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Biomedical subjects

P Vaillant

Publications and source records attributed to P Vaillant.

17 recordsLinked to original sources
PubMed1992

[Plasma beta chorionic gonadotropin between 14 and 20 weeks of amenorrhea: a sign of pregnancy-related hypertension].

A defect of placenta maturation has been described in hypertension of pregnancy. Plasma beta chorionic gonadotropins (beta HCG) of placental origin rise at the onset of pregnancy and reach a peak between 9 and 10 weeks of amenorrhoea. As we were making systematic assays between 14 and 20 weeks in a trisomy detection programme, we looked for differences in plasma beta HCG levels between women with pregnancy-induced arterial hypertension and pregnant women with normal blood pressure. We also studied the predictive value of such assays. Pregnancy-induced hypertension was found in 6 women in a population of 89 nulliparas and in 12 women in a population of 163 multiparas. beta HCG levels were significantly higher in women who later developed hypertension among both nulliparas (52,833 +/- 19,538 IU vs 24,499 +/- 16,485 IU) and multiparas (50,558 +/- 23,597 IU vs 20,911 +/- 11,677 IU). In nulliparas, taking 43,000 IU as threshold of pathology we found that the predictive value of beta HCG was higher than that of other tests which had gone through controlled studies (sensitivity 67 percent, specificity 91.6 percent, positive predictive value 36 percent, negative predictive value 97.4 percent, relative risk 5.4). In multiparas, taking 38,000 as threshold and combining this marker with obstetrical history it was possible to predict the occurrence of hypertension more precisely than with other markers which had gone through controlled studies (sensitivity 66.7 percent, specificity 98 percent, positive predictive value 61.4 percent, negative predictive value 97.3 percent, relative risk 8.4).

Adult↗
PubMed1992

Mechanism for the recruitment of macrophages to cancer site. In vivo concentration gradient of monocyte chemotactic activity.

BACKGROUND: Tumor stroma is characterized by the development of new blood vessels, an inflammatory cell infiltration, and a fibrotic reaction. The inflammatory component of tumor stroma plays an important role in the modulation of tumor expansion. In this respect, macrophages constitute a major part of the inflammatory cell infiltration and can exert cytotoxic activity against tumor cells. The accumulation of macrophages in the vicinity of the tumor suggests their recruitment from circulating blood monocytes through the local release of chemotactic factors for monocytes. METHODS: To detect the existence of a concentration gradient of monocyte chemotactic activity (MCA) between the tumor vicinity and blood vessels, malignant pleural effusions defined by the local presence of cancer cells were evaluated for quantification of MCA. RESULTS: Unlike nonmalignant pleural effusions, malignant pleural effusions were characterized by the presence of increased levels of MCA, and in lung adenocarcinoma (a cancer with high inflammatory cell infiltration), pleural levels of MCA were significantly greater than in small cell lung carcinoma (a cancer with low inflammatory cell reaction). An MCA concentration gradient between pleural fluid and plasma was present in malignant effusions because pleural MCA levels in all cancer types were significantly greater than MCA levels in the plasma of the same patients. CONCLUSIONS: Thus, an increased local level of MCA is a feature of cancers with high inflammatory cell infiltration, and the presence of an in vivo concentration gradient of MCA suggests the direct role of this biologic activity in recruiting blood monocytes to the cancer site.

Adenocarcinoma↗
PubMed1992

Characterization of a tumor necrosis factor-alpha inhibitor activity in cancer patients.

To evaluate the feasibility of tumor necrosis factor-alpha (TNF-alpha) treatment of lung cancer patients, we chose the malignant cells contained in their pleural effusions as a first convenient target. We found, however, that a TNF-alpha inhibitor (TNF-alpha I) activity was present in both patient sera and pleural fluids. We therefore compared the TNF-alpha I activity present in patients with benign or malignant pleural effusions using a bioassay of TNF-alpha inhibition and partially characterized it. A high TNF-alpha I activity characterizes cancer patients with sera levels twice as high as the control level measured for blood bank donors (2.54 +/- 1.28 versus 1.19 +/- 0.38) and with even higher levels in pleural fluids (3.75 +/- 1.83). In contrast, patients with benign pleural effusions present similar levels of TNF-alpha I activity, at about the control level, in both their sera and pleural fluids (1.37 +/- 0.98 versus 1.16 +/- 0.85). A high TNF-alpha I activity is consistently found in cancer patients but is only released in vitro by leukocytes. It is most likely related to recently purified TNF-alpha inhibitors that, as soluble shed fragments of TNF receptors, may function as traps for TNF molecules. This study suggests that tumors may evade TNF cytotoxic action by modulating systemic levels of TNF and implies a reassessment of TNF therapy in cancer patients.

Adult↗
PubMed1992

Presence of elevated levels of platelet-derived growth factor (PDGF) in lung adenocarcinoma pleural effusions.

Significant tumor stroma development is a specific feature of adenocarcinoma of the lung in comparison to small-cell lung cancer (SCLC). The fibrotic component of tumor stroma is thought to result from the migration and local replication of mesenchymal cells in response to the presence of cytokines. One of them, platelet-derived growth factor (PDGF), is a chemotactic and growth factor for mesenchymal cells. Since several lung adenocarcinoma cell lines, but not SCLC cell lines, have been shown in vitro to express PDGF genes, we evaluated pleural effusions for the presence of PDGF in patients with adenocarcinoma of the lung, SCLC, or nonmalignant pleural effusions. In adenocarcinoma of the lung, PDGF levels in pleural effusions were higher than in SCLC and in nonmalignant pleural effusions and were associated with the presence of a growth-promoting activity for fibroblasts due, in part, to the presence of PDGF. This observation suggests the role of PDGF in tumor stroma formation in adenocarcinoma of the lung.

Adenocarcinoma↗
PubMed1992

Dexamethasone modulation of tumour necrosis factor-alpha (cachectin) release by activated normal human alveolar macrophages.

Recurrent infections of the lower respiratory tract are a frequent and serious side-effect of chronic corticosteroid treatment. Since alveolar macrophages (AM) are currently thought to play a central role in the protection of the lower respiratory tract against infectious agents, it is likely that a steroid-induced deficiency of AM is involved in this process. In this respect, when activated, AM are major producers of tumour necrosis factor-alpha (TNF or cachectin), a versatile cytokine with several biological properties including antiviral and anti-infectious activities. A deficit of TNF production induced by corticosteroid may be one mechanism of the sensitivity to infections. Thus normal human AM obtained by bronchoalveolar lavage were pretreated with dexamethasone (DXM) before activation with lipopolysaccharides (LPS) and the amounts of TNF released in culture were quantified. Pretreatment with DXM resulted in a marked decrease of TNF release in a dose-dependent fashion. In contrast, when AM were activated with LPS before DXM treatment, TNF release by AM was suppressed in a more limited fashion. Thus DXM suppression of LPS-activated AM ability to release TNF may play a role in the susceptibility to infections of patients chronically treated with corticosteroids.

Adult↗
PubMed1991

[Mechanisms of pulmonary fibrosis].

Lung fibrosis is characterized by the accumulation of extracellular matrix and mesenchymal cells leading a progressive loss of respiratory functional units. The accumulation of mesenchymal cells results from their migration and local replication. These cellular events are dependent upon the local presence of cytokines with chemotactic and/or mitogenic activity. The sequence of events leading the lung fibrosis is thought to result from a stereotyped response: after an initial injury, an inflammatory reaction develops and controls tissue repair through local production of cytokines. The permanency of these processes results in the development of fibrosis.

Acute Disease↗
PubMed1991

[Biopathology of fibrosing alveolitis].

Fibrosis is a condition where the functional tissue of an organ has been replaced by mesenchymal cells and their extracellular matrix. The process is frequent and may be regarded as univocal and independent of aetiology. An initial tissue damage is responsible for an inflammatory reaction which modulates and controls tissue repair with accumulation of mesenchymal cells, an accumulation which results from their migration and replication under the influence of chemotactic and/or mitogenic mediators (cytokines). Fibrosis occurs as an accentuation of this physiological process and may be understood as a healing process that has succeeded beyond normal expectation. Studies of idiopathic pulmonary fibrosis have improved our understanding of the physiopathology of pulmonary fibrosis. Alveolitis sets in response to an initial injury of undetermined nature, and from then on lymphocytes, neutrophils and macrophages intervene in the pathological process: (1) lymphocytes contribute to the perpetuation of the process by local production of immune complexes and coactivation of other inflammatory cells; (2) neutrophils and, to a lesser extent, eosinophils worsen the initial tissue injury by producing proteases and oxydants; (3) finally, macrophages control the local accumulation of mesenchymal cells by producing chemotactic and growth factors and by modulating the secretion by these cells of extracellular matrix.

Cytokines↗
PubMed1989

[Change in the lymphocyte subpopulations in bronchoalveolar lavage 72 hours after the allergen provocation test in the asthmatic].

Fourteen patients suffering from perennial allergic asthma linked to mono-sensitivity to the house dust mite were studied. An initial bronchoalveolar lavage with standard cytology as well as a study of the T lymphocyte subpopulations (CD3, CD4, CD8, Leu 7) and B cells (CD19) was carried out, representing the basal situation. Four weeks later an allergic bronchial provocation test to purified extracts of the house dust mite was performed taking care to monitor the occurrence of any delayed bronchial response (8 out of 14). A second bronchoalveolar lavage was performed 72 hours after the bronchial provocation test. A significant rise of eosinophils in the bronchoalveolar fluid was registered 72 hours after the provocation test; m +/- sem (%): 3.07 +/- 1.31 vs 7.78 +/- 1.22; p less than or equal to 0.005, Student t test for paired series. This large rise in eosinophils was observed independently of the type of response, whether immediate or biphasic. The CD4 lymphocyte subpopulations were significantly decreased after bronchial provocation tests m +/- sem (%) 12.21 +/- 2.79 vs 6.47 +/- 1.62; p less than or equal to 0.05 Student t test for paired series. There was no overall significant difference after the provocation tests in the CD8 lymphocyte subpopulation. However, a remarkable and significant rise was noted in the CD8 populations after bronchial provocation in 6 subjects presenting with an immediate isolated asthmatic reaction; m +/- sem (%) 10.17 +/- 4.01 vs 34 +/- 7.32, p less than 0.05, paired Wilcoxon test.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

[Severe complications related to metabisulfites].

Metabisulfite intolerance is encountered in 8 p. 100 of cases of extrinsic asthma and in 20 p. 100 of cases of the "aspirin triad" with nasosinusal polyposis, asthma and aspirin sensitivity. The possibility that anaphylactoid shock or acute severe asthma leading to status asthmaticus, might be related to sulfite sensitivity must be well known. Two case reports are set out. The first observation is that of a 35-year-old woman suffering from intrinsic asthma with alcohol intolerance, who developed status asthmaticus a few minutes after intravenous administration of Doxycycline associated with a metabisulfite preservative. The other 33-year-old patient presented with an acute bronchospasm in the course of a fiberoscopy using Lidocaine associated by mishap with epinephrine, as local anesthetic. The authors point to the miscellaneous drugs containing sulfites, that are employed in asthmatics by different routes, i.e. parenteral, oral, inhalational and other local treatments. Heavy metabisulfite intake may also arise from daily alcohol consumption. Sulfite intolerance could contribute to the persistence of chronic inflammatory processes in bronchial asthma and therefore should be systematically investigated.

Adult↗