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Biomedical subjects

P Carré

Publications and source records attributed to P Carré.

At least 19 recordsLinked to original sources
PubMed1995

[Disappearance of emphysematous bullae after infectious episodes].

The authors report 3 cases of peri-emphysematous lung infection associated with the development of air-fluid level in pre-existing emphysematous bullae. Prolonged observation revealed that both bullae and fluid disappeared completely or partially after short antibiotic treatment. The review of literature show that this favourable evolution has not often been described and that these pictures must be to differentiate from lung abscess.

Humans↗
PubMed1994

[Diffuse alveolar hemorrhage and myositis in icterohemorrhagic leptospirosis. Rapid control by a single bolus of corticoids].

Leptospirosis is one of the commonest causes of diffuse alveolar haemorrhage. Despite good sensitivity to penicillin and current techniques of ventilation, there remains a considerable mortality which is particularly linked to the initial pulmonary disease at presentation. The authors describe a new case of a gravely ill patient with leptospirosis and sever hypoxaemia. There was diffuse alveolar haemorrhage and myositis thus a bolus of corticosteroids was used over the first 24 hours complementary to the traditional treatment.

Adrenal Cortex Hormones↗
PubMed1993

Doppler ultrasound assessment of the effects of ketamine on neonatal cerebral circulation.

The effects of a single dose of 5 mg.kg-1 of ketamine administered intravenously to 10 critically ill preterm infants prior to epicutaneo-caval catheterization were analyzed using pulsed-wave Doppler ultrasound. The infants weighed between 670 and 1,885 g and their gestational ages ranged from 26 to 33 weeks. Arterial pressure (MAP), cardiac output (CO), transcutaneous oxygen pressure (TcPO2), transcutaneous carbon dioxide pressure (TcPCO2), end-diastolic velocity (EDV), peak systolic velocity (PSV), mean arterial velocity (MAV) of the cerebral anterior artery as well as Pourcelot's resistance index (PRI) were measured before and after injection of the drug. We observed a significant decrease in arterial pressure at 2 min after injection while heart rate and CO did not vary significantly. TcPO2 and TcPCO2, also remained unchanged throughout the period of measurement. EDV, PSV, and MAV did not vary significantly nor did PRI. As this drug provides major comfort to the baby during painful procedures and considerably facilitates difficult thin vessel catheterization, we believe that it may be used in such conditions.

Cerebrovascular Circulation↗
PubMed1993

[Cytokines and pulmonary fibroses].

Pulmonary fibrosis corresponds to an accumulation of collagens and other proteins of the extracellular matrix in the interstitium and alveoli. Biochemical and cellular mechanisms of pulmonary fibrogenesis remain poorly understood. The cells of the alveolitis (macrophages, lymphocytes and neutrophils) play a key role in producing the factors which regulate the proliferation, chemotactism and secretory activity of the fibroblasts. Amongst these factors the cytokines (interleukins, interferons and growth factors) play a definite but very complex role. Certain cytokines stimulate in vitro the attraction and activation of cells of the alveolitis, as well as the multiplication, migration and secretory activity of fibroblasts. The following cytokines are involved: tumour necrosis factor alpha: (TNF alpha), interleukin 1 (IL-1), interleukin 6 (IL-6) interleukin 8 (IL-8) transforming growth factor beta (TGF beta), platelet derived growth factor (PDGF), insulin like growth factor 1 (IGF-1), fibronectin, monocyte chemotactic protein 1: (MCP-1). Other cytokines, principally the interferons (of alpha, beta or gamma type: IFN alpha, IFN beta, IFN gamma) inhibit in vitro and in vivo the proliferation and the production of collagen by fibroblasts. During the course of human pulmonary fibrosis or in experimental situations, the majority of the cytokines mentioned above are produced in excess in the lung. Without doubt they play an important role in the pathogenesis of fibrosis, even if it is not yet very well known how they interact and contribute in vitro to the process of fibrogenesis. Certain cytokines potentially regulating in the fibrosis are yet to be identified. In the future the use of cytokines and of their inhibitors will perhaps provide new therapies in pulmonary fibrosis.

Animals↗
PubMed1992

[A unilateral hyperlucent lung...].

The occurrence in a young patient of a chronic cough with dyspnoea and restrictive ventilatory failure as shown by respiratory function tests suggested the possibility of a Mac Leod syndrome. However, other aetiologies could be considered such as vascular malformations, bronchial malformations and also tumours. If the chest X-ray sometimes enables an aetiological slant, bronchoscopy remains a first line investigation.

Adolescent↗
PubMed1990

[Therapeutic modalities in pulmonary tuberculosis].

In 1990, specific antituberculous chemotherapy can cure almost 100 p. cent of patients with pulmonary tuberculosis in France, provided practitioners follow strict therapeutic rules and patients' compliance with treatment is perfect. A single standard treatment is proposed for those patients whose tuberculosis has never previously been treated; it consists of a six months' course of isoniazid (5 mg/kg/day) and rifampicin (10 mg/kg/day); combined with ethambutol (20 mg/kg/day) and pyrazinamide (30 mg/kg/day) during the first two months. This treatment must be administered under regular medical supervision, and it must be prolonged for some time after cure has been obtained. In case of relapse or in some special situations (e.g. pregnant women, HIV positive patients, serofibrinous pleurisy, complex anatomico-clinical forms of the disease) treatment is more difficult, but it should always give favourable results.

Adult↗
PubMed1990

[The in vivo penetration of erythromycin into alveolar macrophages].

In order to appreciate the in vivo penetration of erythromycin the alveolar spaces a broncho-alveolar lavage was carried out in 24 guinea pigs, 30 minutes, 1 hour 30 minutes and three hours after a single intraperitoneal injection of 50 mgms. of erythromycin. The erythromycin dose was assessed by a microbiological method in the alveolar macrophages and the supernatant of the broncho-alveolar lavage liquid. The intramacrophage concentrations of erythromycin were 3.9, 11.5 and 12 times higher than the serum concentrations at 30 minutes, 1 hour 30 and three hours respectively. The concentrations in the broncho-alveolar lavage liquid was always higher than the serum concentrations tacking account of the different dilutions estimated with relation to the glucose concentrations. At 30 minutes, 1 hour 30 minutes and three hours the alveolar macrophages contained 1.9; 7.6 and 6 times more erythromycin respectively than the lavage supernatant. From the first half hour of its administration the erythromycin was concentrated in the alveolar spaces, in particular within the macrophages. Already noted in vitro, this rapidity of erythromycin concentration in vivo in alveolar macrophages appears to be one of the reasons to explain its activity against micro-organisms developing within macrophages.

Absorption↗
PubMed1990

[Effects of cotrimoxazole on some macrophage functions: microbicide, tumoricide, production of free oxygen radicals, prostaglandins and leukotrienes].

In order to demonstrate an immunomodulating effect of cotrimoxazole, we investigated its influence on some macrophage (M phi) functions in culture: P815 tumor cells killing, Toxoplasma gondii killing, production of free oxygen radicals by luminol-dependent chemiluminescence, prostaglandins and leukotrienes secretion evaluated after incorporation of tritiated arachidonic acid. In vitro, cotrimoxazole inhibited in a dose-dependent fashion the chemiluminescence of murine resident peritoneal or guinea pig alveolar M phi. Production of prostaglandin (PG) 6-keto-F1 alpha, PGF2 alpha, and 5-hydroxyeicosatetraenoic acid by resident peritoneal M phi was also inhibited. However, PGD2 synthesis by alveolar M phi was enhanced. A second study was performed on peritoneal M phi, resident or elicited in vivo by one intra-peritoneal injection of an extract from Mycobacterium Tuberculosis membranes and obtained from mice pretreated or not by cotrimoxazole per os. Resident M phi from cotrimoxale-treated animals showed increased production of leucotriene B4 compared to M phi from controls. 6-keto-PGF1 alpha and free oxygen radicals production by elicited M phi was greatly enhanced by cotrimoxazole whereas thromboxane B2 was reduced. Finally cotrimoxazole enhanced intracellular killing of Toxoplasma gondii and cytotoxicity for tumor cells P815 by resident but not by elicited M phi. It is concluded that cotrimoxazole can modulate MO activation and some M phi functions involved in immune homeostasis. This data could help to understand why an antibiotic such as cotrimoxazole, which is known to be frequently used in immunocompromised hosts, is also efficient in Wegener's granulomatosis.

Animals↗
PubMed1988

[Current aspects of Goodpasture's syndrome].

Goodpasture's syndrome is an auto-immune disorder with antibodies directed against alveolar and glomerular basement membrane. These antibodies are usually present in the serum but their detection is difficult, requiring a radio-immunological technique which remains uncommon. The fixed antibodies are detected more easily and more constantly in the kidney tissue than in the lung; they appear on a kidney biopsy in the form of linear deposits of immunoglobulins on the basement membrane. Thus, the renal biopsy appears to be the essential requirement to establish a diagnosis of Goodpasture's syndrome, and one should not hesitate to perform a biopsy in the presence of diffuse alveolar haemorrhage without an evident aetiology and even in the absence of any biological evidence of renal disease. Alveolar lavage may be used to confirm a haemorrhage which has been purely alveolar. The treatment for respiratory and renal recovery, using immunological therapy includes corticosteroids, cytotoxic drugs and plasmapheresis. The exact methods are not yet fully defined during the course on certain clinical forms of the disease: for oliguric patients, dialysis is the single treatment; the isolated pulmonary forms have often been treated and improved by corticotherapy alone. The responsible antigen, probably unique, has been recently been identified as collagen type IV of the glomerular basement membrane. The pathogenesis of Goodpasture's syndrome remains unknown. The inhalation of hydrocarbons has been frequently noted. The dismal prognosis in the natural history of the disease and the therapeutic possibilities available make diagnosis an urgency. Currently, renal biopsy represents the most reliable and rapid mean of diagnosis.

Adult↗
PubMed1987

[Primary leiomyosarcoma of the pulmonary artery. Apropos of a case].

A case of leiomyosarcoma of the pulmonary artery in a 64-year old man without previous cardiovascular disease is reported. The clinical picture, which comprised episodes of paroxysmal dyspnoea associated with acute cor pulmonale, suggested pulmonary embolism. Radioisotope perfusion study and pulmonary angiography seemed to confirm this diagnosis, but no improvement was obtained with a prolonged thrombolytic treatment. The presence of a median mass at CT led to exploratory thoracotomy and to the finding of a tumour in the pulmonary artery, which turned out to be a leiomyosarcoma. The disease rapidly took an unfavourable course. Comparison of this case with data from the literature showed that primary tumours of the pulmonary artery are extremely rare, that they are diagnosed with difficulty and often at a late stage and that their prognosis is usually very sombre.

Humans↗
PubMed1987

[Alveolar macrophages and antibiotics. Review].

Although alveolar macrophages play a key role in pulmonary defence against infections, little is known about interactions of these cells with antibiotics. In vitro, some drugs fail to enter alveolar macrophages readily; in contrast, other antimicrobial agents (clindamycin, erythromycin, ethambutol) are highly concentrated by these cells, as well as josamycin, erythromycin and spiramycin in vivo. Moreover, clindamycin, erythromycin, chloramphenicol, rifampin and pefloxacin lead to an increased phagocytosis by alveolar macrophages, either by compromising bacterial antiphagocytic components or stimulating proper phagocytic activity of the cell. The influence of antibiotics upon mechanisms of microorganisms destruction (production of oxygen metabolites, oxygen independent system), upon regulation of lymphocyte functions (interleukin 1, prostaglandin E2) or other secretory activities (enzymes, modulators of cell activities, various bioactive products) have not been extensively studied and require further investigations.

Animals↗
PubMed1987

[Acute primary alveolar hemorrhage or Goodpasture's syndrome?].

We report a case of idiopathic diffuse alveolar haemorrhage with fatal outcome in a 23 year old man. In the absence of any renal abnormality of circulating antiglomerular basement antibody the diagnosis of Goodpasture's syndrome was made taking into account the history and the autopsy evidence of linear deposits of immunoglobulin on the glomerular basement membranes.

Acute Disease↗