Abstract

Clinical & Experimental AllergyVolume 40, Issue 7 p. 957-957 Free Access The Editor takes a closer look at some of this month's articles First published: 10 June 2010 https://doi.org/10.1111/j.1365-2222.2010.03555.xAboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Clinically relevant local IgE production: doubt no more? There is now convincing evidence, much of which is quoted in the Opinions article by Powe and colleagues (pp. 987–997), that tissue production of specific IgE occurs in allergic disease. A number of authorities including Powe et al. as well as Peter Barnes in an Opinions paper last year [1], have argued that this is the explanation for intrinsic allergic disease. In other words the difference between extrinsic allergic disease and non-atopic disease is that in the former the specific IgE gets into the blood and in the latter it doesn't, although if this is the case the reasons remain unknown. If this hypothesis were correct then allergen challenge in intrinsic disease would also result in an early and late response. As inclusion criteria for allergen challenge is a positive skin prick test or circulating specific IgE this is not often done in non-atopic subjects. However Lopez and colleagues (pp. 1007–1014) have convincingly shown that patients who they describe as having ‘local allergic rhinitis’ (defined as people with perennial symptoms to dust mite with negative circulating specific IgE), have both early and late responses to allergen challenge measured by symptoms and mediator release including mast cell tryptase. This is an important and exciting observation, not least because it suggests that anti-allergic therapy including specific immunotherapy and omalizumab would be beneficial in intrinsic disease. [ (see Fig. 1 in Powe et al.) ] Twin studies: worth their weight Two papers in this issue illustrate the considerable value of twin studies, particularly those from the impressive Scandinavian twin registries where detailed information is available on large numbers of subjects. Thomsen et al. (pp. 1054–1061) have used the Danish Twin Registry which contains information on asthma in over 20 000 twins to measure the hereditability of asthma, confirming previous studies of a strong genetic element in young children and adults, and showing that this does not extend to older adults. Lundholm et al. (pp. 1044–1053) have interrogated the Swedish twin registry containing data on allergic disease in over 10 000 twins to definitively show that increased birth weight is a risk factor for the development of eczema, but interestingly not allergic rhinitis, independently of confounding factors such as gestational age and environmental and genetic factors. Two powerful studies generating novel and important data. [ Twins (courtesy of Wikipedia) ] Food allergy: go easy on the antacids There is increasing evidence that neutralization of stomach acid increases the risk of food allergy, presumably by preventing effective protein digestion, which in turn leads to larger amounts of allergen protein reaching the small intestine and being systemically absorbed [2, 3]. Further support for the importance of this pathway comes from Pali-Scholl et al. (pp. 1091–1098). They demonstrated in vitro that increasing the pH prevented the digestion of codfish antigens. They then demonstrated in a mouse model that co-feeding the animals codfish with antacids caused increased production of fish specific IgE and the development of a positive intradermal skin test. As they point out the widespread over-the-counter use of antacid tablets and powders could be one explanation for the increase in the incidence of food allergy, particularly in adults. [ Antacid tablets (courtesy of Wikipedia) ] References 1 Barnes PJ. Intrinsic asthma: not so different from allergic asthma but driven by superantigens? Clin Exp Allergy 2009; 39: 1145– 51. CASPubMedWeb of Science®Google Scholar 2 Kemp AS. Allergy and gastric acid suppression. Clin Exp Allergy 2009; 39: 176– 8. Wiley Online LibraryCASPubMedWeb of Science®Google Scholar 3 Dehlink E et al. First evidence of a possible association between gastric acid suppression during pregnancy and childhood asthma: a population-based register study. Clin Exp Allergy 2009; 39: 246– 53. CASPubMedWeb of Science®Google Scholar Volume40, Issue7July 2010Pages 957-957 ReferencesRelatedInformation

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