Acute respiratory distress syndrome during neutropenia recovery
AP-HP, Hôpital Saint-Louis, Medical ICU, University Paris-7 Paris-Diderot, UFR de Médecine, 1 avenue Claude Vellefaux, 75010 Paris, France. .Critical care (London, England) (Impact Factor: 4.48). 02/2010; 14(1):114. DOI: 10.1186/cc8198
Acute respiratory failure is a life-threatening complication in cancer patients. During neutropenia, patients are at high risk for bacterial pneumonia or invasive fungal infections, when neutropenia is prolonged. A high proportion of patients in whom neutropenia had been complicated by pneumonia will present with substantial respiratory deterioration during neutropenia recovery. Patients with fungal pneumonia and those receiving granulocyte colony-stimulating factor to shorten neutropenia duration may be at higher risk for this acute lung injury/acute respiratory distress syndrome during neutropenia recovery. Routine screening of patient's risk factors is crucial since first symptoms of acute respiratory distress syndrome may occur before biological leukocyte recovery.
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- "Both panels: hematoxylin and eosin (H&E) stain; original objective magnification used: 0.5Â. of the main inciting features of ARDS (X. Zhou, Dai, and Huang 2012; Williams and Chambers 2014), the syndrome also develops in neutropenic patients or those who have recently undergone full-body bone marrow irradiation (Mokart et al. 2012; Azoulay and Darmon 2010; Ognibene et al. 1986; Laufe et al. 1986). This divergence is most likely due to the vast variety of stimuli that can incite the development of ARDS. "
ABSTRACT: Acute respiratory distress syndrome (ARDS) is a severe pulmonary reaction requiring hospitalization, which is incited by many causes, including bacterial and viral pneumonia as well as near drowning, aspiration of gastric contents, pancreatitis, intravenous drug use, and abdominal trauma. In humans, ARDS is very well defined by a list of clinical parameters. However, until recently no consensus was available regarding the criteria of ARDS that should be evident in an experimental animal model. This lack was rectified by a 2011 workshop report by the American Thoracic Society, which defined the main features proposed to delineate the presence of ARDS in laboratory animals. These should include histological changes in parenchymal tissue, altered integrity of the alveolar capillary barrier, inflammation, and abnormal pulmonary function. Murine ARDS models typically are defined by such features as pulmonary edema and leukocyte infiltration in cytological preparations of bronchoalveolar lavage fluid and/or lung sections. Common pathophysiological indicators of ARDS in mice include impaired pulmonary gas exchange and histological evidence of inflammatory infiltrates into the lung. Thus, morphological endpoints remain a vital component of data sets assembled from animal ARDS models. © 2015 by The Author(s).
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ABSTRACT: ABSTRACT Although neutropenia recovery is associated with deterioration of preexisting acute lung injury (ALI), there are few reports of the preventive strategies. Statins have been found to attenuate inflammatory responses in murine models of lipopolysaccharide (LPS)-induced ALI. The aim of this study was to determine whether pravastatin could attenuate ALI during neutropenia recovery in mice. Cyclophosphamide was administered to mice to induce neutropenia. Mice were given intratracheal LPS 7 days after cyclophosphamide administration, after which pravastatin was administered by intraperitoneal injection. In order to study the effects of pravastatin, mice were killed on day 5. Pravastatin attenuated the pulmonary edema and histopathological changes of LPS-induced lung injury. The accumulation of neutrophils and the concentrations of TNF-α, IL-1β, IL-6, and MPO in BAL fluids were also effectively inhibited by pravastatin. The expression levels of Toll-like receptor 4, nuclear factor kappa B, tumor growth factor-β and matrix metalloproteinase-9 were significantly reduced by pravastatin. Taken together, pravastatin significantly attenuated LPS-induced ALI during neutropenia recovery. These results provide evidence for the potential of pravastatin in the treatment of ALI during neutropenia recovery.