[Small-cell bronchogenic carcinoma with ectopic secretion of ACTH: apropos of 2 cases and review of the literature]. / Carcinoma broncogénico de células pequeñas con secreción ectópica de ACTH: a propósito de dos casos y revisión de la literatura.

Described in this report are 2 patients with small-cell bronchogenic carcinoma with ectopic secretion of ACTH, an association that has long been reported in the literature but that is nevertheless rare, with most authors describing small series of patients or reporting retrospective studies. Pathogenic and etiological aspects are reviewed, with emphasis on the scarcity of clinical signs and the biochemical criteria needed for diagnosis. The poor prognosis of the disease is discussed along with the need to try to treat hypercortisolism even before cytotoxic therapy is initiated.

[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)