The unexposed providers anticipated their patients might resist ICS discontinuation because it seems counterintuitive to stop something that is working, patient's fear of worsening symptoms, or if the prescription was initiated by another provider. Forty-eight PCPs returned surveys (24 exposed and 24 unexposed, response rate: 35%). We conducted inductive and deductive content analysis of qualitative data to explore an emergent theme of patient reaction. We interviewed 9 patients within 3 months after their PCP proposed ICS discontinuation. We completed interviews with 16 unexposed providers and 6 intervention-exposed providers. PCPs at two Veterans Health Administration healthcare systems were included. We conducted a mixed-methods analysis in a provider-randomized quality improvement project testing a proactive electronic-consultation from pulmonologists recommending ICS discontinuation when appropriate. We sought to understand Veteran and provider experience when de-implementing guideline-discordant use of inhaled corticosteroids (ICS) in those with mild-to-moderate chronic obstructive pulmonary disease (COPD). Patient reaction is one potential barrier to deprescribing, but little research has assessed this in specific instances of medication discontinuation. This review briefly discusses COPD pathophysiology, and provides an update on the development and clinical testing of novel COPD treatments.ĭespite evidence of possible patient harm and substantial costs, medication overuse is persistent. Therapies directly or indirectly targeting the oxidative imbalance may be promising alternatives. Due to the complexity of its pathophysiology, and the risk of exacerbating symptoms with existing therapies, other specific and effective treatment options are required. However, these therapies do not effectively halt disease progression. Current treatments include inhaled corticosteroids and bronchodilator therapy. ![]() Alteration in cell functions results in the generation of an oxidative and inflammatory microenvironment, which contributes to disease progression. Different cell types, including macrophages, epithelial cells, neutrophils, and T lymphocytes, contribute to COPD pathophysiology. CS exposure causes an imbalance favoring pro- over antioxidants (oxidative stress), leading to transcription factor activation and increased expression of inflammatory mediators and proteases. A hallmark of COPD is progressive airflow obstruction primarily caused by cigarette smoke (CS). The purpose of this review is a complete criticism of pharmacological and clinical aspects related to the use of LAMA/LABA single inhalers for the maintenance treatment of stable COPD, with particular mention to the most debated topics and future prospects in the field.Ĭhronic obstructive pulmonary disease (COPD) is one of the leading global causes of morbidity and mortality. Many LAMA/LABA fixed dose combinations have been licensed in different countries and the clinical use of these drugs stimulated the performance of many clinical trials. Currently the Global initiative for COPD suggests the use of long acting beta agonists (LABAs) and long acting muscarinic antagonists (LAMAs) in combination for the majority of COPD patients, thus great interest is associated with the developing of LAMA/LABA fixed combination in the maintenance treatment of stable COPD. ![]() The cornerstones of treatment are bronchodilator drugs of two different classes: beta agonists and muscarinic antagonists. Great efforts were spent in the development of drugs able to improve symptoms, quality of life, reduce exacerbations, hospitalizations and the frequency of death of patients with COPD. Chronic obstructive pulmonary disease (COPD) is a common disabling disease characterized by progressive airflow obstruction.
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