Correlation of ovalbumin of egg white components with allergic diseases in children.

BACKGROUND: Immunoglobulin E (IgE)-mediated food allergy, such as egg white allergy, is common in young children (<3 years old), but not all young children sensitive to egg white present with allergic symptoms. This study investigated the relationship between sensitization to egg white component allergens and clinical manifestations of allergic diseases in young children. METHODS: From March to December 2010, 2256 children with physician-diagnosed allergic diseases were tested for serum levels of egg white, ovalbumin, and ovomucoid-specific IgE in the Pediatric Allergy and Asthma Center of Chang Gung Memorial Hospital. Serum was analyzed for specific IgE antibodies to egg white, ovalbumin, and ovomucoid by ImmunoCAP (Phadia, Uppsala, Sweden). Allergen-specific IgE levels ≥0.35 kUA/L were defined as positive. RESULTS: There was a significantly higher sensitization rate to egg white and its components in children aged 2-4 years old. The sensitization rate to egg white, ovalbumin, and ovomucoid in this age group was 53.5%, 48.3%, and 37.2%, respectively, and the trend of the sensitization decreased with age (p < 0.001). After adjusting for age, sensitization to egg white and ovalbumin was associated with children with dermatitis [egg white: odds ratio (OR) = 1.28, 95% confidence intervals (CI) = 1.03-1.58, p < 0.05; ovalbumin: OR = 1.30, 95% CI = 1.04-1.62, p < 0.05]. Children with ovomucoid sensitization had no statistically significant risk among different groups in the current study. CONCLUSION: Children aged 2-4 years old have higher sensitivity to egg white, ovalbumin, and ovomucoid. Children with egg white and ovalbumin sensitization have a higher risk for atopic dermatitis, and ovalbumin has a more important contribution. Furthermore, we suggested that in children with atopic dermatitis, if they are aged 2-4 years old and are having egg white and ovalbumin sensitization, avoiding eating raw or slightly heated eggs might have a beneficial effect.

Patterns of sensitization to peanut allergen components in Taiwanese Preschool children.

BACKGROUND/PURPOSE: Peanut allergy is very common in Western countries, although it is seldom encountered in Eastern countries. Peanuts are comprised of at least 11 components, but the contribution to clinical symptoms by each component in each individual is not known. This study investigated the distributions of sensitivity to peanut allergen components among Taiwanese children who were sensitized to peanuts and followed the evolution of sensitization patterns to these components. METHODS: We enrolled 29 preschool children (age=2.11±1.36 years) who were sensitized to peanuts above class 3. Serum was analyzed for specific immunoglobulin E (IgE) antibodies to recombinant Ara h 1, Ara h 2, Ara h 3, Ara h 8, and Ara h 9. Allergen component-specific IgE ≥0.35 kU(A)/L was defined as positive. Eighteen children were retested 22.64±5.1 months later. Peanut allergy symptoms were recorded from detailed questionnaires. RESULTS: The percentages of children sensitized to Ara h 1, 2, 3, 8, and 9 were, respectively, 51.8%, 65.5%, 62.1%, 13.8%, and 24.1%. Regarding changing patterns of peanut component sensitization at follow-up, children with clinical symptoms to peanuts had persistent elevations of Ara h 2-specific IgE: 12.6±1.01 up to 34.15±19.4 kU(A)/L; p=0.144. In contrast, Ara h 2 concentrations decreased significantly in children without clinical symptoms. Ara h 8 and 9 were nonspecific for children with or without symptoms. CONCLUSION: Ara h 1, Ara h 2, and Ara h 3 were major components contributing to peanut sensitization in Taiwanese children. Ara h 2 was probably the most important component that contributed to clinical symptoms and remained steady in children who had peanut allergy.

Autosomal dominant avascular necrosis of femoral head in two Taiwanese pedigrees and linkage to chromosome 12q13.

Avascular necrosis of the femoral head (ANFH) is a debilitating disease that commonly leads to destruction of the hip joint in adults. The etiology of ANFH is unknown, but previous studies have indicated that heritable thrombophilia (increased tendency to form thrombi) and hypofibrinolysis (reduced ability to lyse thrombi), alcohol intake, and steroid use are risk factors for ANFH. We recently identified two families with ANFH showing autosomal dominant inheritance. By applying linkage analysis to a four-generation pedigree, we excluded linkage between the family and three genes related to thrombophilia and hypofibrinolysis: protein C, protein S, and plasminogen activator inhibitor. Furthermore, by a genomewide scan, a significant two-point LOD score of 3.45 (recombination fraction [theta] = 0) was obtained between the family with ANFH and marker D12S85 on chromosome 12. High-resolution mapping was conducted in a second family with ANFH and replicated the linkage to D12S368 (pedigree I: LOD score 2.47, theta = 0.05; pedigree II: LOD score 2.81, theta = 0.10). When an age-dependent-penetrance model was applied, the combined multipoint LOD score was 6.43 between D12S1663 and D12S85. Thus, we mapped the candidate gene for autosomal dominant ANFH to a 15-cM region between D12S1663 and D12S1632 on chromosome 12q13.