[Hypoxic eosinophilic pneumonia in two patients treated with ACE inhibitors]. / Pneumopathie à éosinophiles hypoxémiante sous traitement par IEC.

Diffuse hypoxic pneumonia was found to be caused by angiotensin converting enzyme (ACE) inhibitors in two patients given enalapril and fosinopril for hypertension. Both patients developed sub-acute respiratory failure and lost weight. Imaging explorations showed multiple areas of alveolar consolidation, moderate pleural effusion and in one case linear opacities. In both cases, peripheral eosinophila was found and the bronchoalveolar lavage fluid contained lymphocytes. Progressive improvement was achieved after withdrawal of the ACE and corticosteroid therapy for three months. Subsequent x-rays and respiratory function tests returned to normal apart from persistently low CO diffusion in one patient. In view of other cases reported in the literature, ACE inhibitors should probably be included in the list of drugs capable of inducing pneumonia, notably eosinophilic pneumonia.

[Primary malignant mediastinal melanoma. Apropos of a case]. / Mélanome malin primitif médiastinal. A propos d'un cas.

We report the case of a 57-year-old patient with primary malignant melanoma of the mediastinum who survived nine months despite immunotherapy, radiotherapy and chemotherapy. The primary nature of the intrathoracic melanoma was difficult to prove. Definitive diagnosis was based on the uniform morphology of the melanoma which showed junctional anomalies at the histology examination with tracheo-bronchial and esophageal localizations as well as on the absence of other patent or formerly resected melanocyte-rich localizations (skin, mucosa, ocular) at clinical examination and autopsy.

[Chronic diffuse interstitial pneumonia associated with chronic active hepatitis. 2 cases]. / Pneumopathie interstitielle diffuse chronique associée à une hépatite chronique active. 2 observations.

Two cases of chronic active hepatitis associated with diffuse interstitial pneumonia (lymphoid in one patient, lymphoid and fibrosing in the other) are reported. Histopathological data from the lungs, together with the parallel course of pulmonary and hepatic manifestations observed under corticosteroid therapy, suggest that these two diseases shared a common dysimmune pathogenesis. A few cases identical with these have been found in the literature. The clinical, laboratory and histopathological elements obtained from these cases also suggest an immune cause in most patients.

The penetration of macrolides into bronchial secretions.

Macrolides have shown efficacy in the treatment of a large range of respiratory infections. These antibiotics are well tolerated, have a narrow antibacterial spectrum, and excellent diffusion properties. We have studied the penetration into bronchial secretions of three macrolides, erythromycin, josamycin and oleandomycin. The bronchial concentrations of erythromycin reached an average of 1 mg/l 2 h after oral administration of 1 g; they were lower for josamycin (0.52 mg/l) but the ratio between bronchial and simultaneous serum concentrations was similar for both drugs. Bronchial levels of oleandomycin were rapidly higher than the serum levels, reaching 3 to 4 mg/l, a ratio of more than 100%. Other studies on tissue concentrations of erythromycin and josamycin showed local levels of 4 to 6 mg/l, whereas in bronchial secretions the concentrations were identical to those measured in our study. On the whole, the good diffusion of macrolides into respiratory tissues and secretions as well as in-vitro antibacterial activity against most species responsible for respiratory infections confirm their indication in the treatment of these infections.

Influence of a fluidifying agent (bromhexine) on the penetration of antibiotics into respiratory secretions.

The authors report the results of a study designed to evaluate the possible increase of penetration into bronchial secretions of antibiotics when combined with a fluidifying agent: bromhexine. The study was carried out in a double-blind experiment: erythromycin in 22 patients (group I) or amoxycillin in 26 patients (group II) were administered orally; in both groups several patients were given a placebo, instead of bromhexine. Antibiotics were administered at the usual dosage: 0.5 g X 2 for erythromycin (3 days); 1 g X 2 for amoxycillin (7 days); with the latter, two different doses of bromhexine were administered simultaneously: 48 mg/day and 96 mg/day in ten and eight patients respectively. Samples of bronchial secretions were collected by means of fibreoptic bronchoscopy at the second hour for erythromycin and for amoxycillin; simultaneous serum samples were also collected. The results of the study showed in both groups a significant increase of the ratios between bronchial levels and simultaneous serum concentrations when combined with bromhexine; in patients receiving amoxycillin with 96 mg of bromhexine the percentage penetration was noticeably higher (7.5%) than in those treated with 48 mg bromhexine (4.3%). These results confirm the efficacy of bromhexine as a drug able to disrupt mucopolysaccharides of bronchial secretions and, as a result, to increase the bronchial penetration of antimicrobial drugs as evaluated on the basis of percentage penetration ratio.

Diagnosis of pulmonary histiocytosis X by immunodetection of Langerhans cells in bronchoalveolar lavage fluid.

Based on the finding that Langerhans cells and histiocytosis X cells react with the monoclonal antibody OKT6, raised against a subset of thymocytes, we used this antibody to study the cells collected by bronchoalveolar lavage (BAL) from 131 patients, including 18 with pulmonary histiocytosis X, 43 with pulmonary sarcoidosis, 67 with miscellaneous pulmonary disorders, and 3 controls. Immunofluorescence studies demonstrated the presence of OKT6-reactive cells in all patients with pulmonary histiocytosis X (mean +/- SEM, 5.29% +/- 1.14% of all cells in BAL fluid). Immunoelectron microscopic studies revealed that the cells labeled in these patients (n = 13) contained Langerhans granules. The number of fluorescent cells in the other 113 patients was significantly smaller (mean +/- SEM, 0.20% +/- 0.04% of all cells; P less than 0.001). In the 3 control patients, in the 43 patients with sarcoidosis, and in 61 of the 67 patients with miscellaneous disorders unrelated to histiocytosis X, no cells or less than 1% of the total were labeled; however, in the 6 remaining patients in this miscellaneous group, 1.3 to 2.8% of all cells in BAL were labeled. In 3 of these 6 patients, immunoelectronmicroscopic examination showed that the cells labeled by OKT6 had the general characteristics of Langerhans cells but lacked Langerhans granules. OKT3, OKT4, and OKT8 monoclonal antibodies did not stain histiocytosis X cells in BAL fluid.