Conclusion-Nearly three quarters of patients previously diagnosed as having oesophagitis still had significant morbidity related to gastro-oesophageal reflux disease more than 10 years after diagnosis. Some quality of life scores were significantly lower than those of the general population.
A strong HLA association is seen in coeliac disease [specifically to the DQ(alpha1*0501,beta1*0201 heterodimer], but this cannot entirely account for the increased risk seen in relatives of affected cases. One or more genes at HLA-unlinked loci also predispose to coeliac disease and are probably stronger determinants of disease susceptibility than HLA. A recent study has proposed a number of candidate regions on chromosomes 6p23 (distinct from HLA), 6p12, 3q27, 5q33.3, 7q31.3, 11p11, 15q26, 19p13.3, 19q13.1, 19q13.4 and 22cen for the location of a non-HLA linked susceptibility gene. We have examined these regions in 28 coeliac disease families by linkage analysis. There was excess sharing of chromosome 6p markers, but no support for a predisposition locus telomeric to HLA. No significant evidence in favour of linkage to coeliac disease was obtained for chromosomes 3q27, 5q33.3, 7q31.3, 11p11, 19p13.3, 19q13.1, 19q13.4 or 22cen. There was, however, excess sharing close to D15S642. The maximum non-parametric linkage score was 1.99 (P = 0.03). Although the evidence for linkage of coeliac disease to chromosome 15q26 is not strong, the well established association between coeliac disease and insulin dependent diabetes mellitus, together with the mapping of an IDDM susceptibility locus (IDDM3) to chromosome 15q26, provide indirect support for this as a candidate locus conferring susceptibility to coeliac disease in some families.
We examined the prevalence of IgE and IgG4 class antibodies to the saliva of Aedes communis and Aedes aegypti mosquitoes in the sera of three groups of exposed children using a sensitive immunoblot method. The frequencies of IgE antibodies to the major 36-kD A. communis and A. aegypti saliva antigens ranged from 82 to 90% in the 20 Finnish, 17 Kenyan, and 20 Mexican children. The corresponding IgG4 antibody frequencies were 85, 41, and 20%, respectively. The nonexposed 20 Icelandic children did not show IgE or IgG4 antisaliva antibodies. Several of the Finish children showed also IgE and IgG4 antibodies to a 22-kD A. communis saliva antigen. The Finnish children abnormally sensitive to mosquito bites had frequently IgE and IgG4 antibodies to the 22-kD A. communis saliva antigen, suggesting that these antibodies play a role in the pathogenesis of immediate cutaneous mosquito bite reactions. In contrast to this, no increase was found in the A aegypti antibody frequencies in the Kenyan and Mexican children with papular urticaria, suggesting that humoral immune response to A. aegypti saliva is not involved in the development of this disorder. The present results show that humoral IgE and IgG4 immune responses to Aedes mosquito saliva antigens is common in children living both in temperature and tropical zones. The IgE antibodies seem to be involved in the immediate mosquito bite wheal-ing, and the occurrence of the IgG4 subclass antisaliva antibodies might be an indicator of intense mosquito bite exposure.
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Research Ethics Committee approvalThe study was reviewed and approved by the University of Nottingham Medical School Research EthicsCommittee.
AcknowledgementsThe authors would like to acknowledge the support of the children who took part in this study, their parents / carers, and the staff of the Fairway Primary School and the Long Eaton Sports Acrobatics Club.
AbstractBackground. MRI scans can be distressing for children, often resulting in sedation. Educating children about
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