Parental Smoking Modifies the Relation between Genetic Variation in Tumor Necrosis Factor-α (TNF) and Childhood Asthma

BACKGROUND: Polymorphisms in the proinflammatory cytokine genes tumor necrosis factor-α (TNF) and lymphotoxin-α (LTA, also called TNF-β) have been associated with asthma and atopy in some studies. Parental smoking is a consistent risk factor for childhood asthma. Secondhand smoke and ozone both stimulate TNF production. OBJECTIVES: Our goal was to investigate whether genetic variation in TNF and LTA is associated with asthma and atopy and whether the association is modified by parental smoking in a Mexican population with high ozone exposure. METHODS: We genotyped six tagging single nucleotide polymorphisms (SNPs) in TNF and LTA, including functional variants, in 596 nuclear families consisting of asthmatics 4–17 years of age and their parents in Mexico City. Atopy was determined by skin prick tests. RESULTS: The A allele of the TNF-308 SNP was associated with increased risk of asthma [relative risk (RR) = 1.54; 95% confidence interval (CI), 1.04–2.28], especially among children of non-smoking parents (RR = 2.06; 95% CI, 1.19–3.55; p for interaction = 0.09). Similarly, the A allele of the TNF-238 SNP was associated with increased asthma risk among children of nonsmoking parents (RR = 2.21; 95% CI, 1.14–4.30; p for interaction = 0.01). LTA SNPs were not associated with asthma. Haplotype analyses reflected the single SNP findings in magnitude and direction. TNF and LTA SNPs were not associated with the degree of atopy. CONCLUSIONS: Our results suggest that genetic variation in TNF may contribute to childhood asthma and that associations may be modified by parental smoking

Adjustable maintenance dosing with budesonide/formoterol in a single inhaler - efficacy and safety

info:eu-repo/semantics/publishe

Asthma and COPID: differences and similarities - With special reference to the usefulness of budesonide/formoterol in a single inhaler (Symbicort (R)) in both diseases

Asthma and chronic obstructive pulmonary disease (COPD) both have a high prevalence worldwide and yet each condition remains underdiagnosed. Despite a number of common features, these inflammatory respiratory syndromes have distinct clinical outcomes. COPD represents a greater economic burden than asthma because it has a less favourable prognosis and is associated with greater morbidity and mortality. Therefore, it is important to distinguish between these two diseases at an early stage, so that appropriate therapy can be prescribed to prevent deterioration. However, effective treatments that may be used in both conditions can minimise the effects of misdiagnosis and maximise the impact of treatment without the associated complexity when both conditions occur together. The current review summarises the differences and similarities of asthma and COPD, in terms of risk factors, pathophysiology, symptoms and diagnosis, to provide greater understanding of the role of budesonide/ formoterol in a single inhaler in both diseases