervision at a school, types of allergies, child's temperament, etc.

The additional question is about food being transferred on playground equipment and causing anaphylaxis. I am not aware of specific studies on this subject (and it is not likely that any study could 100% rule out the possibility). However, we took 30 highly peanut allergic children and had them sniff peanut butter for 10 minutes and rubbed a pea sized amount of peanut butter on their skin (J Allergy Clin Immunol. 2003 Jul;112(1):180-2). None reacted to sniffing peanut (an oily substance-the story would likely be different for peanut flour) and only a third had localized skin symptoms, at the touch site only, during the peanut touch. These data, combined with the general experiences of allergist who perform allergy skin tested to peanut and do not routinely cause anaphylaxis from that procedure, would argue that casual skin exposure to peanut butter (excluding intimate kissing), is not likely to cause a severe reaction (again, it is hard for a study to provide a 100% guarantee that this is not an issue for someone). However, it is fairly clear that even a small amount ingested can induce a severe reaction so the question becomes: will the food be transferred into the mouth? Thus, emphasis in schools has been for strict no food sharing (also no utensil sharing or straws, etc) and age-appropriate additional avoidance measures (allergen free-tables, routine cleaning, etc as deemed appropriate). Perhaps cleaning a young, peanut-allergic child's hands and encouraging the child not to lick fingers is another solution (also not studied).

In regard to expected symptoms from touching the food, my bias is that it depends upon the intactness of the skin (e.g., atopic dermatitis) and amount of exposure. For example, small exposures to the eye may lead to significant eye swelling (in our study mentioned above we rubbed intact skin with peanut butter, not the eye). In this regard, food allergens other than peanut, milk for example, may be more likely to splash and cause problems. I would suppose that pollen allergens significantly outweigh food allergens as an issue of concern in regard to casual exposures causing allergic symptoms in a playground setting. In the pollen season I advise my patients who are playing outside to keep their hands out of their eyes and face and wash upon arrival at home.

There are many suggestions available for managing food allergy at school, child care, camps etc, in programs from the Food Allergy and Anaphylaxis Network (www.foodallergy.org). Avoidance is only one component of a complete food allergy care plan. I may also suggest a book that was just released �The complete peanut allergy handbook� (Berkley Health, $6.99) but I wrote that book so I have to declare a potential conflict of interest in discussion expressed in the book (though I receive no payment for the book so there is no financial conflict of interest). In that book I review, for the lay reader, the various data about this (in more detail) and other peanut allergy issues.

10/5/05 re: Cross-reactivity between tomato and grass allergens

We have, surprisingly, a young female adult who appears to be genuinely extremely allergic to tomatoes, lettuce and a variety of fruits. Skin prick tests to tomato induced a 10mm wheal and she recently developed anaphylaxis when a slice of tomato used as a garnish was placed on her plate and then removed before she ate an omelet (she usually eats egg products without problems). I've seen some reports that suggest that particularly soft fruit allergy (oral allergy syndrome) may be reduced by immunotherapy to birch pollen. She has a strongly positive skin prick reaction to grass and a minor response to tree pollen. Would immunotherapy with grass or tree pollen offer some chance of ameliorating this lady's symptoms.

Some earlier studies suggested allergenic cross-reactivity between tomato (and certain other foods) and grasses. This is reviewed in an enclosed abstract. However, more recent studies have suggested that the major cross-reactivity of tomato allergens with those of pollens is related to the profilins a shared group of proteins which bind to actin (see enclosed abstracts). Such profilins are most prominently present in birch pollen (Bet v1 and Bet v2). I have seen some evidence suggesting cross-reactivity of fruits in the family containing tomato with those in Bermuda grass (unrelated to northern grasses), but not with bluegrass, a major ornamental grass in temperate zones. In reviewing such published information, one must be careful to determine what evidence the authors use for the presence of cross-reactivity. For example, it has been shown that homology of linear amino acid sequences is by itself not sufficient evidence of allergenic similarity of fruit vs pollen proteins because allergenic properties may depend on particular tertiary (3-dimensional) structure characteristics. Obviously, the most convincing evidence comes from blinded challenges of the patient with the food and the pollen in question. However, most of the biochemical/molecular biology studies of cross-reactivity I have seen do not include such challenge information. Therefore, my opinion would be that avoidance is still the best approach here. One cannot count on grass extract immunotherapy to reduce the tomato sensitivity in your patient. Of course, if the patient has sufficient grass pollen-induced respiratory symptoms, one could try grass immunotherapy for that indication. If there is a significant reduction in those seasonal respiratory symptoms, one could then try a very cautious tomato challenge starting with minute amounts of tomato under careful observation and with written informed consent obtained in advance.

I have assumed from your lack of mentioning it that the patient is not clinically sensitive to birch pollen. If there is evidence suggesting such sensitivity, one should consider prick testing with birch extract and considering birch immunotherapy.

J Investig Allergol Clin Immunol. 1998 Jan-Feb;8(1):6-16.
Related Articles, Links
Association between pollen hypersensitivity and edible vegetable allergy: a review.
Caballero T, Martin-Esteban M.
Immunoallergy Laboratory, La Paz Children's Hospital, Madrid, Spain.

Over the last three decades several authors have described the existence of an association between sensitivity to different pollens and sensitivity to diverse edible vegetables. An association between ragweed pollinosis and hypersensitivity to Cucurbitaceae vegetables (e.g., watermelon, melon, cucumber) and banana has been reported. Other authors have found a relationship between birch pollinosis and sensitization to hazelnut, apple, carrot, potato, kiwi and other vegetables. Additionally, several papers have shown the association between mugwort pollinosis and sensitization to celery, carrot, spices, nuts, mustard and Leguminoseae vegetables. Later, some studies showed association between grass pollinosis and sensitization to tomato, potato, green- pea, peanut, watermelon, melon, apple, orange and kiwi. Finally, an association between sensitization to plantain pollen and melon hypersensitivity was also described. The association between pollinosis and edible vegetable sensitization has been explained by the combination of different hypotheses, such as the following: 1) presence of lectins in edible vegetables; 2) existence of IgE to carbohydrates of the glycoprotein's (cross-reactive carbohydrate determinants); and, 3) existence of common allergens between pollens and edible vegetables. Up to now three allergens have been identified as responsible for cross-reactivity in these associations: profilin, a 14 kd protein that regulates actin; Bet v 1, the 18 kd birch pollen allergen; and a 60-69 kd allergen. It is important to study in depth these associated sensitizations and the common allergens responsible for them in order to improve diagnostic methods and treatment of these syndromes

Allergy. 2004 May;59(5):526-32. Related Articles, Links
Tomato profilin Lyc e 1: IgE cross-reactivity and allergenic potency.
Westphal S, Kempf W, Foetisch K, Retzek M, Vieths S, Scheurer S.
Department of Allergology, Paul-Ehrlich-Institut, Langen, Germany.

BACKGROUND: To date, very little data are available about the nature of tomato allergens. Immunoglobulin E (IgE) cross-reactive profilins have been suggested to account for allergic symptoms in patients suffering from tomato allergy. METHODS: The cDNA of tomato profilin was amplified by reversely transcribed polymerase chain reaction (RT-PCR) from total RNA extracted from ripe tomato fruit. The gene was cloned into the pET101D expression plasmid and the protein was produced in Escherichia coli BL21. Purification was performed via poly-l-proline (PLP) affinity chromatography. IgE reactivity of recombinant tomato profilin was investigated by immunoblot and enzyme-linked immunosorbent assay. IgE-inhibition studies were performed to analyze cross-reactivity with other profilins. To determine the allergenic activity of the recombinant protein, basophil histamine release assays using sera of patients with adverse reactions to tomato were performed. RESULTS: Profilin was identified as a new minor allergen in tomato fruits. The recombinant tomato profilin comprises 131 amino acids and high sequence identity to other allergenic food and pollen profilins. It was shown to be IgE-reactive with a prevalence of 22% (11/50) in tomato-allergic patients. In patients with tomato allergy and multiple sensitizations to other foods and birch pollen, IgE directed against tomato profilin showed a strong cross-reactivity with profilins from plant food sources and birch pollen. The tomato profilin was able to induce mediator release from human basophils. CONCLUSION: The tomato profilin is a minor allergen in tomato fruit. Thus, it shows biological activity, as confirmed by in vitro histamine release assays with human basophils and thereby has the potential to account for clinical symptoms in tomato-allergic patients.

Int Arch Allergy Immunol. 2003 Aug;131(4):245-55.
Related Articles, Links
Cloning and molecular and immunological characterization of two new food allergens, Cap a 2 and Lyc e 1, profilins from bell pepper (Capsicum annuum) and Tomato (Lycopersicon esculentum).
Willerroider M, Fuchs H, Ballmer-Weber BK, Focke M, Susani M, Thalhamer J, Ferreira F, Wuthrich B, Scheiner O, Breiteneder H, Hoffmann-Sommergruber K.
Department of Chemistry and Biochemistry, University of Salzburg, Salzburg, Austria.

BACKGROUND: Profilins are recognized by IgE of about 20% of patients allergic to birch pollen and plant foods. They are ubiquitous intracellular proteins highly cross-reactive among plant species. Therefore, they were called panallergens and are made responsible for cross-sensitization between plant pollen and food. OBJECTIVES: The aim of the present study was to clone the cDNAs encoding profilins from bell pepper and tomato, to produce and purify the recombinant proteins and to compare their IgE-binding capacities to those of the natural proteins. METHODS: cDNA clones coding for profilin were obtained by RT-PCR from total RNA of tomato and bell pepper fruits, sequenced and expressed as non-fusion proteins in ESCHERICHIA COLI. The recombinant profilins were subsequently purified and tested for IgE-binding and inhibition capacity with sera from 34 food-allergic patients. Possible oligomerisation of recombinant profilins was investigated by HPLC analysis and its influence on IgE binding assayed by ELISA. RESULTS: The open reading frame from both profilins encompasses 393 bp with a predicted molecular mass of 14,184 kD and a pI of 4.44 for bell pepper profilin (Cap a 2) and 14,257 kD and a pI of 4.46 for the profilin from tomato (Lyc e 1). The two protein sequences display 91% identity, whereas tomato profilin from pollen shares only 75% identity with tomato fruit profilin. Eleven out of 34 food-allergic patients (32%) display IgE binding to both purified profilins. Preincubation of a serum pool with either purified rCap a 2 or rLyc e 1 nearly abolished IgE binding to natural Cap a 2 and Lyc e 1, respectively. In addition, purified recombinant Cap a 2 was able to inhibit IgE-binding to rLyc e 1 by approximately 50%, whereas rLyc e 1 completely blocked IgE-binding to rCap a 2 in cross-inhibition assays. HPLC analysis showed that in solution Cap a 2 and Lyc e 1 can be found predominantly as dimers, which can be partially reduced to monomers by addition of dithiothreitol (DTT). In ELISA DTT-treated Lyc e 1 displayed a clearly lower IgE-binding capacity than untreated profilin. CONCLUSIONS: Purified rCap a 2 and rLyc e 1 proved to be valuable tools for studying cross-reactivity to profilins in patients allergic to pollen and food.

J Allergy Clin Immunol. 2003 Aug;112(2):427-32.
Related Articles, Links
Detection of clinical markers of sensitization to profilin in patients allergic to plant derived foods.
Asero R, Mistrello G, Roncarolo D, Amato S, Zanoni D, Barocci F, Caldironi G.
Ambulatorio di Allergologia, Clinica San Carlo, Paderno Dugnano, Milan, Italy.

BACKGROUND: A proper classification of patients allergic to plant-derived foods is of pivotal importance because the clinical features of allergic reactions to fruits and vegetables depend on the nature and characteristics of proteins responsible for sensitization. However, in normal clinical settings this is presently impossible. OBJECTIVE: We sought to detect clinical markers of sensitization to profilin. METHODS: Seventy-one patients allergic to fruits and vegetables but not sensitized to lipid transfer protein or natural rubber latex were studied. Food allergy was ascertained on the basis of clinical history and positive skin prick test responses with fresh foods, commercial extracts, or both. Allergies to foods that had caused less than 2 adverse reactions were confirmed by means of open oral challenge. IgE reactivity to rBet v 1/rBet v 2 and to natural Phleum species profilin were detected. Moreover, IgE to the 30- to 40-kd and 60- to 90-kd birch pollen-enriched fractions, which also can be involved in cross-reactivity phenomena, were measured in sera from 52 patients by means of ELISA.
RESULTS: On the basis of in vitro tests, 24, 18, and 25 patients turned out to be sensitized to Bet v 1, Bet v 2, or both, respectively. Four patients had negative test results for both allergens. Hypersensitivity to Bet v 2 was strongly associated with clinical allergy to citrus fruits (39% in patients monosensitized to Bet v 2 vs 4% in patients monosensitized to Bet v 1, P <.025), melon or watermelon (67% vs 0%, P <.001), banana (66% vs 8%, P <.001), and tomato (33% vs 0%, P <.05), whereas Bet v 1 sensitivity was associated with clinical allergy to apple (100% vs 39%, P <.001) and hazelnut (56% vs 0%, P <.001). The sensitivity of a history of allergy to gourd fruits, citrus fruits, tomato, banana, or a combination thereof as a means to detect profilin-hypersensitive patients was 85% (41/48). The specificity of an allergy to any of these fruits exceeded 85%, with positive predictive values ranging between 68% and 91%. CONCLUSION: In clinical settings in which laboratory investigations are not easily accessible, allergy to melon, watermelon, citrus fruits, tomato, and banana can be used as a marker of profilin hypersensitivity once a sensitization to natural rubber latex and lipid transfer protein is ruled out.

Rocz Akad Med Bialymst. 2004;49:111-5.
Related Articles, Links
Diagnostic value of birch recombinant allergens (rBet v 1, profilin rBet v 2) in children with pollen-related food allergy. Cudowska B, Kaczmarski M. III
Department of Pediatrics, Medical University of Bialystok, Poland. becud@wp.pl

PURPOSE: Pollen-related food allergy to fresh fruits and vegetables is a well-known clinical phenomenon. Bet v 1, the major birch pollen allergen, has been cloned and shows homologies to various food allergens (e.g. hazelnut, apple, celery, tomato). Allergy to profilin Bet v 2 was also described in 10-15% of patients sensitized to birch pollen.
Objective of our work was to assess the diagnostic value of recombinant allergens (rBet v 1, rBet v 2) for diagnosis of children sensitized to birch pollen with associated food allergy.
MATERIAL AND METHODS: The investigations were carried out on the group of 14 children aged 4-17 years, with a history of allergic reactions and sensitized to birch pollen with associated food allergy. Skin prick tests were performed with natural foods and commercial aeroallergens (Bencard). Sera-specific IgE antibodies to recombinant and other allergens (Pharmacia Upjohn) were measured with a fluoroimmunoenzymatic essay (UniCAP). Oral food challenge tests were performed to confirm adverse food reactions. RESULTS: 64% were sensitized to rBet v 1, 14% to rBet v 2, 7% to both of them. 50% of children with allergy to Bet v 1 had also concomitant allergy to other pollens and food allergy to fruits from family Rosaceae. Patients with positive reaction to Bet v 2 represented allergy to vegetables from family Umbelliferae. The most common form of allergic reactions were: allergic rhinitis in 64%, atopic dermatitis in 36%, oral allergy syndrome in 21% of investigated children.
CONCLUSIONS: Use of two recombinant allergens permits the diagnosis of birch pollen sensitization in children with food-pollen related allergy and gives the pattern of possible cross-reactivity between pollen and food allergens in children with allergic diseases.

9/28/05 re: Food allergies as a cause of bloating

I am a 30 year old RN in pretty good general health. I experience abdominal bloating each afternoon that is uncomfortable and makes my clothes not fit. This is relieved by passing wind but it has gotten worse over the last 12 months and upon questioning other nursing friends, have determined that this is not everyone's experience! I have been trying to find out what is causing this and various information points me to food allergies and ELISA testing. Would this be helpful or is it 'overkill' for my problem? Ie: is ELISA testing for overt food reactions/allergies?

I should first say that abdominal bloating as a major/isolated symptom would be a very unusual presentation of food allergy (FA). Such bloating could be due to a number of other disorders. The first that comes to my mind would be motility disorder in the colon such as the irritable colon syndrome. Other considerations include lactase deficiency, dietary factors such as ingestion of large amounts of gas-producing foods. Recently, it has been recognized that Celiac Disease (CD) can present initially in adults with bloating as a manifestation and improvement on a gluten-free diet. Possible CD can be investigated with a screening (snti-endomysial antibody) blood test.

Low levels of anti-foods IgE antibodies detected by ELISA tests will frequently be positive in individuals with no evidence of clinical adverse reactions to such foods. Therefore, any positive results in your case would require confirmation by an appropriate oral challenge with the suspect foods. My opinion is that this approach has a low likelihood of finding a positive response. Therefore, I would look into other diagnostic possibilities first.

9/20/05 re: Cross-reactivity between flaxseed and soy/wheat

I was recently asked by a patient with soy and wheat allergy if there is any known cross-reactivity between Flaxseed and soy and wheat. I was not able to find any references to indicate cross-reactivity. Is there any known cross-reactivity between these foods?

To respond to your question I obtained input from Dr. Stephen Taylor of the Univ. of Nebraska. Dr. Taylor is a leading expert in food allergens and their sources. His response is enclosed below.

Dr. Taylor's comments:

I am not aware of any known cross-reactivity of wheat or soy with flaxseed. Wheat and soy allergies are much more common than flaxseed allergy which is rarely encountered. I would not be too concerned about cross-reaction except that there is always some potential for agricultural contamination of one grain with another from shared farming practices - flaxseed grown on a field previously used to grow wheat. I doubt that such contamination would rise to the level that it would cause allergic reactions though.

9/13/05 re: Food sensitivity in atopic dermatitis

Hypothetically speaking, a patient with moderate atopic dermatitis is tested with ImmunoCAP and found to have low level positives to egg, milk and peanut. Would a targeted elimination diet of one food at a time be prudent to look for clinical improvement in the atopic dermatitis? If no clinical improvement after elimination of one food, would you reintroduce that food and eliminate other positive foods in the same way? What is the recommendation for managing patient with low level positive SPT/CAP RAST tests to peanut? If a patient has atopic dermatitis and shows sensitization, without obvious immediate reaction, is it recommended avoiding peanuts and carrying an Epi-Pen? Again, this is a patient with atopic symptoms and signs but without immediate allergic reactions.

Individuals with atopic dermatitis (AD) will frequently have increased levels of IgE antibodies against a variety of foods detected by the usual in vitro tests. Only some of the positive tests are indicative of current clinical sensitivity to the foods involved as determined by controlled food challenge tests. Careful recent studies by Sampson's group in New York and some groups in Europe have shown that IgE antibodies above a certain level as detected by the CAP-ELISA or similar technique correlate very well with a positive clinical reaction to a double-blind challenge with that food. For example, serum anti-peanut IgE levels of at least 15 kU/L are highly predictive of a positive clinical reaction to an oral peanut challenge.

However, the situation is more complex when low level IgE levels against foods are found. In some, but certainly not all, of these cases, a double-blind oral challenge with the suspect foods will elicit a positive clinical reaction. Therefore, elimination of individual foods in such cases may well not give clear-cut findings. If there is not an impressive clinical improvement following such elimination, it could be that; 1) the food eliminated is not a clinically-relevant offender or 2) sensitivity to multiple foods (and maybe other factors such as staph infection of skin lesions) are present, so that elimination of just one food offender does not lead to impressive improvement.

It would be preferable to do cautious oral challenges using graded increasing amounts of each suspect food in turn. However, one must realize that worsening of the AD may not occur immediately but only after 1-3 days following the challenge (in some children there is immediate onset increased itching after the oral challenge)

With regards to your question about peanut sensitivity, I think that this is a special situation. If the levels of IgE anti-peanut antibodies are low and there is no history of immediate reactions to peanut, I think that there is a very low risk of a severe immediate reaction to minute amounts of peanuts present as �hidden ingredients� in prepared foods. However, I would advise withholding whole peanuts and foods with high peanut content (e.g. peanut butter) from the diet because peanuts are non-essential foods which are such common sensitizers (particularly in �high atopics�) that general avoidance of them would be prudent in such individuals.

Whether the parent should carry an Epi-Pen for use in a child with no history of an anaphylactic reaction is a judgment call, depending on the anxiety level of the parent about a possible food reaction and other factors.

9/12/05 re: Food allergy and eczema

My baby (8 months) has been diagnosed to have allergy to cow's milk. He is on soy milk now, however he has eczema which has been 60 percent cured with the change in milk. I would want your help to find out the other food that he could be allergic to that causes severe itching in the body.

I would not recommend using a soy-based formula if your child still has eczema with severe itching. Although soy-based formula have been commonly substituted for cow's milk formulas in milk-sensitive infants, recent studies have shown that soy is one of the foods most commonly eliciting allergic reactions in highly atopic children. Such soy sensitivity may develop after soy has been substituted for cow's milk, as done in your child.

I suggest that you have levels of IgE antibodies against commonly ingested foods assessed in a reliable lab. If your child is still having pronounced skin manifestations (though less than before) it may also be advisable to use an amino acid-based formula such as Neocate as the sole feeding until there is greater improvement in the skin situation.

9/4/05 re: Oral food challenge protocol

I see many patients with a good history of food allergy but negative skin and RAST tests. I would like to do food challenges. Is there a standard protocol for doing challenges? Is there a source of materials (capsules containing small amount of the common foods) to use in the challenges?

I know that a practice parameter document that deals with food challenges has been under construction. Therefore, I consulted Dr. Scott Sicherer of the Mt. Sinai School of Medicine in New York, a leading expert in food allergy and a participant in the construction of the document referred to above. Dr. Sicherer's response to me is enclosed below.

There are no commercially available pre-packaged "food challenge" capsules. The food allergy practice parameter has not been published as yet. The reader may wish to look at the recent "Practice Paper" about the diagnosis and management of food allergy available in JACI or the AAAAI Web site (Authors Sicherer and Teuber on behalf of the Adverse Reactions to Foods Committee of the AAAAI) that references papers about performing oral food challenges.

9/2/05 re: Peanut ingredients in natural flavorings

I have very concerned parents with peanut allergies questioning whether �natural flavorings� could have traces of peanuts. Many products list these natural flavorings as an ingredient.

I think that the most information related to your question can be obtained through the Food Allergy and Anaphylaxis Network, a lay support group that closely monitors the constantly changing food allergen �hidden ingredient� situation. I suggest that you contact that group through their website (listed as one of the �Other Links� to this AADMC website).

8/19/05 re: Oral allergy syndrome due to pea allergy

Is it common for oral allergy syndrome to include significant conjunctival edema and watery discharge as well as marked nasal congestion (in addition to itchy throat)? Has anyone described oral allergy syndrome with peas (uncooked sugar snap peas, in a bag from Trader Joe's supermarket)? I am a 46 year old pediatrician with a history of oral allergy syndrome since childhood, to carrots, apples and all the usual fruits and vegetables. For the most part I seemed to be outgrowing this, until this episode. I had a very rapid reaction to the peas as described above, which was worse than I had ever experienced.

Although there has been little reported about allergy to peas as a cause of the oral allergy syndrome (OAS), other legumes, including chick peas are commonly incriminated as causes of the OAS. A report (abstract enclosed) included peas as one of the inciting foods in the OAS. Most individuals with the OAS are also sensitive to one or more cross-reacting pollens leading to respiratory symptoms. Also, fresh, fruits and vegetable are much more likely to induce the OAS than when the same foods are thoroughly cooked. Clinical cross-sensitivity among the legumes (including peas) is uncommon despite strong in vitro cross-reactivity of the IgE antibodies against individual legumes. However, there are reports of clinical cross-sensitivity between peas and peanuts (see enclosed abstract). Therefore, I would be careful about ingestion of substantial amounts of peanuts. Although the involvement in the OAS is typically limited to the oral cavity, a number of patients may have symptoms elsewhere, including the eyes, particularly when the ingested dose of the offending food is sizable. If one has respiratory symptoms, you should also look for the presence of sulfites/SO2 as a curing/preservative agent in the pea package. The SO2 liberated from sulfite metabolism can induce asthmatic reactions, particularly if there is a history of underlying asthma.

J Allergy Clin Immunol. 1989 Mar;83(3):683-90.
Comparison of results of skin prick tests (with fresh foods and commercial food extracts) and RAST in 100 patients with oral allergy syndrome.
Ortolani C, Ispano M, Pastorello EA, Ansaloni R, Magri GC. Bizzozero
Medical Division, Allergy and Immunology Center , Ospedale Niguarda Ca' Granda, Milan, Italy.

One hundred adult patients with a history of oral allergy syndrome (OAS) after ingestion of fruits and vegetables, 77 patients with hay fever and 13 with skin prick tests and RAST positive to pollens but without seasonal symptoms, and 32 normal non-allergic control subjects, had Phadebas RAST and skin prick tests with commercial extracts (CSPT) and with fresh foods (FFSPT) to assess the reliability of these three tests. Sensitivity was better with FFSPT for carrot, celery, cherry, apple, tomato, orange, and peach; better with CSPT for peanut, pea, and walnut; and better with RAST for hazelnut. Specificity, negative predictive value, and positive predictive value of the three tests were determined for apple, carrot, hazelnut, orange, pea, peanut, and tomato. Specificity in the patient groups ranged between 40% (pea) and 100% (apple) for CSPT, between 61% (peanut) and 87% (carrot) for RAST, and between 42% (carrot) and 93% (peanut) for FFSPT. However, all tests were negative in the control group. Thus, false positive results may result from cross-reactivity with pollen allergens. The diagnostic accuracy of these tests in the population with OAS proved comparable for peanut, carrot, hazelnut, and pea. FFSPT proved more sensitive than CSPT or RAST in confirming a history of OAS to certain alimentary allergens, such as apple, orange, tomato, carrot, cherry, celery, and peach.

J Allergy Clin Immunol. 2003 Feb;111(2):420-4.
Patients with anaphylaxis to pea can have peanut allergy caused by cross-reactive IgE to vicilin (Ara h 1).
Wensing M, Knulst AC, Piersma S, O'Kane F, Knol EF, Koppelman SJ.
Department of Dermatology/Allergology G02.124, University Medical Centre Utrecht , Heidelberglaan 100, 3584 CX Utrecht, The Netherlands.

BACKGROUND: Serologic cross-reactivity among legumes has been described; however, it is rarely clinically significant. In this study 3 patients with a history of anaphylaxis to pea are described who subsequently had symptoms after ingestion of peanut.
OBJECTIVE: We investigated whether the peanut-related symptoms were due to cross-reactivity between pea and peanut proteins.
METHODS: Peanut-related symptoms were documented according to case history or double-blind, placebo-controlled food challenge results. Skin prick tests were performed, and specific IgE levels were determined for pea and peanut with the CAP system FEIA. IgE-binding proteins in pea and peanut were identified by using immunoblot analysis. Cross-reactivity was studied by means of immunoblot and ELISA inhibition studies with whole extracts and purified allergens. RESULTS: Peanut-related symptoms consisted of oral symptoms in all patients, with additional urticaria and dyspnea or angioedema in 2 patients. All patients had a positive skin prick test response and an increased IgE level to pea and peanut. Immunoblotting revealed strong IgE binding to mainly vicilin in pea extract and exclusively to Ara h 1 in crude peanut extract. Immunoblot and ELISA inhibition studies with crude extracts, as well as purified proteins, showed that IgE binding to peanut could be inhibited by pea but not or only partially the other way around.
CONCLUSION: Clinically relevant cross-reactivity between pea and peanut does occur. Vicilin homologues in pea and peanut (Ara h 1) are the molecular basis for this cross-reactivity.

8/18/05 re: Almond allergens

I've seen ALMONDS classified as part of the PRUNOIDEAE subfamily (peach, apricot, plum, nectarine, cherry, almonds), and I've also seen almonds classified as part of the TREE NUT group. Where do you feel almonds fit in: (1) as a PRUNOIDEAE (with possible cross-reaction to other prunoideae), or (2) as a TREE NUT (with possible cross reaction to other tree nuts)?

I have also seen descriptions of almonds as belonging to the Prunoideae family as well as being a tree nut. Because I am not expert in such classification areas I obtained input from Dr. Stephen Taylor of the Univ of Nebraska. Dr. Taylor is an expert in the nature of food allergens. His prompt and helpful response is enclosed below:

Dr. Taylor's comments

Biologically, there is no doubt that almonds belong in the Prunoideae family (Plum family) with apricot, cherry, peach, plum and sloe. I have also seen this frequent reference to the Rosaceae family but that is actually incorrect and probably an innocent error that simply got proliferated by others who never bothered to look up the right information; the rose family includes blackberry, raspberry, boysenberry, strawberry.

Almonds of course are also considered as tree nuts which is not a biological classification. That is a commerce classification.

I do not believe that the cross-reactivity of almonds has been well investigated and am not sure that I can give a very authoritative answer. Unlike other foods in the Prunoideae family, we essentially eat the pits of the almond fruit while we eat the flesh of the fruit of the others (in fact, peach and cherry pits contain some nasty toxins so don't try eating them - cyanogenic glycosides that release CN on contact with stomach acid). So, allergens could be different between almonds and other Prunoideae fruits. I am not sure that one would expect cross-reactions or that they occur.

With respect to tree nut cross-reactivity, it is my observation that many tree nut-allergic patients do not necessarily know which tree nuts they are allergic to. In skin tests, many allergists use a mixture of tree nuts so a positive test is hard to interpret with respect to individual tree nuts. Most patients are given the advice to avoid all tree nuts. In my experience, some obviously do know from experience that they can safely eat certain ones. However, cross contamination of one tree nut with another is quite possible in commerce because some suppliers handle all of the various nuts (and peanuts) on shared equipment. Thus, avoidance of all tree nuts is probably a reasonable recommendation in many cases.

Clinical cross-reactivity within the tree nut group has not been very extensively studied either. There is a rather old paper by Gillespie et al (Jerry Gleich was a co-author, I think) from Mayo who looked at the issue with a number of patients and found a rather complicated story based upon the RASTs of the day. Of course, they may not have controlled well enough for cross contamination. But, some clinical cross-reactivity does seem to occur; the biological basis for similar allergens in nuts from dissimilar trees is not yet understood.

7/27/05 re: Soybean oil allergenicity

Can a patient with soy Allergy consume products that list either soy lecithin or soybean oil? I read some other comments on your website to questions that addressed lecithin as safe, but not quite too much information on soybean oil commonly found on products.

Allergic reactions to soybean oil are quite unusual but do occur occasionally (see enclosed abstract). There have been somewhat conflicting findings whether proteins found in commercial soy oil preparations are allergenic (react with IgE present in the serum of individuals with documented allergy to soybeans themselves) - see enclosed abstracts. A group in Nancy, France with extensive experience with food allergies has reported two positive out two oral challenges with soybean oil.

Thus, I would have to conclude at this time that there is a very small but present risk for an allergic reaction to soybean oil in someone who is allergic to soybeans themselves. I would imagine that the degree of risk may depend on the degree of sensitivity to soybeans in an individual patient and how the soybean oil is processed.

Clin Exp Allergy. 1998 Dec;28(12):1559-64. Related Articles, Links
Antigenicity of the proteins in soy lecithin and soy oil in soybean allergy.
Awazuhara H, Kawai H, Baba M, Matsui T, Komiyama A.
Department of Home Economics (Food Science), Faculty of Education, Shinshu University, Nishinagano, Nagano, Japan.

BACKGROUND: Soy lecithin and soy oil are usually produced from the hexane extract of soybean. Some of the soybean proteins are included in the extract and are therefore present in small amounts in both soy lecithin and soy oil. The antigenicity of the proteins present in defatted soybean has been studied with respect to soybean allergy, but the antigenicity of those found in the extract is yet to be investigated. OBJECTIVE: The antigenicity of soy lecithin and soy oil proteins with regard to soybean allergy were investigated. METHODS: The proteins present in soy lecithin and soy oil were determined according to already established method and analysed by SDS-PAGE. The IgE- and IgG4-binding abilities of the soy lecithin proteins were investigated by immunoblotting with sera from 30 soybean-sensitive patients, including seven with a positive challenge test. Immunoblotting of soy oil proteins was performed with the sera from some of these patients. RESULTS: In 100 g of sample, the soy lecithin and soy oil contained 2.8 mg and 1.4-4.0 microg of proteins, respectively. The results of SDS-PAGE demonstrated the presence of only three proteins, with molecular weights of about 58-67 kDa in soy oil, and suggested that soy lecithin also contains these proteins. The soy lecithin also contained many proteins besides these. In the soy lecithin, the detection rate of only one protein, with a molecular weight of 31 kDa, by the serum IgE of patients was significantly different compared with controls (detection rate: 40%). The proteins with molecular weights of 58-67 kDa rarely bound to serum IgE. Only one of the patients who presented a positive challenge test had IgE antibodies to soy lecithin proteins. IgG4-binding proteins were found only rarely in soy lecithin. Neither the IgE nor the IgG4 present in the patients' sera reacted to any soy oil protein. CONCLUSION: Proteins present in soy lecithin and soy oil have little antigenicity with regard to soybean allergy

Allergy
Volume 57 Issue 7 Page 648 - July 2002
doi:10.1034/j.1398-9995.2002.23672.x
Allergen in soy oils
Y. Errahali, M. Morisset, D.-A. Moneret-Vautrin, G. Kanny, M. Metche, J.-P. Nicolas, S. FrTmont *

Soy allergy is of particular importance because of the ubiquity of soy proteins in contemporary foods. This allergy appears to affect 6% of atopic children (1) and 14% of children with cow's milk allergy (2). Soy, which has been responsible for several fatal and severe reactions, is probably an underestimated cause of food anaphylaxis (3). Several proteins have been identified in soy oil (4), but to date, the allergenicity of proteins from deodorized soy oil has never been observed. In this paper we show that allergenic proteins are present in both cold-pressed soy oil and deodorized soy oil. The allergenicity of at least one of these proteins has been demonstrated by Western blot.

The serum was taken from a soy-sensitized woman with a high level of soy specific IgE (18.9 kU/l) (RAST, Cap System, Pharmacia, Uppsala, Sweden). Two kinds of soy oil were tested: deodorized (type A) and cold-pressed (type B) soy oils were supplied by the same company. The proteins were extracted from 500 ml of each batch using PBS buffer at 40¦C and stirred for 3 h. The aqueous phase was dialyzed for 2 days.

The total protein contents of oils A and B were 0.32 ¦g/ml and 1.8 ¦g/ml, respectively. The SDS-PAGE of deodorized and cold-pressed soy oils showed the same pattern (Fig. 1a). The immunoblots of batch A and batch B, conducted with the serum of a soy-sensitized patient, showed two bands at 28 and 56 kDa, respectively, the latter being the main band, whereas the immunoblot using serum of a non-sensitized patient did not exhibit any binding (Fig. 1b).

In conclusion, we showed that allergenic proteins were present not only in cold-pressed but also in deodorized soy oil. We are currently trying to find out whether this allergen is clinically relevant.

Clin Exp Allergy. 2003 Aug;33(8):1046-51. Related Articles, Links
Thresholds of clinical reactivity to milk, egg, peanut and sesame in immunoglobulin E-dependent allergies: evaluation by double-blind or single-blind placebo-controlled oral challenges.
Morisset M, Moneret-Vautrin DA, Kanny G, Guenard L, Beaudouin E, Flabbee J, Hatahet R.
Internal Medicine, Clinical Immunology and Allergology, University Hospital Nancy, France.

BACKGROUND: The prevalence of food anaphylaxis due to masked allergens has increased within the last 10 years. Contamination of manufactured products by food allergens is a key concern for food industries. OBJECTIVE: To determine quantities eliciting reactions in patients who have an IgE-dependent food allergy, thanks to standardized oral provocation tests. To evaluate the subsequent levels of sensitivity required for the detection tests of allergens for egg, peanut, milk and sesame. METHODS: Prick-in-prick tests, Cap system RAST, and single or double-blind placebo-controlled food challenges (SBPCFC or DBPCFC) were performed. The doses of natural food were gradually increased from 5 to 5000 mg for solid food and from 1 to 30 mL for peanut oil, sunflower oil, soy oil and sesame oil. RESULTS: Data from 125 positive oral challenges to egg, 103 to peanut, 59 to milk and 12 to sesame seeds were analysed. Haemodynamic modifications were observed in 2%, 3%, 1.7%, and 8% of the oral challenges (OCs) to egg, peanut, milk and sesame, respectively. Respiratory symptoms were observed in 12%, 20%, 10% and 42% of egg, peanut milk and sesame allergies, respectively. A cumulative reactive dose inferior or equal to 65 mg of solid food or 0.8 mL of milk characterized 16%, 18%, 5% and 8% of egg, peanut, milk and sesame allergies, respectively. 0.8% of egg allergies, 3.9% of peanut allergies, and 1.7% of milk allergies reacted to 10 mg or less of solid food or to 0.1 mL for milk. The lowest reactive threshold has been observed at less than 2 mg of egg; 5 mg of peanut, 0.1 mL of milk and 30 mg of sesame seed. Ten out of 29 OC with peanut oil, two out of two OC with soy oil and three out of six OC with sunflower oil were positive. Five out six OC with sesame oil were positive: 1 and 5 mL induced an anaphylactic shock. CONCLUSION: The risk of asthma and anaphylactic shock to sesame and peanut is confirmed. Minimal reactive quantities show that, in order to guarantee a 95% safety for patients who are allergic to egg, peanut and milk, and on the basis of consumption of 100 g of food, the detection tests should ensure a sensitivity of 10 p.p.m. for egg, 24 p.p.m. for peanut and 30 p.p.m. for milk proteins. Oil allergies being considered, the limit of sensitivity should fall to 5 p.p.m.

7/26/05 re: Sesame allergy

I am a registered dietitian with a daughter who was diagnosed with peanut allergy by clinical history (facial rash and swelling after ingestion of a small quantity of peanut butter) at age 15 months, confirmed with prick skin test (4+). At age 2-1/2 she had a pediatric food allergen panel performed, with negative results to corn, almond, coconut, pecan, sesame seed, egg white, cow milk, wheat, and soybean, but positive results for peanut: 13.1 kU/L, ASM Class 4. This year, at age 3-1/2, repeat testing again showed positive result for peanut of 15.0 kU/L, ASM Class 5, as well as a weakly positive result for almonds <0.4 kU/L, ASM Class 1 and sesame seed <0.4 kU/L ASM Class 1. We have avoided all peanuts and tree nuts since the initial diagnosis, but not sesame seeds. I have a couple of questions. Her allergist has advised us, on the basis of the sesame seed result, to avoid sesame seeds and sesame oil. He said she does not have a true allergy to them, but could develop one if she continues to consume them (she has never had an apparent reaction after sesame ingestion). Is this true? Also, does the increase in value for her peanut test mean that her peanut allergy is worsening? Does this decrease her likelihood of outgrowing the allergy? She does not have asthma.

The incidence of sesame allergy appears to be increasing in children, possibly because of increasing exposures to sesame in various food products (see enclosed abstract). The very low level of IgE anti-sesame antibodies your described (0.4 kU/mL) would generally mean that your daughter, as an atopic individual, is more likely to develop higher levels of such antibodies (with increased likelihood of manifesting clinical sensitivity to sesame) than if she had no IgE anti-sesame antibodies at this time. Of course, the likehood of her developing stronger IgE antibody reactivity would depend in part on her level of exposure to sesame. Therefore, avoidance of obvious sesame exposure would be reasonable without the meticulous complete avoidance of tiny amounts that would be indicated if she had documented clinical sensitivity to sesame.

Recent studies have indicated that the levels of IgE anti-peanut antibodies in validated tests can be predictive of an allergic reaction to an oral challenge with peanuts (see enclosed abstract). If one can apply those criteria to the tests done in your daughter, a level of 15kU/mL would strongly predict clinical sensitivity. However, I would not make too much of a difference between 13.5 and 15 kU/mL. Both levels are quite high. Peanut sensitivity in childhood persists into adulthood in about 80% of the cases. Such persistence of peanut allergy is more likely in those with higher levels of anti-peanut IgE antibodies (such as your daughter).

Allerg Immunol (Paris). 2004 Oct;36(8):300-5.
Sesame seed allergy in children
Agne PS, Bidat E, Agne PS, Rance F, Paty E.
Assistance publique-hopitaux de Paris, Hopital Ambroise Pare Boulogne, France.

BACKGROUND: Sesame seed allergy is becoming more common in childhood. The aim of this study is to define the clinical signs and the results of allergological work-up of this food allergy as well as the demographical data in children. Sesame seed allergy outcome is unknown. MATERIALS AND METHODS: 14 children were recruited from 3 allergy centers in France . The diagnosis of food allergy was based on a convincing clinical history and positive skin prick tests and/or an elevated sesame specific IgE. Food challenge test was done when results of history and allergological work-up were conflicting. A reintroduction test was done when a child seemed to outgrow his (or her) food allergy. RESULTS: The median age at the beginning of sesame seed allergy was 5 years (range from 5 months to 16 years old). All patients reacted immediately after sesame seed consumption and presented as a first manifestation: edema (9 cases, 48%), urticaria (5, 27%), and one of each of the following symptoms (vomiting, rhinitis, conjunctivitis, asthma and anaphylactic shock). One patient had recurrent anaphylactic shocks and another an anaphylactic shock after subsequent sesame seed exposure; these 2 patients were asthmatic. The median of the wheal size was 5 mm (range 3 to 15 mm). The commercial sesame seed extract was less sensitive than the native seed. The median of sesame seed IgE was 5.58 kUA/L (range 0.35 to 100 kUA/L). The follow up lasted from a few months to 6 years. Three patients outgrew their food allergy. All of these patients showed a previous drop of sesame seed IgE and skin prick-tests became negative. CONCLUSION: Sesame seed allergy is not very different than other food allergy. We reported the spontaneous outgrowing of sesame seed allergy without being able to define the predictive criteria for a good outcome.

J Allergy Clin Immunol. 2005 Jun;115(6):1291-6. Related Articles, Links
Diagnosing peanut allergy with skin prick and specific IgE testing
Roberts G, Lack G.
Paediatric Allergy, Asthma and Immunology, Imperial College at St. Mary's, St. Mary's Hospital, Praed Street, London W2 1NY, UK.

BACKGROUND: Food allergy is common in childhood. It has been suggested that the magnitude of a skin prick test or specific IgE result can improve diagnostic usefulness, but this has been addressed in only a few tertiary challenge-based studies. OBJECTIVE: To determine the predictive value of a wheal > or = 8 mm or serum specific IgE > or = 15 kU A /L for clinical allergy and investigate whether results are generalizable. METHODS: All subjects, up to 16 years of age, who had been investigated with a peanut or tree nut food challenge were eligible for the study. Subjects were referred from either a tertiary allergy clinic or a community birth cohort. All subjects with a history suggestive of food allergy were offered a challenge unless there were features of anaphylaxis. Details of challenges were prospectively recorded. Results were modeled by using logistic regression. RESULTS: There was a total of 161 peanut challenges. Recent skin prick (longest wheal diameter) and specific IgE data were available for 135 and 136 challenges, respectively. The results suggest that a skin prick result > or = 8 mm and a specific IgE > or = 15 kU A /L have predictive values of 95% (95% CI, 76.2% to 99.9%) and 92.0% (74.0% to 99.0%), respectively, for a positive challenge. Age, the type of nut, and referral pattern of the subject did not appear to alter this relationship.
CONCLUSION: These data suggest that a skin prick result > or = 8 mm or a specific IgE or = 15 kU A /L have a high predictive value for clinical allergy to peanut and that these cutoff figures appear generalizable to different populations of children undergoing an assessment for peanut allergy.

7/22/05 re: Reaction to inhaled peanuts

Is it really possible for someone to have a reaction, especially an anaphylactic reaction, to simply the smell of a food. I am not talking about standing over a pot of boiling food allergen but, say, smelling a peanut butter sandwich that someone next to "you" is eating, assuming "you" have anaphylaxis to peanuts. I have had a couple of people tell me that they react to the smell of certain food allergens.

Some reportedly peanut-allergic individuals have claimed triggering of their allergic reaction when containers of peanuts are opened close to them such as the situation on airplanes when small packages of peanuts are opened. As I understand it, such descriptions played a role in the policy of a number of airlines to discontinue serving peanuts on airplane flights.There is little question that the peanut odor is often discernible by people sitting close to the person opening the peanut package. However, the only study I know of directed to the question whether inhaled peanut "vapors" in non-cooking situations cause problems in peanut-allergic individuals was carried out by the very experienced group at Mt. Sinai School of Medicine in New York. As described in the abstract enclosed below, they found that inhalation of the obvious odors emanating from a portion of peanut butter placed close-by did not induce reactions in a group of peanut-allergic patients.

The authors commented that these findings cannot be extrapolated to the situation when people are exposed to the odors of roasted peanuts. However, it should be noted that almost all peanut-allergic people will have an allergic reaction when a sufficient amount of peanut butter is ingested. Also, as you know, the peanut odor emanating from peanut butter is generally quite strong. Thus, further challenges with exposure to freshly opened packages of roasted peanuts would be worth investigating. However, I would suspect that no systemic reactions to the odors in such challenges would occur in truly peanut-allergic individuals.

I should mention that respiratory reactions to certain inhaled food components have occurred in some non-cooking occupational allergy reactions. For example, this type of reaction is a fairly common occurrence in workers in snow-crab processing facilities.

J Allergy Clin Immunol. 2003 Jul;112(1):180-2.
Relevance of casual contact with peanut butter in children with peanut allergy.
Simonte SJ, Ma S, Mofidi S, Sicherer SH.
Department of Pediatrics, Mount Sinai School of Medicine, New York, NY 10029-6574, USA.

BACKGROUND: Casual skin contact or inhalation of peanut butter fumes is reported and feared to cause allergic reactions in highly sensitive children with peanut allergy but has not been systematically studied. OBJECTIVE: We sought to determine the clinical relevance of exposure to peanut butter by means of inhalation and skin contact in children with peanut allergy.
METHODS: Children with significant peanut allergy (recent peanut-specific IgE antibody concentration >50 kIU/L or evidence of peanut-specific IgE antibody and one of the following: clinical anaphylaxis, a reported inhalation-contact reaction, or positive double-blind, placebo-controlled oral challenge result to peanut) underwent double-blind, placebo-controlled, randomized exposures to peanut butter by means of contact with intact skin (0.2 mL pressed flat for 1 minute) and inhalation (surface area of 6.3 square inches 12 inches from the face for 10 minutes). Placebo challenges were performed by using soy butter mixed with histamine (contact), and scent was masked with soy butter, tuna, and mint (inhalation).
RESULTS: Thirty children underwent the challenges (median age, 7.7 years; median peanut IgE level, >100 kIU/L; 13 with prior history of contact and 11 with inhalation reactions). None experienced a systemic or respiratory reaction. Erythema (3 subjects), pruritus without erythema (5 subjects), and wheal-and-flare reactions (2 subjects) developed only at the site of skin contact with peanut butter. From this number of participants, it can be stated with 96% confidence that at least 90% of highly sensitive children with peanut allergy would not experience a systemic-respiratory reaction from casual exposure to peanut butter. CONCLUSIONS: Casual exposure to peanut butter is unlikely to elicit significant allergic reactions. The results cannot be generalized to larger exposures or to contact with peanut in other forms (flour and roasted peanuts).

I have a 41 YO male military officer present with tachycardia and elevated blood pressure. Patient arrived in Germany in March 2005 with no previous symptomology. The patient describes mild chest pain or discomfort. The patient has experienced 8-9 episodes where he has developed progressive fatigue and profound malaise in addition to a warm sensation in his chest that will radiate towards his head. After the onset of symptoms during his initial episode, he presented for evaluation to a German hospital where he was noted to be markedly hypertensive (174/112) on presentation in addition to tachycardia. No acute ischemic changes were noted on his ECG. He was admitted for observation, and his symptoms and vitals gradually improved during the period of observation. Additional testing included serial cardiac enzymes which were negative for evidence of ischemia, normal CRP and TSH. An echocardiogram was noted to be normal. His symptoms eventually attributed to a GI etiology, and he was treated with increased doses of rabelprazole. Since that time, he has experienced similar episodes on 8 additional occasions. When evaluated, he has demonstrated significant hypertension and tachycardia without other evidence of ischemia. In retrospect, the patient describes moderate ingestion of wine/beer on all of the occasions within 24 hours of the onset of symptoms, but recall one episode that was not related to Etoh ingestion. On other occasions, he has been able to drink wine or beer without problems. Otherwise, the patient has no prior history of cardiac disease or prior cardiac evaluation. He has been in general good health. Current medications: Lisinopril, Zocor, Rabeprazole, Aciphex. Conducted normal stress test with noted resting tachycardia with accelerated heart rate. CBC/DIFF, Metabolic panel, T4 Free, Thyrotropin, urinalysis, 24 hr urinalysis û all labs normal. Echo û normal. LSL Allergy consult results: SKT pos to mite, pollen, hazelnut, hops. Recommended additional tests and Tx.

From your description, the first condition that comes to my mind is pheochromocytoma which should be looked for by appropriate chemical tests. Other chemically-mediated reactions such as carcinoid may also be considered. However, carcinoid is manifested more by flushing and wheezing rather than by prominent systemic hypertension.

Interaction of MAO inhibitors with certain foods can induce a somewhat similar picture. However, the medication list you sent does not look suspicious in that regard (incidentally,- I believe that Rabeprazole and Aciphex listed by you are the same medication).

I suspect that your message was sent to us for advice concerning possible food allergy because of the reported associated of episodes with ingestion of wine or beer. Your statement that such ingestion occurred within 24 hours before the episodes is not sufficient to make a clinical impression in this regard. True allergic reactions to alcoholic beverages practically always start within 2 hours after ingestion, particularly because such products are absorbed rapidly into the blood stream. Alcoholic beverages also interact with certain medications but such interactions would also likely be within 2-4 hours after ingestion. Therefore, if the patient ingested the wine/beer the evening before the episodes, it is highly unlikely that such ingestion caused the reactions.

7/19/05 re: Corn allergy questions

I am a pediatric dietitian working with many children with food allergies. I'm seeing an increase in the number of children with corn allergies (identified via patch testing). I'm looking for definitive information regarding treatment of this allergy - corn sources to avoid, etc. We allow soybean oil for our soy allergic kids, what is the stance on corn oil for corn allergy and does it matter if the oil is partly hydrogenated? What about corn syrup solids, maltoedextri, starch etc? What about paper packaging that contains corn? With the kids I see with multiple food allergies it's often necessary to put them on one of the Neocate products, which do contain a corn derivitave, but is typically well tolerated.

Dr. Scott Sicherer, a leading expert in food allergy matters, has just responded to me that the dietitian in their unit was not successful in getting a definitive statement from any food manufacturing companies. However, Dr. Sicherer and Ms Mofidi have constructed a response that they hope will be helpful to you. I have enclosed their very thoughtful response below.

As you will see, there is not much in the way of published information about the tolerance of presumably corn-allergic individuals to various corn products or by-products contained in foods.

You had mentioned that the diagnosis of corn allergy was based on findings in a patch test. As Dr. Sicherer mentioned in his response, if this was a delayed reaction to a patch test and not the immediate reaction in a traditional prick skin test to food allergens, it should be mentioned that the clinical relevance of such patch test reactions to foods is still an investigational area not well-defined to date.

ANSWER FROM Scott H. Sicherer M.D. and Shideh Mofidi, MS RD CSP at the Jaffe Food Allergy Institute at Mount Sinai, New York.

IgE mediated allergy to corn has been documented, in some cases, to relate to heat stable lipid transfer proteins from corn (e.g., Pastorello et al J Allergy Clin Immunol. 2003 Oct;112(4):775-83). However, corn, like any food, is a collection of proteins and the complete array of corn proteins that may be responsible for allergic responses, presumably including labile proteins, has not been established. Based upon studies of other foods and allergens, we know that people may become sensitized to various combinations of proteins, and specific areas of proteins (epitopes), and that the specific pattern of response may be reflected in clinical outcomes. Some proteins of corn would presumably be more stable to processing (e.g., lipid transfer proteins) and digestion than others. Therefore, depending upon a persons "corn allergy profile" and the processing through which a corn ingredient went, one may predict clinical reactions would occur in some instances and not others. These variables, not explored in a comprehensive way, could impact the clinical implications of having a "corn derived" ingredient in a food and so we cannot give an absolutely firm answer to each query posed. Specifically, one may hypothesize that a product made from less-cooked ground corn may behave differently compared to a food with a more processed corn derivative. Further ambiguity is brought in to this query because the relationship of clinical allergy to foods such as corn as reflected by results of patch tests are just now beginning to be explored.

As a quick example regarding the issue of clinical relevance of residual proteins in the context of IgE antibody associated allergy, Frisner et al (Pediatr Allergy Immunol 2000;11(2):106-10) identified a corn protein in an hypoallergenic infant formula based upon IgE binding from patient's sera; however, no clinical reactions were documented. To give "definitive" answers about residual proteins after processing would require studies of large groups of corn-allergic individuals tested against various corn products and at various doses (for threshold determination); these studies do not exist so we are left to some degree with educated opinion.

Corn products are used widely in the food industry since they possess functional qualities that enhance the final product. Corn by products such as corn syrup and corn syrup solids, corn starch, maltodextrin, and corn oil are used in a variety of different products taking advantage of each of these products' unique qualities. These products, depending the manufacturing process and depending on the food they are utilized in and level of processing or refining, may have more or less corn protein, but they presumably have potentially relevant doses. Corn syrup and corn syrup solids can help prevent crystal formation and therefore are used in ice creams and frozen desserts. They also have a positive effect on viscosity which helps with the flow of salad dressings and condiments when poured. Corn syrup is also used in canned fruits since it improves texture and enhances the color of the fruit without masking any of the natural flavors. Corn starch is used as a thickener and has an infinite number of uses in the food industry since it is flavorless.

Corn oil has excellent frying quality, is resistant to discoloration and developing off-flavors, contains have high levels of healthy poly-unsaturated fatty acids instead of the undesirable saturated fats.

Corn oil is usually processed by a combination of mechanical and solvent extractions which is then refined and filtered into the finished oil. This process generally denatures most if not all the corn protein present in the oil. In our practice, we do not limit corn oil for corn allergic individuals. The process of hydrogenation (addition of hydrogen to change the oil from a liquid to a semi-solid state) does not change the allergenicity of corn oil; hence hydrogenated corn oil found in margarines would also be tolerated by corn allergic individuals.

Studies have not looked at all of the specific corn products and their allergenicity. There are a dearth of clinical studies on corn allergy that include blinded oral food challenges (e.g., Tanaka et al J Allergy Clin Immunol. 2001 Apr;107(4):744). Pasini and colleagues (Allergy. 2002 Feb;57(2):98-106) reported on an effort to verify the clinical significance of positive prick skin and serum tests for IgE to corn. Six out of the sixteen subjects with positive tests to corn had a positive challenge with cooked corn flour with symptoms of asthma (1/6), angioedema (1/6), gastrointestinal symptoms (2/6), oral allergy syndrome (2/6) and urticaria (5/6). They suggest an oral challenge to verify the accuracy of the positive skin and blood test to corn.

In our practice, we have experience with many individuals requiring elemental diets for gastrointestinal disorders and have been able to use the elemental amino acid formulas that are currently available on the market (EleCare(r) and Neocate(r) powders) without any problems. Since corn is used so widely in the food industry it is prudent to be concerned with cross contamination of corn containing products such lollipops with other food allergens such as milk and egg. Identification of "clean" products and contacting manufacturers in relation to their practices is a critical step in the appropriate management of individual with gastrointestinal allergies where elimination diets are utilized.

7/18/05 re: Food allergies and G-I manifestations. MMR immunizations

I am a family physician and have a 14 month old patient with delayed GI-type reactions (mucoid stools, vomiting, abdominal pain) since infancy to cow's milk, soy and multiple other foods through mother's breastmilk, most severe reactions noted with eggs, rice, citrus, milder reactions with oats, barley etc... He has been on Neocate formula accounting for the majority of his nutrition.The child is slowly dropping off weight percentiles (started at 75th, now down to 10th) despite adequate Neocate intake, and aside from other possible causes of not gaining weight which we are investigating, the mother is interested in adding more calories to his solids intake. We have been doing slow food introductions over a week period with least allergenic foods first, but since the symptoms are only GI related (never hives or any respiratory problems) it has been difficult recognizing reactions at times.

What is the sensitivity and specificity of skin vs. Rast vs. Immunocap testing in non-IgE mediated food allergies in a 14 month old? The results would be useful if fairly accurate in picking the new foods to introduce and removing some of the "guess work". I also understand that there are false negatives involved with each test and that reaction history is a better guideline, but at this point any help would be appreciated.

In addition, the child has never had any eggs or egg products and the mother is concerned about giving MMR. I have done extensive searches and have found somewhat conflicting information, although when I contacted CDC they advised that MMR is not contraindicated and to just proceed with the immunizations. Would it be useful to have skin testing for MMR prior to giving the vaccine or simply administer in and observe closely? Any information you may have will be grately appreciated. Thank you.

Your questions deal with a quite complex subject. I have obtained input from Dr. Scott Sicherer of the Mt. Sinai School of Medicine in New York. Dr. Sicherer and his colleagues are among the leading experts in food allergy in the world. His comments are enclosed below. I do not know where you are located geographically. However, if it feasible to have your patient seen for evaluation by the group in the Mt. Sinai Medical Center in New York, that may be quite beneficial (likely several visits would be required).

Dr. Sicherer's comments

This family physician presents a patient with a complex clinical presentation that is difficult (and inappropriate) to try to completely address in this format. I will provide a few points that may be helpful.

There are a number of gastrointestinal manifestations of food allergy in infants (proctocolitis syndrome, enteropathy syndrome, food protein-induced enterocolitis syndrome, eosinophilic gastroenteropathies, reflux syndromes, etc). Most of the disorders, particularly ones that are isolated to the gut and occur in a delayed manner after ingestion, are presumed to be cell-mediated. More specifically, tests for IgE antibodies to foods are usually negative. Thus, a negative test (serum food-specific IgE or a prick skin test to the food) would not rule-out a problem with a particular food.

Conversely, a positive test may or may not be informative. People have been looking into using "patch tests" to foods (similar to tests used for contact dermatitis) to predict outcomes; while studies so far show some promise, this is still at this time in the experimental stages.

In diagnosing and treating a patient like this, I have to suggest that direct (e.g., full history, physical, testing, etc) expert input from an allergist, gastroenterologist, and likely both types of specialists, and ideally also a dietitian is extremely helpful and really necessary. The type of illness described could be Food Protein-Induced Enterocolitis Syndrome. Some children with this disorder have quite severe reactions (even though they are not IgE antibody mediated) with vomiting, lethargy, pain, hypotension and even acidemia and methemoglobinemia about 2 hours following ingestion of the food. Therefore, a definitive diagnosis, various tests, careful dietary evaluations (for calories and also possible milk/soy contamination of the diet that could cause subclinical problems with failure to thrive), possible oral food challenges, etc would be needed for care of this child. In addition, persons knowledgeable about gastrointestinal allergic disorders would suggest particular low risk foods to try or high risk foods to avoid (or perform oral food challenges) and follow the child over time for possible resolution of the allergy.

In regard to the MMR, the RED BOOK is an excellent resource for Pediatricians and Family Practice physicians in regard to vaccines that are or are not an issue for children with food allergies. Specifically in regard to egg and MMR, the book indicates, based upon original research articles, that the MMR does not contain significant egg protein and is therefore not a particular risk for persons with egg allergy (there are other vaccines with appreciable egg protein). Children with egg allergy had about the same risk of an immediate allergic reaction to the vaccine as persons without an egg allergy (e.g., anyone could have a reaction to a vaccine, those with egg allergy were not at extra risk).

The data is really about IgE mediated egg allergy (anaphylaxis), but I am not aware of gastrointestinal reactions or systemic reactions to the vaccine in persons with gastrointestinal, non-IgE mediated food allergy.

Here are several references that may be helpful:

(1) Sampson HA, Anderson JA. Summary and recommendations: Classification of gastrointestinal manifestations due to immunologic reactions to foods in infants and young children. J.Pediatr.Gastroenterol.Nutr. 30, S87-S94. 2000.

(2) Sicherer SH. Food protein-induced enterocolitis syndrome: case presentations and management lessons. J Allergy Clin Immunol 2005; 115(1):149-56.

(3) Sicherer SH. Clinical aspects of gastrointestinal food allergy in childhood. Pediatrics 2003; 111(6 Pt 3):1609-16.

(4) Nowak-Wegrzyn A, Sampson HA, Wood RA, Sicherer SH. Food protein-induced enterocolitis syndrome caused by solid food proteins. Pediatrics 2003; 111(4 Pt 1):829-35.

(5) Sampson HA, Sicherer SH, Birnbaum AH. AGA technical review on the evaluation of food allergy in gastrointestinal disorders. American Gastroenterological Association. Gastroenterol 2001; 120(4):1026-40.

7/14/05 re: Skin test vs RAST in the diagnosis of food allergy

I am a dietitian and have a child with severe (anaphylactic) food allergies-known are pistachios and cashews and peanuts. Peanuts were tested in '98 with the RAST and came out #1116 or class I. 2 years later I had her tested with a skin prick test and she came out with an MT of 12-30. Histamine was MT 8-27. Is there a table of values for the skin prick? I ask because I did not even realize that her allergy to peanuts had gotten so much worse until her allergist (different than the one who gave her the skin prick test-although he had the records of it) told me LAST YEAR that my dau is "reactive" to peanuts and prescribed EpiPen for them also. I, obviously, don't recall the other allergist nforming me of the severe peanut allergy and although I had looked at the test results more than once, I just figured it was probably getting worse but had no idea how much worse as there are no reference ranges given, such as with the RAST testing.My second question is concerning antihistamines and food allergies. I have tried to look this up but found nothing. If antihistamine helps to block the histamine from releasing, shouldn't taking an antihistamine daily help prevent or lesson the severity an anaphylactic reaction if the anaphylaxis-causing allergen is ingested in small amounts, by accident? Thank you so much in advance! This is a fabulous, educational website!

I do not know where the RAST tests in 1998 were done in your daughter's case but the results you describe are not the usual way such tests are reported. Most labs state the levels in kU/L of IgE antibodies against the food tested. I have enclosed below portions of an excellent review of food allergy by Dr. Hugh Sampson of the Mt. Sinai Med Center in New York, one of the leading food allergy experts in the world. As Dr. Sampson points out, there has been considerable progress in the past few years in the blood test techniques used to measure IgE antibodies against food allergens. Therefore, most experts use results of a quantitiative CAP-FEIA or similar tests instead of the older (qualitative) RAST test for the reasons given by Sampson . Thus, it would be quite difficult to compare results in the previous RAST with that obtained with current techniques. Levels of IgE antibodies by CAP-FEIA higher than a certain level (with the cut-off level varying with the particular food involved), are strongly correlated with clinical reactivity to that food. These exact levels are shown in Table VI of Dr. Sampson's review article.

However, occasionally, an individual can be clinically sensitive to a food such as peanuts in face of a negative blood test for IgE antibodies. The skin prick test may be more sensitive diagnostically in such cases. Your description suggests that your daughter's skin test response to peanuts was positive (see Dr. Sampson's description of food skin tests enclosed). One cannot quantify the degree of such reactivity using screening skin tests, as you requested, for several reasons (which would require a detailed immunologic explanation). One can semi-quantitate the degree of skin test reactivity by doing skin tests with a set of carefully prepared dilutions of the usual testing material. However, this is not generally done in usual clinical practice.

Thus, one cannot reliably compare the degree of sensitivity in current investigation of your daughter with that done back in 1998. It is certainly conceivable that your daughter is more sensitive to peanut than in 1998 but one cannot say this with certainty. In practical terms, if the history suggests peanut allergy and the skin test is positive, I would assume that she is clinically sensitive and act accordingly. If the history does not suggest peanut sensitivity, one might consider a cautious oral challenge starting with minute amounts of peanut. However, such challenges should be done under special observation with emergency equipment on hand. It may not be advisable if the previous reaction in your daughter was truly anaphylactic.

In response to your other question, the antihistamines used clinically do not inhibit the release of histamine as you suggested. They work by competing with histamine for binding to a particular receptor on tissues. Because such competition occurs for only a limited period of time after each dose of the antihistamine, it may not prevent a reaction if a large amount of histamine is released in an anaphylactic reaction. Also, there is evidence that allergic mediators other than histamine may be released during anaphylactic reactions. Therefore, taking non-sedating antihistamines all the time should do no harm and may help. However, one cannot rely on such an approach to completely prevent an anaphylactic reaction. One should not stop taking steps to avoid offending food allergens because one is taking antihistamines.

From Sampson, H- J.
Allergy Clin Immunol 2004; 113: 805-19

For IgE-mediated disorders, skin prick tests p