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J Cadranel

Publications and source records attributed to J Cadranel.

At least 127 records · Page 7Linked to original sources
PubMed1991

Expression of 1,25(OH)2D3 receptors on alveolar lymphocytes from patients with pulmonary granulomatous diseases.

1,25(OH)2D3 is known to be produced at sites of granulomatous reactions. In order to characterize the cell types that are targets for this immunoregulatory hormone, we have evaluated the expression of 1,25(OH)2D3 receptors on peripheral blood T-lymphocytes and those recovered from the lung by bronchoalveolar lavage from patients with pulmonary granulomatous diseases (tuberculosis and sarcoidosis) and from normal control subjects using combined autoradiographic and immunohistochemical techniques. Lavage T-lymphocytes from patients with tuberculosis or with sarcoidosis, but not those from normal control subjects, expressed 1,25(OH)2D3 receptors as demonstrated by binding of [3H]1,25(OH)2D3, which was inhibited by the presence of excess unlabeled 1,25(OH)2D3, but not by the presence of unlabeled 25(OH)D3 (receptor-positive lymphocytes: sarcoidosis, 20 +/- 12%; tuberculosis, 31 +/- 17%). In contrast, blood lymphocytes from patients with granulomatous diseases did not express detectable 1,25(OH)2D3 receptors. The percentage of lavage T-lymphocytes expressing 1,25(OH)2D3 receptors was significantly greater for patients with tuberculosis presenting with isolated hilar adenopathy than for patients with pulmonary infiltrates and/or cavities. 1,25(OH)2D3 receptors were expressed to a greater extent on CD8+ T-lymphocytes than on CD4+ T-lymphocytes in sarcoidosis, whereas a greater proportion of CD4+ than of CD8+ T-lymphocytes from patients with tuberculosis were receptor-positive. These findings support the conclusion that the interaction of 1,25(OH)2D3 with its receptor on T-lymphocytes may play an important role in the regulation of granulomatous reactions, but because these receptors are expressed on different lymphocyte populations, the net effect of this potent immunoregulatory molecule is likely different in sarcoidosis and tuberculosis.

Adult↗
PubMed1991

Antigen-induced proliferative response of lavage and blood T lymphocytes. Comparison of cells from normal subjects and patients with sarcoidosis.

To evaluate the mechanisms responsible for anergy in sarcoid patients, we studied the ability of highly purified lavage and blood T lymphocytes from control subjects and patients with sarcoidosis to proliferate in response to recall antigens, and compared the results of antigen-induced lymphocyte proliferation with the clinical characteristics of the patients. Both blood and lavage T lymphocytes from all control subjects proliferated in response to purified protein derivative (PPD) and candida antigens, and no significant difference was observed comparing the proliferation of lymphocytes from the two sources. The antigen-induced proliferation of blood and lavage T lymphocytes from sarcoid patients was reduced compared with that of the corresponding cell populations from normal subjects (p less than 0.01 for PPD, Candida, and tetanus), and the proliferative response of sarcoid lavage lymphocytes was significantly lower than that of blood T lymphocytes from these patients. No evidence for inhibition of T lymphocyte proliferation by accessory cells (blood monocytes) or CD8+ T lymphocytes was observed, and the refractory state could not be overcome by adding exogenous recombinant human IL-2 or IL-4. An inverse correlation was observed between the PPD-induced proliferation of sarcoid lavage T lymphocytes and criteria associated with "active" disease, including lymphocytes/ml lavage fluid (p less than 0.003), 67Ga uptake (p less than 0.005), and serum angiotensin converting enzyme activity (p less than 0.005). Lavage lymphocytes from patients studied early in the course of the disease proliferated better than those from patients with more long-standing disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

[Respiratory involvement in AIDS].

This review paper is divided into three parts. The first two parts are devoted to an analytical description of the clinical, diagnostic, prognostic and therapeutic aspects of the various bronchopulmonary and pleural lesions observed in AIDS. The third part presents an overall view of the main diagnostic and therapeutic approaches in the main clinical situations covering all respiratory disorders.

Acquired Immunodeficiency Syndrome↗
PubMed1991

[Pulmonary infection with Mycobacterium szulgai].

Mycobacterium szulgai is a newly recognised species of mycobacteria whose pathogenicity in man can only be confirmed following certain criteria. We report a new observation comprising three points of interest. M. szulgai appears to be directly responsible for pulmonary infection and the clinical and radiological progress is very rapid. The human disease probably comes from infected water in aquaria. We have reviewed other cases of M. szulgai in the literature and for two out of three amongst these there is pulmonary involvement resembling tuberculosis; in the other cases cutaneous disease, synovial disease and bone disease have been described.

Humans↗
PubMed1991

[Interstitial pulmonary involvement of polymyositis and dermatomyositis. Apropos of 3 cases. Review of the literature].

The authors report 3 new cases of myositis associated with pulmonary lesions that preceded or succeeded the muscular disorder. In one of these cases, which was particularly difficult to diagnose, the patient's serum was positive for the anti-Jo1 antibody. These 3 cases have encouraged the authors to review the literature with particular attention to the diagnostic approach, the latest physiopathological data and the therapeutic basis of the "specific" pulmonary lesions associated with polymyositis and dermatomyositis.

Adult↗
PubMed1990

Nodular regenerative hyperplasia of the liver, peliosis hepatis, and perisinusoidal fibrosis. Association with angioimmunoblastic lymphadenopathy and severe hypoxemia.

Three different liver lesions were found in a 20-year-old woman with angioimmunoblastic lymphadenopathy. The lesions included nodular regenerative hyperplasia of the liver, perisinusoidal fibrosis, and peliosis hepatis. It is suggested that the association of angioimmunoblastic lymphadenopathy with this broad spectrum of liver lesions was not fortuitous.

Adult↗
PubMed1990

In vitro production of tumour necrosis factor and prostaglandin E2 by peripheral blood mononuclear cells from tuberculosis patients.

We investigated the production of tumour necrosis factor-alpha (TNF-alpha) and prostaglandin E2 (PGE2) by peripheral blood mononuclear cells (PBMC) from tuberculosis patients and healthy controls. PBMC from tuberculosis patients generated constitutively more TNF-alpha than did control PBMC. This production was significantly higher for patients with high-grade fever and cachexia. The increase of TNF-alpha production by PBMC from tuberculosis patients was associated with a comparatively weaker elevation of PGE2 synthesis which did not parallel fever or weight loss. In vitro treatment of control PBMC with the tuberculin purified protein derivative (PPD) promoted an increased TNF-alpha production which was similar to that of untreated PBMC from tuberculosis patients. Thus, the increased TNF-alpha production in tuberculosis could be explained by the in vivo exposure of PBMC to mycobacterial antigens. In contrast, the concentration of PGE2 was weaker in the medium of untreated PBMC from tuberculosis patients than in the medium of PPD-treated control PBMC, suggesting that PGE2 synthesis by PBMC was limited in tuberculosis by unidentified factors.

Adult↗
PubMed1990

1,25(OH)2D2 production by T lymphocytes and alveolar macrophages recovered by lavage from normocalcemic patients with tuberculosis.

To compare extra-renal 1,25(OH)2D3 production in different types of granulomatous disease, and to identify the cell types responsible, we have evaluated the conversion of 25(OH)D3 in 1,25(OH)2D3 by uncultured cells recovered by bronchoalveolar lavage and blood mononuclear cells from normocalcemic patients with sarcoidosis and tuberculosis. 1,25(OH)2D3 was produced both by lavage cells (12/12 tuberculosis patients, 2/6 sarcoidosis patients) and blood mononuclear cells (3/5 tuberculosis patients, 0/3 sarcoidosis patients) from patients but not controls, but significantly greater amounts were produced by lavage cells from tuberculosis patients than those of sarcoidosis patients (P less than 0.001). 1,25(OH)2D3 production by lavage cells from tuberculosis patients correlated with the number of CD8+ T lymphocytes present but not other cell types. T lymphocytes appeared to be an important source of 1,25(OH)2D3 production, since purified T lymphocytes from all patients with tuberculosis produced 1,25(OH)2D3, and 1,25(OH)2D3 production by these cells correlated closely with that produced by unseparated lavage cells. Because 1,25(OH)2D3 can improve the capacity of macrophages to kill mycobacteria, our results support the conclusion that macrophage-lymphocyte interactions, mediated at least in part by 1,25(OH)2D3, may be an important component of a successful antituberculous immune response.

Adult↗
PubMed1990

[Serum neuron-specific enolase in small cell bronchial cancers].

Despite its very good specificity, serum neuron-specific enolase (SNE) cannot be relied upon to diagnose small cell carcinoma. However, this marker is of interest owing to the double correlation observed between it and tumoral extension and between its rapid elevation under chemotherapy and clinical response to chemotherapy. Repeated SNE assays help in determining this response when SNE returns to normal level, and in predicting the progression of the disease several weeks in advance when SNE levels increase. Early and later SNE assays therefore have prognostic value.

Carcinoma, Bronchogenic↗
PubMed1990

[Pulmonary and pleural localizations of Kaposi's sarcoma in AIDS].

Intrathoracic Kaposi's sarcoma (KS) in AIDS is remarkable for its frequency and severity. It is responsible for 10% of "pneumonias" and almost 50% of pleurisies observed in these patients. The time elapsed between the discovery of the lesion and the patient's death does not exceed a few months on average. The initial manifestations of pulmonary KS are usually discreet and consist of cough and/or dyspnoea in patients with KS of the skin and mucosae. Fever is lacking or moderate. The most suggestive radiological findings are dense, nodular, tumour-like opacities and bilateral linear and/or micronodular opacities around the bronchi and vessels. The diagnosis rests on bronchial fibroscopy which shows red, non friable lesions which, to a trained endoscopist, are very characteristic. When these lesions are absent, thoracotomy may be necessary for diagnostic purposes. Treatment essentially consists of chemotherapy; zidovudine therapy and prophylaxis of pneumocystosis are indicated if the circulating CD 4 cell count falls below 200/mm3. When its symptoms are predominant, pleural KS is typically progressive, with normal or slightly elevated temperature, associated parenchymal lesions that are clearly visible on CT scans and copious, bilateral, blood-stained serous or chylous pleural fluid. When these signs are absent throacoscopy or thoracotomy may be necessary. Future advances in this field will be due not only to improvements in chemotherapy but also to a better understanding of the physiopathology of intrathoracic Kaposi's sarcoma.

Acquired Immunodeficiency Syndrome↗
PubMed1990

[Bronchial cancer in patients infected with human immunodeficiency virus (HIV). Report of 3 cases].

We report 3 cases of bronchial carcinoma in patients with human immunodeficiency virus (HIV) infection. Like the other 13 cases found in the literature, these were characterized by their occurrence in young subjects, their often adenocarcinomatous nature and their abnormally severe course. These clinical features raise the problem of the role played by HIV in the development and, above all, the clinical expression of bronchial carcinoma.

Adenocarcinoma↗
PubMed1990

[Specificity and serum concentrations of tumor necrosis factor in septic shock].

Several lines of evidence implicate tumor necrosis factor (TNF), a cytokine produced by monocytes-macrophages, in the systemic manifestations of shock induced by Gram-negative bacteria. Whether the increase of circulating TNF levels is specific to septic shock as compared to sepsis without shock or to non-septic shock is still unclear. Since TNF values recorded at the time of admission to the hospital vary widely, statistical analysis has not been possible. Therefore, we postulated that the evolution of a patient's TNF serum level as compared to his initial value may better distinguish the survivor from the non-survivor than a single initial determination. Using a radioimmunoassay, we measured the TNF concentrations in the sera of 7 patients with severe infections without shock, 16 patients with septic shock and 8 patients with non-septic shock. Blood samples were drawn within the first 12 hours after the onset of shock. Patients with cancer, HIV infection, or under steroid therapy were excluded. Repeated measurements were made during the first 3 days of septic shock in 10 patients. The circulating TNF level, determined upon admission, appears to be neither specific nor predictive of the outcome of septic shock. In contrast, persistently high levels of circulating TNF seem to be well correlated with a poor prognosis, since 5 out of 6 patients with elevated TNF values died of septic shock.

Adult↗