Expert review of respiratory medicine
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Expert Rev Respir Med · Oct 2015
ReviewDual bronchodilator therapy with aclidinium bromide/formoterol fumarate for chronic obstructive pulmonary disease.
Inhaled bronchodilator therapy is a mainstay of treatment for chronic obstructive pulmonary disease (COPD). Despite the number and types of treatments available, the control of symptoms and exacerbations remains suboptimal, and adherence to, and persistence with, inhaled therapy is generally poor. ⋯ Several combinations of a LAMA plus a LABA have recently become available in a single inhaler for maintenance therapy for adults with moderate-to-severe COPD, including aclidinium bromide/formoterol fumarate, glycopyrronium/indacaterol and umeclidinium/vilanterol. Here, we review clinical data demonstrating significant improvements in bronchodilation, 24-h symptoms, and health status with aclidinium/formoterol twice daily, and discuss how this treatment can be implemented in clinical practice as part of a patient-focused approach to disease control.
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Expert Rev Respir Med · Aug 2015
ReviewShould we treat chronic obstructive pulmonary disease as a cardiovascular disease?
Chronic obstructive pulmonary disease (COPD) is characterized by largely irreversible airflow limitation and is associated with several extrapulmonary manifestations and co-morbidities. Cardiovascular diseases are among the most frequent co-morbid conditions affecting patients with COPD and have important prognostic implications for hospitalization and mortality. In turn, COPD shares common risk factors with several cardiovascular diseases (i.e., smoking habit), while several features of COPD can predispose to cardiovascular disease (i.e., gas exchange abnormalities, polycythemia, systemic inflammation and sedentary lifestyle). ⋯ This review will discuss the increased prevalence and prognostic implications of cardiovascular co-morbidities in patients with COPD. The effect of COPD on the outcomes in cardiovascular disease will also be highlighted and the pathogenic mechanisms that underlie cardiovascular co-morbidities in patients with COPD will also be reviewed. Finally, options for the management of cardiovascular co-morbidities in patients with COPD will be discussed.
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Expert Rev Respir Med · Aug 2015
Permanent alveolar collapse is the predominant mechanism in idiopathic pulmonary fibrosis.
Alveolar epithelial cell loss and impaired epithelial cell regeneration are currently accepted as central initiating events in idiopathic pulmonary fibrosis (IPF), but subsequent downstream effects remain uncertain. The most accepted downstream effect is aberrant and dysregulated mesenchymal cell proliferation and excess extracellular matrix (ECM) accumulation. ⋯ Loss of tissue aeration is a consequence of alveolar collapse, which occurs in IPF as a result of apposition and septal incorporation of denuded basal lamina. Permanent alveolar collapse is well-documented following epithelial injury, has the ability to mimic interstitial fibrosis radiologically and histologically, and is a better supported explanation than dysregulated fibroblast proliferation and excess ECM accumulation for the constellation of findings in patients with IPF.
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Expert Rev Respir Med · Jun 2015
ReviewOxygen therapy in acute exacerbations of chronic obstructive pulmonary disease.
During the last decade, there have been major advances in knowledge of the effects of oxygen therapy in patients with acute exacerbations of chronic obstructive pulmonary disease. This includes a randomised controlled trial of oxygen therapy in the pre-hospital setting, which showed that high concentration oxygen therapy leads to a 2.4-fold increased risk of mortality compared with titrated oxygen therapy to maintain oxygen saturations (SpO2) within a target range of 88-92%. ⋯ The aim of this review is to provide an overview of the evidence base that underpins these recommendations. We suggest that their implementation will require important changes to current clinical practice in which there is an entrenched culture of the use of high concentration oxygen therapy.
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Pulmonary alveolar proteinosis (PAP) is categorized into hereditary, secondary and autoimmune PAP (aPAP) types. The common pathogenesis is the ability of the alveolar macrophages to catabolize phagocytized surfactant is affected. Hereditary PAP is caused by mutations involving the GM-CSF signaling, particularly in genes for the GM-CSF receptor and sometimes by GATA2 mutations. ⋯ Myeloid cells' immunity deteriorates, increasing the risk of infections. Treatment of PAP is based on its etiology. In aPAP, recent therapeutic advances might shift the treatment option from the whole lung lavage procedure under general anesthesia to the inhalation of GM-CSF 'as needed'.