Expert review of respiratory medicine
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Expert Rev Respir Med · Jun 2010
ReviewPirfenidone: antifibrotic agent for idiopathic pulmonary fibrosis.
Idiopathic pulmonary fibrosis (IPF) is a devastating disease with rare incidence but high mortality, and the pathogenesis of which is still poorly understood. Available treatment options have been empirically applied but evidence-based benefits have not yet been confirmed. Pirfenidone is an antifibrotic agent that is potentially effective for IPF treatment. ⋯ The efficacy is demonstrated in patients with mild-to-moderate impairment of pulmonary functions, but not confirmed for patients with severe impairment. Major adverse events are photosensitivity and anorexia, but the treatment was generally safe and well tolerated. In this article, the usefulness and limitations of pirfenidone in IPF treatment are discussed to determine its potential for the management of IPF progression.
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Transfusion-related acute lung injury (TRALI) remains the deadliest complication of transfusion. Consensus definitions of TRALI have been developed but remain controversial. Recent evidence supports a strong relationship between blood transfusion and the development of acute lung injury in the critically ill and trauma population. ⋯ The 'two hit' model may best explain the immune and nonimmune pathogenesis of TRALI. Current treatment remains largely supportive; effective measures for decreasing the incidence of TRALI include the use of predominantly male plasma and apheresis platelets. Greater understanding of the blood component and patient risk factors for TRALI will hopefully lead to novel treatment and preventive strategies for reducing the risk of this life-threatening syndrome.
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Although mechanical ventilation (MV) is a life-saving intervention for patients with acute respiratory distress syndrome (ARDS), it can aggravate or cause lung injury, known as ventilator-induced lung injury (VILI). The biophysical characteristics of heterogeneously injured ARDS lungs increase the parenchymal stress associated with breathing, which is further aggravated by MV. ⋯ Several attempts have been made to identify clinical surrogate measures of lung stress/strain (e.g., density changes in chest computed tomography, lower and upper inflection points of the pressure-volume curve, plateau pressure and inflammatory cytokine levels) that could be used to titrate MV. However, uncertainty about the topographical distribution of stress relative to that of the susceptibility of the cells and tissues to injury makes the existence of a single 'global' stress/strain injury threshold doubtful.