[Recurrent pneumonia secondary to idiopathic bronchomalacia]. / Neumonías recurrentes secundarias a broncomalacia idiopática.

Bronchomalacia in adults develops secondary to bronchial disease processes (chronic bronchitis, tuberculosis, neoplasm) or to lesions resulting from prolonged intubation, surgery, trauma, or lung transplantation. We report the case of an 84-year-old woman with no history of any of the aforementioned associations in whom we detected severe idiopathic bronchomalacia of the main left bronchus. The identified lesion caused recurrent pneumonias leading to death. We show images obtained by bronchoscopy, revealing the severity of the lesion and its functional repercussions.

[Pulmonary function tests at different stages of toxic oil syndrome]. / Exploration fonctionnelle pulmonaire aux différents stades du syndrome dû à l'huile toxique.

The toxic oil syndrome is a new multisystemic disease, caused by ingestion of adulterated olive oil; this oil had a part of rapeseed oil, which was denatured with aniline for industrial use, and then re-refined. It is estimated that 20,000 people were more or less affected, the mortality being 1.7%. There is no clear pathogenetic mechanism, but the most probable is the generation of free radicals, caused by anilides. The clinical picture began with fever, acute interstitial pneumonia, pruritus, exanthems, myalgias and eosinophilia. The main pathological findings were generalized endothelial lesions, septal oedema, mild inflammatory mononuclear infiltrates and hydropic degeneration of type I and II pneumocytes with desquamation of type I. The pneumonic syndrome had a favourable evolution, except in 5% of the patients who went into acute respiratory distress and suffered an important mortality. In 10% of the patients, a moderate hypoxaemia remained with normal chest film; in these cases, a transbronchial biopsy showed more severe endothelial lesions and, in some of these patients, it was possible to find clinical signs of pulmonary hypertension, which was moderate and did not improve with oxygen or vasoactive agents. The neurological symptomatology was progressive, leading to very severe muscular atrophy and, in some cases, to alveolar hypoventilation. The neuromyopathy, as the other clinical manifestations, improved slowly during the following months. A year after the onset, a pulmonary restriction with a low transfer factor of CO remained, and some patients had residual neuromyopathy and severe scleroderma-like lesions of the skin. (ABSTRACT TRUNCATED AT 250 WORDS)