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There have been reports of increased prevalence of certain food allergies in patients with Type I latex allergy (LA). A detailed food allergy history was obtained from 137 patients with LA. Latex allergy was defined by positive history of IgE mediated reactions to contact with latex and positive skin prick test to latex and/or positive in vitro test (AlaSTAT and/or Pharmacia CAP). Food allergy was diagnosed by a convincing history of possible IgE mediated symptoms occurring within 60 minutes of ingestion. We identified 49 potential allergic reactions to foods in 29 (21.1%) patients. Foods responsible for these reactions include banana 9 (18.3%), avocado 8 (16.3%), shellfish 6 (12.2%), fish 4 (8.1%), kiwi 6 (12.2%), tomato 3 (6.1%), watermelon, peach, carrot 2 (4.1%) each, and apple, chestnut, cherry, coconut, apricot, strawberry, loquat, one (2.0%) each. Reactions to foods included local mouth irritation, angioedema, urticaria, asthma, nausea, vomiting, diarrhea, rhinitis, or anaphylaxis. Our study confirms the earlier reports of increased prevalence of food allergies in patients with LA. We also report increased prevalence of shellfish and fish allergy not previously reported. The nature of cross reacting epitopes or independent sensitization between latex and these foods is not clear.
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PMID:Prevalence of food allergy in 137 latex-allergic patients. 1020 85

The prevalence of atopic diseases is increasing worldwide for reasons that are not clear. Food allergies are the earliest manifestations of atopy. This review defines the foods most commonly involved in allergic reactions and identifies an emerging group of syndromes in which food allergy is involved. A study of the frequency of food allergies in Australia and South-East Asia has recently shown that egg, cow's milk and peanut are the most common food allergens in Australia, but there were divergent results from different regions of South-East Asia. It is not clear whether the differences in reactivity to foods are due to genetic or cultural factors, but the findings raise the possibility that genetic susceptibility to food allergy may operate at the T-cell level modulated by the major histocompatibility complex. The Melbourne Milk Allergy Study defined a wide range of clinical symptoms and syndromes that could be reproduced by dietary challenge. A subsequent analysis of the infants with hypersensitivity to cow's milk and other multiple food proteins identified a new syndrome, multiple food protein intolerance of infancy. Food challenges demonstrated reactions developing slowly days after commencement of low-allergen soy formula or extensively hydrolysed formula. Follow-up at the age of 3 years showed that most children with this disorder tolerated most foods apart from cow's milk, egg and peanut. Atopic dermatitis affects about 18% of infants in the first 2 years of life. In a community-based study we have shown a very strong association (RR 3.5) between atopic dermatitis and infants with immunoglobulin E allergy to cow's milk, egg or peanut. Family studies on these infants have shown a link between atopic dermatitis and the genomic region 5q31 adjacent to the interleukin-4 gene cluster. Infantile colic (distress) affects 15-40% of infants in the first 4 months of life. Many theories of causation have been proposed, but a study from our centre showed that dietary modification, particularly that of breastfeeding mothers whose infants present with colic before the age of 6 weeks, alleviated symptoms. Colic associated with vomiting has been attributed to gastro-oesophageal reflux (GOR). This has been considered primarily a motility disorder, but a secondary form resulting from food protein intolerance has been described recently. We have also recently identified a group of infants with distressed behaviour attributed to GOR who have failed to respond to H2-receptor antagonists, prokinetic agents and multiple formula changes. Symptoms resolved on commencement of an elemental amino acid-based formula. In two-thirds of the patients, symptoms relapsed when challenged with low-allergen soy formula or extensively hydrolysed formula. We propose that a period of food protein intolerance is a part of the normal development of the immune system as it encounters common dietary proteins in infancy and early childhood. Future targets for research are development of appropriate dietary and management strategies for these entities and identification of genetic markers for these disorders.
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PMID:Clinical spectrum of food allergy in children in Australia and South-East Asia: identification and targets for treatment. 1048 Jul 58

Adverse reactions to foods involving abnormal immune reactions to food antigens occur in 2-7% of the North American population; the numbers are perhaps higher in children. Both IgE-mediated and non-IgE-mediated allergic responses occur. IgE-mediated allergic responses to foods are the most dramatic and perhaps the most easily diagnosed type of food allergy. Non-IgE-mediated food hypersensitivity is more chronic, less acute, less obvious in its clinical presentation, and often more difficult to diagnose. It usually presents in infants between one week and three months of age with vomiting and diarrhea, although irritability, poor feeding, and failure to thrive are not uncommon. A thorough history and physical examination are often key in establishing a diagnosis of food protein hypersensitivity. In non-IgE-mediated disease, skin tests and immunological studies are not helpful. Eliminating the food allergen is the only means of dealing with a food allergy in most patients. About 85% of infants who have formula protein intolerance will outgrow their symptoms somewhere between 1 month and 3 years of age, older children and adults are somewhat less likely to lose their sensitivity, although approximately one-third will after 1-2 years of dietary restriction.
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PMID:Food hypersensitivity in children. 1056 87

Eating disorders are serious illnesses affecting 1-2% of young women. Patients may present to any doctor, sometimes atypically (e.g. unexplained weight loss, food allergy, infertility, diarrhoea), delaying diagnosis and leading to needless investigation. The cardinal signs are weight loss, amenorrhoea, bingeing with vomiting and other compensatory behaviours, and disturbances in body image with an exaggeration of the importance of slimness. When other causes have been excluded, useful investigations are serum potassium, bone mineral density scanning and pelvic ultrasound. In emaciated patients multiple systems may fail with pancytopaenia, neuromyopathy and heart failure. Clinical assessment of muscle power is used to monitor physical risk. Treatment may involve individual, group or family sessions, using cognitive-behavioural, psychodynamic and family approaches. More severe or intractable illness is treated with day care, with in-patient care in a medical or specialist psychiatric unit reserved for the most severely ill patients. Antidepressants have a place in the treatment of bulimia nervosa unresponsive to psychological approaches, and when severe depressive symptoms develop. The children of people with eating disorders may have an increased risk of difficulties. Support for the patient and family, and effective liaison between professionals, are essential in the treatment of severe eating disorders.
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PMID:Review article: recognition and treatment of eating disorders in primary and secondary care. 1075 15

There have frequently been doubts as to the relevance of food allergy, in particular as far as the involvement of the intestinal tract is concerned. Several studies, however, have confirmed the existence of allergic reactions in the gut, with an estimated prevalence of about 1-2% in adults. Clinical symptoms are unspecific and include nausea, vomiting, abdominal pain, cramping and diarrhea. Intestinal mast cells, as well as intestinal eosinophils, have been shown to be involved in the pathogenesis of food-allergy-related enteropathy. In addition to classical IgE-dependent degranulation, further agonists have been demonstrated for mast cell activation, for example IL-4. The methods used to confirm the diagnosis of intestinal allergy are still insufficient. Until now, blinded oral challenge procedures with food antigens have been accepted as the 'gold standard' in diagnosing food allergy, although these tests have practical problems. Therefore, new test systems have been developed, such as endoscopic provocation tests, that may improve diagnostic procedures. Elimination diet still presents the main basis of therapy. Aspects to be focused on in the future are the role fo IgE-independent allergic mechanisms in intestinal allergy, the impact of cross-reactivity with other allergens and the relationship to other inflammatory bowel diseases such as Crohn's disease, ulcerative colitis, celiac disease and irritable bowel syndrome.
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PMID:Allergy and the gut. 1082 17

Food intolerance is a reproducible adverse reaction to a specific food ingredient that is not psychologically based. Food allergy is a form of food intolerance in which there is evidence that the response is caused by an immunological reaction to food. Other mechanisms of food intolerance include enzyme defects (e.g. lactase deficiency), pharmacological effects (e.g. histamine), toxic properties (e.g. haemagglutinating lectins) and irritants (e.g. spices). Food allergy in children is a highly contentious subject and there is often a striking lack of published evidence from which to base clinical decisions. The true prevalence of food allergy in children is unknown, although there is evidence of an increasing incidence of allergic reactions to some foods, especially peanuts. Our understanding of why some children are unable to tolerate certain foods (e.g. cow's milk, egg), or how they grow out of this intolerance, is very poor. Symptoms of food allergy in children are diverse and include vomiting, poor weight gain, abdominal pain, malabsorption, cough, wheeze, rhinitis, atopic eczema, urticaria and angioedema. Despite the lack of objective data to support the notion that food intolerance contributes to behaviour in children, this is a belief firmly held by many parents and some professionals. The gold standard for diagnosing food intolerance is the double-blind placebo-controlled food challenge (DBPCFC). There is often a poor correlation between the results of food provocation tests and those of skin prick tests of radioallergosorbent tests for specific food antibodies. For proven food allergy, elimination diets are the mainstay of management. In children these must be closely supervised to avoid nutritional deficiency and compromise of growth. Some children who have had severe (anaphylactic) reactions after food need to have a supply of self-injectable adrenaline made available to their parents and teachers and must also practice strict avoidance of the offending food.
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PMID:Food allergy and food intolerance in childhood. 1113 67

Adverse reactions to food may be toxic or non toxic, depending on the susceptibility to a certain food; non toxic reactions that involve immune mechanisms are termed allergy if they are IgE-mediated. If no immunological mechanism is responsible, it is termed intolerance. The following disorders are considered a consequence of food allergy: gastrointestinal reactions (oral allergy syndrome, vomiting, diarrhea, protein-induced enterocolitic syndrome, eosinophilic gastroenteritis); respiratory reactions (rhinitis, asthma, laryngeal edema); cutaneous reactions (urticaria-angioedema, atopic dermatitis); anaphylaxis. There is much recent evidence to consider celiac disease an immunological disorder. Food allergy diagnosis is based on history, SPT, specific IgE, food challenges. DBPCFC is fundamental for diagnosing true food allergy; patients who have had anaphylaxis to food must not undergo DBPCFC. Rapidly progressive respiratory reactions and anaphylactic shock are life-threatening reactions that can be caused by food allergy. The doses of food inducing anaphylaxis can be very low, therefore commercial cross-contamination with an unsuspected food during food processing can be risky for the food allergic patient. The prevention of severe anaphylactic food reactions may lie in interdisciplinary collaboration among allergologists, chemists, food technologists, and experts in food industry research.
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PMID:Introducing chemists to food allergy. 1129 97

Atopic dermatitis is a typical chronic inflammatory skin disease that usually occurs in individuals with a personal or family history of atopy. Children with atopic dermatitis frequently present IgE-mediated food sensitization, the most commonly involved foods being egg and cow's milk. However, controversy currently surrounds whether food allergy is an etiological factor in atopic dermatitis or whether it is simply an associated factor, accompanying this disease as one more expression of the patient's atopic predisposition. Approximately 40 % of neonates and small children with moderate-to-severe atopic dermatitis present food allergy confirmed by double-blind provocation tests but this allergy does not seem to be the cause of dermatitis since in many cases onset occurs before the food responsible for allergic sensitization is introduced into the newborn's diet.Studies of double-blind provocation tests with food in patients with atopic dermatitis demonstrate mainly immediate reactions compatible with an IgE-mediated allergy. These reactions occur between 5 minutes and 2 hours and present mainly cutaneous symptoms (pruritus, erythema, morbilliform exanthema, wheals) and to a lesser extent, digestive manifestations (nausea, vomiting, abdominal pain, diarrhea), as well as respiratory symptoms (wheezing, nasal congestion, sneezing, coughing). However, these reactions do not indicate the development of dermatitis.Some authors believe that responses to the food in provocation tests may also be delayed, appearing mainly in the following 48 hours, and clinically manifested as exacerbation of dermatitis. However, delayed symptoms are difficult to diagnose and attributing these symptoms to a particular foodstuff may not be possible.Delayed reactions have been attributed to a non-IgE-mediated immunological mechanism and patch tests with food have been proposed for their diagnosis. In our experience and in that of other authors, the results of patch tests with cow's milk do not seem very specific and could be due, at least in part, to the irritant effect of these patches on the reactive skin of children with atopic dermatitis.The involvement of foods in atopic dermatitis will always be difficult to demonstrate given that an exclusion diet is not usually required for its resolution. Food is just one among several possible exacerbating factors and consequently identification of its precise role in the course of the disease is difficult. Further double-blind prospective studies are required to demonstrate the effectiveness of exclusion diets in the treatment of atopic dermatitis.Apart from the controversy surrounding the etiological role of foods, the most important point in atopic dermatitis is to understand that the child is atopic, that is, predisposed to developing sensitivity to environmental allergens; in the first few years of life to foods and subsequently to aeroallergens. Consequently, possible allergic sensitization to foods should be evaluated in children with atopic dermatitis to avoid allergic reactions and to prevent the possible development of allergic respiratory disease later in life.
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PMID:[Etiologic implication of foods in atopic dermatitis: evidence against]. 1198 42

BACKGROUND: Eosinophilic gastritis is related to eosinophilic gastroenteritis, varying only in regards to the extent of disease and small bowel involvement. Common symptoms reported are similar to our patient's including: abdominal pain, epigastric pain, anorexia, bloating, weight loss, diarrhea, ankle edema, dysphagia, melaena and postprandial nausea and vomiting. Microscopic features of eosinophilic infiltration usually occur in the lamina propria or submucosa with perivascular aggregates. The disease is likely mediated by eosinophils activated by various cytokines and chemokines. Therapy centers around the use of immunosuppressive agents and dietary therapy if food allergy is a factor. CASE PRESENTATION: The patient is a 31 year old Caucasian female with a past medical history significant for ulcerative colitis. She presented with recurrent bouts of vomiting, abdominal pain and chest discomfort of 11 months duration. The bouts of vomiting had been reoccurring every 7-10 days, with each episode lasting for 1-3 days. This was associated with extreme weakness and cachexia. Gastric biopsies revealed intense eosinophilic infiltration. The patient responded to glucocorticoids and azathioprine. The differential diagnosis and molecular pathogenesis of eosinophilic gastritis as well as the molecular effects of glucocorticoids in eosinophilic disorders are discussed. CONCLUSIONS: The patient responded to a combination of glucocorticosteroids and azathioprine with decreased eosinophilia and symptoms. It is likely that eosinophil-active cytokines such as interleukin-3 (IL-3), granulocyte macrophage colony stimulating factor (GM-CSF) and IL-5 play pivotal roles in this disease. Chemokines such as eotaxin may be involved in eosinophil recruitment. These mediators are downregulated or inhibited by the use of immunosuppressive medications.
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PMID:Eosinophilia in a patient with cyclical vomiting: a case report. 1514 61

Gastroesophageal reflux (GER), defined as passage of gastric contents into esophagus, and GER disease (GERD), defined as symptoms or complications of GER, are common pediatric problems encountered by both primary and specialty medical providers. Clinical manifestations of GERD in children include vomiting, poor weight gain, dysphagia, abdominal or substernal pain, esophagitis and respiratory disorders. On the other hand, recurrent vomiting is the symptom of hydronephrosis, brain tumor, food allergy, uremia, other metabolic disease, obstruction of intestine etc. It is very important for clinicians dealing with children and infants to understand GERD. The evaluation and treatment of gastroesophageal reflux in infants and children were reviewed here.
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PMID:[Evaluation and treatment of gastroesophageal reflux in infants and children]. 1534 50


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