Respirology : official journal of the Asian Pacific Society of Respirology
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Fibrosing interstitial lung diseases (f-ILDs) represent a heterogeneous group of disorders in which the aetiology may be identified or, not infrequently, remain unknown. Establishing a correct diagnosis of a distinct f-ILD requires a multidisciplinary approach, integrating clinical profile, physiological and laboratory data, radiological appearance and, when appropriate, histological findings. Surgical lung biopsy is still considered the most important diagnostic tool as it is able to provide lung samples large enough for identification of complex patterns such as usual interstitial pneumonitis (UIP) and nonspecific interstitial pneumonitis. ⋯ The introduction of less invasive methods such as transbronchial cryobiopsy show great promise to clinical practice as they can be used to obtain samples large enough to morphologically support a diagnosis of IPF or other idiopathic interstitial pneumonias, along with fewer complications. Recent advances in the field suggest that less invasive methods of lung sampling, without significant side effects, in combination with other diagnostic methods could replace the need for surgical lung biopsy in the future. Indeed, these new multidisciplinary procedures may become the main diagnostic work-up method for patients with suspected idiopathic interstitial pneumonia.
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Polymicrobial aetiology in community-acquired pneumonia (CAP) is more common than previously recognized. This growing new entity can influence inflammation, host immunity and disease outcomes in CAP patients. ⋯ The observed rate of polymicrobial cases may also lead to new antibiotic therapy considerations. In this review, we discuss the pathogenesis, microbial interactions in pneumonia, epidemiology, biomarkers and antibiotic therapy for polymicrobial CAP.
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The natural history of chronic obstructive pulmonary disease (COPD) is usually described with a focus on change in forced expiratory volume in 1 s (FEV1 ) over time as this allows for exploration of risk factors for an accelerated decline-and thus of developing COPD. From epidemiological studies we have recognized important risk factors such as smoking, exposure to biomass and occupational exposures, but we have also learnt about features such as chronic bronchitis, airway hyper-responsiveness and asthma that seem to accelerate decline in FEV1 independent of exposures. In addition we are gradually beginning to better link early life events to subsequent risk of disease in adulthood. Although more complicated, our current understanding of COPD has come a long way from being a simple image of smoking leading to poor lungs.