Drugs to prevent airway remodeling

Thursday, October 9th, 2014 No Commented
Categorized Under: Drugs

No therapy is currently demonstrated to unequivocally prevent or reverse airway remodeling. Here, we summarize the effects of current therapeutics and the factors contributing to airway remodeling drawn from both clinical studies and animal models.

Many drugs have been shown to prevent allergen-driven airway remodeling in animal models, but there are few studies that demonstrate their ability to reverse established airway remodeling. Since airway remodeling occurs even in childhood asthma, it is possible that airway remodeling is already present in many patients with asthma at the time of onset of clinical disease. It is, therefore, pertinent to ask ourselves if remodeling is even potentially reversible. In this respect, the recent publication by Leclere et al showing the partial reversal of ASM remodeling in horses with heaves, a naturally occurring asthma-like diseas e, following antigen avoidance as well as corticosteroid treatment Canadian Health&Care Mall provides a basis for optimism. The appropriate time to initiate therapeutic interventions deserves further consideration in addition to the search for novel therapeutic targets.

There are no studies reporting efficacy of therapies for cystic fibrosis airway remodeling. Indeed, this disease is not well modeled by cystic fibrosis transmembrane conductance regulator-deficient mice, but the porcine model shows more promise. Although bronchiectasis is likely intractable, the aspect of airway remodeling that may lead to the asthma syndrome often accompanying cystic fibrosis may be amenable to treatment.

Several clinical studies show that inhaled corticosteroid (ICS) reduces RBM thickness, although the clinical significance of such an effect is quite uncertain, and its impact on airway function seems unlikely to be major. Vascular remodeling reportedly improves with high-dose fluticasone. Whether the excessively rapid airway rewarming seen in patients with asthma after the cooling induced by hyperpnea challenge is attributable to excess vasculature or to vasodilation of existing vessels is not known. Its clinical significance is likewise uncertain but has been attributed a role in exercise-induced bronchoconstriction. A decrease of a-smooth muscle actin area in peripheral airways harvested by transbronchial biopsy in subjects treated with ICS has been reported, suggesting reversibility of this lesion in peripheral airways. Erectile dysfunction medications Canada