Revue des maladies respiratoires
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Primary pulmonary arterial hypertension (PPH) is a rare disorder with a predilection for young subjects (most commonly of 20-40 years) and of the female sex. The prognosis is very poor because the average life expectancy is of the order of two to three years from the time of diagnosis. ⋯ A very recent case-control study has shown that any use of anorexic drugs (mainly fenfluramine derivatives) was associated with an increased risk of PPH (odds ratio: 6/1), and particularly when the duration of treatment exceeds 3 months. Outside the group of appetite suppressants few medications are capable of favouring the development of PPH, the cases are sporadic and the relationship between cause and effect is hardly established.
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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.