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eosinophiliC oesophaGitis


									                          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
 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,

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.
                                                              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. Eosinophilic esophagitis in children and adults: a systematic
                                                                 review and consensus recommendations for diagnosis and treat-
                                                                 ment. Gastroenterology 2007; 133: 1342-1363.
                                                              6. Pentiuk SP, Miller CK, Kaul A. Eosinophilic esophagitis in infants and
                                                                 toddlers. Dysphagia 2007; 22: 44-48.
                                                              7. Croese J, Fairley SK, Masson JW, et al. Clinical and endoscopic
                                                                 features of eosinophilic esophagitis in adults. Gastrointest Endosc
                                                                 2003; 58: 516-522.
                                                              8. Noel RJ, Putnam PE, Rothenberg ME. Eosinophilic esophagitis.
                                                                 N Engl J Med 2004; 351: 940-941.
                                                              9. Jyonouchi S, Brown-Whitehorn TA, Spergel JM. Association of eo-
                                                                 sinophilic gastrointestinal disorders with other atopic disorders. Im-
                                                                 munol Allergy Clin North Am 2009; 9: 85-97.
                                                             10. Odze RD. Pathology of eosinophilic esophagitis: what the clinician
                                                                 needs to know. Am J Gastroenterol 2009; 104: 485-490.
                                                             11. Gonsalves N, Policarpio-Nicolas M, Zhang Q, Rao MS, Hirano I.
                                                                 Histopathologic variability and endoscopic correlates in adults with
                                                                 eosinophilic esophagitis. 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. Aceves SS, Dohil R, Newbury RO, Bastian JF. Topical viscous
     18. Kelly KJ, Lazenby AJ, Rowe PC, Yardley JH, Perman JA, Sampson                 budesonide suspension for treatment of eosinophilic esophagitis.
         HA. Eosinophilic esophagitis attributed to gastroesophageal reflux:           J Allergy Clin Immunol 2005; 116: 705-706.
         improvement with an amino acid-based formula. Gastroenterology            28. Liacouras CA, Wenner WJ, Brown K, Ruchelli E. Primary eosino-
         1995; 109: 1503-1512.                                                         philic esophagitis in children: successful treatment with oral corti-
     19. Markowitz JE, Spergel JM, Ruchelli E, Liacouras CA. Elemental diet            costeroids. J Pediatr Gastroenterol Nutr 1998; 26: 380-385.
         is an effective treatment for eosinophilic esophagitis in children and    29 Schaefer ET, Fitzgerald JF, Molleston JP, et al. Comparison of oral
         adolescents. Am J Gastroenterol 2003; 98: 777-782.                           prednisone and topical fluticasone in the treatment of eosinophilic
     20. Gonsalves N. 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.
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 (
                                                 SPONSORED BY MSD AND NETCARE
                                         Refreshments and a light dinner will be served.

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