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eosinophiliC oesophaGitis ME Levin, MB ChB, FCPaed, Dip Allergy, MMed food allergy is more common, has well-defined patho- (Paed), PhD logical mechanisms and has a rapid onset and thus a Asthma and Allergy Clinic, Red Cross War Memo- clear link between exposure and symptoms. This, and rial Children’s Hospital, School of Child and Adolescent the ready availability of validated tests results in a rela- Health, University of Cape Town, Rondebosch, South tively easy diagnosis. Non-IgE-mediated food allergy, on Africa the other hand, may have unclear mechanisms of initia- tion of response and has a delayed onset of symptoms. There may therefore be no clear link between exposure to the offending food and the adverse reaction. In addi- ABSTRACT tion, tests are not well validated for non-IgE food allergy Eosinophilic oesophagitis (EO) is a mixed IgE-medi- and it is therefore far harder to diagnose. ated and non-IgE (cell)-mediated food allergy. Adults Recent literature classifies the mechanisms of initiation present predominantly with dysphagia and food im- of the symptoms of food allergy into (i) IgE-mediated, (ii) paction. Children present predominantly with vomit- mixed IgE-mediated and non-IgE-mediated (cell-mediat- ing, gastro-oesophageal reflux that does not respond ed) food allergy and (iii) non-IgE, entirely cell-mediated to medical treatment, food refusal and failure to food allergy.1 Table I lists disorders in these categories. thrive. The hallmark of the condition is oesophageal biopsy showing >15 eosinophils per high power field Eosinophilic oesophagitis (EO), an isolated eosinophilic and exclusion of other similar disorders especially inflammation of the oesophagus, is the most common gastro-oesophageal reflux disease (GORD). Skin- of the eosinophilic gastrointestinal disorders. The in- prick and patch testing are useful to identify food cidence of these diseases has increased over recent allergens responsible for triggering EO. Dietary ma- years in both adults2 and children,3 and this seems to nipulation has the best long-term results but almost be a real increase rather than an increase in diagnosis equivalent results can be achieved with topical ste- due to increased awareness of the disorders. roid administration or systemic steroids. There is ur- Older children and adults may present with food impac- gent need for study of EO in South Africa, assessing tion whereas children present with symptoms of gas- the prevalence in high-risk groups, the role of food tro-oesophageal reflux that does not respond to anti- allergies and the success of alternative methods of reflux treatment. In addition they may have feeding dif- treatment. ficulties, food refusal and failure to thrive. Patients with EO have a higher risk of associated allergic disorders such as asthma and atopic dermatitis. INTRODUCTION The mechanism of EO is not clearly elucidated but True food allergy is an immune-mediated adverse reac- both IgE- and non-IgE-mediated food allergy play a role. tion to food. Food allergy is usually divided into IgE-me- Foods such as cow’s milk, hen’s egg, soya and wheat diated and non-IgE-mediated food allergy. IgE-mediated are commonly implicated. A number of reports sug- gest familial clustering and preliminary evidence has emerged for a role of the gene encoding the eosinophil- Table I. Food allergy disorders specific chemo-attractant eotaxin-3.4 IgE-mediated Gastrointestinal Oral allergy syndrome, gastrointestinal anaphylaxis CASE VIGNETTE Cutaneous Urticaria, angio-oedema, HM presented to the asthma and allergy clinic at age morbilliform rashes and flushing 1½ years. Presenting problems were eczema, im- Respiratory Acute rhinoconjunctivitis, mediate food allergies and failure to thrive. Eczema bronchospasm (wheezing) had an early onset at the age of weaning, typical of Generalised Anaphylactic shock that related to food allergies. She had experienced itching and flaring with ingestion of peanuts. She had Mixed IgE- and cell-mediated been breastfed and her mother ate peanuts every Gastrointestinal Allergic eosinophilic oesophagitis, day. Specific IgE to peanuts was 1.6 kU/l which is allergic eosinophilic gastroenteritis raised but not above the range at which it can be Cutaneous Eczema held to be strongly predictive of IgE-mediated food allergy (14 kU/l). She had experienced urticarial skin Respiratory Asthma rashes within an hour of ingestion of milk. Specific Cell-mediated IgE to milk was 24 kU/l and skin test was 4 mm to Gastrointestinal Food protein induced enterocolitis, milk extract and 13 mm to fresh milk, both strongly food protein induced proctocolitis, suggestive of IgE-mediated food allergy (>5 kU/l and food protein induced enteropathy 6 mm respectively). She had never ingested egg, syndromes, coeliac disease but a specific IgE to hen’s egg was 6.1 kU/l and skin Cutaneous Contact dermatitis, dermatitis herpe- testing was 13 mm to fresh egg white, confirming tiformis IgE-mediated food allergy (>2 kU/l and 5 mm respec- tively). She was on a diet excluding milk, egg and Respiratory Food-induced pulmonary haemo- peanuts under the supervision of a dietician. siderosis (Heiner syndrome) Correspondence: Dr M Levin, firstname.lastname@example.org 22 Current Allergy & Clinical Immunology, March 2010 Vol 23, No. 1 The differential diagnosis of oesophageal eosinophilia includes GORD, food allergy, candida oesophagitis, eo- Feeding was a significant problem. The mother was sinophilic gastroenteritis, inflammatory bowel disease, struggling to get her to drink her soya milk. She was coeliac disease and parasitic infection. Rarer causes refusing to eat foods and when she did ingest solids include connective tissue disease, drug allergy, hyper- she took a very long time to eat. She had occasional eosinophilic syndrome, autoimmune enteropathy, viral vomiting. Stools were normal. oesophagitis (herpes or cytomegalovirus) and Churg- At this stage the differential diagnosis was gastro- Strauss syndrome. oesophageal reflux disease (GORD) and EO with resulting malnutrition and rickets. The following spe- cial investigations were performed. Blood chemistry Endoscopy tests showed normal electrolytes, calcium, mag- Endoscopic appearance may be grossly abnormal, have nesium and phosphate and a raised alkaline phos- subtle abnormalities or be macroscopically normal. phatase level of 1430 (upper limit of normal up to Common features include concentric rings and linear 140 in children) with normal liver function tests, sug- furrows. When these coexist a cobblestoned appear- gestive of early rickets. She had a white cell count ance is produced. White plaques of eosinophilic infiltra- of 11.3 with an eosinophil count of between 4% tion may be mistaken macroscopically for candidal in- and 8% on repeated samples (normal range 0-4%). fection. Aggregates of eosinophils may produce visible A barium swallow revealed reflux to the thoracic micro-abscesses. Normal endoscopy does not exclude inlet. An upper gastrointestinal endoscopy was nor- EO, thus all endoscopic evaluation of EO must be fol- mal macroscopically and biopsy of the oesophagus lowed up with biopsies even when endoscopy is mac- and stomach was performed. Oesophageal biopsy roscopically normal.5 showed a peak concentration of 35 eosinophils per high power field (hpf). Figure 1 shows another oe- Biopsies sophageal biopsy. The hallmark of EO is eosinophilic infiltration of the squamous epithelium. There is no consensus as to what quantity of eosinophils is pathognomonic of the EOSINOPHILIC OESOPHAGITIS condition with some studies using as few as 5 per hpf Eosinophilic oesophagitis (EO) has been described in and others up to 30 per hpf, but a recent consensus patients from all ethnic backgrounds in studies origi- statement uses 15 as a cut-off level.5 Other minor fea- nating in all continents apart from Africa.5 There is no tures on biopsy may include basal zone hyperplasia, clear ethnic, racial or socioeconomic predilection. EO increased papillary size, intercellular oedema, lamina does have a male predilection and has been reported in propria fibrosis and layering of eosinophils resulting in paediatric and adult populations. In children, the mean aggregates or micro-abscesses.10 age of presentation is 7-10 years and in adults 30-40 GORD can also result in eosinophilic infiltration but at years, but these data may reflect the age at which the a lower level of up to 10 per hpf. In addition the dis- diagnosis is most commonly made as a result of patient tribution of infiltration in the oesophagus will be pre- complaints raising the possibility, rather than reflecting dominantly distal, starting from the gastro-oesophageal the true peak age of the condition. EO may occur in junction spreading proximally with increased severity of very young infants and toddlers.6 Adults often complain disease, whereas in EO the histological abnormalities of dysphagia, food impaction, reflux symptoms, chest typically involve longer lengths of the oesophagus, af- pain, abdominal pain and vomiting and 25-50% have fect the proximal equally, or even more, than the distal concomitant allergies.7 Children experience abdominal oesophagus, and the pathological findings are often pain, vomiting, gastro-oesophageal reflux that does not patchy in distribution.10 For this reason it is highly rec- respond to medical treatment, and failure to thrive. Food ommended to take biopsy specimens from the distal, refusal or intolerance is the presenting complaint in chil- mid and proximal oesophagus to assess the distribu- dren too young to complain of symptoms. Other con- tion of pathology as well as from macroscopically nor- comitant allergic diseases are present in 50-80%.8,9 mal and abnormal areas. Taking 1 biopsy specimen has a sensitivity of 55% in contrast to a sensitivity of 100% from 5 specimens.11 Biopsy specimens should also be taken from the duodenum and stomach to rule out other diseases such as eosinophilic gastroenteritis and inflammatory bowel disease. The concept of a cut-off level for eosinophil count per hpf is therefore an oversimplification as the number of eosinophils varies according to the site of the biopsy. In addition there may be many patients whose symptoms are typical of EO, who respond to treatment for EO rather than GORD and who therefore should be con- sidered as fulfilling the case definition for EO despite not qualifying according to the degree of eosinophilic infiltration on biopsy. Brigger et al.12 assessed the accu- racy of histopathological diagnosis in distinguishing EO from GORD in children by repeating the assessment of biopsy specimens in 31 patients with EO, GORD or Fig. 1. Oesophageal biopsy of a different patient show- neither, with the pathologist blinded as to the clinical ing squamous epithelium (light pink) interspersed with presentation and response to therapy. Diagnostic con- many eosinophils (granular red cytoplasm and bilobed currence between the masked pathological diagnosis blue nuclei). (Material provided by Dr Komala Pillay, De- and the established clinicopathological diagnosis was partment of Histopathology, National Health Laboratory 64% in children with EO, 70% in children with GORD, Services and University of Cape Town). and 100% in children with neither. Current Allergy & Clinical Immunology, March 2010 Vol 23, No. 1 23 The distinction between EO and GORD can therefore Dietary modification not be reliably made on histopathological evidence Controversy exists over the choice of a targeted diet alone. All biopsy specimens should be interpreted in that eliminates suspected foodstuffs or a totally ele- the light of the clinical findings on history and examina- mental diet. Because EO is a mixed IgE- and cell-me- tion and patients with typical findings whose biopsies diated process, history, skin tests and allergen-specific do not reveal >15 eosinophils per hpf may also benefit IgE tests alone are insufficient to guide an elimination from a trial of therapy. In addition biopsy specimens diet. Patch tests may give additional information about revealing isolated oesophageal eosinophilia while the cell-mediated allergic food hypersensitivity. patient is on an adequate dose of acid suppression is virtually pathognomonic of EO. Targeted food avoidance Spergel et al.’s13 use of skin and patch tests to identify Laboratory features foods suspected of triggering EO allowed targeted food The sensitivity and specificity of laboratory tests are not avoidance to be instituted with 18 patients experienc- known. Peripheral eosinophilia is reported to be pres- ing complete resolution and 6 partial resolution. The ent in 10-50% of adults and 20-100% of children.5 This most common foods were milk, egg, soya, chicken and and raised total IgE may indicate background atopic wheat. A follow-up study15 identified 146 children with predisposition and not be specific or sensitive for EO. EO and eliminated foods based on skin and patch tests Antigen specific IgE may be raised due to specific im- (including 14% who required elemental diets because mediate food allergies or due to involvement of food as of multiple positive food tests). Seventy-seven per cent a trigger for EO, but no positive or negative predictive of subjects in this study had resolution on biopsy and values for any foods have been elucidated. Skin-prick in a 10-year review16 a 98% clinical response rate to test and patch tests are commonly positive in subjects dietary restriction was observed. with EO. Elemental diet Skin-prick testing Kagalwalla et al.17 compared a standard 6-foods avoid- Approximately two-thirds of all paediatric patients have ance diet with elemental diet in 50 children with EO. positive skin tests to at least one food. The number of Seventy-four per cent of children on the specific avoid- foods tested in studies typically ranges from an aver- ance diet had symptom resolution and histological age of 13 to a maximum of 42 foods.5 In adults, the response, compared with 88% of the children on the presence of positive skin tests to foods is uncommon elemental diet. The post-treatment eosinophil counts unless there is a history of immediate food hypersensi- were much lower in the extensively hydrolysed group tivity to a particular food. The most common foods re- (3.7 per hpf vs 13.6 per hpf), but the initial eosinophil ported to be positive by skin test include peanuts, eggs, count in this group was also somewhat lower at 58.8 soya, cow’s milk, wheat, beans, rye and beef. per hpf vs 80.2 per hpf. Kelly et al.18 placed 10 children on elemental (amino acid) formula for a minimum of 6 weeks with partial or Patch testing complete resolution in all 10. On follow-up biopsies, Patch testing to foods has primarily been studied in median eosinophil counts decreased markedly. All chil- eczema. Spergel’s group13 identified food allergens in dren relapsed on open food challenge. Markowitz et 26 children with EO using skin-prick and patch testing. al.19 used elemental formula on 51 children. Forty-nine Skin-prick testing identified 68 suspect foods in 19 chil- had symptom resolution and reduced eosinophil counts dren and patch testing 67 suspect foods in 21 patients. on repeat biopsies. The median time to improvement Although overlap existed between foods identified in was 8.5 days. individual patients, skin-prick in combination with patch These data suggest that elemental diet may be superi- testing revealed more suspect foods (average 2.7) per or, but that specific food avoidance guided by skin-prick patient. Patch testing is poorly standardised14 and the and patch tests or specific ‘few-foods’ diets may be protocol used by Spergel et al. for patch testing differs alternative options. Failure to respond to an elemental from that of other investigators. Notably, larger (12 mm) diet does not exclude food antigens as triggers, but es- Finn chambers are used and foods are prepared where tablishes, at a minimum, that something besides food available in dry powder form (milk, soy, potato, rice, oat, also triggers eosinophilic infiltration. The link between wheat, corn, egg, barley and rye) or jarred baby foods. food allergens and EO is not clear in adults because This may result in a higher concentration of food aller- of limited data. An abstract by Gonsalves20 reported a gen in the chamber, possibly accounting for the higher 50% response rate in adults to a 6-foods elimination rate of positive foods identified by patch testing in their diet and near 100% resolution on an elemental diet. studies compared with results of other investigators. In children elemental formula may be necessary as a supplement to a few-food restricted diet to maintain Treatment nutritional adequacy. Because of poor palatability the Gastric acid is not thought to be the primary cause formula may need to be administered via a nasogas- of EO. Patients with oesophageal eosinophilia whose tric tube or even a gastrostomy. In selecting a diet, the symptoms resolve with acid inhibition have GORD, not patient’s lifestyle and family resources need to be con- EO. Despite this, acid suppression may have a poten- sidered and consultation with a dietician is necessary to tial role in patients with EO. Lack of a response to ad- aid in adherence to the diet and to ensure its nutritional equate acid suppression with symptoms and isolated adequacy. oesophageal eosiniphilia is diagnostic of EO. In addition acid suppression may be considered as cotherapy to Topical steroids relieve symptoms of GORD that may occur secondary Swallowed steroids are used for the treatment of EO. to established EO. Definitive treatment relies on avoid- In this modality of treatment inhaled steroids are given, ance of food triggers either with specific targeted food usually by metered dose inhaler without a spacer, while elimination or institution of an elemental diet, as well as the patient is not inhaling. The patient is instructed to immune modulation with oral steroids, topical steroids avoid food or drink for half-an-hour after administration. or leukotriene-receptor antagonists. Fluticasone is the most well-studied formulation21-23 in- 24 Current Allergy & Clinical Immunology, March 2010 Vol 23, No. 1 1. Confirm diagnosis by biopsy after PPI 2. Allergy testing (skin prick and patch tests) to foods 3. Educate family and negotiate treatment options 4. Choose one of next steps → → → Pharmacotherapy with “topical” steroids. Directed Elimination diet OR Elemental diet Fluticasone or Budesonide. six foods elimination diet. Replace diet with elemental formula and Follow up scope in 3 months Follow up scope in 3 months Follow up scope in 3 months → → → → → → Drug therapy Drug therapy Directed elimination Elimination diet Elemental diet Elemental diet does NOT DOES diet does NOT does NOT does NOT DOES result in remission result in remission result in remission result in remission result in remission result in remission → → → → → → Medication dose Medication dose Empiric six foods Maintain current diet Drug therapy Maintain elemental increased Remains the same elimination diet Scope only if and follow diet Scope in 3 months Scope in 12 months Scope in 3 months diet changes pharmacotherapy path Scope in 3 months Scope in 3 months OR OR OR OR OR Discontinue steroid and Medication dose reduction Elemental diet Re-introduction Begin phase of institute diet therapy To achieve “maintenance” selected foods food trials (elimination or elemental) Scope in 3 months Scope in 3 months Scope 3 months Scope to be Scope in 3 months (resume original dose for after new food determined by clinical symptoms or recurrences) OR circumstances Drug therapy and follow pharmacotherapy path Scope in 3 months Fig. 2. Treatment flow algorithm. Reprinted from Putnam PE,33 with permission from Elsevier, Dr Putnam and the Cincinnati Center for Eosinophilic Disorders. (PPI – proton pump inhibitor). cluding a randomised double-blinded placebo-controlled group receiving oral steroids. Systemic adverse effects study.24 were noted in 40% of the subjects receiving oral ste- Arora et al. 21 treated 21 adult patients with swallowed roids, whereas oesophageal candidal overgrowth was fluticasone for 6 weeks. All patients had complete seen in 15% of the subjects receiving topical flutica- symptomatic relief for at least 4 months. The only side- sone. There was no statistical difference between the effect was dry mouth, with no oral candidiasis reported. groups in terms of symptom resolution, relapse rates, Oral candidiasis has been reported in a small minority or time to relapse. Symptom relapse was common to of patients.5 Remedios et al.25 treated 19 adult patients both groups upon therapy discontinuation, highlighting with dysphagia and food bolus obstruction with swal- the need for maintenance treatment protocols. lowed fluticasone propionate. All had symptom resolu- tion and a histological response. Leukotriene receptor antagonists Budesonide may also be used26 and recently orally Schwartz et al.30 first documented the use of mon- administered viscous budesonide27 (nebuliser solution telukast as a steroid-sparing maintenance therapy in a mixed with sucralose) has been used. In 20 children patient with recurrent relapsing EO, but some subse- treated with viscous budesonide,27 there were 16 re- quent studies have been unsuccessful.31 Only 1 study sponders, 1 partial responder, and 3 non-responders. has been published on a small series of 8 adult patients. Morning cortisol levels were within normal limits. Attwood et al.32 used higher than usual doses of mon- telukast starting at 10 mg orally once daily and titrated if necessary up to 100 mg daily. All patients had symp- Oral steroids tomatic improvement, with only 2 having residual dis- The use of oral steroids was first documented in children comfort. Once symptoms were relieved, the dose was by Liacoras et al.28 After 4 weeks of steroid therapy, 19 reduced to 20-40 mg/day to maintain symptom reso- of 20 children responded and 13 had complete symp- lution. Side-effects included nausea and myalgias and tom resolution. Steroids and anti-reflux medications, treatment did not change the density of eosinophils on such as proton pump inhibitors, were then tapered and repeat biopsy. withdrawn after 6 weeks. The average time to improve- ment was 8 days. Comparison between strategies A prospective randomised trial comparing oral steroids A prospective trial has compared targeted dietary re- to topical fluticasone29 showed excellent effectiveness striction and swallowed fluticasone in children.22 Di- of both modalities, with all of 32 and 35 of 36 patients etary restriction did not induce clinical improvement in being free of presenting symptoms at week 4. Histolog- any patients, whereas all children who completed treat- ical improvement was seen in 30 of 32 patients on oral ment with fluticasone had resolution of symptoms. Re- steroids and 34 of 36 patients taking topical fluticasone, peat biopsy in the fluticasone group showed a signifi- with a greater degree of histological improvement in the cant reduction in eosinophils. Current Allergy & Clinical Immunology, March 2010 Vol 23, No. 1 25 Treatment flow algorithm ing despite medical management, children with reflux The algorithm (Fig. 2) describes the scheme followed and other atopic diseases or failure to thrive, or adults for management of children who have EO at the Cincin- and children with swallowing difficulties. A high index nati Center for Eosinophilic Disorders.33 Many centres of suspicion must exist for investigating for EO in these perform follow-up scope and repeat biopsies as the subgroups. A consensus statement defines EO as be- definitive method for assessing response to treatment, ing present where there are symptoms compatible but there have been few studies to guide the biopsy with EO, >15 eosinophils per hpf and exclusion of other protocol or to clarify baseline fluctuation in the density similar disorders especially GORD. Biopsy is the most of eosinophils with time. Endoscopy and biopsy may important diagnostic modality and it is critical to take also be associated with the potential for complications. multiple biopsy specimens from different sites, both If repeat endoscopy with biopsy is planned it should be normal and abnormal in macroscopic appearance. It is performed no less than 4 weeks after the last therapeu- highly recommended to perform biopsies after institut- tic intervention. Repeat biopsies may not be practical ing acid suppression treatment to exclude the possibil- in all settings because of cost constraints and patient ity of confounding biopsy results due to reflux. If exper- refusal. Repeat biopsies may be better indicated after a tise is present (or can be developed) in patch testing, change in symptoms or a change in therapy, rather than this is recommended to broaden the range of possible on a routine basis. dietary treatment strategies or at the very least to help guide the re-introduction of foods after the institution of an elemental diet. Dietary manipulation (with the help of a registered dietician) has the best long-term results CASE VIGNETTE CONTINUED but almost equivalent results can be achieved with topi- A short course of oral prednisone (2 mg/kg daily) and cal steroid administration or systemic steroids. In either maintenance swallowed fluticasone (125 µg twice case a course of systemic steroids can be used at ini- daily) was commenced. In addition montelukast tiation of treatment to achieve rapid control. Treatment was added at a dose of 5 mg daily. Elemental diet options should be guided by the wishes of the patient was instituted with Neocate. On follow up after 2 and family in order to achieve better adherence to the weeks symptomatic improvement was noted with chosen strategy. Repeat biopsies are the gold standard less vomiting and better appetite. The patient was for assessing response to treatment. Should one treat- weaned off oral steroids. Fruit and vegetables were ment option fail, another may be tried. There is urgent reintroduced into the diet and were eaten more eas- need for a study of EO in South Africa assessing the ily and better tolerated. After 3 months growth had prevalence in high-risk groups, the role of food allergies improved and eczema had improved substantially. and the success of alternative methods of treatment. Patch tests (Fig. 3) were performed which revealed additional suspect foods that had not been identified Declaration of conflict of interest with specific IgE and skin-prick testing. This has al- The author declares no conflict of interest. lowed a targeted elimination diet and the re-introduc- tion of other solid food. REFERENCES 1. Sampson HA. Update on food allergy. J Allergy Clin Immunol 2004; 113: 805-819 2 Whitney-Miller CL, Katzka D, Furth EE. Eosinophilic esophagitis: a retrospective review of esophageal biopsy specimens from 1992 to 2004 at an adult academic medical center. Am J Clin Pathol 2009; 131: 788-792. 3. Lee JJ, Baker RD, Khan AR, Baker SS. Childhood esophagitis: then and now. J Pediatr Gastroenterol Nutr 2009; 48: 37-40. 4. Blanchard C, Wang N, Stringer KF, et al. Eotaxin-3 and a uniquely conserved gene-expression profile in eosinophilic esophagitis. J Clin Invest 2006; 116: 536-547. 5. Furuta GT, Liacouras CA, Collins MH, et al. First International Gas- trointestinal Eosinophil Research Symposium (FIGERS) Subcommit- tees. 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Gastrointest Endosc 2006; 64: 313- 319. 12. Brigger MT, Misdraji J, Hardy SC, Hartnick CJ. Eosinophilic esophagi- tis in children: a pathologic or clinicopathologic diagnosis? Arch Oto- Fig. 3. Patch tests. laryngol Head Neck Surg 2009; 135: 95-100. 13. Spergel JM, Beausoleil JL, Mascarenhas M, Liacouras CA. The use of skin prick tests and patch tests to identify causative foods in eo- CONCLUSION sinophilic esophagitis. J Allergy Clin Immunol 2002; 109: 363-368. Although EO is considered rare in South Africa, no 14. Du Toit G. Atopy patch testing for the diagnosis of food hypersen- large studies have been performed looking for EO in sitivity disorders. Current Allergy & Clinical Immunology 2006; 19: high-risk groups, such as children with reflux persist- 196-198. 26 Current Allergy & Clinical Immunology, March 2010 Vol 23, No. 1 15. Spergel JM, Andrews T, Brown-Whitehorn TF, Beausoleil JL, Lia- 25. Remedios M, Campbell C, Jones DM, Kerlin P. Eosinophilic couras CA. Treatment of eosinophilic esophagitis with specific food esophagitis in adults: clinical, endoscopic, histologic findings, and elimination diet directed by a combination of skin prick and patch response to treatment with fluticasone propionate. Rev Gastroen- tests. Ann Allergy Asthma Immunol 2005; 95: 336-343. terol Disord 2006; 6: 245-247. 16. Liacouras CA, Spergel JM, Ruchelli E, et al. Eosinophilic esophagi- 26. Maples KM, Henderson SC, Graham M, Irani AM. Treatment of eo- tis: a 10-year experience in 381 children. Clin Gastroenterol Hepatol sinophilic esophagitis with inhaled budesonide in a 7-year-old boy 2005; 3: 1198-1206. with concomitant persistent asthma: resolution of esophageal sub- 17. Kagalwalla AF, Sentongo TA, Ritz S, et al. Effect of six-food elimi- mucosal fibrosis and eosinophilic infiltration. Ann Allergy Asthma nation diet on clinical and histologic outcomes in eosinophilic Immunol 2007; 99: 572-574. esophagitis. Clin Gastroenterol Hepatol 2006; 4: 1097-1102. 27. 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A prospective clinical trial of allergy testing and food esophagitis: a randomized trial in children. Clin Gastroenterol Hepa- elimination diet in adults with eosinophilic esophagitis (EE) [ab- tol 2008; 6: 165-173. stract]. Digestive Disease Week 2007 (conference). 30. Schwartz DA, Pardi DS, Murray JA. Use of montelukast as steroid- 21. Arora AS, Perrault J, Smyrk TC. Topical corticosteroid treatment of sparing agent for recurrent eosinophilic gastroenteritis. Dig Dis Sci dysphagia due to eosinophilic esophagitis in adults. Mayo Clin Proc 2001; 46: 1787-1790. 2003; 78: 830-835. 31. Daikh BE, Ryan CK, Schwartz RH. Montelukast reduces peripheral 22. Teitelbaum JE, Fox VL, Twarog FJ, et al. Eosinophilic esophagitis in blood eosinophilia but not tissue eosinophilia or symptoms in a pa- children: immunopathological analysis and response to fluticasone tient with eosinophilic gastroenteritis and esophageal stricture. Ann propionate. Gastroenterology 2002; 122: 1216-1225. Allergy Asthma Immunol 2003; 90: 23-27. 23. Noel RJ, Putnam PE, Collins MH, et al. Clinical and immunopatho- 32. Attwood SE, Lewis CJ, Bronder CS, Morris CD, Armstrong GR, logic effects of swallowed fluticasone for eosinophilic esophagitis. Whittam J. Eosinophilic oesophagitis: a novel treatment using mon- Clin Gastroenterol Hepatol 2004; 2: 568-575. telukast. Gut 2003; 52: 181-185. 24. Konikoff MR, Noel RJ, Blanchard C, et al. A randomized, double- 33. Putnam PE. Evaluation of the child who has eosinophilic esophagi- blind, placebo-controlled trial of fluticasone propionate for pediatric tis. Immunol Allergy Clin North Am.2009; 29: 1-10. eosinophilic esophagitis. Gastroenterology 2006; 131: 1381-1391. ALLSA ALLERGY MASTER CLASSES PRESENTED BY PROFESSOR EUGENE WEINBERG You are invited to attend a series of practical allergy teaching sessions in Gauteng presented and hosted by Prof Eugene Weinberg. COURSE CONTENT: The sessions will follow a structured allergy learning curriculum. It will offer a practical learning opportunity for medical practitioners, registrars and nurses with an interest in allergy. Sessions are planned for the following dates: 15 March Allergy in SA and taking an allergic history 3 May Approach to the allergic child 7 June The allergic march 19 July Allergic rhinitis and its complications in children 6 September Asthma and wheezing in children 18 October Atopic eczema in children 29 November Insect allergy, anaphylaxis and immunotherapy VENUE: Suite 200, Netcare Clinton Hospital, Alberton – 15 March only. Thereafter – all meetings will be held at the Netcare Union Hospital Boardroom TIME: 9h00 RSVP: Ethel Matlala: 082 904 3935 (email@example.com) CPD POINTS AND LOGBOOK POINTS WILL BE ACCREDITED SPONSORED BY MSD AND NETCARE Refreshments and a light dinner will be served.
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