Cigarette smoking is common in asthma and is associated with poor symptom control and a reduced therapeutic response to inhaled and oral corticosteroids as compared with nonsmokers with asthma. This review examines the range of adverse health effects of smoking in asthma, the inflammatory mechanisms that may influence the efficacy of current drugs and discusses potential future therapeutic directions.
"The majority of adults with asthma have mild or moderate disease that can be controlled by inhaled corticosteroids either alone or in combination with inhaled long-acting ß2 agonist bronchodilators [1-3]. Questionnaire surveys however indicate that a considerable proportion of these patients , as well as most with severe asthma , or who are cigarette smokers [6,7] have poorly controlled asthma. Systematic evaluation can help identify patients with severe asthma from those with difficult-to-treat asthma due to poor adherence, untreated co-morbidities, dysfunctional breathing or psychological problems [8,9]. "
[Show abstract][Hide abstract] ABSTRACT: Many patients with asthma have poorly controlled symptoms, and particularly for those with severe disease, there is a clear need for improved treatments. Two recent therapies licensed for use in asthma are omalizumab, a humanized monoclonal antibody that binds circulating IgE antibody, and bronchial thermoplasty, which involves the delivery of radio frequency energy to the airways to reduce airway smooth muscle mass. In addition, there are new therapies under development for asthma that have good potential to reach the clinic in the next five years. These include biological agents targeting pro-inflammatory cytokines such as interleukin-5 and interleukin-13, inhaled ultra long-acting β2-agonists and once daily inhaled corticosteroids. In addition, drugs that block components of the arachidonic acid pathway that targets neutrophilic asthma and CRTH2 receptor antagonists that inhibit the proinflammatory actions of prostaglandin D2 may become available. We review the recent progress made in developing viable therapies for severe asthma and briefly discuss the idea that development of novel therapies for asthma is likely to increasingly involve the assessment of genotypic and/or phenotypic factors.
BMC Medicine 09/2011; 9(1):102. DOI:10.1186/1741-7015-9-102 · 7.25 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: In developed countries approximately one-quarter of adults with asthma are active cigarette smokers. These individuals have poorly controlled symptoms, impaired therapeutic responses to corticosteroids, and increased rates of health care utilization compared to nonsmokers with asthma. Persistent airflow obstruction can develop in asthma, particularly in smokers. Accelerated loss of lung function in adulthood as well as genetic, environmental risk factors (other than smoking), and submaximal lung growth in childhood may also contribute to the development of persistent airflow obstruction in smokers with asthma. The best strategy for managing symptoms due to persistent airflow obstruction in smokers with asthma is uncertain and, in particular, which recommendations from international guidelines for asthma or COPD are most appropriate for the management of this patient group.
[Show abstract][Hide abstract] ABSTRACT: In a previous study, we reported a new pyrroloquinazoline derivative, 3-(4'-acetoxy-3',5'-dimethoxy)benzylidene-1,2-dihydropyrrolo[2,1-b]quinazoline-9-one (PQ), which inhibited human purified 5-lipoxygenase activity and prostaglandin E2 release in lipopolysaccharide-stimulated RAW 264.7 cells. In the present work, we show that PQ inhibits cyclo-oxygenase-2 activity in intact cell assays (human monocytes) and purified enzyme preparations (ovine isoenzymes) without affecting cyclo-oxygenase-1 activity. This behaviour was confirmed in vivo by using the zymosan-injected mouse air pouch model, where PQ caused a marked reduction in cell migration and leukotriene B4 levels at 4 h, as well as inhibition of prostaglandin E2 levels without affecting cyclo-oxygenase-2 expression at 24 h after zymosan stimulation. In addition, oral administration of this compound significantly reduced carrageenan-induced mouse paw oedema and phenyl-p-benzoquinone-induced writhings in mice. These results indicate that oral PQ exerts analgesic and anti-inflammatory effects, which are related to dual inhibition of cyclo-oxygenase-2 and 5-lipoxygenase activities.
European Journal of Pharmacology 02/2002; 434(3):177-85. DOI:10.1016/S0014-2999(01)01539-4 · 2.53 Impact Factor
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