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While breast feeding should be promoted for children at risk for atopy, mothers can be encouraged to stay on normal diet during pregnancy and the breast feeding period.

Background: In order to investigate, whether atopic and nonatopic children show differences in their specific IgE and IgG4 immune responses to tetanus (T) and diphtheria (D) antigens, we studied 538 children who had been followed from birth on and from whom records had been kept of all immunizations. Methods: The prevalence of eczema and asthma was registered at regular intervals and the cumulative incidence of symptoms was determined at 24 months of age. Total serum IgE and specific IgE to a panel of nine allergens as well as T-and D-specifíc IgE and IgG4 were determined from the 24-month blood samples. Results: Our results show that both atopic and nonatopic children are capable of mounting high levels of toxoid-specific IgE antibody responses. Children with cord blood IgE > 0.9 kU/l, serum IgE 10–100 kU/l and > 100 kU/l and at least one sensitization to an allergen at 24 months of age have significantly higher IgE responses to T and D (p < 0.001). In contrast, specific IgG4 antibody concentrations to T and D were not significantly different in children with elevated total IgE levels at 24 months. No differences in subgroups of children with or without early symptoms of atopy were observed. Conclusions: Our data indicate that IgE responses to toxoids such as T and D are not limited to infants with clinical manifestations of atopy in the first 2 years of life but are related to immunological parameters of atopy.

Pertussis (P) toxin acts as adjuvant for IgE formation against simultaneously administered Ags in animal models. P vaccination may also have an adjuvant impact on IgE formation against coadministered diphtheria (D) and tetanus (T) Ags in humans. Sera of 103 D-T-P-immunized and 319 D-T-immunized children aged 2 years were analyzed for IgE, IgG4, and IgG to D and T (radioallergosorbent test), total IgE and IgE against common inhalant allergens (CAP radioallergosorbent test fluoroenzyme immunoassay). Fewer D-T-P- than D-T-immunized children had sera positive for T-IgE (12.6 vs 53.6%, p &lt; 0.001), T-IgG4 (71.6 vs 89.2%, p &lt; 0.001), D-IgE (31.0 vs 70.5%, p &lt; 0.001), and D-IgG4 (85.2 vs 93.4%, p = 0.039). Suppression of T-IgE was not dependent on the cutoff chosen for a positive test result, but was dependent on the proportion of D-T immunizations given with P. The risk for sensitization to common environmental allergens did not differ (odds ratio 0.953, 95% confidence interval 0.815–1.114). No significant differences between D-T- and D-T-P-immunized children were found with regard to T-IgG or D-IgG. In summary, IgE and IgG4 (but not IgG) serum levels to coadministered D- and T-Ags are suppressed among P-immunized children as compared with nonimmunized children. These results suggest that the presence of a microbial product during Ag exposure can down-regulate an IgE/IgG4 response in humans.

Nearly all patients had symptoms of MS, and 40% had MS showing that this highly health-threatening condition is quite common. Therefore, effective therapy and prevention efforts must be developed for this high risk group. More migration-specific research regarding insulin resistance, MS and Type 2 DM is needed.

OBJECTIVE: Several studies have shown that obese children and adolescence seem to have an increased risk to develop a disturbed glucose metabolism as already known for obese adults. This might result in the same disastrous outcomes of cardiovascular diseases as it has been shown for adult obese patients. The most sensitive measurement for detecting changes in glucose metabolism in obese children seems to be an oral glucose tolerance test (OGGT) which is not practical for all daily outpatient clinics. DESIGN: Cross-sectional study. SUBJECTS AND MEASUREMENTS:We therefore made a preselection from a cohort of 491 subjects according to the American Diabetes Association (ADA) criteria for the diagnosis of diabetes. In the selected high-risk subgroup (n ¼ 102) of obese pediatric subjects, we measured the prevalence of impaired glucose tolerance (IGT) by OGTT. RESULTS: We diagnosed six patients with type 2 diabetes and 37 patients with impaired glucose tolerance. In addition, we found a close correlation of IGT to disturbances of triglyceride and cholesterol parameters. This prevalence was comparable to a similar study group that was screened without preselection. CONCLUSIONS: These prevalence data further underline the need to diagnose children with obesity-associated risk factors in terms of an insulin resistance syndrome. The preselection of a high-risk subgroup by ADA criteria might be a practical approach.

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Over the past two decades, obesity in children has been increasing worldwide, leading to serious complications. The treatment for childhood obesity remains largely ineffective; therefore preventive measures are crucial. The prevalence of obesity depends on the BMI-percentiles used. Recent BMI-percentiles may underestimate the problem. Currently, the only representative cross-sectional BMI-data are obtained at the school entry examination. These data reveal certain risk groups (migrants, low socioeconomic status). More representative longitudinal data are needed to study the progression of obesity during childhood. Our obesity clinic provides multidisciplinary therapy programs (group or individual) and is also focused on the diagnosis and treatment of comorbidity, especially of the metabolic syndrome. Almost 60% of our severely obese patients are already affected. The molecular diagnosis of rare monogenetic or syndromal forms of obesity may be helpful in providing additional support for these patients. In general, most obesity programs are successful only in families without severe psychosocial problems and with motivation for lifestyle changes. This can be expected in only 3% of our families. Therefore, a substantial societal effort is needed to facilitate prevention for all children, and effective therapies have to be tailored depending on biological and psychosocial risk factors.