[Note on the therapy of suppurating infarction of the lung].
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Biomedical subjects
Publications and source records attributed to C Boutin.
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The present radiological status of 133 exworkers (mean age: 58 +/- 0.7 yr) of the chrysotile mine of Canari (Corsica) was compared to that recorded in 1965, when the mine was closed. The mean time since first exposure is 27 +/- 0.4 yr, and the mean time since termination of asbestos exposure equals 16 +/- 0.3 yr. This study showed an evolution of radiographic changes: in 1965 only 14% of the subjects had grade 1/1 or more parenchymal fibrosis, and 6% had bilateral pleural lesions; in 1979 these percentages reached 40% and 27%, respectively. Subjects who had a given parenchymal change in 1965 (e.g., 1/1 grade lesions) were older and had a more intensive dust exposure and tobacco consumption than exminers who developed the same parenchymal changes much later. A progression of parenchymal changes was observed in 39% of the subjects with normal findings in 1965, and in 63% of the subjects with grade 1/1 or more changes in 1965. Those who progressed (46% of the cohort) were older, had a longer exposure, and a more intensive dust exposure and cigarette smoking than nonprogressors.
After intratracheal injection of 0.5 mg of UICC chrysotile, rats were sacrificed at various time intervals over a 1-month period, and their pleural cavity washed with saline. Samples were examined by means of transmission electron microscopy for identification, quantitation, and sizing of chrysotile fibers. No fibers were found in control rats injected with saline. The size and quantity of fibers that reached the pleural cavity of test rats was time-dependent, with two peaks on day 7 (mean number = 9.6 X 10(4); mean length = 1.3 micron) and on day 21 (mean number = 1.3 X 10(5); mean length = 0.3 micron). Such variations are compatible with a heterogeneous migration of chrysotile fibrils toward the pleura.
We determined the toxicity and pharmacokinetics of high-dose intrapleural cisplatin (CDDP) as a treatment of malignant pleural effusions (MPE). Fourteen patients with MPE were enrolled in this study. After complete drainage of the fluid, a catheter was inserted into the pleural cavity during a thoracoscopy. CDDP (300 mg) was administered via the catheter in a 6-h infusion. Peak levels, the areas under the concentration curve (AUC), and drug half-lives were measured in pleural fluid and plasma samples collected at 0 (baseline), 6, and 24 h as well as 4, 14, and 21 days after intrapleural administration. The dosage of CDDP ranged from 153 to 203 mg/m2. The time interval between infusion was prolonged until a maximum of 109 days. Only 7/40 infusions were associated with adverse effects in 4 patients (18%). Residual concentrations in pleural fluid (0.66+/-0.07 microgram /ml) were three-fold higher than in plasma (0.13+/-0.07 microgram/ml). In pleural fluid, maximal concentration (Cmax) varied from 19 to 900 microgram/ml and in plasma from 0.34 to 3.65 microgram/ml. AUC in plasma during the three courses was 112+/-49 microgram/ml/d. The T1/2 was 31+/-33 days higher than that previously reported after intravenous administration (8-15 days). Although intrapleural CDDP has the potential advantage of treating the underlying malignancy in addition to controlling the malignant effusion with a good tolerance, it cannot be recommended for the standard control of malignant pleural effusion. Indeed we observed a great variability of intrapleural CDDP concentration depending on the extent of pleural invasion and plasma diffusion. Further studies are needed to determine the value of high-dose intrapleural CDDP for the treatment of MPE.