YOU ARE NOW CONNECTED TO THE TOXLINE (1981 FORWARD, NON-ROYALTY) FILE. ==ECZEMA, INFANT - HANDS== 2 AUTHOR Dotterud LK TITLE [Role of food in atopic eczema] SOURCE Tidsskr Nor Laegeforen; VOL 116, ISS 28, 1996, P3335-40 (REF: 59) ABSTRACT Some new aspects of adverse reactions to food are reviewed. People quite often blame food for the development of allergic symptoms. These true reactions can be divided into three groups: Immunological (food allergy--type I-IV reactions), non-immunological (intolerance--result of non-immunologic mechanisms) and toxic/biochemical reactions. The patterns of adverse food reactions are age dependent, especially allergy to cow's milk, hen's egg-white and soya, and symptoms appear most frequently in children under three years of age. 10-20% of children report adverse reactions to food, but only 3-5% have IgE-mediated reactions. In children with moderate to severe atopic dermatitis as many as 30% are reported to have food allergies. In adults, it is believed that 3-12% may have some kind of adverse reaction to specific foods, but only 1-2% have food allergy. The most common symptoms of adverse food reactions appear in the skin and in the gastrointestinal tract, but respiratory symptoms are also observed. Once food allergy has been proven conclusively the identified food should be totally eliminated from the diet. If important foods are eliminated the patient's sensitivity should be reevaluated again after a time. 3 AUTHOR Hogan PA TITLE Atopic eczema in children: what to do when treatment fails to work. SOURCE Australas J Dermatol; VOL 37, ISS 3, 1996, P119-22; quiz 123-4 (REF: 25) ABSTRACT Atopic eczema in infants and children usually responds to a management programme involving patient education, the avoidance of environmental irritants, the regular use of emollients and the application of topical steroids. If a child fails to respond to this management programme, the dermatologist should initially ensure that the diagnosis is correct and exclude a coexistent disease process (for example, infection or immunodeficiency) that may be hampering response to treatment. The next step is to ensure that environmental irritants have been identified and eliminated from the child's environment and that prescribed medication is being used as instructed. Allergy assessment and ancillary therapy are reserved for those infants and children with severe disease not responding to basic therapy. 4 AUTHOR Sporik R AUTHOR Platts-Mills TA TITLE Epidemiology of dust-mite-related disease. SOURCE Exp Appl Acarol; VOL 16, ISS 1-2, 1992, P141-51 (REF: 50) ABSTRACT For many years it has been suggested that allergens derived from the house dust mite played a major role in the pathogenesis of asthma, eczema and some cases of allergic rhinitis. Recently, house dust mite allergens have been purified and specific immunoassays developed with which exposure to house dust mites and their allergens can be more easily determined. Using these tools, epidemiological studies have provided confirmatory evidence that not only is house dust mite exposure associated with the majority of cases of asthma in children and young adults, but that it is causally related to the development of asthma. 5 AUTHOR Sampson HA TITLE Food hypersensitivity and dietary management in atopic dermatitis. SOURCE Pediatr Dermatol; VOL 9, ISS 4, 1992, P376-9 (REF: 19) ABSTRACT Although immune dysfunction is known to play an integral role in the development of atopic dermatitis, no clear delineation of the underlying pathogenic mechanism(s) responsible for this disorder has been proposed. Several factors are known to trigger flares of atopic dermatitis. In the extrinsic form of this disorder, food and airborne allergens may provoke flares of eczema. Research implicating food hypersensitivity in the pathogenesis of atopic dermatitis includes studies of food allergen avoidance in newborn infants at high risk for atopic disease, investigations of children with blinded food challenges, and therapeutic trials of allergen-elimination diets. Taken together, these studies demonstrate a significant pathogenic role for food hypersensitivity in about one-third of children with atopic dermatitis. 6 AUTHOR David TJ TITLE Short stature in children with atopic eczema. SOURCE Acta Derm Venereol Suppl (Stockh); VOL 144, 1989, P41-4 (REF: 34) ABSTRACT Short stature, defined as a standing height below the third centile when corrected for mid-parental height, was found in 22% of children with atopic eczema troublesome enough to cause regular attendance at hospital. The cause of this short stature is unknown in most cases, but contributory factors comprise topical steroid therapy, co-existing asthma, inhaled or oral steroid therapy, malnutrition due to unsupervised dietary restriction, loss of sleep, and vitamin D deficiency. If the short stature is simply associated with severe disease and not attributable to steroid therapy, and if the disease remits before puberty, then catch-up growth can be expected. If the short stature is caused by steroid therapy, or if severe disease persists into adult life, then permanent growth stunting may occur. 7 AUTHOR Rystedt I TITLE Hand eczema and long-term prognosis in atopic dermatitis. SOURCE Acta Derm Venereol Suppl (Stockh); VOL 117, 1985, P1-59 (REF: 196) ABSTRACT A follow-up study of 1177 adult patients who had had atopic dermatitis (AD) (Groups 1 and 2) or respiratory allergy (Group 3) in childhood is reported. Patients who had had AD in childhood had received in-patient (Group 1) or out-patient treatment (Group 2) for their dermatitis. 183 patients in Group 1 and 162 in Group 2 were examined clinically. Further, 445 patients who had recently been treated for hand eczema at a department for occupational dermatoses were studied (Group 5). A group of 199 people who had no personal or family history of atopy served as controls (Group 4). The essential findings were as follows: The healing rate was lower (38%) in patients with severe (Group 1) than in those with moderate (60%) childhood dermatitis (Group 2). Although the healing rate was comparatively low in both groups, persistent eczema was in most cases of mild degree. The commonest localization of persistent dermatitis was the hands. The AD had developed earlier in patients who had had severe childhood dermatitis than in those whose childhood AD was moderate. Severe childhood AD was also associated with a significantly higher frequency of family history of atopy and associated respiratory allergy. The inheritance pattern was specific for the different types of atopic disease. A family history of AD was significantly commoner in people with AD than in people with respiratory allergy, and, conversely, people with a family history of respiratory allergy had developed asthma or allergic rhinitis rather than AD. The serum IgE level was raised in 45% and 26% of the clinically examined individuals in Groups 1 and 2, respectively. A comparatively large proportion of patients with persistent or recurrent dermatitis had normal IgE values. There was a strong correlation between the extent of persistent dermatitis and serum IgE levels. It is concluded that the serum IgE cannot be used to establish the diagnosis of atopic dermatitis. The number of contact sensitized people was greater in Group 2 (23%) than in Group 1 (17%). Occurrence of contact sensitivity, which was demonstrable in a total of 20% of the patch tested individuals from Groups 1 and 2, was not correlated to prevalence of healing at the time of examination. Fragrance-mix and balsam of Peru were the commonest contact sensitizers. People with a history of AD showed a higher incidence of recurrent (greater than 5 episodes per year) cold sores, upper respiratory infection, and herpes zoster than non-atopic controls.(ABSTRACT TRUNCATED AT 400 WORDS) 8 AUTHOR Atherton DJ TITLE Diagnosis and management of skin disorders caused by food allergy. SOURCE Ann Allergy; VOL 53, ISS 6 Pt 2, 1984, P623-8 (REF: 14) ABSTRACT A major aetiologic role for foods has been demonstrated in urticaria, atopic eczema and dermatitis herpetiformis. In some patients with urticaria, whealing occurs within minutes of the ingestion of a particular food. In most, but not necessarily all cases, this appears to be a consequence of IgE-mediated cutaneous mast cell degranulation, i.e. a classical type I hypersensitivity response. In other patients with recurrent urticaria, the whealing may be provoked by foods by a much slower and more insidious reaction. This type of reaction has been established in the case of several common food additives, notably azo dyes, but other foods may be able to cause urticaria in a similar fashion. Foods appear to play an important provocative role in many patients with atopic eczema. The reaction in such cases appears to be slow and insidious, almost always unrecognized by the patient and not detected by skin testing or tests for IgE antibodies. There can be no real doubt that dietary gluten is responsible for most, if not all dermatitis herpetiformis, though this relationship was revealed only by the finding of concurrent and usually asymptomatic jejunal villous atrophy in affected individuals. The mechanisms responsible for the slow food reactions in urticaria, atopic eczema and dermatitis herpetiformis remain largely unknown, but are likely to be different in each case.