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In this issue

There is increasing controversy about the possibility that allergic sensitization can occur in the prenatal period (1). This has been the topic of many papers and reviews in the journal (2, 3). We have a paper on fetal sensitization to cow milk protein resulting in a non-IgEmediated enteropathy. While one case does not make a story, it certainly sustains the argument. Much of the discussion on this topic has focussed on month of birth studies in relation to preor post-natal allergen exposure. However, other climatological factors during both periods could also influence the development of allergies as highlighted in a study from Japan. Furthermore, raised cord blood IgE is a highly specific although insensitive marker of subsequent allergy (4, 5). We have another paper from the Isle of Wight birth cohort, this time showing a relationship between an IL-13 gene polymorphism and cord IgE. There are likely to be a number of polymorphisms associated with a higher risk of raised cord IgE and subsequent allergy (6). The key issue to now address is whether these polymorphisms have an effect if present in the mother rather than infant (7). Gene polymorphism studies in established allergic disease have covered most chromosomes and many mediators and we have another, namely brain-derived neurotrophic factor which again has a gender-specific affect (6). While serum IgE is often raised in advanced HIV disease a study from New York has shown that perinatally acquired HIV infection does not increase the risks of allergy. In relation to allergy prevention, recent work has moved from pro-biotics to pre-biotics (8) and we have a paper on the effects of oligosaccharides, as found in human breast milk, in the enhancement of murine Th-1 responses. Trials in humans will be difficult with the current attitudes to infant milk formula companies but are essential (9). Large population studies sometimes identify unexpected associations with allergic diseases and we have such an observation from Sweden, suggesting a link between severe asthma and neonatal photo-therapy/jaundice. Does the measurement of allergen-specific IgG subclasses and IgA have any value in clinical practice? A study from Turkey shows an association between raised levels of IgG1 and 4 and IgE house-mite-specific antibodies in asthmatics with higher levels in those with a longer duration of disease. The value of steroids in virus-associated wheeze in infancy remains in doubt, but a trial of prednisolone from Finland suggested benefits in those with particular viral infections. Future trials will need to be more precise about the viruses involved, as in this study, because it is clear that different mechanisms will be involved in the elimination of the virus from the airway. Atopic eczema remains a difficult condition to treat, and many recommendations are not well evidence based particularly in relation to clothing. We have a very nice controlled trial of a silk fabric with an anti-bacterial ingredient which produced significant improvements compared with cotton. Perhaps silk is more sensuous on the skin, because a study from Iran suggests that atopic eczema infants show higher scores for soothability and pleasure than controls. We have a paper on VEGF in lupus as a marker of disease activity and of eosinophilia in Kawasaki disease as a marker of responsiveness to intravenous immunoglobulin. Finally, we have the second in our educational series, this time on non-IgE-mediated enteropathies. J. O. Warner Professor of Paediatrics, Imperial College London London, UK