APC is an effective method for tumor devitalization and reduction in tumor size, making it a viable and less costly therapeutic option for the treatment of benign endobronchial tumors.
Benign pulmonary tumors are a rare entity but have been historically managed with surgical resection. When located endobronchially, they may be amenable to endoscopic therapy. We reviewed the literature for studies addressing endobronchial management of benign endobronchial tumors. We discovered an assortment of case series and retrospective cohorts describing innovative treatment modalities for patients with endobronchial disease that can be attempted before contemplating surgical options. When modalities are carefully selected and executed by an experienced operator, adverse events are minimal. Endobronchial devitalizing and debulking offers an effective method of removing benign endobronchial tumors that can spare the symptomatic patient invasive surgery.
Asthma is a common, chronic disease of the airways that is treated with a combination of different therapies. The combination of LABA and ICS therapy results in a synergistic interaction that is efficacious in improving asthma symptom control; however, genetic variation has the potential to alter therapeutic efficacy. Both agents mediate complex molecular pathways consisting of gene variation that has been investigated with the analysis of candidate genes in the β2-adrenergic receptor and glucocorticoid pathway. These pharmacogenetic studies have been limited to retrospective analyses of clinical trial cohorts and a small number of prospective, genotype-stratified trials. More recently, genome-wide association studies in combination with replication in additional cohorts and in vitro cell-based models have been used to identify novel pathway-related pharmacogenetic variations. This review of the pharmacogenetics of the β2-adrenergic receptor and glucocorticoid pathways highlights the genotypic effects of variation in multiple genes from interacting pathways which may contribute to differential responses to inhaled beta agonists and glucocorticoids. As our understanding of these genetic mechanisms improves, panels of biomarkers may be developed to determine which combination therapies are the most effective with the least risk to an individual asthma patient. Before we can usher in an era of personalized medicine for asthma, it is first important to improve our ability to analyze large volumes of genetic data in large clinical trial cohorts using a combination of study designs, analytical methods, and in vitro functional studies.
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