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S Labrune

Publications and source records attributed to S Labrune.

17 recordsLinked to original sources

[Treatment of fibrosing interstitial lung diseases].

In fibrosing pneumonitis, respiratory insufficiency is due to both fibrosis and inflammation induced pulmonary fibrosis. There is no treatment that can suppress fibrosis, so the current treatment of fibrosing pneumonitis--corticosteroid and/or immunosuppressive drugs--aims at reducing pulmonary inflammation and thus at slowing down the development of fibrosis which cannot regress. Therefore, it is necessary to determine the respective parts of inflammation, potentially reversible, and of fibrosis which is not. Most of the time, respiratory insufficiency cannot be prevented and requires long-term oxygen therapy. In a few patients, lung transplantation must be discussed.

Follow-Up Studies

[Sleep apneas].

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Humans

Drug-induced lung disease: 1990 review.

Numerous drug-induced pulmonary manifestations have been reported but studies of their pathogenic mechanisms are still rare. These mechanisms should, however, be precisely determined in order to identify subjects at risk and to prevent some of these complications by the proper use of certain drugs in more appropriate conditions. The possibility of an iatrogenic manifestation should always be considered in patients developing pulmonary symptoms. Data from biological investigations, although not specific, contribute to the understanding of lung injury mechanisms.

Asthma

Lung function declines in patients with pulmonary sarcoidosis and increased respiratory epithelial permeability to 99mTc-DTPA.

Respiratory epithelial clearance of 99mTc-DTPA (RC-Tc-DTPA) and pulmonary function tests (PFT) were determined at intervals of 6 or 12 months in 37 untreated, nonsmoking patients with sarcoidosis over a period of 6 to 36 months. PFT included the measurements of total lung capacity (TLC), vital capacity (VC), FEV1, and diffusing capacity for carbon monoxide. No difference was found between the respiratory clearance of 113mIn-DTPA (2.25 +/- 1.00%/min) and RC-Tc-DTPA (2.29 +/- 1.11%/min) in eight patients with pulmonary sarcoidosis. Pulmonary function decreased 15% or more in at least 2 function tests during 11 follow-up periods, but it remained stable during 47 follow-up periods. In patients whose lung function deteriorated, RC-Tc-DTPA increased to 3.51 +/- 1.55%/min; in contrast, in patients whose lung function remained stable, regardless of the initial values, RC-Tc-DTPA was normal (1.00 +/- 0.50%/min; p less than 0.001). In eight patients who were treated with corticosteroids, RC-Tc-DTPA decreased from 3.48 +/- 1.31%/min to 1.56 +/- 0.64%/min (p less than 0.001), and PFT improved. We conclude that in nonsmokers with pulmonary sarcoidosis, increased RC-Tc-DTPA is not related to dissociation of 99mTc from DTPA, RC-Tc-DTPA is increased when pulmonary function decreases, and, when increased, RC-Tc-DTPA decreases with corticosteroid therapy.

Adult

[Diffuse familial interstitial pulmonary fibrosis. Study of a family].

A study of the genealogy of a 53 year old lady (A.M...) suffering from diffuse interstitial pulmonary fibrosis (FID) has revealed several cases of FID in her forbears and relations. Two brothers of A.M... died of histologically proven FID; FID was also discovered in one of their daughters. A sister died young of some unclassified respiratory problem. Two cousins died likewise at a young age of acute FID proven histologically. The level of spontaneous pneumothorax was particularly elevated in this family which represented a clinical peculiarity when compared to sporadic FID. The most probable mode of transmission of familial FID is autosomal dominant with variable penetrance. The HLA group seen in A.M... showed the A2 and B12 alleles. The B12 allele was also present in the niece of A.M...

Bronchi

[Combined treatment of small cell bronchopulmonary cancer. Results of a retrospective study of 59 patients].

Fifty-nine patients with small cell bronchial tumours (36 localized, 17 diffuse, in the absence of marrow biopsy) were treated by a protocol combining chemotherapy and radiotherapy between October 1978 and October 1982. The chemotherapy consisted of three courses of Adriamycin (60 mg/m2 on day 1), Methotrexate (40 mg/m2 on day 2), Cyclophosphamide (800 mg/m2 on day 3), CCNU (60 mg/m2 on day 4). Six patients died during the first month of treatment and can not be evaluated; 53 patients completed the initial course of chemotherapy. The radiotherapy was administered after 3 courses of chemotherapy in 14 patients in complete remission and to 14 patients in incomplete remission with residual thoracic tumour. Of the 22 patients in complete remission following this combined treatment, 8 received a re-induction chemotherapy similar to the induction chemotherapy and 14 were simply followed up. The median follow-up of the survivors is 15 months. The actuarial one year survival rate of the 53 evaluable patients is 35% and the 2 year survival is 9%. There are certain hopes for the future: 1) the actuarial one year survival rate for the 22 patients in complete remission (67%) is significantly higher than that for the 31 patients who did not obtain complete remission (24%); 2) the actuarial one year survival rate for the 8 patients who received re-induction chemotherapy (87%) is significantly higher than that for the 14 patients who did not receive this treatment, although both groups were otherwise comparable. It is therefore possible that multiplication or intensification of the courses of treatment will improve the prognosis.

Adult