Atopic eczema is the most common inflammatory skin disease of childhood in developed countries. We performed a systematic review of randomized controlled trials to assess the effects of dietary exclusions for the treatment of established atopic eczema. Nine trials (421 participants) were included, most of which were poorly reported. Six were studies of egg and milk exclusion (n = 288), one was a study of few foods (n = 85) and two were studies of an elemental diet (n = 48). There appears to be no benefit of an egg- and milk-free diet in unselected participants with atopic eczema. There is also no evidence of benefit in the use of an elemental or few-foods diet in unselected cases of atopic eczema. There may be some benefit in using an egg-free diet in infants with suspected egg allergy who have positive specific IgE to eggs - one study found 51% of the children had a significant improvement in body surface area with the exclusion diet as compared with normal diet (95% CI 1.07-2.11) and change in surface area and severity score was significantly improved in the exclusion diet as compared with the normal diet at the end of 6 weeks (MD 5.50, 95% CI 0.19-10.81) and end of treatment (MD 6.10, 95% CI 0.06-12.14). Despite their frequent use, we find little good quality evidence to support the use of exclusion diets in atopic eczema.

BACKGROUND & AIMS: Adults with eosinophilic esophagitis (EoE) typically present with dysphagia and food impaction. A 6-food elimination diet (SFED) is effective in children with EoE. We assessed the effects of the SFED followed by food reintroduction on the histologic response, symptoms, and quality of life in adults with EoE.

METHODS: At the start of the study, 50 adults with EoE underwent esophagogastroduodenoscopies (EGDs), biopsies, and skin-prick tests for food and aeroallergens. After 6 weeks of SFED, patients underwent repeat EGD and biopsies. Histologic responders, defined by≤5 eosinophils/high-power field (eos/hpf) (n = 32), underwent systematic reintroduction of foods followed by EGD and biopsies (n = 20). Symptom and quality of life scores were determined before and after SFED.

RESULTS: Common symptoms of EoE included dysphagia (96%), food impaction (74%), and heartburn (94%). The mean peak eosinophil counts in the proximal esophagus were 34 eos/hpf and 8 eos/hpf, before and after the SFED, and 44 eos/hpf and 13 eos/hpf in the distal esophagus, respectively (P<.0001). After the SFED, 64% of patients had peak counts≤5 eos/hpf and 70% had peak counts of ≤10 eos/hpf. Symptom scores decreased in 94% (P<.0001). After food reintroduction, esophageal eosinophil counts returned to pretreatment values (P<.0001). Based on reintroduction, the foods most frequently associated with EoE were wheat (60% of cases) and milk (50% of cases). Skin-prick testing predicted only 13% of foods associated with EoE.

CONCLUSIONS: An elimination diet significantly improves symptoms and reduces endoscopic and histopathologic features of EoE in adults. Food reintroduction re-initiated features of EoE in patients, indicating a role for food allergens in its pathogenesis. Foods that activated EoE were identified by systematic reintroduction analysis but not by skin-prick tests.

Celiac disease, eosinophilic esophagitis, and urticaria are 3 manifestations of food allergy with different pathogenic mechanisms. We report the case of a 2-year-old child with digestive symptoms, slow growth, and severe asthma. The results of skin prick tests were positive to several foods. Endoscopy revealed eosinophilic esophagitis and celiac disease. Treatment consisted of a gluten-free diet and a 1-month course of oral corticosteroids. Endoscopy and biopsy findings were normal at 5 years of age. A gluten-free diet is the basis of treatment of celiac disease, but the role of an elimination diet in eosinophilic esophagitis is not well established. Our patient also developed urticaria when exposed to milk and egg.We present, to our knowledge, the first report of a patient with celiac disease, eosinophilic esophagitis, and immediate-type immunoglobulin E-mediated food allergy.

The aims of this study were to evaluate the implication of food allergy as a cause of paediatric constipation and to determine the diet period needed to tolerate the constipation-causing foods. Fifty-four children aged 6 months to 14 years (median, 42 months) suffering from chronic constipation (without anatomic abnormalities, cοeliac disease or hypothyroidism), unresponsive to a 3-month laxative therapy, were prospectively evaluated. All participants were evaluated for allergy to cow's milk, egg, wheat, rice, corn, potato, chicken, beef and soy, using skin tests (SPT), serum specific IgE and atopy patch test (APT). A withdrawal of the APT-positive foods was instructed. Thirty-two children had positive APT; 15 were positive to one; six, to two and 11, to three or more food allergens, wheat and egg being the commonest. After withdrawing the APT-positive foods for an 8-week period, constipation had improved in 28/32 children, but a relapse of constipation was noticed after an oral food challenge, so they continued the elimination diet. Tolerance to food allergens was achieved in only 6/28 after 6 months, compared to 25/28 after 12 months and to all after a 2-year-long elimination. Food allergy seems to be a significant etiologic factor for chronic constipation not responding to treatment, in infants and young children. APT was found to be useful in evaluating non-IgE allergy-mediated constipation, and there was no correlation of APT with IgE detection. Tolerance was adequately achieved after 12 months of strict food allergen elimination.

BACKGROUND AND AIM:Food-related symptoms are commonly described by patients with functional bowel disorders, but dietary change as an evidence-based therapy has not been part of routine management strategies. This reviews aims to discuss strategies commonly applied.

METHOD:Published literature was reviewed.

RESULTS:Traditional approaches involve elimination diets followed by placebo-controlled reintroduction of specific foods, which is tedious at best and not applied in routine practice. Pathogenically-based approaches include determining what food components are inducing food hypersensitivity responses using specific biomarkers, but this is probably applicable to a small proportion of patients only and has met with only limited success. Food bioactive chemicals, such as salicylates, have been targeted, but there is a paucity of quality evidence for or against this approach. In contrast, targeting poorly absorbed dietary components that might induce luminal distension via osmotic effects and rapid fermentation (FODMAPs) has been successful and the efficacy of the dietitian-delivered low FODMAP diet is now supported by high quality evidence. Improvement of all symptoms of FBD in three out of four patients has been achieved. The diet may potentially improve stool frequency in patients with an ileal pouch or a high output ileostomy, or functional symptoms in patients with inflammatory bowel disease. FODMAPs in enteral formulas may also be responsible for diarrhoea induced by enteral nutrition.

CONCLUSION:Dietary restriction of FODMAPs is an effective therapy in the majority of patients with functional bowel symptoms and, provided dietitians are trained in the technique, should be first line therapy.

BACKGROUND:Eosinophilic esophagitis (EE) is a recently described disorder identified in patients with symptoms suggestive of gastroesophageal reflux disease (GERD) but unresponsive to conventional reflux therapies. Therapies have included corticosteroids, elemental diet, and diet restriction. We report our experience with skin prick and atopy patch testing and food elimination diets in patients diagnosed as having EE.

OBJECTIVE:To identify food antigens that cause EE and the characteristics of patients who respond to food elimination vs those who are unresponsive.

METHODS:Patients diagnosed as having EE had restricted diets based on skin prick and atopy patch testing results. Additional biopsies were performed after 4 to 8 weeks of restricted diet. Demographics, atopic tendencies, and food antigens were identified retrospectively in our food allergy database.

RESULTS:A total of 146 patients diagnosed as having EE were evaluated with skin prick and atopy patch testing. Thirty-nine patients had unequivocal demonstration of food causing EE, with normalization of biopsy results on elimination and reoccurrence on reintroduction. An additional 73 patients, for a total 112 (77%) of 146 patients, had resolution of their EE as demonstrated by biopsy results. Fifteen (10%) of 146 patients were nonresponders manifested by no significant reduction in esophageal eosinophils despite restricted diet based on skin prick and atopy patch testing. Egg, milk, and soy were identified most frequently with skin prick testing, whereas corn, soy, and wheat were identified most frequently with atopy patch testing.

CONCLUSION:In more than 75% of patients with EE, both symptoms and esophageal inflammation can be significantly improved with dietary elimination of foods. Skin prick and atopy patch testing can help identify foods in most patients.

BACKGROUND:Epidemiological evidence has shown that pediatric food allergy is more prevalent in regions further from the equator, suggesting that vitamin D insufficiency may play a role in this disease.

OBJECTIVE:To investigate the role of vitamin D status in infantile food allergy.

METHODS:A population sample of 5276 one-year-old infants underwent skin prick testing to peanut, egg, sesame, and cow's milk or shrimp. All those with a detectable wheal and a random sample of participants with negative skin prick test results attended a hospital-based food challenge clinic. Blood samples were available for 577 infants (344 with challenge-proven food allergy, 74 sensitized but tolerant to food challenge, 159 negative on skin prick test and food challenge). Serum 25-hydroxyvitamin D levels were measured by using liquid chromatography tandem mass spectrometry. Associations between serum 25-hydroxyvitamin D and food allergy were examined by using multiple logistic regression, adjusting for potential risk and confounding factors.

RESULTS:Infants of Australian-born parents, but not of parents born overseas, with vitamin D insufficiency (≤50 nmol/L) were more likely to be peanut (adjusted odds ratio [aOR], 11.51; 95% CI, 2.01-65.79; P=.006) and/or egg (aOR, 3.79; 95% CI, 1.19-12.08; P=.025) allergic than were those with adequate vitamin D levels independent of eczema status. Among those with Australian-born parents, infants with vitamin D insufficiency were more likely to have multiple food allergies (≥2) rather than a single food allergy (aOR, 10.48; 95% CI, 1.60-68.61 vs aOR, 1.82; 95% CI, 0.38-8.77, respectively).

CONCLUSIONS:These results provide the first direct evidence that vitamin D sufficiency may be an important protective factor for food allergy in the first year of life.