Revue des maladies respiratoires
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Pulmonary fibrosis is a frequent and serious complication of scleroderma whose pathophysiology remains poorly understood. The alveolar structures are infiltrated by activated chronic inflammatory cells, alveolar macrophages and polymorphonuclear neutrophils in particular and these could play a determining role. We have studied the state of activation of alveolar macrophages and monocytes circulating in these patients who presented with scleroderma and interstitial pulmonary involvement and also in healthy subjects. ⋯ The neutrophil alveolitis is accompanied by a breakdown in the equilibrium of elastase-antielastase which could participate in the development of alveolar lesions leading to fibrosis. In addition to the activation of macrophages, there is an activation of monocytes marked by the increase in secretion of interleukin-6 and interleukin-8 in vitro during the progression of the disease of scleroderma. Thus, alveolar inflammation is integrated with the overall systemic inflammation whose causes remain unknown.
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Respiratory mechanics abnormalities in patients with chronic obstructive pulmonary disease (COPD) in acute respiratory failure (ARF) consist of the followings : 1) expiratory flow limitation, 2) marked increase in airway resistance, 3) dynamic hyperinflation. As a results, both resistive and elastic loads to the respiratory muscles are increased. These abnormalities, which are already present in stable COPD patients, are considerably more marked in ARF. ⋯ Shortening the inspiratory time could result not only to reduce the hyperinflation but also to increase expiratory flow through the increased dynamic pulmonary elastance. The inspiratory work was twice higher in COPD than in normals because of the PEEPi and the resistive components. Due to their flow and volume dependence, the results of resistances and elastances should be standardized.
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A young man without any past history of note had taken isotretinoin for disfiguring acne before the summer season. He presented with a severe bilateral pneumonia, associated with dyspnoea two months after the start of treatment. ⋯ The elevated level of eosinophils (54% in 564,000 cells/ml) in the alveolar lavage lead to a diagnosis of allergic pneumonia. The rapidly favourable outcome following the cessation of the medication and with the addition of corticosteroids seemed to us a supplementary argument in favour of a diagnosis of eosinophilic pneumonia, due to isotretinoin which seemed the primary initiating factor.
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To examine three typical disease states seen in intensive care, sepsis, Fulminant purpura and acute respiratory distress syndrome (ARDS) to assess the implication of cytokines in their pathogenesis and particularly in the clinical applications of possible cytokine inhibitors. ⋯ Future clinical strategies designed to combat. Future clinical strategies designed to fight against the most critical diseases in intensive care medicine require some use of any kind of immunotherapy. In animal studies, convincing data are available showing that immunotherapy improves the prognosis of sepsis, whereas in humans, to date, the results appear to be deceiving. Future research in this direction is mandatory, in sepsis and in other disease states, like ARDS, because no other hope for treating these patients seems to appear in a near future.