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Abstract
Cow’s milk allergy (CMA) is defined as an immunologically mediated adverse reaction to cow’s milk proteins. In industrialized nations, CMA affects approximately 2% of infants under 2 years of age, and is the most common food allergy in this age group. Parents may overestimate milk as a cause of symptoms, but unrecognized reactions may also occur. br About 2% of the general population and up to 6% of children suffer -#102;-#114;-#111;-#109; food allergy. Cow’s milk is charged with a important role in infancy after weaning, since conventional formula are based on its procession. br Cow’s milk is often the first major food protein ingested by formula-fed infants, and may lead to early allergic sensitization. CMA can also occur in exclusively breast-fed infants. CMA in infancy and early childhood can be regarded as a model of food allergies, as a significant number of sensitized infants have other allergies. It is uncertain to what extent the development of food allergies and atopy can be prevented by dietary allergen avoidance. br CMA presents with a broad range of clinical symptoms and syndromes. The clinical spectrum extends -#102;-#114;-#111;-#109; acute anaphylactic manifestations to diverse dis-#111;-#114;-#100;-#101;-#114;s, such as atopic dermatitis, food-associated wheeze, infantile colic, gastro-oesophageal reflux (GOR), oesophagitis, cow’s milk enterocolitis, food-associated proctocolitis and constipation. The mechanisms underlying the various clinical manifestations are poorly understood. -#119;-#104;-#101;-#114;-#101;as food allergies in older children are mainly caused by IgE hypersensitivity, in young children non-IgE-mediated mechanisms are increasingly being recognized. br Milk contains more than 40 proteins and all of them may act like human species antigens. The main allergens are beta lactoglobulin, casein, alpha lactoalbumin and seroalbumin; beta lactoglobulin is a protein not existing in human species and is found in maternal milk in minimal quantities (mcg) due to milky products ingested by the mother, these small quantities are responsible of the highest number of sensitizations to this protein . br The diagnosis of CMPA is based on one or more of the following: a detailed clinical history, allergy test results (skin prick testing [SPT] and/or specific immunoglobulin E [IgE]) and, if required, supervised incremental milk challenges. The majority of UK primary care centres do not have access to these tests and may also be unfamiliar with the interpretation or result. br A comprehensive history (including a family history of atopy) and careful physical examination form the foundation of both algorithms. The risk of atopy increases if a parent or sibling has atopic disease (20–40% and 25–35%, respectively), and is higher still if both parents are atopic (40–60%). br Differential diagnoses include, among others: metabolic dis-#111;-#114;-#100;-#101;-#114;s, anatomical abnormalities, coeliac disease and other (rare) enteropathies, pancreatic insufficiency (such as in cystic fibrosis), non-immunological adverse reactions to food (such as fructose malabsorption or secondary lactose intolerance, mostly with an onset in older children), allergic reactions to other food allergens (such as hen’s eggs, soy, wheat, etc) or other substances (such as animal dander, moulds, dust), malignancy, and infections (particularly gastrointestinal and urinary tract infections) and sepsis. A role for allergy in recurrent otitis media has been heavily discussed in some of the literature. br The clinician should also assess whether the child suffers -#102;-#114;-#111;-#109; concurrent conditions. For example, 15–21% of children with suggested or proven gastro-oesophageal reflux disease (GORD) or CMPA suffer -#102;-#114;-#111;-#109; both conditions. Furthermore, 16–42% of children with a history of GORD show signs or symptoms of CMPA. CMPA has also been related to infantile colic. However, colic has numerous aetiologies which should be considered during the differential diagnosis. However, there is a subgroup of about 10% of colicky formula-fed infants in whom the colic episodes are a manifestation of CMPA. br In addition, they do not have the facilities for supervised food challenges. Empirical treatment is often required pending confirmation of allergy or referral to a specialist centre, but requires clear guidelines. No consensus guidelines currently exist for the diagnosis and management of CMPA in the UK. An international task force has recently published proposed guidelines for the management of CMPA. These provide separate algorithms covering the diagnosis and management of CMPA for both breast-fed and formula-fed infants and discuss the use of hypoallergenic formulae, elimination diets and diagnostic tests. Revisions and adaptations for the UK market are required and are discussed in this article. br Breast-feeding is generally considered to be the most appropriate form of infant feeding as it may reduce the risk of the subsequent development of atopic disease. However, a large study of 6209 infants, found that prolonged breast-feeding may increase the risk of IgE-sensitization. Allergic IgE sensitization can occur as early as during the fetal period. br Breast feeding should be promoted for the primary prevention of allergy, but breast-fed infants with proven CMPA should be treated by allergen avoidance. There is evidence that food proteins -#102;-#114;-#111;-#109; milk, egg, peanut and wheat are excreted in breast milk and may cause adverse reactions during exclusive breast feeding in sensitised infants. Due to the many benefits of breast feeding to the infant and the mother, clinicians should advise mothers to continue breast feeding but avoid the causal foods in their own diet.