International consensus on (ICON) pediatric asthma.

Asthma is the most common chronic lower respiratory disease in childhood throughout the world. Several guidelines and/or consensus documents are available to support medical decisions on pediatric asthma. Although there is no doubt that the use of common systematic approaches for management can considerably improve outcomes, dissemination and implementation of these are still major challenges. Consequently, the International Collaboration in Asthma, Allergy and Immunology (iCAALL), recently formed by the EAACI, AAAAI, ACAAI, and WAO, has decided to propose an International Consensus on (ICON) Pediatric Asthma. The purpose of this document is to highlight the key messages that are common to many of the existing guidelines, while critically reviewing and commenting on any differences, thus providing a concise reference. The principles of pediatric asthma management are generally accepted. Overall, the treatment goal is disease control. To achieve this, patients and their parents should be educated to optimally manage the disease, in collaboration with healthcare professionals. Identification and avoidance of triggers is also of significant importance. Assessment and monitoring should be performed regularly to re-evaluate and fine-tune treatment. Pharmacotherapy is the cornerstone of treatment. The optimal use of medication can, in most cases, help patients control symptoms and reduce the risk for future morbidity. The management of exacerbations is a major consideration, independent of chronic treatment. There is a trend toward considering phenotype-specific treatment choices; however, this goal has not yet been achieved.

Metropolitan home living conditions associated with indoor endotoxin levels.

BACKGROUND: Household endotoxin exposure in allergy and asthma has been gaining attention for its dual potential to exacerbate these conditions in individuals with established disease and to abrogate atopy before disease onset. OBJECTIVE: We sought to better understand the home environmental and lifestyle factors influencing house dust endotoxin levels. METHODS: From the homes of 86 infants with wheeze in metropolitan Denver, Colorado, house dust endotoxin (detected with a standardized Limulus Amebocyte Lysate assay) and common indoor allergen (Fel d 1, Can f 1, Der p 1, Der f 1, and Bla g 1) contents were quantified. Comprehensive home environment and lifestyle questionnaires were completed during home visits by trained study staff and parents. RESULTS: House dust endotoxin levels were associated with only 2 home environmental features: animals in the home and the presence of central air conditioning. The strongest positive associations were found with animals in the home. Interestingly, the homes without cats or other animals revealed a negative correlation between house dust Fel d 1 and endotoxin (P =.03). Central air conditioning, especially during months of typical use, was associated with lower house dust endotoxin levels. No significant associations between house dust endotoxin levels and home dampness, number of household inhabitants or young children, cleaning frequency, or presence of tobacco smokers in the home were found. CONCLUSIONS: Indoor endotoxin exposure can be increased by the presence of animals in the home and decreased with central air conditioning. In some homes without animals, where allergen exposure adequate for sensitization still occurs, there are lower levels of house dust endotoxin. Therefore in homes without animals, factors that influence allergen and endotoxin levels in house dust probably differ. Households with detectable allergen levels but low endotoxin levels may provide a predisposing environment for animal allergen sensitization.

Relation between house-dust endotoxin exposure, type 1 T-cell development, and allergen sensitisation in infants at high risk of asthma.

BACKGROUND: Bacterial endotoxin is known to induce interferon gamma and interleukin 12 production, and therefore has the potential to decrease allergen sensitisation. To find out the role of early chronic endotoxin exposure in the development of allergen sensitisation and asthma, we compared concentrations of endotoxin in house dust with allergen sensitisation in infants at high risk for developing asthma. METHODS: 61 infants 9-24 months old with at least three physician-documented episodes of wheezing were studied. Concentrations of house-dust endotoxin and allergens were measured in the infants' homes. Allergen sensitisation was measured by skin-prick testing with a panel of common inhalant and food allergens. In a subset of these infants, proportions of T lymphocytes producing interferon gamma, and interleukins 4, 5, and 13 were calculated by cell-surface and intracellular cytokine staining, with flow cytometry. FINDINGS: House-dust endotoxin concentrations ranged from 104 to 10,000 endotoxin units (EU) per mL (geometric mean 912 EU/mL). Concentrations did not vary significantly over a 6-month interval. Ten infants (16%) were sensitised to at least one allergen. The homes of allergen-sensitised infants contained significantly lower concentrations of house-dust endotoxin than those of non-sensitised infants (mean 468 vs 1035 EU/mL, respectively; p=0.01). Increased house-dust endotoxin concentrations correlated with increased proportions of interferon-gamma-producing CD4 T cells (p=0.01). Such concentrations did not correlate with proportions of cells that produced interleukins 4, 5, or 13. INTERPRETATION: This study may provide the first direct in-vivo evidence that indoor endotoxin exposure early in life may protect against allergen sensitisation by enhancing type 1 immunity.

Neonatal presentation of Gordon syndrome.

Gordon syndrome, the association of hypertension with hyperkalemic acidosis, has been described in older children and adults. We report an affected family in which two of the members had exhibited the metabolic manifestations of the disease since infancy. Both patients responded well to thiazides. To our knowledge, these are the youngest patients with documented cases of Gordon syndrome.