Expert review of respiratory medicine
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Expert Rev Respir Med · Dec 2010
ReviewViral infection and aging as cofactors for the development of pulmonary fibrosis.
Idiopathic pulmonary fibrosis (IPF) is a disease of unknown origin and progression that primarily affects older adults. Accumulating clinical and experimental evidence suggests that viral infections may play a role, either as agents that predispose the lung to fibrosis or exacerbate existing fibrosis. ⋯ In addition, we review mechanistic studies in animal models that highlight the fibrotic potential of viral infection, and explore the different mechanisms that might be responsible. We also review early evidence to suggest that the aged lung may be particularly susceptible to viral-induced fibrosis and make recommendations for future research directions.
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Lipoid pneumonia is an uncommon disease caused by the presence of lipid in the alveoli. It is classified into two major groups, depending on whether the lipid/oil in the respiratory tract is from an exogenous (exogenous lipoid pneumonia) or endogenous/idiopathic (endogenous lipoid pneumonia) source. The usual presentation occurs with insidious onset and nonspecific respiratory symptoms such as dyspnea and/or cough. ⋯ Pathologically, lipoid pneumonia is a chronic foreign body reaction to fat, characterized by lipid-laden macrophages. Diagnosis of this disease requires a high index of suspicion and can be confirmed by demonstration of lipid-laden macrophages in respiratory samples such as sputum, bronchoalveolar lavage fluid or fine-needle aspiration cytology/biopsy from lung lesions. Treatment protocols for this illness are poorly defined.
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Expert Rev Respir Med · Dec 2010
Animal models of cigarette smoke-induced chronic obstructive pulmonary disease.
Chronic exposure of laboratory animals to cigarette smoke reproduces many of the anatomic/physiologic lesions (emphysema, small-airway remodeling and pulmonary hypertension) of human chronic obstructive pulmonary disease, although smoke-exposed laboratory animals are not good models of chronic bronchitis or acute exacerbations, as these are conditions based upon symptoms that are not recapitulated in animals. Many types of antiproteolytic and anti-inflammatory interventions, such as use of drugs or genetic modifications, are highly effective in preventing emphysema in these models, and some also prevent small-airway remodeling and pulmonary hypertension. ⋯ Recent data from our laboratory suggest that the parenchyma can repair smoke-induced damage for some period, but then switches to a mode where it fails to repair; these observations suggest that the timing of an intervention in humans may be crucial to its success. The various different anatomic lesions induced by smoke appear to be largely independent effects and may require different therapeutic approaches.
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Expert Rev Respir Med · Oct 2010
ReviewAutophagy in cigarette smoke-induced chronic obstructive pulmonary disease.
The molecular and cellular mechanisms underlying the pathogenesis of chronic obstructive pulmonary disease (COPD) remain incompletely understood. We have investigated the potential role of macro-autophagy, a cellular homeostatic mechanism, in COPD and cigarette smoke-induced lung-cell injury. Autophagy is a dynamic process for the turnover of organelles and proteins, which regenerates metabolic precursors through the lysosomal-dependent catabolism of cellular macromolecules. ⋯ We have found elevated autophagy in COPD lung specimens, as well as in response to cigarette smoke exposure in vitro and in vivo. In our studies, the activation of autophagic proteins was associated with epithelial cell apoptosis in response to cigarette smoke, with pathogenic implications in COPD. Further studies are needed to determine the functional significance of autophagy in COPD and other diseases of the lung.
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Up to 20% of patients requiring mechanical ventilation will suffer from difficult weaning (the need of more than 7 days of weaning after the first spontaneous breathing trial), which may depend on several reversible causes: respiratory and/or cardiac load, neuromuscular and neuropsychological factors, and metabolic and endocrine disorders. Clinical consequences (and/or often causes) of prolonged mechanical ventilation comprise features such as myopathy, neuropathy, and body composition alterations and depression, which increase the costs, morbidity and mortality of this. ⋯ Physiotherapy is an important component of weaning protocols. Weaning success depends strongly on patients’ complexity and comorbidities, hospital organization and personnel expertise, availability of early physiotherapy, use of weaning protocols, patients’ autonomy and families’ preparation for home discharge with mechanical ventilation.