Allergia alimentare ed esofagite eosinofila. Imparare cosa evitare


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Allergia alimentare ed esofagite eosinofila. Imparare cosa evitare

  1. 1. REVIEWCME EDUCATIONAL OBJECTIVE: Readers will be familiar with the mechanisms, diagnosis, and current treatmentCREDIT of food allergies Sandra Hong, Md nicola M. Vogel, Md Respiratory Institute, Allergy Associates of New Hampshire, Cleveland Clinic PortsmouthFood allergy and eosinophilicesophagitis: Learning what to avoid■ ■ABSTRACT Min thechildren various foodsontheseriseto than ore be allergic to and even adults seem past. Also apparently the days is Food allergies have increased in prevalence significantly in the past decade and so, apparently, has eosino- a linked condition, eosinophilic esophagitis. philic esophagitis. Although the cause of eosinophilic The reason for these increases is not clear. esophagitis is unknown, allergic responses including This article confines itself to what we know about the mechanisms of food allergies and eo- food allergies have been implicated. This article reviews sinophilic esophagitis, how to diagnose them, both conditions, focusing on how to detect and manage and how to treat them. them.■ ■KEY POINTS ■ FOOD ALLERGIES ARE COmmOn, AnD mORE pREvALEnt thAn EvER Food allergies can be classified as mediated by immuno- globulin E (IgE-mediated), non-IgE-mediated, or mixed. Food allergies—abnormal immune responses Their clinical presentation can vary from life-threatening to food proteins1—affect an estimated 6% to anaphylaxis in IgE-mediated reactions to chronic, de- 8% of young children and 3% to 4% of adults layed symptoms as seen in eosinophilic esophagitis (a in the United States,2,3 and their prevalence mixed reaction). appears to be rising in developed countries. Studies in US and British children indicate that peanut allergy has doubled in the past de- The diagnosis of an IgE-mediated food allergy is made cade.4 by taking a complete history and performing directed Any food can provoke a reaction, but only testing—skin-prick testing or measurement of food- a few foods account for most of the significant specific IgE levels in the serum, or both. allergic reactions: cow’s milk, soy, wheat, eggs, peanuts, tree nuts, fish, and shellfish. Despite promising developments, food allergies continue The prevalence of food allergy is greatest to be treated primarily by telling patients to avoid aller- in the first few years of life (Table 1).2 Allergies gens and to initiate therapy if ingestion occurs. to milk, egg, and peanuts are more common in children, while allergies to tree nuts, fish, and shellfish are more common in adults.2,5 Because most patients with eosinophilic esophagitis Approximately 80% of allergies to milk, have a strong history of atopic disease and respond to egg, wheat, and soy resolve by the time the pa- allergen-free diets, a complete evaluation by a specialist tient reaches early adolescence.6 Fewer cases in allergy and immunology is recommended. resolve in children with tree nut allergies (ap- proximately 9%) or peanut allergy (20%),7,8 and allergies to fish and shellfish often develop or persist in adulthood. A family history of an atopic disease such doi:10.3949/ccjm.77a.09018 as asthma, allergic rhinitis, eczema, or food al- CL EVEL AND CL I NI C J O URNAL O F M E DI CI NE V O L UM E 77 • NUM BE R 1 J ANUARY 201 0 51
  2. 2. FOOD ALLERGY AND EOSINOPHILIC ESOPHAGITIS gamma-delta T cells, and CD8+ suppressor tAbLE 1 cells can all contribute to suppressing allergic Prevalence of food allergies responses.10 Dendritic cells also help induce in the United States tolerance by stimulating CD4+ T cells to se- crete transforming growth factor beta, which FOOD ChILDREn ADULtS leads to the production of interleukin 10 and milk 2.5% 0.3% additional transforming growth factor beta.11 Egg 1.3% 0.2% Factors that contribute to food allergy peanut 0.8% 0.6% Many factors may contribute to whether a tree nuts 0.2% 0.5% person becomes tolerant to or sensitized to a Fish 0.1% 0.4% specific food protein. The dose of antigen. Tolerance can devel- Shellfish 0.1% 2.0% op after either high or low doses of antigens, Overall 6% 3.7% but by different mechanisms. FROM SAMpSON HA. UpDAtE ON FOOD ALLERgY. J ALLERgY CLIN The antigen structure. Soluble antigens are IMMUNOL 2004; 113:805–819; WItH pERMISSION FROM ELSEVIER, WWW.SCIENCEDIRECt.COM/SCIENCE/JOURNAL/00916749 less sensitizing than particulate antigens.12,13 Processing of foods. Dry-roasted peanuts are more allergenic than raw or boiled pea- lergy is a risk factor for developing a food aller- nuts, partly because they are less soluble.13 gy.3 Considering that the rate of peanut allergy The route of initial exposure. Sensiti- has doubled in children over the past 10 years, zation to food proteins can occur directly environmental factors may also play a role.3 through the gut or the skin. Alternatively, it can occur indirectly via the respiratory tract. how we tolerate foods Skin exposure may be especially sensitizing in or become allergic to them children with atopic dermatitis.14,15 The gut, the largest mucosal organ in the The gut flora. When mice are raised in aMost common body, is exposed to large quantities of foreign germ-free environment, they fail to developfood allergens: proteins daily. Most protein is broken down by normal tolerance.16 They are also more likely stomach acid and digestive enzymes into less- to become sensitized if they are treated withcow’s milk, antigenic peptides or is bound by secretory antibiotics or if they lack toll-like receptorssoy, wheat, immunoglobulin A (IgA), which prevents it that recognize bacterial lipopolysaccharides.17 from being absorbed. Further, the epithelial Furthermore, human studies suggest that pro-eggs, peanuts, cells lining the gut do not allow large mole- biotics promote tolerance, especially in pre-tree nuts, fish, cules to pass easily, having tight intracellular venting atopic dermatitis, although the stud-shellfish junctions and being covered with mucus. ies have had conflicting results.18–21 For these reasons, less than 2% of the pro- The gastric pH. Murine and human stud- tein in food is absorbed in an allergenic form.9 ies reveal that antacid medications increase The reason food allergies are more prevalent the risk of food allergy.22,23 in children is most likely that children have Genetic susceptibility. A child with a sib- an immature gut barrier, lower IgA levels, a ling who is allergic to peanuts is approximate- higher gastric pH, and lower proteolytic en- ly 10 times more likely to be allergic to pea- zyme levels. nuts than predicted by the rate in the general When dietary proteins do cross the gut population. Although no risk-conferring gene barrier, the immune system normally suppress- has been identified, a study of twins showed es the allergic response. Regulatory T cells, concordance for peanut allergy in 64.3% of dendritic cells, and local immune responses identical twins vs 6.8% of fraternal twins.24 play critical roles in the development of toler- ance. Several types of regulatory T cells, such three types of immune responses to food as Tr1 cells (which secrete interleukin 10), About 20% of all people alter their diet be- TH3 cells (which secrete transforming growth cause of concerns about adverse reactions to factor beta), CD4+CD25+ regulatory T cells, foods.3 These adverse reactions include meta- 52 CLEV ELA N D C LI N I C JO URNAL OF MEDICINE VOL UME 77 • NU M BE R 1 J ANUARY 2010
  3. 3. HONG AND VOGELbolic disorders (eg, lactose intolerance), a re- tAbLE 2action to a pharmacologic component such ascaffeine or a toxic contaminant of a food (eg, Classification of adverse reactions to foodsbacterial food poisoning), psychological re-actions (eg, food aversion), and documented Intolerance (nonallergenic)immunologic responses to a food (eg, food al- Lactose intolerancelergy) (Table 2).2,3,25 Galactosemia Alcohol Immunologic reactions to foods can be di-vided into three categories: mediated by im- pharmacologicmunoglobulin E (IgE), non-IgE-mediated, and Caffeinemixed. Therefore, these disorders can present Tyramine in aged cheesesas an acute, potentially life-threatening reac- Alcoholtion or as a chronic disease such as eosino- toxicphilic gastoenteropathy. Bacterial food poisoning IgE-mediated reactions are immediate hy- Food allergypersensitivity responses. In most patients, an Mediated by immunoglobulin E (IgE) (acute onset)IgE-mediated mechanism can be confirmed by Urticaria, angioedemaa positive skin test or a test for food-specific Rhinitis, asthmaIgE in the serum. In this article, the term “food Anaphylaxisallergy” refers to an IgE-mediated reaction to a Food-associated exercise-induced anaphylaxisfood, unless otherwise indicated. Pollen-food allergy syndrome Non-IgE-mediated reactions have a de- (oral allergy syndrome)layed onset and chronic symptoms. Com- Non-IgE-mediated (delayed-onset, chronic symptoms)monly, they are confined to the gastrointesti- Celiac disease, dermatitis herpetiformisnal tract; examples are food-protein-induced Contact dermatitisenterocolitis, proctitis, and proctocolitis and Dietary protein enterocolitisceliac disease.3,26,27 However, other diseases Dietary protein proctitis and proctocolitissuch as contact dermatitis, dermatitis herpeti- Heiner syndrome (food-induced pulmonary hemosiderosis)formis, and food-induced pulmonary hemosid- Mixed (IgE-mediated and non-IgE-mediated)erosis (Heiner syndrome) are also considered Eosinophilic gastroenteropathiesnon-IgE-mediated allergies. (including eosinophilic esophagitis) Mixed-reaction disorders are chronic and Atopic dermatitisinclude the eosinophilic gastroenteropathies,ie, eosinophilic proctocolitis, eosinophilic Symptoms similar to food allergy Auriculotemporal syndromegastroenteritis, and eosinophilic esophagitis.28 Scombroid fish poisoningThe pathophysiology of these diseases is poor-ly understood. Many patients have evidence ADAptED FROM SICHERER SH, SAMpSON HA. FOOD ALLERgY.of allergic sensitivities to food or to environ- J ALLERgY CLIN IMMUNOL 2006; 117:S470–S475; WItH pERMISSION FROM ELSEVIER, WWW.SCIENCEDIRECt.COM/SCIENCE/JOURNAL/00916749.mental allergens, or both, but whether thesesensitivities have a causal role in these disor-ders is not clear. Atopic dermatitis, another complicated prit foods, the quantity eaten, the timing ofdisease process, may be associated with mixed- the onset of symptoms, and related factorsreaction food allergy, as approximately 35% of such as exercise, alcohol intake, or medica-young children with moderate to severe atopic tion use. Symptoms of an IgE-mediated reac-dermatitis have food allergies.29 tion are generally rapid in onset but may be delayed up to a few hours, while non-IgE me-Diagnosis of IgE-mediated food allergies diated symptoms may present several hours to A thorough history and physical exami- days later.nation are key to diagnosing an IgE-mediated Food challenge. A double-blind, placebo-food allergy. controlled oral food challenge is the gold stan- The history should include potential cul- dard for the diagnosis of food allergies. (The CL EVEL AND CL I NI C J O URNAL O F M E DI CI NE V O L UM E 77 • NUM BE R 1 J ANUARY 201 0 53
  4. 4. FOOD ALLERGY AND EOSINOPHILIC ESOPHAGITIS Immunoassays are generally less sensitive tAbLE 3 and more costly than skin-prick tests, and their results are not immediately available, Predictive values of specific immunoglobulin E unlike those of skin-prick testing. However, for selected food allergens these in vitro tests are not affected by anti- ALLERGEn ImmUnOGLObULIn E (kIU/L) a histamine use and are useful in patients with mEAn AGE 5 YEARS, mEAn AGE 5 YEARS, AGE ≤ 2 YEARS, severe dermatologic conditions or severe ana- 50% REACt 95% REACt 95% REACt phylaxis, for whom skin-prick testing would Egg 2 7 2 not be appropriate. milk 2 15 5 As with the response size in the skin- prick test, the higher the concentration of a peanut 2 (convincing history) 14 — food-specific IgE, the higher the likelihood 5 (unconvincing history) of a clinical reaction.29 Threshold values a Measured by Pharmacia CAP system fluorescent enzyme immunoassay of food-specific IgE have been established FROM SICHERER SH, SAMpSON HA. FOOD ALLERgY.J ALLERgY CLIN IMMUNOL 2006; 117:S470–S475, above which the likelihood that the patient WItH pERMISSION FROM ELSEVIER; WWW.SCIENCEDIRECt.COM/SCIENCE/JOURNAL/00916749. will experience an allergic reaction is greater than 95% (Table 3).3,29,31 However, unlike a negative skin-prick food to be tested is hidden in other food or in test, an undetectable serum food-specific IgE capsules.) However, this test poses significant level has a low negative predictive value, and risks, and other diagnostic methods are more an undetectable level may be associated with practical for screening. symptoms of an allergic reaction for 10% to Skin-prick tests with commercially avail- 25% of patients.29 Therefore, if one suspects able extracts are a rapid and sensitive method an allergic reaction but no food-specific IgE of screening for allergy to several foods. can be detected in the serum, confirming the Negative skin-prick tests have an esti- absence of a clinical allergy must be done with mated negative predictive value of more than a skin-prick test or with a physician-supervisedIgE-mediated 95% and can therefore exclude IgE-mediated oral challenge, or both.reactions are food allergies. A positive test indicates the presence of IgE managing food allergyusually against a specific food allergen and suggests a by avoiding the allergenimmediate; clinical food allergy, although the specificity Food allergies are managed by strictly avoiding of the test is only about 50%, making a posi- food allergens and by taking medications suchnon-IgE and tive result difficult to interpret. Although the as self-injectable epinephrine for anaphylacticmixed reactions size of the skin-test response does not neces- symptoms.are delayed sarily correlate with the potential severity of Patients and caregivers must be educated a reaction, a response larger than 3 mm does about reading food labels, avoiding high-riskor chronic indicate a greater likelihood of clinical reac- situations such as eating at buffets and other tivity. A positive test is most helpful in con- restaurants with high risk of cross-contami- firming the diagnosis of IgE-mediated food al- nation, wearing a medical-alert bracelet, rec- lergy when combined with a clear history of ognizing and managing early symptoms of an food-induced symptoms. allergic reaction, and calling for emergency The proteins in commercially based ex- services if they are having an allergic reaction. tracts of most fruits and vegetables are often Since January 2006, the US Food and Drug labile; therefore, skin testing with fresh fruits Administration has required food manufac- and vegetables may be indicated.30 turers to list common food allergens on food Immunoassays. Radioallergosorbent tests labels (cow’s milk, soy, wheat, egg, peanut, (RASTs) and fluorescent enzyme immuno- tree nuts, fish, and shellfish), and the labeling assays are used to identity food-specific IgE must use simple, easily understood terms, such antibodies in the serum. The commercially as “milk” instead of “whey.” However, it is still available tests do not use radioactivity, but the prudent to read all ingredients listed on the term “RAST” is still commonly used. label. 54 CLEV ELA N D C LI N I C JO URNAL OF MEDICINE VOL UME 77 • NU M BE R 1 J ANUARY 2010
  5. 5. HONG AND VOGELExperimental treatments for food allergies field in at least one esophageal biopsy Humanized monoclonal anti-IgE antibod- specimenies such as talizumab (also known as TNX- • No response to a proton-pump inhibi-901) and omalizumab (Xolair) have been de- tor in high doses (up to 2 mg/kg/day) forveloped, but their use in food allergy has been 1 to 2 months, or normal results on pHlimited. In a study in patients with peanut probe monitoring of the esophagus (theallergy, injections of talizumab increased the reason for this criterion is that patientsthreshold for sensitivity to peanuts in most with gastroesophageal reflux disease canpatients, but 25% of the patients did not have also have large numbers of eosinophils inany improvement.32 A study of omalizumab in the esophagus—more than 100 per high-patients with peanut allergy was stopped after power field38)adverse reactions developed during oral pea- • Exclusion of other causes.nut challenges.33 Though the cause of eosinophilic esopha- Oral immunotherapy. Recent studies gitis is not completely understood, atopy hassuggest it may be possible to induce oral been strongly implicated as a factor. Moretolerance in patients with IgE-mediated than 50% of patients with eosinophilicfood allergy. Pilot studies have shown that esophagitis also have an atopic condition (eg,frequent, increasing doses of food aller- atopic dermatitis, allergic rhinitis, asthma), asgens (egg, milk, and peanut) may raise the well as positive results on skin-prick testingthreshold at which symptoms occur.34–36 or measurement of antigen-specific IgE in theThough these studies suggest that oral im- serum.39–41 Also, since most patients improvemunotherapy may protect some patients with either dietary restriction or elementalagainst a reaction if they accidentally ingest diets, food sensitization appears to play a con-a food they are allergic to, some patients siderable role.could not reach the goal doses because al- As with atopic conditions such as asth-lergic symptoms were provoked. ma, atopic dermatitis, allergic rhinitis, and At this early stage, these strategies must be food allergy, eosinophilic esophagitis hasconsidered investigational, and more random- been linked with immune responses involv- Skin-prick plusized, placebo-controlled studies are needed. ing helper T cell 2 (TH2). Adults and chil- patch testingFurther studies will also be needed to assess dren with eosinophilic esophagitis have beenwhether oral immunotherapy induces only found to have elevated eosinophil counts may be moreshort-term desensitization (in which case the and total IgE levels in peripheral blood.37 effective thanallergen needs to be ingested daily to prevent In the esophagus, patients have elevatedreactions) or sustained tolerance (in which levels of the TH2 cytokines often seen in skin-prickcase the antigenic protein can be ingested atopic patients (eg, interleukins 4, 5, and testing alonewithout symptoms despite periods of absti- 13) and mast cells.42,43 In mice, eosinophilic in identifyingnence). esophagitis can be induced by allergen expo- sure and overexpression of TH2 cytokines.44,45 potential food■ thE ROLE OF FOOD ALLERGY Expression of eotaxin-3, a potent eosinophil triggers In EOSInOphILIC ESOphAGItIS chemoattractant, was noted to be higher in children with eosinophilic esophagitis thanEosinophilic esophagitis has been recognized in controls.46with increasing frequency in both children Of interest, some patients with eosino-and adults over the past several years. Symp- philic esophagitis say their symptoms varytoms can include difficulty feeding, failure to with the seasons, correlating with seasonalthrive, vomiting, epigastric or chest pain, dys- changes in esophageal eosinophil levels.47,48phagia, and food impaction. Diagnostic criteria for eosinophilic esophagi- Studies linking eosinophilic esophagitistis are37: and food allergy in children• Clinical symptoms of esophageal dysfunc- A link between food allergy and eosinophilic tion esophagitis was initially suggested when pa-• At least 15 eosinophils per high-power tients who had eosinophilic esophagitis im- CL EVEL AND CL I NI C J O URNAL O F M E DI CI NE V O L UM E 77 • NUM BE R 1 J ANUARY 201 0 55
  6. 6. FOOD ALLERGY AND EOSINOPHILIC ESOPHAGITIS tAbLE 4 Response to dietary manipulation in patients with eosinophilic esophagitis StUDY n AGE DIEt SYmptOmS DECREASE In ImpROvED OR EOSInOphILS (%) RESOLvED (%) Kelly et al (1995)49 10 8 mo–12.5 yr Elemental 100 100 Markowitz et al (2003) 50 51 8.3 ± 3.1 yr Elemental 96 96 Liacouras et al (2005) 39 247 10.4 ± 5.2 yr Restricted 57 a 57 8.1 ± 4.3 yr Elemental 97 97 Kagalwalla et al (2006)51 60 6.3 yr (mean) Six-food elimination b 97 74 Elemental 100 88 Gonsalves et al (2008)52 18 19–70 yr Six-food elimination 94 78 Simon et al (2006) 53 6 25.8 ± 9.0 yr No wheat or rye 17 0 a Of 132 patients, 75 improved with dietary restriction; 57 patients who did not respond were included in the 172 patients started on an elemental diet; 160 of the 164 patients compliant with the elemental diet had significant improvement of symptoms and a significant decrease in the number of eosinophils in the esophagus. b Six-food elimination: milk, soy, wheat, egg, peanut, and seafood proved when put on an elemental or allergen- food was reintroduced into the diet. free diet (Table 4).39,49–53 Most of the studies In a retrospective study, Kagalwalla et al51 linking food allergy and eosinophilic esophagi- reported that 60 children with eosinophilic tis have been in children. esophagitis were treated with either an ele-It may be Kelly et al49 reported that 10 children with mental diet or a six-food elimination diet (nopossible to chronic symptomatic gastroesophageal reflux milk, soy, wheat, egg, peanut, or seafood). The and eosinophilic esophagitis all had partial two groups showed similar clinical and histo-induce oral or complete resolution of symptoms on an el- logic improvements.tolerance emental diet. Collectively, these studies in pediatric pa- found that symptomsin patients with of Markowitz et aldisease and eosinophilic tients imply that food allergy is a significant 50 chronic reflux factor in the pathogenesis of eosinophilicIgE-mediated esophagitis improved in 49 of 51 children on allergy an elemental diet, and the number of eosino- phils in the distal esophagus decreased signifi- Studies in adults cantly. Fewer studies of the link between food allergy Liacouras et al39 reported similar findings and eosinophilic esophagitis have been done in a 10-year experience. Of 132 children who in adults. had eosinophilic esophagitis, 75 improved In a preliminary study, 18 adults followed with dietary restriction based on results of the six-food elimination diet. Symptoms im- skin-prick and patch testing. The 57 patients proved in 17 (94%), and histologic findings who did not respond and 115 others were improved in 14 (78%).52 started on an elemental diet. Of the 164 pa- On the other hand, in six adult patients tients who complied with the elemental diet, with eosinophilic esophagitis, Simon et al53 160 had significant improvement of symptoms found that only one had improvement in symp- and a significant decrease in the number of toms after eliminating wheat and rye from the eosinophils in the esophagus. Individual foods diet, and none had significant changes in the were reintroduced approximately every 5 days, number of eosinophils in the esophagus. and esophagogastroduodenoscopy with biop- In a 37-year-old man with eosinophilic sies was performed 4 to 8 weeks after the last esophagitis, symptoms improved after elimi- 56 CLEV ELA N D C LI N I C JO URNAL OF MEDICINE VOL UME 77 • NU M BE R 1 J ANUARY 2010
  7. 7. HONG AND VOGELnating egg from his diet.54 Atopy patch testing. The combination Yamazaki et al55 measured expression of of skin-prick testing and atopy patch testinginterleukin 5 and interleukin 13 in 15 adult may be more effective than skin-prick test-patients with eosinophilic esophagitis. Food ing alone in identifying potential food trig-and aeroallergens that included milk, soy, gers. Atopy patch testing has been used in thedust mite, ragweed, and Aspergillus induced diagnosis of non-IgE cell-mediated (delayed)significantly more interleukin 5 production immune responses, in which T cells may playin these patients than in atopic controls, sug- a significant role.gesting that both foods and aeroallergens may Atopy patch testing is similar to patchhave a role in the pathogenesis of eosinophilic testing for contact dermatitis. It involvesesophagitis in adults. placing a small quantity of food on the skin and evaluating for a local delayed reactionhow to identify potential food triggers after a set time.of eosinophilic esophagitis In two studies,50,57 146 children with biop-Though elemental diets have been associated sy-proven eosinophilic esophagitis had foodswith a decrease in symptoms and esophageal eliminated from the diet on the basis of posi-eosinophilia, elemental formulas are expen- tive skin-prick tests and atopy patch tests.sive and unpalatable and pose a risk of nu- Approximately 77% of the children had sig-tritional deprivation. Identifying specific nificant reduction of esophageal eosinophilsfood allergens to eliminate from the diet in in biopsy specimens (from 20 per high-powerpatients with eosinophilic esophagitis may be field to 1.1). The foods most commonly im-less expensive and more desirable than a very plicated by skin-prick testing were cow’s milk,limited or elemental diet. egg, wheat, peanut, shellfish, peas, beef, fish, However, potential food triggers have been rye, and tomato; those identified by atopyhard to identify in eosinophilic esophagitis. A patch testing were cow’s milk, egg, wheat,recent consensus report did not recommend corn, beef, milk, soy, rye, chicken, oats, andin vitro food allergy testing,37 owing to a lack potato. The combination of both types ofof positive or negative predictive values for testing had a negative predictive value of More studiesfood-specific IgE level testing in eosinophilic 88% to 100% for all foods except milk, while are neededesophagitis. Furthermore, the absence of IgE the positive predictive value was greater thandoes not eliminate a food as a potential trigger, 74% for the most common foods causing eo- to validatesince non-IgE mechanisms may play a role. sinophilic esophagitis.58 atopy patch Skin-prick testing is one of the currently Though atopy patch testing shows somevalidated diagnostic methods. Several stud- usefulness in identifying foods that may elicit testing inies have used skin-prick testing of foods in non-IgE-mediated reactions, currently these patients withpatients with eosinophilic esophagitis. In tests are not validated and have been evaluat- eosinophilicthese studies, approximately two-thirds of pa- ed in only a small number of studies. Currently,tients had positive test reactions to at least no standardized testing materials, methods of esophagitisone food, most often to common food aller- application, or interpretation of results exist,gens such as cow’s milk, egg, soy, wheat, and and no studies have included a control popu-peanut, but also to rye, beef, and bean.37 In lation to validate atopy patch testing. Morea recent article,56 81% of adult patients with studies are needed to validate atopy patch test-eosinophilic esophagitis had one or more al- ing as a reliable diagnostic tool before it can belergens identified by skin-prick testing, and recommended as a component of routine diag-50% of the patients tested positive for one or nostic evaluation in patients with eosinophilicmore food allergens. esophagitis. ■■ REFEREnCES 3. Sicherer SH, Sampson Ha. 9. Food allergy. J Allergy Clin Immunol 2006; 117(suppl 2):S470–S475. 1. bruijnzeel-Koomen C, Ortolani C, aas K, et al. Adverse reactions to 4. Sicherer SH, Munoz-Furlong a, Sampson Ha. Prevalence of peanut food. European Academy of Allergology and Clinical Immunology Subcommittee. Allergy 1995; 50:623–635. and tree nut allergy in the United States determined by means of 2. Sampson Ha. Update on food allergy. J Allergy Clin Immunol 2004; a random digit dial telephone survey: a 5-year follow-up study. J 113:805–819. Allergy Clin Immunol 2003; 112:1203–1207. CL EVEL AND CL I NI C J O URNAL O F M E DI CI NE V O L UM E 77 • NUM BE R 1 J ANUARY 201 0 57
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  9. 9. HONG AND VOGEL Back by popular demand—in a new edition! Proceedings of the improvement with an amino acid-based formula. Gastro-50. enterology 1995; 109:1503–1512. Markowitz Je, Spergel JM, Ruchelli e, liacouras Ca. 4th annual Elemental diet is an effective treatment for eosinophilic esophagitis in children and adolescents. Am J Gastroen- Perioperative Medicine Summit terol 2003; 98:777–782.51. Kagalwalla aF, Sentongo Ta, Ritz S, et al. Effect of six- Supplement to food elimination diet on clinical and histologic outcomes in eosinophilic esophagitis. Clin Gastroenterol Hepatol Cleveland Clinic Journal of Medicine52. 2006; 4:1097–1102. Gonsalves N, Yang GY, Doerfler b, et al. A prospective november 2009 clinical trial of six food elimination diet and reintro- duction of causative agents in adults with eosinophilic Quality esophagitis [abstract]. Gastroenterology 2008; 134(suppl 1):A104–A105.53. Simon D, Straumann a, Wenk a, Spichtin H, Simon HU, braathen lR. Eosinophilic esophagitis in adults—no clinical relevance of wheat and rye sensitizations. Allergy Evidence-based 2006; 61:1480–1483. perioperative54. antón Remirez J, escudero R, Caceres O, Fernandez-ben- medical Care itez M. Eosinophilic esophagitis. Allergol Immunopathol (Madr) 2006; 34:79–81.55. Yamazaki K, Murray Ja, arora aS, et al. Allergen-specific Safety Outcomes in vitro cytokine production in adult patients with eo- sinophilic esophagitis. Dig Dis Sci 2006; 51:1934–1941.56. Penfield JD, lang DM, Goldblum JR, lopez R, Falk GW. Supplement Editor: The role of allergy evaluation in adults with eosinophilic Amir K. Jaffer, MD esophagitis. J Clin Gastroenterol 2009 (Epub ahead of print). University of Miami School of Medicine57. Spergel JM, andrews T, brown-Whitehorn TF, beausoleil Jl, liacouras Ca. Treatment of eosinophilic esophagitis Associate Editors: with specific food elimination diet directed by a combina- tion of skin prick and patch tests. Ann Allergy Asthma David L. Hepner, MD Immunol 2005; 95:336–343. Brigham and Women’s Hospital58. Spergel JM, brown-Whitehorn T, beausoleil Jl, Shuker M, liacouras Ca. Predictive values for skin prick test and Franklin A. Michota, MD atopy patch test for eosinophilic esophagitis. J Allergy Clin Immunol 2007; 119:509–511. Cleveland ClinicADDRESS: Sandra Hong, MD, Respiratory Institute, ST10,Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; 20 full-length articles covering the spectrume-mail of perioperative management 132 pages • CME-certified Faculty of national and international experts: • Lee Fleisher on preop cardiac risk stratification Visit our web site at http:// • Don poldermans and p. J. Devereaux debate perioperative beta-blockade contact us by e-mail at • Gerald Smetana on postop pulmonary complications • Challenging clinical cases from Steven Cohn and bobbieJean Sweitzer • Many more limited supply available. order copies today at or 216-444-2661 CL EVEL AND CL I NI C J O URNAL O F M E DI CI NE V O L UM E 77 • NUM BE R 1 J ANUARY 201 0 59