PubMed · 14342140
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J CULLINAN. 1965-08-27. REFLECTIONS ON ELECTIONS.. https://pubmed.ncbi.nlm.nih.gov/14342140/
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Food allergies in children present with a wide spectrum of clinical manifestations, including anaphylaxis, urticaria, angioedema, atopic dermatitis and gastrointestinal symptoms (such as vomiting, diarrhoea and failure to thrive). Symptoms usually begin in the first 2 years of life, often after the first known exposure to the food. Immediate reactions (occurring between several minutes and 2 hours after ingestion) are likely to be IgE-mediated and can usually be detected by skin prick testing (SPT) or measuring food-specific serum IgE antibody levels. Over 90% of IgE-mediated food allergies in childhood are caused by eight foods: cows milk, hens egg, soy, peanuts, tree nuts (and seeds), wheat, fish and shellfish. Anaphylaxis is a severe and potentially life-threatening form of IgE-mediated food allergy that requires prescription of self-injectable adrenaline. Delayed-onset reactions (occurring within several hours to days after ingestion) are often difficult to diagnose. They are usually SPT negative, and elimination or challenge protocols are required to make a definitive diagnosis. These forms of food allergy are not usually associated with anaphylaxis. The mainstay of diagnosis and management of food allergies is correct identification and avoidance of the offending antigen. Children often develop tolerance to cows milk, egg, soy and wheat by school age, whereas allergies to nuts and shellfish are more likely to be lifelong.
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We report ten infants (mean gestational age: 30 weeks; range: 25 to 40 weeks) with zinc deficiency dermatitis who developed erosive, impetiginized periorificial dermatitis at 10 weeks of age (corresponding to a mean gestational age of 41.4 weeks, with a range of 36-44 weeks), but who were otherwise well. Cutaneous symptoms were initially misdiagnosed as eczema or impetigo in 8/10 (80%) children who received either topical (4/8) and/or systemic (6/8) antibiotics. Topical corticosteroids were applied in 4/10 infants for a mean time of 4 weeks (range: 2 to 5 weeks) before the correct diagnosis was established by decreased serum zinc levels; skin atrophy (telangiectasia, thinning) as a complication of topical steroid treatment (class II steroids) was observed in two infants. All children responded to oral therapy with zinc sulfate or zinc gluconate (1.5-4 mg/kg/d). Skin lesions started to clear within 24 h after the initiation of therapy and had completely cleared in all infants after 14 days of therapy (range: 3-14 days). We conclude that nutritional zinc deficiency is a frequently misdiagnosed problem in thriving, fully breast-fed preterm babies. It is attributable to the decreased zinc content of human milk as compared to cow's milk, and the increased demand of zinc in rapidly thriving preterm infants. It seems advisable to routinely check serum zinc levels in fully breast-fed preterm infants who do not receive regular oral zinc supplementation once they reach a gestational age of 40 weeks.