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Keywords:

  • AEDS;
  • child;
  • diet;
  • eczema;
  • food allergy;
  • therapy

Abstract

  1. Top of page
  2. Abstract
  3. Aims and methods
  4. Data retrieval and inclusion criteria
  5. Results
  6. Interpretation of the results
  7. Conclusions
  8. References

Objective:  This review summarizes the research and clinical evidence in favour of dietary intervention aimed at eliminating allergenic foods in the management of atopic eczema/dermatitis syndrome (AEDS).

Data sources:  The data source was PubMed, using a search algorithm selecting for clinical studies of AEDS, diet therapy and food allergy in all children to October 2003. Also included is a commentary based on the authors' clinical experience in the allergy unit of a university hospital in Italy.

Results:  Fourteen prospective studies matched the entry criteria. Diverse trial designs, diagnostic criteria, types of dietary intervention and length of observation periods precluded meta-analytic methods. Allergenic food exclusion claimed efficacy in 13 of the 14 studies and was most useful in infants, in patients with elevated immunoglobulin E levels and/or multiple food sensitization and in patients with a diagnosis of food allergy.

Conclusion:  Dietary intervention in the form of an elimination diet is efficacious in children with AEDS when a specific diagnosis of food allergy has been made. Diagnostic evaluation of food allergy should be performed in all children with eczema, particularly in younger children and those with severe forms of the disease.

Abbreviations
AD

atopic dermatitis

AEDS

atopic eczema/dermatitis syndrome

CMA

cow's milk allergy

DBPCFC

double-blind placebo-controlled food challenge

eHF

extensively hydrolysed formula

SPT

skin prick test

New cases of atopic eczema/dermatitis syndrome (AEDS) (1) are increasing dramatically (2, 3). A chronic condition which peaks in infancy with onset during the first 3 months of life, AEDS often anticipates the progression of atopic disease (4–6). Food allergy also peaks during the first year and food allergen sensitization at 12 months predicts allergic sensitization to common inhalant allergens at 3 years of age (7,8). The association of food-specific immunoglobulin E (IgE) antibody and ‘atopic dermatitis’ has enhanced the expectation among patients, their parents and their caregivers that restricted diets may alter the course or severity of disease. Common food allergens, such as egg, cow's milk or tomatoes, are frequently implicated (9,10). Food triggers of allergic skin symptoms, however, cannot account for the whole clinical spectrum and course of AEDS. Diagnosis must rest on a clinical, multifactor assessment basis. Diagnostic systematics varies (11) but pruritus, chronic/relapsing disease and personal/family history of atopy are considered major criteria (12,13). At least 47 different types of intervention against AEDS were reviewed from the literature in 2000 (14). However, there was no consensus [and, earlier, even opposition (15)] regarding the efficacy of allergen dietary restriction, although food allergy as an etiological factor in AEDS was not at issue (16–19).

Data retrieval and inclusion criteria

  1. Top of page
  2. Abstract
  3. Aims and methods
  4. Data retrieval and inclusion criteria
  5. Results
  6. Interpretation of the results
  7. Conclusions
  8. References

Literature was retrieved from the NCBI Pub Medical database using the following search algorithm to select for evidence linking pathogenic role of allergic sensitization to foods and assess the efficacy of dietary restriction in the treatment of infants and children with AEDS.

  • #  1 atopic dermatitis http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db = PubMed

  • #  2 OR atopic eczema/

  • #  3 or AEDS/

  • #  4 OR/neurodermatitis/

  • #  5 OR neurodermitis constitutionalis atopica

  • #  6 AND food allergy/

  • #  7 AND cow's milk allergy/

  • #  8 AND egg allergy/

  • #  9 AND wheat allergy/

  • # 10 AND multiple food allergy/

  • # 11 diet therapy/

  • # 12 prevention and control/

  • # 13 child/

  • # 14 OR infant/

  • # 15 1975 January – 2003 October

  • # 17 clinical studies.

Date of last search: 28 November 2003

Studies of all children up to 18 years diagnosed by a clinician using the criteria of Hanifin and Rajka (12) or their modification (20) were considered, regardless of the terminology used (atopic eczema, atopic dermatitis, or AEDS). The primary outcome measure to assess the efficacy of elimination of food(s) was improvement in clinical symptoms and secondary outcome measures were time off school, improvement in quality of life and need for topical steroids, antihistamines and emollients. Owing to the type of intervention reviewed (diet and nonpharmacological therapy), there are few controlled trials of dietary restriction efficacy in AEDS in the literature and thus blindedness of studies was not among the inclusion criteria. No language parameter was set.

Results

  1. Top of page
  2. Abstract
  3. Aims and methods
  4. Data retrieval and inclusion criteria
  5. Results
  6. Interpretation of the results
  7. Conclusions
  8. References

Fifteen studies fulfilled the inclusion criteria (21–35) and were tabulated. These papers differed so markedly in study populations (Table 1), types of intervention, trial design, duration (Table 2) and outcome assessment methods (Table 3) as to withstand systematization or meta-analysis. Definition of atopic dermatitis was defined according to clinical criteria in all studies, sometimes with a specific reference (e.g. Hanifin's criteria). In three studies ‘severe’ eczema was considered an inclusion criterion whereas three other considered ‘refractory’ eczema as sole entry criterion. A selection bias appeared in all studies as children with eczema were referred for assessment to either dermatological or paediatric allergy clinics. Their caseloads are not representative of the whole population of infants and children with AEDS. The disparity between entry criteria was matched by differences in sample size. In total, 823 children were assessed; 142 in caseloads recruited on the ‘refractory’ disease criterion (25,28,30), 137 in studies concerned with ‘severe’ disease (22,29,33) and 544 in studies which did not specify the severity of symptoms for enrolment (21,23,24,26,27,29,31,32) (Table 1). There was no uniformity in the exclusion/trial of foods as part of the dietary intervention. Two studies eliminated cow's milk and egg (21,23), two prohibited only eggs (27,34), four studies substituted formulae [either elemental (25,31,36) or cow's milk hydrolysates (31,32,36) to their patients while two others excluded cow's milk and eggs from the diet of the nursing mother (24,27)]. The elimination of cow's milk and/or eggs (22), of ‘suspect’ foods (26), of three (28), or six (29) foods has also been recommended as well as an elemental diet based on a small number of foods (30,33) (Table 2). The main limitation of published trials in this field is the lack of blindedness. One study (24) compared the effect of an exclusion diet with a placebo under double-blinded conditions but only in a subset of patients. Another study (32) carried out a blinded comparison of probiotic supplementation, but the allergy arm of the study was open. In mitigation, it must be said that finding suitable placebo is difficult. An amino acid elemental formula could substitute for cow's milk, but the two studies assessing its use against a whey hydrolysate are open studies (31,35) (Table 2). Well-controlled, prospective assessment of cow's milk restriction is ruled out by ethical concerns. Other confounding factors present in all these studies are not always acknowledged. The most conspicuous is a method for evaluating eczema for which a consensus is yet to be reached, although specific scoring systems have been devised (36,37). Thus studies rely on home-made scores, but some are difficult to use (38) and evidence or consensus on which is the best are still lacking (39,40). Another confounder is the method used for diagnosing food allergy in these children. In some studies, children are sensitized to one or two foods but do not undergo formal demonstration of food allergy by oral provocation tests (22,25,34). In other studies children are sensitized by multiple foods (33) or are described as suffering from atopic dermatitis but without specifically referring to the foods they are sensitized by or allergic to. Only two studies enjoy the ideal situation when an allergic reaction to the study food is confirmed at double-blind, placebo-controlled food challenge (DBPCFC) (31,35). A third factor is the problem of the evaluation of compliance with dietary advice. Dietary restrictions are increasingly hard to enforce among older children and in children undergoing stringent dietetic prescriptions the phenomenon ought to be taken into account. Of further limitation are the high drop-out rates [reported as 44 (21), 25 (23) and 41% (30)]. All told, 112 out of 823 children (or 13.6%) were lost to follow-up in the studies considered. A further confounder of study interpretation is the concomitant administration of nondietetic therapeutic intervention, e.g. pharmacological treatment (Table 1) and environmental measures (25,29). The limited duration of many of the studies is also a drawback: most studies investigated only short- to medium-term effects. Three studies evaluated patients 6 (35), 9 (31) and 12 (25) months into diet therapy, each with favourable conclusions. In a disease with marked seasonal variations, it can be impossible to draw conclusions from studies of 2, 4 (21,28,32–34) or 6 weeks (29,30). Finally, many of these studies have a lack of statistical power because of poor study design and only in one study of cow's milk allergy in children (31) was the effect of a substitute assessed against placebo use. Case-controlled cross-over studies can be fitted to logistic regression models but these studies may not have sufficient statistical power to evaluate the multiple outcomes of an exclusion diet on AEDS (14). A few studies focused on the risks of exclusion diets in AEDS. We know that children with eczema show a reduced pattern of growth during the first year of life (41) and this can reflect a nutritional disorder because of food allergy. These disorders may be aggravated by inappropriate diet, sometimes with dramatic effects (42). Another case in which eczema can develop in the absence of food allergy even in little children is phenylketonuria (PKU), when the appropriate metabolic diet can prevent both atopic eczema and the allergic sensitization to foods (43). A study showing that feeding an amino acid formula resulted in improved growth compared with feeding an eHF suggests that the more anallergic are the diet substitutes, the more adequate is their nutritional value (35). Thus, a full nutritional history has to be taken when exclusion diets are planned for children with AEDS.

Table 1.  Overview of dietetic interventions in the literature on cow's milk allergy (CMA): caseload characteristics
StudyOutcome measuresSample size and demographics
  • *

    Percentages indicate body area.

(21)clinical diagnosis of ‘atopic eczema’36 children (20 completed the trial)
Age 2–8 years attending a dermatology clinic
(22)clinical diagnosis of ‘severe atopic dermatitis’59 children. No age reported
No dropout reported.
(23)atopic eczema53 children and young adults (40 completed the trial)
Age 1–23 years
(24)established atopic eczema19 breast-fed infants
(25)severe, refractory, widespread atopic eczema37 children
(26)atopic dermatitis91 children 0–5 years (referrals to dermatological clinic)
16 healthy controls
61 SAFT-positive (including 38 lost at follow-up)
(27)atopic dermatitis138 children 0–3 years (33 aged 3–6 months; 25 aged 7–11 months; 46 aged 11–24 months; 34 aged 24–36 months)
(28)severe atopic dermatitis unresponsive to topical treatment12 children aged 0.8–4.1 years (mean 2.64; SD 0.95)
(29)severe atopic dermatitis (>30%*) with poor response to conventional therapy or with clear history of food intolerance62 children (median 2.9 years).
37 with exceptionally severe AD
(30)refractory atopic dermatitis (>12%*)85 nonbreast-fed children (median age 2.3 years; range 0.3–13.3 years)
(31)atopic dermatitis45 nonbreast-fed children allergic to cow's milk and requiring a substitute formula for at least 6 months (mean age 14 months; range not reported)
(32)atopic dermatitis (Hanifin's criteria)27 children aged 2.5–15.7 months (median age not reported)
(33)suspected multiple-food induced severe atopic dermatitis16 children aged 5–24 months (median age not reported) outpatients attending dermatology clinic
(34)atopic dermatitis specific IgE to egg62 ‘young children’ (age reported only as mean ± SD; 11.3 months in the diet group and 17.2 months in the control group)
(35)atopic dermatitis73 infants
CMA at DBPCFCAge 1.6–9 months (median 5.7 months)
Table 2.  Dietary interventions in cow's milk allergy: design of intervention and study
StudyDietary intervention [concomitant treatment]Trial design and duration
(21)egg and cow's milk elimination diet (soy as substitute) [antihistamine]double-blind, crossover, placebo [soy]-controlled.
Two 4-week periods separated by a 4-week period of free diet.
(22)exclusion of milk and/or egg [not reported]open design; observations of various duration.
(23)egg and cow's milk elimination diet (soy as substitute). [antihistamine + topical steroids]double-blind controlled crossover trial
Two 6-week periods separated by a 6-week period of free diet.
(24)egg and cow's milk elimination from the mother's diet (soy as substitute).2 groups:
(n = 19) double-blind, crossover trial with exclusion of egg and cows' milk
(n = 18) open exclusion of 11 foods followed by double-blind challenge to mothers whose infants seemed to respond.
(25)antigen avoidance (hospitalization, exclusive elemental formula feeding for 30 days (median) [reduction of pet and dust mite antigens at home]open for 12 months. After eczema clearance, food challenges at 7-day intervals
(26)elimination of foods causing food immediate-contact hypersensitivity [FICH] (cow's milk, egg, peanut or soy).open, variable observation period
(27)egg elimination diet in infants and breast-feeding mothers [use of concomitant medication not reported]single-blind, controlled trial
(28)2–4-week egg, wheat and cow's milk elimination diet [use of concomitant medication not reported]open for 2–4 weeks. Results confirmed with open reintroduction of foods in 8/12 children.
(29)six-food elimination diet. In subgroup with exceptionally severe disease: hospitalization and exclusive feeding with an elemental formula (Vivonex) for a median duration of 30 days [antihistamine + topical steroids]open for 6 weeks
(30)elemental diet (eliminating all but five to eight foods) + n = 27: whey hydrolysate; n = 32 casein hydrolysate formula vs. n = 26 unrestricted diet. [antihistamine + topical steroids]parallel, single-blinded (6 weeks)
(31)n = 22 infantsparallel, randomized, prospective study (9 months)
 median age 6 months: extensively hydrolysed whey formula 
 median age 17 months: amino acid-derived formula. 
(32)cow's milk elimination diet without (group a) and with (group b) Lactobacillus GGparallel, randomized, prospective (group a)
substitute: extensively hydrolysed whey formula.open (group b) (1 month)
(33)elemental diet (home-made meat-based formula)open for (4 weeks) followed by DBPCFC with cow's milk, egg and wheat
(34)general advice + egg exclusion diet vs general advice vs.randomized controlled trial
general advice only [emollients + topical steroids]open to parents but blinded to assessor. (4-weeks)
(35)Extensively hydrolysed whey formula (Alfaré of Pepti-Tutteli, n. 42)Open, randomized, controlled multicenter trial
Amino acid-derived formula. (Neocate, n. 31)(6 months)
Table 3.  Dietary interventions in cow's milk allergy in children with AEDS: selection criteria and evaluation of food-allergy
StudyOutcome measuresFood allergy diagnosis
(21)unpublished composite score including the number of areas affected, itching, sleeplessness and use of antihistaminesnot reported
(22)clinical improvementSPT and clinical history
(23)areas affected, day- and night-time itch and use of topical steroidnot reported
(24)unpublished 60-point numerical scorenot reported
(25)unpublished combined disease severity score of surface area plus erythema score topical corticosteroids as per British National Formularytotal and specific IgE
(26)unpublished clinical score [described in the study]skin application food test [SAFT]
(27)clinicalspecific IgE (RAST) – no oral provocation test
(28)unpublished dermatological score, based on distribution and severity of lesionsSPT, RAST confirmed sensitization in 8/12 patients. single-blinded, chal lenge with egg, cow's milk and wheat after the exclusion diet
(29)clinicalhistory of food intolerance
(30)unpublished skin severity score (extent and severity) plus parental record of itch, sleep loss and global improvementnot reported
(31)SCORAD indexcow's milk allergy confirmed at DBPCFC
(32)SCORAD index. Other outcome measures were the concentrations of fecal α1-antitrypsin, tumour necrosis factor-α, eosinophil cationic protein before and after dietary intervention.cow's milk allergy: clinical history confirmed at SPT in 30%, RAST in 37% of infants. no challenge confirmation
(33)previously published (62) severity score based on skin lesion interpretationmultiple food allergy (more than three positive SPT responses to foods)
(34)previously published (63) composite severity score based on readings of 16 body sites; eczema in extent percentageRAST positive to egg (unspecified cut-off point). No SPT. Suggestive history in 7 cases.
(35)SCORAD indexcow's milk allergy confirmed at DBPCFC

Interpretation of the results

  1. Top of page
  2. Abstract
  3. Aims and methods
  4. Data retrieval and inclusion criteria
  5. Results
  6. Interpretation of the results
  7. Conclusions
  8. References

With such limitations, the task of sifting meaningful clinical data from the literature appears daunting and it is not surprising that the claims of proponents of diet therapy in atopic dermatitis have been considered optimistic. Primary outcomes (improvement in signs and symptoms as rated by the clinician) are consistently reported in the literature (Table 4). Secondary outcomes are sometimes omitted and thus defy analysis. One study (30), though limited by a dropout rate of 46%, does not mention reduction in severity of eczema or extent of lesions in children treated with an elemental diet and a casein hydrolysate. A nonstatistically significant (but still clinically important) reduction of symptoms was however, observed in children treated with an elemental formula and a whey hydrolysate. In studies claiming efficacy of dietary treatment, this is reported within a 25–100% range, which suggests that allergen restriction is effective in at least some subsets of children with AEDS. Peak efficacy was reported in children under 2 years of age (22,24,25), while older children had a lower rate of response (21,23,30). This supports the observation that, among infants, food allergy is a more relevant trigger of AEDS. Furthermore, the response rate is higher in children with the more severe presentation of atopic dermatitis (44). In studies of ‘severe’ or ‘refractory’ forms of disease (25,28,29,33), diet therapy was found to be effective in 52–80% of cases. Surprisingly, several authors have considered the effects of dietary intervention in whole populations of children with AEDS irrespective of aetiology. Thus, one study (28) considered eliminating cow's milk, egg and wheat in children with severe AEDS but only single-blinded provocation tests were carried out with these foods after the elimination diet. The two studies evaluating children with a challenge-confirmed diagnosis of food allergy (31,35) report clinical improvement in all children. An unconfirmed diagnosis but strong sensitization indices also characterized positive outcomes for diet therapy (22,33). That children with a confirmed food allergy diagnosis respond better to an elimination diet is suggestive that indication predicated on a precise food allergy work-up may have yielded better results elsewhere also. Five studies investigated the efficacy of single food elimination [egg (27,34) and cow's milk (31,32,35)] although this kind of intervention is relatively easier to implement in a family setting but interest in this avenue of research seems to have waned (only one of such studies appeared during the last 5 years) while the attention of researchers regarding the diet therapy for AEDS has focused on treatments the biopathogenesis of which remains at the pure research biology level. Although metabolic alterations at the core of atopic dermatitis have been postulated (45,46), pathophysiological confirmation is still lagging behind empiric attempts to capitalize on the comparatively harmless effects of essential fatty acid supplements (47). There is, however, recent negative randomized controlled trial evidence against the efficacy of oil of borage in atopic dermatitis (48), a situation reminiscent of similar attempts using gamma-linolenic acid (49). Another dietary approach to the treatment for AEDS predicated on basic research axiomatization (or lack thereof) is through a ‘probiotic effect’ conferred by viable bacteria supplementation. The rationale underpinning this empiric treatment is derived from the indirect evidence of epidemiological studies in turn predicated on the hygiene hypothesis (50) that reduced colonization by enterobacteria and intestinal mucosal alterations are involved in the pathogenesis of AEDS, a postulate that also awaits microbiological, pathophysiological and randomized clinical trial evidence confirmation. Furthermore, studies of probiotic bacteria supplements in AEDS are based on limited populations (32,51,52) and their authors rely on future research to clarify their mechanisms of action (53). Thus, sheer lack of scientific and clinical evidence of the efficacy of ‘probiotic’ bacteria in the treatment (54) or prevention (55) of AEDS argues against recommending these supplements. As an endnote, reviewing the literature on diet therapy for atopic dermatitis has revealed as wide a spectrum of opinion and advice as there is on its description. Denial of the role of food allergy in AEDS, evidence of which, avowedly, is not incontrovertible, has been put forward by some researchers who claim that ‘although many patients with atopic dermatitis do have an allergic constitution (56), the contribution of allergy and IgE-mediated hypersensitivity reactions to the pathogenesis and the clinical severity of atopic dermatitis remains controversial’ (51).

Table 4.  Dietary interventions in cow's milk allergy: results and comments
StudyResultsComments
(21)13 improved; 1 worsened; 6 no change SPT unrelated to clinical responseevaluation method similar to SCORAD. The possibility of soy [placebo] allergy was not excluded. High dropout rate (16/36)
(22)clinical improvement in 80% after dietary exclusion. younger children did best. Severity of the eczema did not matterdefinition of food allergy and evaluation of eczema unclear. Variable duration of the observation period
(23)clinical improvement in 25% of cases after dietary exclusionno definition of food allergy. high dropout rate. Adults included.
(24)clinical improvement in 23%.poor blinding method. Small sample.
(25)improvement in 73%. Severity score fell to 27% of pretreatment. 3/27 patients required topical corticosteroids.open design, lack of definition of food allergy. 4/37 patients responded by anaphylactic shock to reintroduction.
(26)(FICH) egg: 72%, cow's milk: 47%, peanut: 34%; soy: 1.7%. (SAFT +) 39% response to elimination dietopen design, 62% dropout rate, nonstandardized test. Interesting for the evaluation of FICH as predictor response to diet.
(27)effect only in 3–6-month-old infants old with egg allergyblinded evaluation of egg allergy in children allergic to various foods including egg.
recruitment throughout the year, excluding seasonal variation.
(28)effect on 8 children (66%). 3 had diagnosis confirmed at the reintroduction.small sample. Open design. Results confirmed by open reintroduction
(29)whole group: effect in 52% (14% drop-out).subgroup: effect in 73% (no drop-out).good sample size. No evaluation of food sensitization. Open design. Good observation method (during hospitalization). Excellent evaluation of the relative weight of different steroids. Modest dropout rate. Mixed interventions.
(30)46% dropout rate (35 in the diet group, 4 in the control group). median reduction in percentage surface area whey hydrolysate group = 17.8%; casein hydrolysate group 5%; control group 4.9%. skin severity score: whey hydrolysate group, 21.8%; casein hydrolysate group, 13.5%; control, 15.9%.a specific calculation should be produced for the whey hydrolysate group. Good randomization. One of the few blinded studies (though single-blind).
improvement in the skin severity score was more than 20% in 58% of the diet group vs. 73% in control group.no diagnosis of food allergy.
diets were found ineffective.most of the drop-outs are in the diet group
(31)atopic eczema improved significantly and progressively all round: from 17 to 5 in We group and from 21 to 4 in Aa group.SCORAD indicated that children were mainly affected by mild AD. selected population diagnosis of cow's milk allergy.
(32)SCORAD improved from 21 to 19 in group a, from 26 to 15 in group b.the only study with laboratory evaluation of efficacy.
 concentrations of α1-antitrypsin and fecal TNF-α decreased only in group b.these data contradict the data of the previous paper (in a similar group and study design) suggesting that diet is effective only when associated with Lactobacillus GG.
concentration of fecal ECP unaltered.no blinding of L GG
(33)severity score improved in 100% of casesopen, unblinded.
no statistical evaluation.
(34)affected surface area 3% vs. 8.7% (p = 0.02).egg avoidance can be useful but effect magnitude is not great.
severity score 3.2% vs. 9.9% (p = 0.04). 
(35)SCORAD decreased from 24.6 to 12.2 at three months and 10.7 at 6 months. No difference between AA and eHF groupsthe study is mainly designed to evaluate growth. It shows an improvement in both groups, but there is not a control group (infants kept on CM diet)

Conclusions

  1. Top of page
  2. Abstract
  3. Aims and methods
  4. Data retrieval and inclusion criteria
  5. Results
  6. Interpretation of the results
  7. Conclusions
  8. References

Previous reviews have been confined to particular aspects of the dietetic treatment of infants and children with atopic dermatitis, such as the effect of exclusion of egg and milk from the diet of breast-feeding mothers of children suffering from eczema, the conclusions being that maternal avoidance of dietary antigen may reduce the severity of eczema but that larger trials are needed (57).

At the moment, however, no Cochrane review has been mounted into the effect of dietetic restrictions in children suffering from AEDS. Studies assessing the effect of an elemental or few-foods diet in atopic dermatitis report different types of interventions and are unable to support their use (14). There is little evidence to support an egg- and milk-free diet in unselected atopic eczema patients (14), but the use of specific food-free diets can be advocated on the grounds of the experience with an egg-free diet in infants with suspected egg allergy whose blood contains plasma egg-specific IgE (34).

Future studies on the efficacy of exclusion of specific food allergens in diet should be longer-term trials, focusing less on children than on infants who have dermatitis severe enough to require dietetic intervention and who are allergic to one or two foods. Food allergy must be demonstrated before the study and only specific triggers should be excluded from the diet. Objective parameters should be used in these studies, for instance the SCORAD (35), SASSAD (58), or ADASI (59) scoring system. The quality of life can now be estimated using specific scores as the Dermatology life quality index (60), developed for adults or specific paediatric questionnaires measuring the impact of the disease in children (61). As the evaluation should be performed blinded, children allergic to cow's milk form the ideal population for such trials but the blindedness is seriously hampered by ethical considerations. Finally, assessment of the magnitude of diet responsiveness requires infants from a general population of children with eczema, not selected populations of children sent to tertiary care, to be studied.

References

  1. Top of page
  2. Abstract
  3. Aims and methods
  4. Data retrieval and inclusion criteria
  5. Results
  6. Interpretation of the results
  7. Conclusions
  8. References
  • 1
    Johansson SG, Hourihane JO, Bousquet J, Bruijnzeel-Koomen C, Dreborg S, Haahtela T, et al. A revised nomenclature for allergy. An EAACI position statement from the EAACI nomenclature task force. Allergy 2001;56: 813824.
  • 2
    Isaac Steering Committee. Worldwide variation in prevalence of symptoms of atopic eczema in the international study of asthma and allergy in childhood. J Allergy Clin Immunol 1999;103: 12538.
  • 3
    Leung DYM, Bieber T. Atopic dermatitis. Lancet 2003;361: 151160.
  • 4
    Bergmann RL, Bergmann KE, Lau-Schadendorf S, Wahn U. Atopic diseases in infancy. The German multicenter atopy study (MAS-90). Pediatr Allergy Immunol 1994;5: 1925.
  • 5
    Kulig M, Bergmann R, Klettke U, Wahn V, Tacke U, Wahn U. Natural course of sensitization to food and inhalant allergens during the first 6 years of life. J Allergy Clin Immunol 1999;103: 11731179.
  • 6
    Nickel R, Lau S, Niggemann B, Gruber C, Von Mutius E, Illi S, et al. Messages from the German Multicentre Allergy Study. Pediatr Allergy Immunol 2002;13: 710.
  • 7
    Nickel R, Kulig M, Forster J, Bergmann R, Bauer CP, Lau S, et al. Sensitization to hen's egg at the age of twelve months is predictive for allergic sensitization to common indoor and outdoor allergens at the age of three years. J Allergy Clin Immunol 1997;99: 613617.
  • 8
    Wahn U, Bergmann R, Kulig M, Forster J, Bauer CP. The natural course of sensitisation and atopic disease in infancy and childhood. Pediatr Allergy Immunol 1997;8: 1620.
  • 9
    Steinman HA, Potter PC. The precipitation of symptoms by common foods in children with atopic dermatitis. Allergy Proc 1994;15: 203210.
  • 10
    Eggesbo M, Halvorsen R, Tambs K, Botten G. Prevalence of parentally perceived adverse reactions to food in young children. Pediatr Allergy Immunol 1999;10: 122132.
  • 11
    Tofte SJ, Hanifin JM. Current management and therapy of atopic dermatitis. J Am Acad Dermatol 2001;44: 1316.
  • 12
    Hanifin JM, Raijka G. Diagnostic features of atopic dermatitis. Acta Dermatovener (Stockholm) 1980;92: 4447.
  • 13
    Sampson HA. Atopic dermatitis. Ann Allergy 1992;69: 469479.
  • 14
    Hoare C, Li Wan Po A, Williams H. Systematic review of treatments for atopic eczema. Health Technol Assessment 2000;4: 1191.
  • 15
    Allen R. Role of diet in treating atopic eczema: dietary manipulation has no value. BMJ 1988;197: 14591460.
  • 16
    Eigenmann PA, Sicherer SH, Borkowski TA, Cohen BA, Sampson HA. Prevalence of IgE-mediated food allergy among children with atopic dermatitis. Pediatrics 1998;101: E8.
  • 17
    Eigenmann PA, Calza AM. Diagnosis of IgE-mediated food allergy among Swiss children with atopic dermatitis. Pediatr Allergy Immunol 2000;11: 95100.
  • 18
    Roehr CC, Reibel S, Ziegert M, Sommerfield C, Wahn U, Niggemann B. Atopy patch tests, together with determination of specific IgE levels, reduce the need for oral food challenges in children with atopic dermatitis. J Allergy Clin Immunol 2001;107: 548553.
  • 19
    Niggemann B, Reibel S, Roehr CC, Felger D, Ziegert M, Sommerfield C, et al. Predictors of positive food challenge outcome in non-IgE-mediated reactions to food in children with atopic dermatitis. J Allergy Clin Immunol 2001;108: 10531058.
  • 20
    Williams HC, Wüthrich B. Atopic Dermatitis. Cambridge: Cambridge University Press, 2000.
  • 21
    Atherton DJ, Sewell M, Soothill JF, Wells RS, Chilvers CE. A double-blind controlled crossover trial of an antigen-avoidance diet in atopic eczema. Lancet 1978;1: 401403.
  • 22
    Businco L, Businco E, Cantani A, Galli E, Infussi R, Benincori N. Results of a milk- and/or egg-free diet in children with atopic dermatitis. Allergol Immunopathol (Madr) 1982;10: 283288.
  • 23
    Neild VS, Marsden RA, Bailes JA, Bland JM. Egg and milk exclusion diets in atopic eczema. Br J Dermatol 1986;114: 117123.
  • 24
    Cant AJ, Bailes JA, Marsden RA, Hewitt D. Effect of maternal dietary exclusion on breast fed infants with eczema: two controlled studies. BMJ 1986;293: 231233.
  • 25
    Devlin J, David TJ, Stanton RH. Elemental diet for refractory atopic eczema. Arch Dis Child 1991;66: 9399.
  • 26
    Oranje AP, Aarsen RS, Mulder PG, Van Toorenenbergen AW, Liefaard G, Dieges PH. Food immediate-contact hypersensitivity (FICH) and elimination diet in young children with atopic dermatitis. Preliminary results in 107 children. Acta Derm Venereol (Suppl.)(Stockh) 1992;176: 4144.
  • 27
    Aoki T, Kojima M, Adachi J, Okano M. Effect of short-term egg exclusion diet on infantile atopic dermatitis and its relation to egg allergy: a single-blind test. Acta Dermatol Venereol (Suppl.)(Stockh) 1992;176: 99102.
  • 28
    Broberg A, Engstrom I, Kalimo K, Reimers L. Elimination diet in young children with atopic dermatitis. Acta Dermatol Venereol 1992;72: 365369.
  • 29
    David TJ. Extreme dietary measures in the management of atopic dermatitis in childhood. Acta Dermatol Venereol (Suppl.)(Stockholm) 1992;176: 113116.
  • 30
    Mabin DC, Sykes AE, David TJ. Controlled trial of a few foods diet in severe atopic dermatitis. Arch Dis Child 1995;73: 202207.
  • 31
    Isolauri E, Sutas Y, Makinen-Kiljunen S, Oja SS, Isosomppi R, Turjanmaa K. Efficacy and safety of hydrolyzed cow milk and amino acid-derived formulas in infants with cow milk allergy. J Pediatr 1995;127: 550557.
  • 32
    Majamaa H, Isolauri E. Probiotics: a novel approach in the management of food allergy. J Allergy Clin Immunol 1997;99: 179185.
  • 33
    Martino F, Bruno G, Aprigliano D, Agolini D, Guido F, Giardini O, et al. Effectiveness of a home-made meat based formula (the Rezza–Cardi diet) as a diagnostic tool in children with food-induced atopic dermatitis. Pediatr Allergy Immunol 1998;9: 192196.
  • 34
    Lever R, MacDonald C, Waugh P, Aitchison T. Randomised controlled trial of advice on an egg exclusion diet in young children with atopic eczema and sensitivity to eggs. Pediatr Allergy Immunol 1998;9: 1319.
  • 35
    Niggemann B, Binder C, Dupont C, Hadji S, Arvola T, Isolauri E. Prospective, controlled, multi-center study on the effect of an amino-acid-based formula in infants with cow's milk allergy/intolerance and atopic dermatitis. Pediatr Allergy Immunol 2001;12: 7882.
  • 36
    European Task Force on Atopic Dermatitis. Severity scoring of atopic dermatitis: the SCORAD index. consensus report of the European Task Force on Atopic Dermatitis. Dermatology 1993;186: 2331.
  • 37
    Hanifin JM, Thurston M, Omoto M, Cherill R, Tofte SJ, Graeber M. The Eczema Area and Severity Index (EASI): assessment of reliability in atopic dermatitis. Exp Dermatol 2001;10: 1118.
  • 38
    Sugarman JL, Fluhr JW, Fowler AJ, Bruckner T, Diepgen TL, Williams ML. The objective severity assessment of atopic dermatitis score. an objective measure using permeability barrier function and stratum corneum hydration with computer-assisted estimates for extent of disease. Arch Dermatol 2003;139: 14171422.
  • 39
    Gutgesell C, Frolich JC, Neumann C. Comparison of different activity parameters in atopic dermatitis: correlation with clinical scores. Br J Dermatol 2002;147: 914919.
  • 40
    Gelmetti C, Colonna C. The value of SCORAD and beyond. Towards a standardised evaluation of severity? Allergy 2004;59(Suppl. 78):6165.
  • 41
    Agostoni C, Grandi F, Scaglioni S, GiannÌ ML, Torcoletti M, Radaelli G, et al. Growth pattern of breastfed and nonbreastfed infants with atopic dermatitis in the first year of life. Pediatrics 2000;106: E73.
  • 42
    Nguyen J, Cazassus F, Atallah A, Baba N, Sibille G, Coriatt D. Kwashiorkor after an exclusion diet for eczema. Presse Med 2001;30: 14961497.
  • 43
    Riva E, Fiocchi A, Agostoni C, Biasucci G, Sala M, Banderali G, et al. PKU-related dysgammaglobulinemia. The effect of diet therapy on IgE and allergic sensitization. J Inher Metab Dis 1994;17: 710717.
  • 44
    Guillet G, Guillet M. Natural history of sensitizations in atopic dermatitis. Arch Dermatol 1992;128: 187192.
  • 45
    Wright S. Essential fatty acids and the skin. Br J Dermatol 1991;125: 503515.
  • 46
    Melnik BC, Plewig G, Tschung T. Disturbances of essential fatty acid- and prostaglandin E-mediated immunoregulation in atopy. Prostaglandins Leukot Essent Fatty Acids 1991;42: 125130.
  • 47
    Van Gool CJ, Thijs C, Henquet CJ, Van Houwelingen AC, Dagnelie PC, Schrander J et al. Gamma-linolenic acid supplementation for prophylaxis of atopic dermatitis – a randomized controlled trial in infants at high familial risk. Am J Clin Nutr 2003;77: 943951.
  • 48
    Takwale A, Tan E, Agarwal S, Barclay G, Ahmed I, Hotchkiss K, et al. Efficacy and tolerability of borage oil in adults and children with atopic eczema: randomised, double blind, placebo controlled, parallel group trial. BMJ 2003;327: 13851388.
  • 49
    Berth-Jones J, Graham-Brown RAC. A review of the use of essential fatty acid supplementation in atopic dermatitis with emphasis on the methodology of trial design. In: Maibach, HI, Schwindt, DA, editors. Cutaneous Biometrics. New York: Plenum Publishing Corporation 2000: 109117.
  • 50
    Wold AE. The hygiene hypothesis revised. Is the rising frequency of allergy due to changes in the intestinal flora? Allergy 1999;83: 2025.
  • 51
    Rosenfeldt V, Benfeldt E, Nielsen SD, Michaelsen KF, Jeppesen DL, Valerius NH, et al. Effect of probiotic Lactobacillus strains in children with atopic dermatitis. J Allergy Clin Immunol 2003;111: 389395.
  • 52
    Isolauri E, Arvola T, Sutas Y, Moilanen E, Salminen S. Probiotics: a novel approach in the management of food allergy. J Allergy Clin Immunol 1997;99: 179185.
  • 53
    Laiho K, Hoppu U, Ouwehand AC, Salminen S, Isolauri E. Probiotics: ongoing research on atopic individuals. Br J Nutr 2002;88: S19S27.
  • 54
    Matricardi PM, Bjorksten B, Bonini S, Bousquet J, Djukanovic R, Dreborg S, et al. Microbial products in allergy prevention and therapy. Allergy 2003;58: 461471.
  • 55
    Fiocchi A, Martelli A, De Chiara A, Moro G, Warm A, Terracciano L. Dietary primary prevention of food allergy. Ann Allergy Asthma Immunol 2003;91: 313.
  • 56
    Halbert A, William L, Morelli JG. Atopic dermatitis. is it an allergic disease? J Am Acad Dermatol 1995, 2003;33: 10081018.
  • 57
    Kramer MS, Kakuma R. Maternal dietary antigen avoidance during pregnancy and/or lactation for preventing or treating atopic disease in the child (Cochrane Review). In: The Cochrane Library, Issue 4. Chichester: John Wiley & Sons, Ltd.
  • 58
    Berth-Jones J. Six area, six sign atopic dermatitis (SASSAD) severity score: a simple system for monitoring disease activity in atopic dermatitis. Br J Dermatol 1996;135: 2530.
  • 59
    Bahmer FA. ADASI score: atopic dermatitis area and severity index. Acta Dermatol Venereol (Suppl )(Stockh) 1992;176: 3233.
  • 60
    Sowden JM, Berth-Jones J, Ross JS, Motley RJ, Marks R, Finlay AY, et al. Double-blind, controlled, crossover study of cyclosporin in adults with severe refractory atopic dermatitis. Lancet 1991;338: 137140.
  • 61
    Sicherer SH, Noone SA, Munoz-Furlong A. The impact of childhood food allergy on quality of life. Ann Allergy Asthma Immunol 2001;87: 461464.
  • 62
    Businco L, Benincori N, Nini G, Businco E, Cantani A, De Angelis M. Double-blind crossover trial with oral sodium chromoglycate in children with atopic dermatitis due to food allergy. Ann Allergy 1976;57: 433438.
  • 63
    Lever L, Hadley K, Downey D, MacKie R. Staphylococcal colonisation in atopic dermatitis and the effect of topical mupirocin therapy. Br J Dermatol 1988;119: 189198.