few food diets in the treatment atopic eczema · admission for eczema. fifty nine children (91%)...

Archives of Disease in Childhood, 1989, 64, 1691-1698

Few food diets in the treatment of atopic eczema

M G PIKE, C M CARTER, P BOULTON, M W TURNER, J F SOOTHILL, ANDD J ATHERTON

Departments of Dermatology and Immunology, Hospital for Sick Children, London

SUMMARY Sixty six children with severe atopic eczema were treated with highly restricted ('fewfood') diets followed, if they improved, by serial reintroduction of excluded foods. Twenty fourpatients (36%) improved considerably during the few food phase of the diet. Fifteen of these(23% of the study group) maintained this improvement on dietary treatment, of whom threeabandoned the diet after periods ranging from six to 10 months, despite continued benefit,because they found the dietary restrictions too arduous. Thus 12 out of 66 children (18%) withsevere eczema experienced prolonged and useful benefit from this dietary manoeuvre. Doubleblind food challenges performed in 10 patients failed to establish that parental identification ofprovoking foods is reliable. A search for historical and in vitro predictors of diet responsivenesswas unsuccessful in this series.

A number of studies, both uncontrolled'-3 andcontrolled,4 5 have examined the therapeutic effectof 'simple' empirical diets excluding a few foods(cows' milk and egg in particular) in atopic eczema.We are aware of seven published studies of highly

restricted diets in the treatment of atopic eczema.Three of these deal with 'oligoantigenic' or 'fewfood' diets. Hathaway and Warner described prob-lems of compliance in 40 children whose eczemaimproved on milk and egg exclusion (n=7), fewfood diets (n=30) or 'elemental' diets (n=3).6However, it is not clear what proportion of all thosetreated with diets, these 40 diet responsive childrenrepresent. Graham et al treated 26 children with amoderately restricted diet for two weeks followed bya few food diet for a final week.7 Twenty twochildren completed the dietary protocol of whom 18showed benefit, and 16 of these experienced somebenefit from the few food phase of the diet.Armstrong et al used a similar protocol to assess agroup of eczematous adults and children, startingwith a simple exclusion diet followed, if improve-ment did not occur, by a few food diet.8 Of 28children who did not benefit from a simple exclusiondiet, 12 proceeded to a few food diet and two ofthese 12 improved. The study by Juto et al dealsexclusively with infants under 16 months and theeffect of delayed sequential weaning in this group.9The other three studies assessed the therapeutic

effect of 'elemental' (theoretically antigen free)diets; one placebo controlled study in adults'0

showed no benefit while another open and uncon-trolled study suggested improvement in five out ofsix adults on an elemental diet." Hill and Lynchreported improvement in eight out of 10 eczematouschildren in an uncontrolled study of an elementalfeed (Vivonex).'2No published study to date has examined the

effect of few food diets in a large number of childrenwith atopic eczema. We have used such diets to treat66 children of varying ages with atopic eczemasevere enough to justify such a disruptive measure.Our aims were: (i) to assess the therapeutic value ofsuch diets, (ii) to identify the most frequent provok-ing foods by serial reintroduction, (iii) to confirmthat improvement and deterioration in eczema wasgenuinely food related by administering doubleblind placebo controlled food challenges, (iv) toevaluate parental history, skin prick tests, and IgEantibodies as tests for the identification of provokingfoods and, finally (v) to seek out any identifiablecharacteristics of diet responsive patients.

Patients and methods

Sixty six children (mean age 4-2 years, range0-6-16-8 years; 36 boys) were selected from thedermatology outpatient clinic at the Hospital forSick Children, Great Ormond Street during theperiod from late 1983 to early 1985. All had severeatopic eczema inadequately controlled by standardtopical treatment and families who were judged to

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1692 Pike, Carter, Boulton, Turner, Soothill, and Atherton

be capable of managing complex dietary manipula-tions. Sixty children (91%) had first degree relativeswith atopic disease. Thirty two children were fromsocial classes I and II, 26 from social class III, andeight from social classes IV and V. Twenty eightchildren (42%) had had at least one hospitaladmission for eczema. Fifty nine children (91%)were woken by itching on more than 50% of nights ifthe mean of the best and worst months of the latestsix months was taken. Thirty five children (53%)had undergone previous dietary treatment for theireczema and in 13 this was said to have beenbeneficial. Thirty four children (52%) were alreadyexcluding one or more foods at the start of thestudy.

Parents were questioned as to the history of thedisease in their child, observed dietary and environ-mental factors, and previous treatments. Whereboth the child's compliance and the severity of theeczema allowed, children were skin prick tested withextracts of cows' milk, egg, dog fur, cat fur, housedust mite, and Timothy grass pollen (Bencard).Blood was taken to measure circulating IgE anti-bodies using a modification of the radioallergosor-bent test (RAST) technique described by Ceska etalt3 and antigens obtained from Sigma Chemical Co(ovalbumin and lactoglobulin) and Bencard(house dust mite, cat fur, and Timothy grass pollen).Gastrointestinal permeability, a possible marker offood allergic disease, 14 was measured using thelactulose:rhamnose excretion ratio before and afterthe few food phase of the diet.Each child was prescribed an individual few food

diet after discussion with the parents. Dietaryconstituents were selected according to the follow-ing criteria: (i) foods generally regarded as commonlyexacerbating atopic eczema were excluded, (ii)foods implicated on history in the exacerbation of

the individual child's eczema were excluded, (iii)foods frequently eaten by the child were excluded,(iv) the diet was nutritionally adequate for theperiod concerned and, (v) the diet was judged by theparents, dietitian, and doctor to be as strict as thechild could tolerate and palatable enough to ensurecompliance. The diets therefore varied in strictnessand constitution from child to child (diets A, B, andC in table 1 give an indication of the degree of thisvariation). The mean (SD) number of foods in thefew food phase was 8*76 (3.76) with a range fromone food (a casein hydrolysate for an infant aged 7months) to 19 foods.Eczema severity was assessed by a single clinician

(MGP) before and after the few food phase of thediet. A modification of the visual score system usedby Atherton et al was completed4: the body surfacewas divided into 20 areas (10 anterior and 10posterior); for each area, the degree of redness,surface damage, and lichenification were assessedusing firstly a numerical scale of severity (0 to 3)and, secondly, a figure expressing the percentage ofthe area concerned affected by the characteristicbeing assessed. These two figures were multipliedtogether and the products for all three characteristicsfor all 20 areas were added to give an overall scoreof severity. Twenty children had their visual eczemascore assessed by one clinician (MGP) on twooccasions not less than an hour apart as an indicationof the variability of this measurement; the coefficientof variation calculated from these duplicate scores

was 5-1%. Parents kept diary cards on which itch,redness, and sleep disturbance were each scoreddaily (0, 1, 2, 3 in order of increasing severity) andthe amount of treatment used was documented.Dietary mistakes-that is excluded foods eaten inerror-were also recorded on the diary card.The median duration of the initial phase of the

Table 1 Examples of the kind of diet prescribed

A B C

Lamb Rabbit VenisonDuck

Rice* Potato Rice*Potato and/or buckwheat, sago, yam

Cascin hydrolysatet Brassicas (cabbage, Parsnips, carrots, cucumbers, courgettescauliflower, sprouts, broccoli)

Peaches. apricots, grapes, raisins Dates, guava, lycheeOlive oil Sunflower oil

Sugar

These examples indicate the range of few food diets used in order of decreasing strictness. Note frequent use of uncommon foods to whichchildren were unlikely to have been previously exposed.*Included additive and malt free rice krispies' produced by Kellogg Co Great Britain, Manchester.tNutramigen. Bristol-Myers.



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Few food diets in the treatment of atopic eczema 1693

Stop (or proceed to seconddiet)

Few food diet

3-6 Weeks

Inadequate improvement

Double blindplacebo controlled trial

Active Washout Placebo

Useful improvement

Serial reintroduction of single foods at weekly intervals(foods judged to exacerbate eczema excluded)

Placebo Washout Active

Fig 1 Protocol for few food diet, serial reintroduction of foods and double blind placebo controlled food challenge.

diet was 26 days (range 19-44 days, the longerduration resulting from a desire on some occasionsto see whether a mild initial improvement wouldincrease with time). At the end of this phase thedoctor judged whether sufficient improvement hadoccurred to justify continuing dietary treatment (fig1). This decision was a clinical one (to which visualscore chart and diary card data were contributorybut not fundamental) and judged whether improve-ment had occurred of such a degree as to justifycontinuing with what is a very difficult and protractedform of treatment.

Children who were not judged to have improvedadequately either discontinued dietary treatment orproceeded to a second diet, similar in type but withentirely different constituents. Diet responsivechildren continued, with parental agreement, to theserial reintroduction of individual foods at weeklyintervals. Foods being introduced were initiallytaken in small quantities to minimise the chance ofan unexpected severe allergic reaction but from thesecond day in full helpings at least once a day. If thechild's eczema remained apparently unaffected bythe introduction of a food it was incorporated intothe diet. If a deterioration occurred that progressedduring exposure to the food and improved on itswithdrawal, the food was judged to exacerbate theeczema and withdrawn. Sometimes a number ofreintroductory and withdrawal periods were neces-

sary to establish whether a food was exacerbating orinnocuous.

In children who successfully completed the foodreintroduction phase, double blind, placebo con-trolled food challenges were performed, (i) toconfirm that the child's eczema improved anddeteriorated in response to dietary manipulationand (ii) to validate parental identification of exacer-bating foods.A food identified by parents as exacerbating was

disguised in a mixture with an innocuous food('active') and the effect was compared with that ofthe innocuous food alone ('placebo'). Active andplacebo components of the challenge were confir-med to be indistinguishable from one another by agroup of 10 adult volunteers. Each mixture wastaken daily in the same quantity and form, and forthe same period as had been necessary to produceexacerbation on open introduction. When benzoicacid and tartrazine were tested, doses of 50 mg/dayand 20 mg/day respectively (these doses being of thesame order of magnitude as the daily intake of anormal child in the United Kingdom) were con-cealed in opaque capsules (Elanco). The order ofactive and placebo challenges was randomised andthere was a one week wash out period between theactive and the placebo periods.Eczema was assessed by visual score chart before

and after each challenge period and diary cards were



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kept by parents throughout the challeiBoth parent and doctor indicated i

thought to be the exacerbating compoithe mixtures were decoded.Data from questionnaires, and from in

vitro testing, were evaluated as predicresponsiveness.Informed consent was obtained from

and approval for the study was obtainehospital's standing committee on ethical

Results

OUTCOME OF FEW FOOD DIETARY TREATM

Forty three children performed one fev20 performed two, and two patientsthree. Children failed to complete thphase of the diet on five occasions; thiwere second diets in children who tcompleted a first diet without benefit; ondiet in which chicken pox supervened aisubsequently successfully completed a da first diet in an infant who was care(extended family in which it proved inobtain compliance by all family membern

Worthwhile improvementon few food diet:(Doctor's opinion) 24 (36%)

Coincident non-dietary factorsidentified: 4

Started reintroductory phase: 20 (30%)

Deterioration of eczemaafter 1-3 months withoutimplicating dietary factors: 5

Worthwhile long term 15 (23%)

inprovement:

Diet abandoned despitepersistent improvement(after6-l0months) 3

Continued on diet withpersistent improvement: 12 (18%)

(Median duration 47-9 weeks,range 264--71-1 weeks)

Fig 2 Outcome of dietary treatment (numbefood diet=66).

nge period. 65 out of 66 children completed at least one few foodwhich they diet.nent before Thirty children (46%) were felt by the parents to

have improved sufficiently to justify continuing tovivo and in food reintroduction, but the doctor concurred withtors of diet this opinion in only 24 cases (36%) (in no case where

the doctor thought sufficient improvement hadall parents occurred did the parents disagree). Only in the 24

zd from the cases in whom the doctor judged sufficient improve-I practice. ment to have occurred was a reintroductory phase

considered. In four of this group of 24, however,coincident factors were thought by the doctor orparents, or both, to be important: two were admit-

IENT (fig 2) ted to hospital for intensive topical treatmentv food diet, because of exacerbations of their eczema during partperformed of the few food phase of the diet and in two other

e few food children a change of washing powder and seasonalree of these factors respectively were thought to have contri-lad already buted significantly to the improvement.ie was a first Twenty children (30%) therefore proceeded tond this child the reintroductory phase. In five of these 20 childrenLiet; one was the eczema deteriorated during the first one to threed for by an months of the reintroductory phase. Renewednpossible to exclusion of foods they had reintroduced produceds. Therefore no benefit; it was therefore not possible to ascribe

their deterioration to dietary factors. These childrentherefore withdrew from the study leaving 15children (23%) who maintained worthwhile im-provement on dietary treatment. Three of this groupof 15, however, abandoned dietary treatment despite

(Parental persisting improvement after periods ranging fromopinion 46%) six to 10 months. These children and their families

found the diets too burdensome despite theirbeneficial effects. A review of the historical and testdata for these three children did not identify anydistinguishing features; in particular they were notolder than the children who persisted with dietarytreatment.

Therefore, ultimately, 12 of 66 children (18%)persisted with dietary treatment with long termbenefit. At the end of the study the mean durationof dietary treatment in these children was 47-9weeks (range 264-471-1 weeks).

OPEN REINTRODUCTION OF FOODSThe 15 children who improved on dietary treat-ment had reintroduced without deterioration amean of 15-3 foods each by the end of the study(range 6-37). The overall rate of successful foodreintroduction was one food per three weeks (rangeone food in seven weeks to one food in one and ahalf weeks).The foods most often judged to exacerbate

r starting few atopic eczema on open reintroduction are listed intable 2.



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Table 2 Proportion of times individual foods reintroduced were identified as causing a deterioration in eczema

Food Exacerbations/total Food Exacerbations/totalreintroductions reintroductions

Meat/poultry/fish VegetablesLamb 2/11 Pea/runner bean 3/10Beef 6/13 Carrot/parsnip 3/10Pork 3/13 Brassicas 1/11Rabbit 0/3 Tomato* 6/9Chicken* 6/12 Onion/leek 3/5Turkey 1/5 Courgette/cucumber 0/1Cod* 4/8 Potato 1/8Mackerel 1/1 Lentil 1/1Plaice 3/4

Fruit

Milks and soya Apple/pear 3/13Cows' milk* 10/14 Apricot/peach 1/10Goats' milk* 6/11 Plum/nectarine 0/2

Sheeps' milk /15 Grape/raisin 2/7Soya 'milk' formula* 5/7 Orange* 6/11

Banana* 8/12

Eggs ~~~~~~~~~~~~Pineapple 3/7Eggs Blackcurrant 2/4Hens' egg* 6/9 Melon 0/2

Grains/yeast/malt AdditivesWheat* 7/13 Colourings/Corn 5/12 preservatives 6/14Oats 4/13Rice 1/8 OtherRye 0/2 Sugar 0/7Yeast 1/7 Chocolate ('plain') 2/5Malt 0/6 Tea 0/4

*Foods reintroduced by seven or more children and identified as exacerbating eczema on 50% or more of these reintroductions.

DOUBLE BLIND, PLACEBO CONTROLLED FOODCHALLENGESTen of the 15 diet responsive patients completeddouble blind food challenges. The active andplacebo components of these challenges are shownin table 3.When the child had completed both active and

placebo parts of the double blind challenge, parentsand doctor each indicated which they thought hadbeen the 'active' period; parents and doctor eachidentified the active period incorrectly on fiveoccasions and correctly on five occasions. Parentsand doctor were in agreement with each other ineight of these decisions.

Visual eczema scores were analysed both compar-ing the end of the active period with the end of theplacebo period and also comparing the change fromthe beginning to the end of the active period withthe analogous change in the placebo period. Diarycard scores for itch, redness, sleep disturbance,steroid usage, and emollients were each analysed as

follows: (1) the score for each variable for the wholeof the active period was compared with the placeboperiod (paired t test). (2) The change in score foreach variable from the start (first two days) to the

finish (last two days) of the active period was

compared with the same change in the placeboperiod (paired t test). There was no significantdifference between active and placebo periods on

any of these analyses.During the interval between open introduction

and double blind challenge there is a theoretical riskthat the child's response to the food will alter. Themean interval from the identification of an exacer-

bating food on open introduction to double blindchallenge was 45-4 days (range 16-181 days). Therewas no significant difference in the duration of this

Table 3(n=1O)

Constituents of double blind food challenges

No of Active Placebopatients component component

4 Cows' milk Goats' milk2 Cows' milk 'Nutramigen'1 Cows' milk Soya 'milk'2 Benzoic acid and Calcium gluconate

tartrazine1 Benzoic acid Calcium gluconate



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interval between the double blind challenges inwhich the active component was correctly identified,whether by doctor or patient, and those in which itwas incorrectly identified (p>0.01, Mann-WhitneyU test in both analyses).

CHARACTERISTICS OF DIET RESPONSIVE PATIENTSData for the 15 diet responsive patients werecompared with that for 41 unequivocally unrespon-sive patients. Excluded from this analysis were thechild who did not complete a diet, the four childrenin whom concurrent non-dietary factors may havebeen responsible for the improvement, and the fivechildren whose eczema deteriorated early in thereintroductory period without an apparent dietarycause. No significant differences were found withthe exception of positive associations between re-sponse to diet and positive IgE antibody to ovalbu-min, and larger number of 'slow' (occurring morethan two hours after ingestion) cutaneous reactionsto foods reported on history (t test, p<005 in both

Table 4 Data compared in diet responsive and dietunresponsive patients

Personal data: Age. Sex. Age at onset of eczema.Severity of eczema (judged by visual score)at start of few food diet.

Breast feeding (history of/duration of)Environmental History of seasonal fluctuation of eczema.

factors: Presence of dog or cat in home with relevantskin prick test/IgE antibody positive.

History of inhalent allergy.Dietary Previous dietary treatment with or without

factors: benefit.Milk and egg already excluded at start of diet.History of food induced exacerbation ofeczema.

Number of reported 'immediate' (withintwo hours of ingestion) reactions to foodscutaneous and non-cutaneous).

Number of reported 'slow' (more than twohours after ingestion) reactions to foods(cutaneous* and non-cutaneous).

Reported reactions to non-foods (immediateand slow; cutaneous and non-cutaneous).

Duration of few food phase of diet.Number of foods allowed in few food phase of

dict.In vivo and Skin prick test to foods/inhalants.

in vitro Presence of IgE antibodies to:test data: Ovalbumin*

lactoglobulinHouse dust miteCat furTimothy grass pollen

Gastrointestinual permcability tooligosaccharides at start of diet.

Change in gastrointestinal permeability withdiet.

*Significant difference between diet responsive and diet unrespon-sive groups (p<005).

cases, table 4). The number of analyses performedwas such that two results significant at the 5% levelwould be expected to occur by chance.

PREDICTORS OF EXACERBATING FOODSNo useful assessment could be made of the predic-tive value of skin prick tests and IgE antibody tests(RASTs) in the identification of exacerbating foods,as the double blind challenge trial failed to validatethe exacerbating effect of these foods.

VISUAL SCORE CHART AND DIARY CARD DATAIn the diet responsive group over the few food phaseof the diet, the visual scores showed a meanimprovement of 32-4% (range, 62-4% improvementto 1*3% deterioration) and the cumulative diarycard symptom score (itch, redness, and sleep dis-turbance combined) showed a mean improvementof 209% (range, 57-9% improvement to 39-6%deterioration) if the first and last seven days of thefew food phase of the diet were compared. Para-doxical deterioration in one or other measurementoccurred in three children; two showed an appreci-able improvement in visual score but a deteriorationin symptom score; one child had a visual score thatwas marginally worse (1-3%) with a 31% improve-ment in symptom score.

Topical steriod usage increased slightly and emol-lient use decreased during the few food phase, inneither case being significantly different from thechanges in treatment in diet unresponsive patients.

Discussion

These data suggest that few food diets are of limitedbenefit to children with severe atopic eczema.Although it may be argued that our sample wasselected for diet unresponsiveness (as 54% con-tinued to have severe eczema despite past dietarytreatments), the response to the present dietaryprotocol was not in fact better in children who hadnot previously experienced dietary treatment than inthose who had (table 4).Our few food diets were of varied composition but

excluded foods identified, from previous reports, asexacerbating eczema and observed as exacerbatingeczema in the individual child concerned. Compari-son of the two outcome groups (diet responsive anddiet unresponsive) does not suggest that, within therange of diets used in this study, extremely strict orprolonged diets are more effective than shorter lessstrict diets (table 4).Of particular interest in the present study was the

identification of a group of four children whoseimprovement could be ascribed to non-dietaryfactors and a further five children who deteriorated



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in the first one to three months after improving onthe few food diet without dietary factors appearingto be responsible for their deterioration. Thesechildren, if they had been classified as diet respon-sive, would have increased our diet responsivegroup by 38%; clearly careful review of coincidentnon-dietary factors and follow up to confirm thatimprovement is maintained should be part of anyfuture dietary study of this type.Three children in the group judged to have shown

considerable improvement in fact showed a deterio-ration in one of the indices of severity, in thepresence of an appreciable improvement in theother. These cases emphasise the difficulty ofquantifying the severity of this condition. Diary cardsymptom scores may be affected by extraneousfactors (for example, sleep disturbance due tointercurrent illness), and both the weight allocatedto individual symptoms and the periods at thebeginning and end of the few foods phase of the dietfor which cumulative scores are calculated (in thisstudy seven days) are arbitrary. Visual scores at thetime of consultation may not invariably reflect asymptomatic improvement-long standing licheni-fication is unlikely to change measurably over threeweeks and erythema may be exacerbated transientlyby ambient irritants, temperature, or emotion. Forthese reasons decisions as to dietary outcome on thebasis of preset numerical criteria may misallocatepatients.The poor response rate in this study meant that

our double blind trial was small. Furthermore, theinterval between open reintroduction and doubleblind challenge was long in some cases and theoreti-cally an alteration of the effect of the active food (orindeed of the placebo) might have occurred duringthis interval. However, the results as they standhave two implications. Firstly, parental identifica-tion of provoking foods in atopic eczema is unreli-able, presumably'because of the fluctuating natureof the disease and the multiplicity of confound-ing influences (environmental, emotional, etc.).Secondly, the results do not demonstrate exacer-bation of these children's eczema by foods. There-fore, by implication, the improvement observed, onan open uncontrolled basis during the few foodphase of the diet, cannot be ascribed with any confi-dence to food exclusion.

It is of interest that, though analysed differently,the double blind trial described in the study ofArmstrong et al also showed correct identification ofthe active component in only half of the challenges.8In this context, Wilson and Silverman's demonstra-tion that asthmatic children may respond to aller-genic foods, not by simple bronchospasm, but by anincrease in bronchial lability rendering them more

susceptible to a second agent, may be relevant.15Should a similar two stage mechanism occur inatopic eczema, simple provocation tests of the kindused in these studies would not necessarily identifyit.The list of foods implicated on open introduction

(table 2) therefore remains unvalidated. The simi-larity to the foods implicated by the patients inHathaway and Warner's study6 and in the study ofArmstrong et a!8 is of note, however, as is thefrequent implication of soya which, though used as aplacebo a ent in milk and egg exclusion studies inthe past,4 may now be viewed as an unsatisfactorychoice for such a role.Numerous comparisons of historical and test data

for diet responsive and diet unresponsive patientsshowed only two weak associations with diet respon-siveness; however, as stated above, the number ofanalyses performed was such that two results signifi-cant at the 5% level would be expected to occur bychance. Neither association would have usefullyimproved the response rate if used as the criterionfor dietary treatment in our study group. Ofparticular interest was the absence of any associa-tion between increased intestinal permeability andresponse to diet and the absence of a significantchange in permeability over the dietary period inchildren whose eczema improved considerably ondietary treatment; though increased permeabilityhas been shown to occur in childhood atopiceczema16 and in association with food inducedhypersensitivity reactions of probable IgE mediatedtype,14 it does not appear to usefully predictresponse to exclusion diets of the type we haveassessed.

'Simple' empirical diets such as that studied byAtherton et al are a well established part of thetreatment of childhood atopic eczema.4 Furtherwork is needed to clarify the role of elemental dietsin a controlled fashion in larger numbers of childrenwith extreme eczema than have been studied hitherto.Given the burden, both emotional and financial, ofthe few food diet, the eagerness (well illustrated inour study) of parents to pursue such diets even whenthe benefits are marginal, and our failure to achieveeven a small response group validated by doubleblind challenge, it would seem prudent to restrictthe use of such diets unless and until furtherevidence is forthcoming.

MGP was supported by a grant from the National Eczema Society.

References

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1698 Pike, Carter, Boulton, Turner, Soothill, and Atherton2 Rowe A, Rowe AH. Atopic dermatitis in infants and children.J Pediatr 1951;39:80-6.Hammar H. Provocation with cows' milk and cereals in atopicdermatitis. Acta Derm Venereol (Stockh) 1977;57:159-63.Atherton DJ, Sewell M, Soothill JF, Wells RS, Chilvers CED.A double-blind controlled crossover trial of an antigen avoidancediet in atopic eczema. Lancet 1978;i:401-3.

5 Neild VS, Marsden RA, Bailes JA. A double-blind crossovertrial of egg and milk exclusion diets in atopic eczema. Br JDermatol 1984;114:117-23.

6 Hathaway MJ, Warner JO. Compliance problems in the dietarymanagement of eczema. Arch Dis Child 1983;58:463-4.

7 Graham P, Hall-Smith SP, Harris JM, Price ML. A study ofhypoallergenic diets and sodium cromoglycate in the manage-ment of atopic eczema. Br J Dermatol 1984;1 10:457-67.

8 Armstrong D, Neild VS, Bailes JA, Marsden RA. Exclusiondiets in atopic eczema. In: Chandra RK, ed. Food allergy.St John's, Newfoundland: Nutrition Research EducationFoundation, 1987:267-72.

9 Juto P, Engberg S, Winberg J. Treatment of infantile atopicdermatitis with a strict elimination diet. Clin Allergy 1978;8:493-500.

'° Munkvard M, Danielsen L, Hoj L, et al. Antigen-free diet in

adult patients with atopic dermatitis. Acta Dern Venereol(Stockh) 1984;64:524-8.

" Villaveces JW, Heiner DG. Experience with an elemental diet(Vivonex R). Anin Allergy 1985;55:783-9.

12 Hill DJ, Lynch BC. Elemental diet in the management of severeeczema in childhood. Clin Allergy 1982;12:313-5.

13 Ceska M, Eriksson R, Varga JM. Radioimmunosorbent assay ofallergens. J Allergy Clin Immunol 1972;49:1-9.

14 Andre C. Diagnosis of food allergy and evaluation of thera-peutic efficacy by measurement of intestinal permeability.Presse Med 1986;15:105-8.Wilson N, Silverman M. Diagnosis of food sensitivity inchildhood asthma. J R Soc Med 1985;78(suppl 5):11-6.

16 Pike M, Heddle RJ, Boulton P, Turner AW, Atherton DJ.Increased intestinal permeability in atopic eczema. J InvestDermatol 1986;86:101-4.

Correspondence to Dr DJ Atherton, Department of Dermatology,Hospital for Sick Children, Great Ormond Street, London WCIN3JH.

Accepted 20 June 1989



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few food diets in the treatment atopic eczema · admission for eczema. fifty nine children (91%)...

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