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Biomedical subjects

F Basset

Publications and source records attributed to F Basset.

At least 37 records · Page 2Linked to original sources
PubMed1987

Role of mast cells in the pathogenesis of hypersensitivity pneumonitis.

To examine the possibility that mast cells have a central role in the pathogenesis of hypersensitivity pneumonitis, 20 patients with this disease were studied with the aim of seeking evidence for mast cell degranulation. The number of mast cells recovered by bronchoalveolar lavage from patients with hypersensitivity pneumonitis was more than 1,000 times greater than those recovered from normal individuals. Furthermore, discontinuation of antigen exposure resulted in an increase in the number of mast cells observed, consistent with the possibility that antigen exposure had induced mast cell degranulation. Cessation of antigen exposure also resulted in a rapid decrease in the number of neutrophils and eosinophils recovered by lavage, followed by an increase in the number of T8+ T lymphocytes present. In each case the time course of the changes was consistent with the possibility that mast cell degranulation had been important in regulating the number of the immune and inflammatory cells present in the lung. Histamine was present in lavage fluid supernatant from patients with hypersensitivity pneumonitis. The amount of histamine present was, however, closely correlated with the number of mast cells present and not with the interval since last antigen exposure. Delay in separating cells from lavage fluid supernatant resulted in an increase in histamine content. These results suggest that the free histamine in lavage fluid resulted from the degranulation of mast cells induced by the lavage procedure as histamine released in vivo has a short half life. We suggest that hypersensitivity pneumonitis results from a "late phase reaction" initiated by antigen induced mast cell degranulation.

Alveolitis, Extrinsic Allergic↗
PubMed1987

Acute and latent pneumonitis after subcutaneous injections of silicone in transsexual men.

We evaluated 13 transsexual men who were hospitalized for symptoms resulting from illicit subcutaneous injections of silicone. Patients with acute silicone pneumonitis were admitted because of fever, bilateral pulmonary infiltrates, and hypoxemia (mean PaO2, 58 +/- 14 mm Hg). Most patients in this group had received new silicone injections within hours of admission, but one presented with the same clinical syndrome a few hours after a brawl. The alveolitis of acute silicone pneumonitis was characterized by increased numbers of alveolar macrophages, neutrophils, and eosinophils (p less than 0.05 compared with those in normal persons with a similar smoking history). Evidence of alveolar hemorrhage was also present in some cases. Alveolar macrophages contained large, pleomorphic, cytoplasmic inclusions, which were identified as silicone by atomic absorption and infrared spectrometry. Patients with latent silicone pneumonitis underwent clinical study at much longer times after the silicone fluid injections because they developed local inflammatory phenomena at the sites of previous injections. Pulmonary function studies usually showed slight restrictive changes, and bronchoalveolar lavage disclosed abnormalities similar to those found in patients with acute silicone pneumonitis, although to a lesser degree. Thus, illicit silicone fluid injection carries a serious respiratory risk since it can induce pneumonitis, followed in some patients by respiratory failure.

Acute Disease↗
PubMed1987

Pulmonary fibrosis following pneumonia due to acute Legionnaires' disease. Clinical, ultrastructural, and immunofluorescent study.

During a recent nosocomial outbreak, 20 critically ill patients with acute Legionnaires' disease were admitted to the intensive care unit of Hopital Bichat, Paris. Pulmonary specimens were obtained at surgery or immediately after death in 12 patients and were examined by light, immunofluorescent, and electron microscopy. Five of these 12 patients showed evidence of pulmonary fibrosis. In all of these five patients, infection with Legionella pneumophila was evidenced by bacteriologic methods, and other diseases known to cause fibrosis were excluded. The condition of four patients deteriorated rapidly with respiratory failure, and they died with pulmonary fibrosis. Only one patient finally recovered but was left with pulmonary sequelae. Two distinctive morphologic patterns were observed, one in which interstitial fibrosis was predominant and one in which intra-alveolar organization and fibrosis were also present. The alveolar epithelial lining and the basement membranes were disrupted in all patients, as evidenced by ultrastructural observations and by immunofluorescent studies showing gaps in the distribution of type 4 collagen and laminin. Types 1 and 3 collagen accumulated in areas corresponding to thickened interstitium and intra-alveolar fibrosis. Thus, some patients who survive the acute pneumonia of Legionnaires' disease may develop pulmonary fibrosis, and this process may lead to functional impairment or death despite prompt and appropriate treatment.

Adult↗
PubMed1987

[Stewart-Treves pseudo-syndrome caused by cutaneo-lymphatic metastases of contralateral breast carcinoma].

The pathogenesis of Stewart-Treves syndrome remains controversial: angiosarcoma or epithelial cell metastases from a mammary carcinoma? The case reported here, with clinical signs of Stewart-Treves syndrome on one side and mastectomy for carcinoma on the other side of the body, revives the debate. Case-history. The patient was an 89-year old woman whose left breast had been removed in June, 1981 for carcinoma with lymph node involvement. One year after the operation, multiple lymphadenopathy developed in her right armpit and subclavian region. In December, 1984, her right arm became swollen by lymphoedema, while Kaposi-like and nodular skin lesions appeared on her right upper chest and upper back and on her right shoulder and arm. Radiography of the chest showed right pleural effusion, bronchial lymph node enlargement and a reticulate image in the right lung. In spite of chemotherapy, the patient died in April, 1985. Pathology. Pathological examinations included standard histology (HPS, PAS and Gordon-Sweet staining), immunohistochemistry, using anti-factor VIII, anti-keratin KL1 and anti-EMA antisera, and electron microscopy. Results. Irrespective of the skin area biopsied, the histological images were always the same, showing carcinomatous lymphangitis with a varying degree of invasion of the surrounding dermis. Staining of the reticulum enhanced the vascular basal membranes but did not mark the intraluminal tumoral cell population. Post-mortem examination confirmed that the malignant lymphangitis extended to the lung tissue, the oesophageal wall and the adrenal glands, and that the axillary and subclavian lymph nodes were invaded by metastases.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Smoking and interstitial lung disease. The effect of cigarette smoking on the incidence of pulmonary histiocytosis X and sarcoidosis.

Cigarette smoking produces marked alterations in the lung parenchyma and in the population of immune and inflammatory cells present in the lower respiratory tract. These cigarette-induced changes appear to influence the incidence of two different interstitial lung diseases, histiocytosis X and sarcoidosis. Smoking is a strong risk factor for the development of pulmonary histiocytosis X, since the incidence of smoking is very high among patients with histiocytosis X: 90% of the patients with histiocytosis X were smokers; 46% of the controls were smokers (p less than .001). In contrast, smoking appears to reduce the incidence of sarcoidosis: 31% of the patients with sarcoidosis were smokers (p less than .05 compared to controls). In an effort to understand how cigarette smoking influences the incidence of these two disorders, we compared the numbers and types of immune and inflammatory cells recovered by bronchoalveolar lavage from nonsmoking and smoking controls and patients with histiocytosis X and sarcoidosis. Although nonsmoking patients with histiocytosis X did not have a significant increase in the number of alveolar macrophages recovered by lavage (p greater than .2 compared to normals), smoking patients had an increase in the number of alveolar macrophages similar to that observed in the control population. In contrast, the number of macrophages recovered from patients with sarcoidosis who smoked was considerably less than that observed in normal smokers (p less than .05 comparing patients with sarcoidosis and controls who smoked 1-20 cigarettes/day). This difference in the intensity of the cigarette-induced macrophage alveolitis observed in the two patient groups may be important in explaining the opposite effects of cigarette smoking on the incidence of histiocytosis X and sarcoidosis.

Adult↗
PubMed1986

Intraluminal fibrosis in interstitial lung disorders.

The histopathologic and ultrastructural features of intraluminal organizing and fibrotic changes were studied in open lung biopsies and autopsy specimens from 373 patients with interstitial lung disorders, including hypersensitivity pneumonitis (n = 44), idiopathic pulmonary fibrosis (n = 92), collagen-vascular diseases (n = 20), chronic eosinophilic pneumonia (n = 10), pulmonary histiocytosis X (n-90), pulmonary sarcoidosis (n = 62), pneumoconioses (n = 25), Legionnaire's disease (n = 5), drug- and toxin-induced pneumonitis (n = 4), radiation-induced pneumonitis (n = 2), lymphangioleiomyomatosis (n = 11), and chronic organizing pneumonia of unknown cause (n = 8). Three patterns of intraluminal organization and fibrosis were recognized: 1) intraluminal buds, which partially filled the alveoli, alveolar ducts and/or distal bronchioles; 2) obliterative changes, in which loose connective tissue masses obliterated the lumens of alveoli, alveolar ducts or distal bronchioles, and 3) mural incorporation of previously intraluminal connective tissue masses, which fused with alveolar, alveolar ductal, or bronchiolar structures and frequently became reepithelialized. All three patterns had common morphologic features, suggesting that, regardless of their severity, they resulted from a common pathogenetic mechanism, ie, the migration of activated connective tissue cells, through defects in the epithelial lining and its basement membrane, from the interstitial into the intraluminal compartment. Intraluminal buds were observed most frequently in hypersensitivity pneumonitis, chronic eosinophilic pneumonia, and organizing pneumonia of unknown cause. Mural incorporation and, to a lesser extent, obliterative changes were observed in most interstitial disorders and were very prominent in idiopathic pulmonary fibrosis. Mural incorporation and obliterative changes play an important role in pulmonary remodeling, especially when several adjacent alveoli and/or other air spaces are involved. Under these circumstances, intraluminal organization can mediate the fusion of adjacent alveolar structures by intraluminal connective tissue.

Alveolitis, Extrinsic Allergic↗
PubMed1985

Cytochrome b-245 in human alveolar macrophages.

To kill microorganisms, phagocytes exhibit an oxidative burst with, in particular, a NADPH-dependent, superoxide-generating system that consists, in polymorphonuclear leukocytes (PMN), of a flavin enzyme and cytochrome b-245 (cyt b-245). We investigated the existence of this cytochrome in human alveolar macrophages (AM) because its presence would support its wide-spread occurrence in phagocytes and would raise the possibility of similarities in the oxygen-dependent killing mechanisms in AM and PMN. Moreover, we compared the amount of cyt b-245 in AM from patients with lung disorders with that from healthy subjects, by a differential spectroscopic measurement of its 558 to 559 nm characteristic band. This spectrum showed that cyt b-245 was present in AM. In AM of healthy subjects, the amount was similar to that found in PMN of blood. In AM of patients with miscellaneous lung diseases and in Am of infected lungs, the data were not modified.

Cytochrome b Group↗
PubMed1985

Immunocytochemical characterization of pulmonary histiocytosis X cells in lung biopsies.

Morphologic and immunohistochemical studies were made of open lung biopsies from 9 patients with pulmonary histiocytosis X (HX) and 12 patients with other conditions, and of skin biopsies from patients with cutaneous sarcoidosis, Chester-Erdheim disease, and eruptive histiocytoma. The monoclonal antibody OKT6 was detected with the use of goat anti-mouse IgG labeled with fluorescein (FITC) for light microscopy, and sheep antimouse Fab'2 fragment of IgG labeled with horseradish peroxidase (HRP) for immunoelectron microscopy. The presence of S-100 protein was revealed by an antibody prepared against bovine S-100 protein, using sheep anti-rabbit IgG labeled with FITC for light microscopy and with HRP for immunoelectron microscopy. OKT6 antibody and S-100 protein were detected simultaneously by double labeling with FITC and rhodamine. In all patients with pulmonary HX, the major cellular components (HX cells) of the granulomas showed labeling of the plasma membranes by OKT6 and of the cytoplasm by the anti S-100 protein antibody. The double-labeling technique demonstrated that the same cells carried both reactivities. Immunoelectron microscopy showed that the reactive cells had all the structural characteristics of Langerhans cells, including Langerhans cell granules. Cells reacting with OKT6 showed discrete internal labeling in some of the Langerhans granules, especially those in continuity with the plasma membranes. However, internal labeling of Langerhans granules was not demonstrated in preparations for the localization of S-100 protein. Control samples of sarcoid lesions and other pulmonary lesions unrelated to HX did not show any reactivity except in Langerhans cells; a skin lesion from a patient with eruptive histiocytoma contained OKT6-positive cells which did not have Langerhans granules.

Antibodies, Monoclonal↗
PubMed1984

[Exploratory bronchoalveolar lavage].

Bronchoalveolar lavage is a simple technique, complementary to fiberoptic bronchoscopy. The material yielded comprises cells and supernatant, and both components may provide information about the distal lung structures. A few counter-indications should be respected. Normally, the cell differential comprises: 93 +/- 5% alveolar macrophages, 7 +/- 1% lymphocytes and about 1% neutrophils, eosinophils and basophils. Total cellularity and cell differentials are altered in many conditions, according to different patterns, which permits a classification. The increase in numbers may relate to macrophages (smokers, pneumoconiotic disorders...), to lymphocytes (sarcoidosis, hypersensitivity pneumonitis...) and to neutrophils and/or eosinophils (fibrotic disorders, chronic eosinophilic pneumonia, histiocytosis X...). In the last disease, the diagnosis may be established by detecting Langerhans cells. In other conditions, bronchoalveolar lavage mostly provides a trend to diagnosis. Usually well tolerated, bronchoalveolar lavage may usefully be repeated for monitoring patients with chronic interstitial lung disorders. It also gives an insight into the pathogenesis of many pulmonary pathological processes.

Bronchi↗
PubMed1984

Accurate quantification of cells recovered by bronchoalveolar lavage.

Quantification of the differential cell count and total number of cells recovered from the lower respiratory tract by bronchoalveolar lavage is a valuable technique for evaluating the alveolitis of patients with inflammatory disorders of the lower respiratory tract. The most commonly used technique for the evaluation of cells recovered by lavage has been to concentrate cells by centrifugation and then to determine total cell number using a hemocytometer and differential cell count from a Wright-Glemsa-stained cytocentrifuge preparation. However, we have noted that the percentage of small cells present in the original cell suspension recovered by lavage is greater than the percentage of lymphocytes identified on cytocentrifuge preparations. Therefore, we developed procedures for determining differential cell counts on lavage cells collected on Millipore filters and stained with hematoxylin-eosin (filter preparations) and compared the results of differential cell counts performed on filter preparations with those obtained using cytocentrifuge preparations. When cells recovered by lavage were collected on filter preparations, accurate differential cell counts were obtained, as confirmed by performing differential cell counts on cell mixtures of known composition, and by comparing differential cell counts obtained using filter preparations stained with hematoxylin-eosin with those obtained using filter preparations stained with a peroxidase cytochemical stain. The morphology of cells displayed on filter preparations was excellent, and interobserver variability in quantitating cell types recovered by lavage was less than 3%.(ABSTRACT TRUNCATED AT 250 WORDS)

Bronchi↗
PubMed1984

Diagnosis of pulmonary histiocytosis X by immunodetection of Langerhans cells in bronchoalveolar lavage fluid.

Based on the finding that Langerhans cells and histiocytosis X cells react with the monoclonal antibody OKT6, raised against a subset of thymocytes, we used this antibody to study the cells collected by bronchoalveolar lavage (BAL) from 131 patients, including 18 with pulmonary histiocytosis X, 43 with pulmonary sarcoidosis, 67 with miscellaneous pulmonary disorders, and 3 controls. Immunofluorescence studies demonstrated the presence of OKT6-reactive cells in all patients with pulmonary histiocytosis X (mean +/- SEM, 5.29% +/- 1.14% of all cells in BAL fluid). Immunoelectron microscopic studies revealed that the cells labeled in these patients (n = 13) contained Langerhans granules. The number of fluorescent cells in the other 113 patients was significantly smaller (mean +/- SEM, 0.20% +/- 0.04% of all cells; P less than 0.001). In the 3 control patients, in the 43 patients with sarcoidosis, and in 61 of the 67 patients with miscellaneous disorders unrelated to histiocytosis X, no cells or less than 1% of the total were labeled; however, in the 6 remaining patients in this miscellaneous group, 1.3 to 2.8% of all cells in BAL were labeled. In 3 of these 6 patients, immunoelectronmicroscopic examination showed that the cells labeled by OKT6 had the general characteristics of Langerhans cells but lacked Langerhans granules. OKT3, OKT4, and OKT8 monoclonal antibodies did not stain histiocytosis X cells in BAL fluid.

Antibodies, Monoclonal↗
PubMed1983

[Histiocytosis].

Current ideas about the histiocyte-macrophage system are briefly reviewed and the functions attributed to the system are defined. An anatomico-clinical classification of histiocytic diseases into four categories is suggested: - secondary of associated histiocytosis illustrating, in particular, macrophage function in immune response; - histiocytosis due to dystrophia or overload illustrating mainly phagocyte function and ability to store fats; - Langerhans histiocytosis characterized by the presence of numerous Langerhans cells. - Neoplastic histiocytosis, which is the only genuine malignant tumoral proliferation of the histiocyte-macrophage system.

Bone Diseases↗