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Biomedical subjects

B Wallaert

Publications and source records attributed to B Wallaert.

At least 19 recordsLinked to original sources
PubMed1992

[Physiopathology of asthma].

Asthma is a multifactorial disease where genetic predisposition, environmental factors (allergens and pollutants) and endogenous factors intervene to varying degrees. Among the disturbances involved in the physiopathology of asthma dysfunction of the autonomic nervous system and development of bronchial inflammation are now known to play the major roles. From the adrenergic system, the role of which is now controverted, the attention of pharmacologists has shifted to the cholinergic central nervous system responsible for bronchial tone and the non adrenergic non cholinergic (NANC) nervous system. The more recently known NANC system is complex and mediated by neuropeptides, and it can alternately induce bronchodilatation and bronchoconstriction, as well as vasoconstriction and vasodilatation. The inhibitory NANC system acts through the bronchodilator VIP. The excitatory NANC system is mediated by tachykinins as which are potent bronchoconstrictors. Interaction of this system with the inflammatory cells induces a "neurogenic inflammation". Local inflammatory reaction is an almost constant element of asthma, irrespective of the cause of the disease. Although mast cells are the initial cells of the inflammatory reaction, there are important and complex cellular interactions with eosinophils, macrophages, lymphocytes and epithelial cells. Owing to their direct cytotoxic actions on the bronchial epithelium, eosinophils play a key-role in the inflammatory reaction. Cytokines secreted by alveolar macrophages, lymphocytes and mast cells amplify and maintain the inflammatory process.

Asthma↗
PubMed1992

Effects of nickel hydroxycarbonate on alveolar macrophage functions.

The metabolic effects of different concentrations of nickel hydroxycarbonate (NiHC) on guinea pig alveolar macrophages (GPAMs) were investigated. Exposure to high concentrations of NiHC (6.25 and 12.5 micrograms 10(-6) cells) led to cell vacuolization. Morphological changes were associated with a dramatic reduction in the steady-state level of cellular adenosine triphosphate (ATP), i.e. ATP levels were reduced by 35% (P less than 0.001) and 53% (P less than 0.01), respectively. Low concentrations of NiHC (0.0625 and 0.125 microgram 10(-6) cells) did not induce morphological changes but increased cellular ATP content by 19% (P less than 0.01) and 12% (P less than 0.05), respectively. Effects of NiHC (0.125 and 6.25 micrograms 10(-6) cells) on cell oxidative metabolism were studied. The chemiluminescence was significantly increased (P less than 0.001) by the lower but not the higher concentration. A slight inhibition of total superoxide dismutase (P less than 0.05) and a decrease of catalase activity were demonstrated (P less than 0.05) for the high dose, while the low dose decreased the levels of reduced and total glutathione. In conclusion, the effects of NiHC on alveolar macrophages are characterized by an overproduction of free radicals for low concentrations and the depletion of cellular reserve energy, particularly ATP, for high concentrations.

Adenosine Triphosphate↗
PubMed1992

Levels of soluble IL-2 receptor in plasma from asthmatics. Correlations with blood eosinophilia, lung function, and corticosteroid therapy.

Evidence now suggests that eosinophils and T lymphocytes infiltrating bronchial tissues may play a key role in the pathophysiology of asthma. Circulating eosinophils, lung function, and plasma soluble IL-2 receptor (sIL-2R) were measured in 42 asthmatic patients referred for symptomatic asthma. The patients were divided into two groups based on the presence or absence of atopy. The group of non-atopic asthmatics was further divided according to the patients' requirement for long term oral corticosteroids. The mean sIL-2R +/- s.d. was 36.3 +/- 9.9 pM in the control group, 28.9 +/- 9.2 pM in the atopic asthmatics, 43.3 +/- 18.07 pM in the non-atopic asthmatics without oral steroid therapy, but was increased in the steroid-treated group (62.2 +/- 19.3 pM, P less than 0.01). A significant correlation was found between FEV1 and circulating eosinophils in atopic asthmatics and in non-atopic asthmatics without oral corticosteroid therapy, but not in the steroid-treated group. Furthermore, significant correlations were found between sIL-2R and FEV1, and between sIL-2R and blood eosinophils, in the group of non-atopic asthmatics not on oral steroid therapy. No such correlations were evidenced in the other groups of asthmatics. Similar results were obtained during the clinical course of three non-atopic patients followed for more than 1 year. These data suggest that T cell activation appears more prominent in non-atopic asthma than in atopic asthma. Moreover, it appears that T cell activation can occur in severe forms of asthma despite steroid treatment. Finally, the results suggest a possible link between T cell activation, eosinophils, and lung function, which may reflect a particular pathogenetic mechanism involved in non-atopic asthma.

Adrenal Cortex Hormones↗
PubMed1992

Increased pulmonary and intestinal permeability in Crohn's disease.

We tested the hypothesis that an increased epithelial permeability may affect sites other than the intestine in patients with Crohn's disease by simultaneously evaluating their pulmonary and intestinal permeability. Pulmonary and intestinal permeability were measured by clearance of inhaled technetium-99m diethylene triamine pentacetate (99mTc-DTPA) and by urinary recovery of chromium-51 ethylene diamine tetracetate respectively in 22 patients with Crohn's disease. The half time clearance of 99mTc-DTPA from lung to blood (t1/2LB) was decreased--that is pulmonary permeability increased--in the whole group of patients with Crohn's disease as compared with 13 controls (median 45.5 minutes (8-160) v 85 minutes (34-130) (p less than 0.003)). When analysed separately only patients with active Crohn's disease (n = 15) had a decreased t1/2 lung to blood v controls (42 minutes (8-160) v 85 minutes (34-130) (p less than 0.0025)). Among patients with active Crohn's disease, six were studied again when their disease was quiescent and their t1/2 lung to blood did not differ significantly. The intestinal permeability was increased in the whole group of Crohn's disease patients as compared with 15 controls (5.25% (1.2-24) v 1.7% (0.65-5.75) (p less than 0.0002)). When analysed separately both patients with active and inactive Crohn's disease had increased intestinal permeability v controls (8.1% (1.6-24) and 3.5% (1.2.9.2) v 1.7% (0.65-5.75)) (p less than 0.0001, p = 0.05 respectively). Six patients with active Crohn's disease were studied again when their disease was quiescent and their intestinal permeability decreased significantly p less than 0.04). Pulmonary permeability was increased in patients with Crohn's disease but was not greatly influenced by Crohn's disease activity as opposed to intestinal permeability. The mechanism of this increase is unknown, but may be related in some patients to the presence of an alveolitis.

Adolescent↗
PubMed1992

Increased intestinal permeability in active pulmonary sarcoidosis.

Altered permeability of the gut is a well-described feature in Crohn's disease. Because of pathologic similarities between Crohn's disease and sarcoidosis, we initiated this study to evaluate the permeability of the gut mucosal lining in patients with pulmonary sarcoidosis. A group of 18 patients with biopsy-proven pulmonary sarcoidosis (active n = 8, inactive n = 10) were included in the study. Control groups included 22 patients with Crohn's disease (active n = 12, inactive n = 10), nine untreated patients with recent pulmonary tuberculosis, six patients with coal worker's pneumoconiosis (CWP), eight patients with idiopathic pulmonary fibrosis (IPF), and 16 healthy subjects. All were nonsmokers. The 24-h urinary excretion of 100 microCi 51Cr-ethylenediaminetetraacetic acid (51Cr-EDTA) was used to test the intestinal permeability (IP). As previously demonstrated, patients with active Crohn's disease demonstrated a dramatic increase in IP (7.7 +/- 1.4%) that was clearly reduced in inactive CD (2.34 +/- 0.54%). Patients with active pulmonary sarcoidosis exhibited a marked increased IP to 51Cr-EDTA (4 +/- 0.54%), which was not found in patients with inactive sarcoidosis (1.6 +/- 0.17%). IP was normal in patients with pulmonary tuberculosis (1.03 +/- 0.25%), CWP (2.1 +/- 0.54%), and IPF (1.9 +/- 0.33%) and did not differ from the control group (1.76 +/- 0.23%). In addition, in 6 patients with active pulmonary sarcoidosis, the concentrations of albumin and hyaluronan were measured in jejunal perfusion fluid and compared with those obtained from 10 patients with active Crohn's disease and 16 control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗
PubMed1992

Long-term prognosis of near-fatal asthma. A 6-year follow-up study of 145 asthmatic patients who underwent mechanical ventilation for a near-fatal attack of asthma.

The objective of the present study was to investigate the long-term prognosis of near-fatal asthma. A retrospective cohort study design was used. Cases were defined as any asthmatic individual requiring mechanical ventilation for the first time for an asthma exacerbation between January 1, 1983 and December 31, 1988. The consecutive sample of patients was drawn from four study sites, specifically four intensive care units (ICU), based in a large urban area (1 million inhabitants). These four ICU total approximately 5,000 admissions per year and are the referral centers for more than 95% of patients requiring respiratory intensive care in the area. Data collection was obtained by questionnaires addressed to the patients and to their attending physicians and was completed by telephone calls if necessary. A total of 147 patients entered the study. The long-term outcome could be evaluated in all but two patients. The follow-up period ranged from 1 to 75 months. In-hospital mortality was 16.5%. Among the 121 patients discharged from the ICU, 18 subsequently died, 17 of whom died from a new attack of asthma. Post-hospitalization mortality was 10.1% (95% CI, 5.9 to 16.8%) after 1 yr, 14.4% (CI, 9 to 22.3%) after 3 yr, and 22.6% (CI, 12.7 to 36.8%) after 6 yr. Nearly two-thirds (61.5%) of these secondary deaths occurred within the year following discharge from the ICU. Smoking was associated with a higher in-hospital mortality, as well as with a higher posthospitalization mortality. Age was also independently associated with a higher posthospitalization mortality. It is noteworthy that the secondary deaths were mostly observed in patients over 40 yr of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1992

Tumor necrosis factor alpha and interleukin-6 production by human mononuclear phagocytes from allergic asthmatics after IgE-dependent stimulation.

We have previously demonstrated the production of tumor necrosis factor alpha (TNF) and interleukin-6 (IL-6) by alveolar macrophages (AM) from allergic asthmatics developing a late asthmatic reaction after bronchial allergen challenge. In order to explain the modalities of this monokine synthesis, we tested in vitro the effect of an IgE-dependent stimulation on blood monocytes (BM) and AM from control and asthmatic subjects. TNF and IL-6 secretions were evaluated in 24-h supernatants by radioimmunoassay and by the 7TD1 cell proliferation test, respectively. AM from allergic asthmatics secreted spontaneously higher concentrations of TNF and IL-6 than did BM or AM from control subjects. BM from asthmatics also produced spontaneously increased levels of TNF, but at a lesser degree than did AM. The addition of anti-IgE induced a significant increase of TNF and IL-6 secretions by mononuclear phagocytes from control subjects only after previous sensitization with IgE-rich medium. In contrast, the direct stimulation by allergen or anti-IgE of AM and BM from asthmatics enhanced significantly the production of TNF and IL-6 when compared with cells cultured in medium alone. In these conditions, IgE-dependent activation of cells from allergic asthmatics compared with those from control subjects increased monokine production in a similar manner. Costimulation by recombinant human interferon gamma and IgE-dependent triggering had a synergistic effect on TNF production, but it had only an additive action on IL-6 synthesis (respective increase index: 9.8 compared with 2.9 and 9.8 compared with 2.1, respectively, for BM from control and asthmatic subjects).(ABSTRACT TRUNCATED AT 250 WORDS)

Asthma↗
PubMed1992

Bronchoalveolar lavage in alcoholic liver cirrhosis. T-lymphocyte subsets and immunoglobulin concentrations.

The purpose of this study was to determine the phenotype profiles of immune effector cells and the concentrations of immunoglobulins in the lower respiratory tract of non-smoking patients with alcoholic liver cirrhosis (ALC). Nine nonsmoking patients with liver biopsy-proved ALC (grade B or C cirrhosis in Child's classification), free of clinical pulmonary symptoms, and with normal chest roentgenogram were included in the study. The control group included 12 healthy nonsmokers. Each patient had fiberoptic bronchoscopy with bronchoalveolar lavage (BAL). The number of T cells and of lymphocyte subpopulations was determined by immunofluorescence studies using monoclonal antibodies that were specific for CD3, CD4, and CD8 markers. Patients with ALC exhibited a dramatically increased percentage of CD8+ cells in BAL that induced a low CD4/CD8 ratio (0.96 +/- 0.15 vs 1.8 +/- 0.12 in healthy controls). Further characterization of lymphocyte subsets' dual immunofluorescence analysis demonstrated that most of the CD8+ alveolar lymphocytes had a phenotype of cytotoxic cells (CD8+ CD11b-; 48 percent +/- 13 in ALC vs 10 percent +/- 5 in controls). ALC was associated with an appreciable alveolar-capillary "leak" as demonstrated by a significant increase in BAL fluid albumin. In addition, the concentrations of immunoglobulins in BAL fluid were significantly greater in ALC than in controls. However, the relative (to albumin) coefficient of excretion of IgG, A, and M in and alpha 2-macroglobulin BAL fluid was not significantly different between controls and ALC. Our results indicate that increased proportions of CB8+ and especially of CD8+ CD11b- cells are a common feature in the lower respiratory tract of nonsmoking patients with ALC. These changes may be of potential functional importance in the regulation of the local pulmonary immune response in ALC.

Adult↗
PubMed1992

[The multifocal form of bronchocentric granulomatosis].

Bronchocentric granulomatosis is a rare entity and has only recently been characterised. We report a case of a forty-three year old man presenting with multifocal bronchocentric granulomatosis which was revealed following some oto-rhino-laryngological and bronchopulmonary symptoms. The open lung biopsy confirmed the diagnosis. Treatment was by bolus doses of corticosteroids (30 mg/kg) and of methotrexate in low dosage (7.5 mg/week, then 15 mg/week) which checked the initially unfavourable outcome.

Adrenal Cortex Hormones↗
PubMed1992

[Broncho-alveolar lavage. From technical aspects to standards of interpretation].

Broncho-alveolar lavage is a simple investigation to carry out and enables the gathering of biological information such as inflammatory and immuno-competent cells, tumour cells, microorganisms as well as mineral particles which are found in the biological milieux present in the distal air spaces. The performance of LBA assumes a mastering of the correct technical aspects of this method of investigation, particularly in the phase of injecting and recovering of physiological saline and an understanding of the indications and contraindications of the technique. The interpretation of the information gathered by cytological, microbiological, mineralogical and biochemical study of the bronchoalveolar lavage liquid should comply with a strict set of rules and justifies a close working contact between the clinician and the biological scientist.

Bronchi↗
PubMed1992

[Occupational dust exposure and chronic obstructive bronchopulmonary disease. Etiopathogenic approach to the problem of compensation in the mining environment].

In order to support the hypothesis of a causal relationship between exposure to respirable coal mine dusts and chronic obstructive pulmonary disease (COPD), investigations were performed to assess the biological disorders affecting the distal air spaces in coal workers with pneumoconiosis. Broncho alveolar lavage studies demonstrated a continual influx of mononuclear phagocytes loaded with mineral particles, associated with neutrophils in small number, in smokers as well as in non smokers. The alveolar macrophages were in activated state, spontaneously releasing various mediators, particularly interleukin I, Tumor necrosis factor alpha and superoxide anion. So, they appeared as responsible both for a chronic inflammation of the distal airways and for a protease-antiprotease imbalance leading to pulmonary emphysema, partly due to an oxidative inactivation of alpha 1 antiprotease inhibitor. In spite of additive effect of tobacco smoke, as shown by longitudinal studies of lung function in coal miners, it is now reasonable to consider the evidence of association between coal mine exposure and COPD to be sufficiently strong to infer causality, and to justify compensation for COPD in coal miners with or without radiological evidence of pneumoconiosis.

Coal↗
PubMed1991

[Value of bronchoalveolar lavage in the diagnosis and management of diffuse interstitial fibrosing lung diseases].

Bronchoalveolar lavage (BAL) is an exploratory technique which is easy to perform and collect cellular constituents, notably inflammatory and immunocompetent cells, as well as biological elements that are present in the distal airways. In patient with chronic diffuse infiltrative lung disease, analysis of these parameters reveals various disturbances such as neutrophilia frequently associated with eosinophilia and, in some cases, lymphocytosis. These features are not specific, but they differentiate chronic diffuse infiltrative lung diseases from sarcoidosis and hypersensitivity lung diseases. Alveolar inflammation (alveolitis) correlates with the evolutive potential of the lesions and their ability to respond to treatment. The presence of lymphocytosis is usually associated with response to corticosteroid therapy, whereas the presence or persistence of neutrophilia and, even more, eosinophilia is characteristic of patients who do not respond to corticosteroids but are amenable to the cyclophosphamide-corticosteroid combination. BAL therefore increasingly appears as an irreplaceable tool to understand the physiopathology of chronic diffuse infiltrative lung diseases.

Bronchoalveolar Lavage Fluid↗
PubMed1991

Increased secretion of tumor necrosis factor alpha and interleukin-6 by alveolar macrophages consecutive to the development of the late asthmatic reaction.

The late asthmatic reaction (LAR), consecutive to bronchial allergen challenge, is characterized both by the influx of various cells in proximal and distal airways and by the enhancement of bronchial hyperresponsiveness. However, the exact conditions for the development of the inflammatory reaction during the LAR remain to be specified. Since monokines play a key role in inflammatory processes, particularly in the lung, the production of tumor necrosis factor-alpha (TNF-alpha), interleukin; 1-beta (IL-1-beta) and interleukin-6 (IL-6) by alveolar macrophages (AM), collected 18 to 20 hours after exposure to allergen, was evaluated in 15 allergic subjects with asthma submitted to a challenge test with Dermatophagoides pteronyssinus (N = 6) or with wheat flour (N = 9) and in three healthy subjects. After bronchial provocation test, four patients presented no bronchial response (group 1), and six patients, a single early reaction (group 2). In contrast, five patients developed successively an immediate plus a late response (group 3). The monokine production was compared to that from nine allergic subjects with asthma studied at baseline (group 0) and from 11 unchallenged healthy subjects (control subjects). Measurements of cytokines were evaluated for TNF-alpha and IL-1-beta by a specific immunoradiometric assay, whereas IL-6 levels were appreciated by the proliferation of 7TD1 cells. No detectable amounts of TNF-alpha, IL-1-beta, and IL-6 were in bronchial alveolar lavage fluid, even after a tenfold concentration. In contrast, a significant increase of TNF-alpha (10,642 +/- 3127 U/ml) and IL-6 (1250 +/- 427 U/ml) concentrations was noted in AM supernatants from patients exhibiting an LAR (group 3) compared to cells recovered from groups 2, 1, and 0 and to challenged or unchallenged control subjects (805 +/- 244, 995 +/- 521, 1269 +/- 524, 688 +/- 85, and 445 +/- 74 pg of TNF-alpha per milliliter, respectively; 190 +/- 64, 114 +/- 91, 242 +/- 95, 80 +/- 9, and 54 +/- 19 U/ml of IL-6 per milliliter, respectively). No modification of IL-1-beta contents could be detected between the different groups. A significant correlation was detected between concentrations of TNF and IL-6 (r = 0.92; p less than 0.001). These results demonstrate TNF-alpha and IL-6 secretion by AM consecutively to the development of LAR in allergic subjects with asthma, confirming that AMs are activated after allergen challenge.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1991

Human alveolar macrophage antibacterial activity in the alcoholic lung.

Alcoholic individuals are predisposed to respiratory infections. However, mechanisms of perturbations leading to increased susceptibility to lung infections of individuals with alcoholic liver cirrhosis (ALC) are not fully understood. We studied the antibacterial activity and oxidant generation (before and after stimulation by phorbol myristate acetate or opsonized zymosan) of alveolar macrophages from 16 patients with ALC. Our results were compared with those obtained from 12 healthy control subjects, from 8 patients with primary biliary cirrhosis (PBC), and from 8 alcoholic individuals without cirrhosis. All were nonsmokers, had normal chest X-rays, and did not present evidence of lung infection 3 months before. The total number of cells recovered by bronchoalveolar lavage did not significantly differ between control subjects and patients. The cellular viability of alveolar macrophages (trypan blue exclusion) was greater than 90% in all cases. The antibacterial activity of alveolar macrophages versus Staphylococcus aureus was severely impaired in ALC (-21 +/- 8.2%) whereas it was normal in PBC (52 +/- 4.2%), in alcoholic subjects (44.6 +/- 5.4%), and in control subjects (60 +/- 5.5%). The same pattern of results was observed versus Escherichia coli (-47.7 +/- 10,28 +/- 8,28 +/- 12, and 29 +/- 8.5%, respectively). Previous incubation of normal alveolar macrophages with serum or BAL fluid from ALC patients or with normal serum or normal BAL fluid did not result in a significant decrease in antibacterial activity of normal alveolar macrophages. To distinguish ingested bacteria from adherent extracellular bacteria, cells that had been incubated with bacteria for 90 min were then incubated with lysostaphin (1 microgram/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Production of tumor necrosis factor-alpha and interleukin-6 by human alveolar macrophages exposed in vitro to coal mine dust.

Following our previous demonstration of cytokine secretion by alveolar macrophages (AM) from coal miners and from patients with coal workers' pneumoconiosis, we investigated the effect of in vitro exposure to coal dust and to its silica content on tumor necrosis factor-alpha (TNF), interleukin (IL)-1 beta, and IL-6 production by normal human AM. TNF and IL-1 beta concentrations were estimated by a specific radioimmunoassay, while IL-6 levels were evaluated by the proliferation of 7TD1 cells. After 24-h culture, coal dust triggered a significant release of TNF and IL-6 at the dose of 0.1 mg/ml and more obviously at 1 mg/ml in comparison with titanium dioxide (TiO2), used as a biologically inert control dust (with 1 mg/ml of dust: 3,526 +/- 3,509 versus 330 +/- 138 pg TNF/ml and 224 +/- 74 versus 72 +/- 34 U IL-6/ml, respectively; P less than 0.01 in both cases). After 3-h culture, a significant TNF secretion as well as an increased TNF mRNA expression were also detected for AM stimulated by coal dust at variance with TiO2. In contrast, no modification of IL-1 beta concentration could be evidenced in AM exposed to coal dust, although we detected an increased expression of specific mRNA expression. In order to define the role of silica among the main components of coal dust in AM activation, we evaluated the effect of silica (alpha-quartz, 30 micrograms/ml, which is the concentration and the type of silica present in our coal dust) alone or mixed with TiO2 (1 mg/ml) on monokine production.(ABSTRACT TRUNCATED AT 250 WORDS)

Cells, Cultured↗
PubMed1991

Oxidative inactivation of alpha 1-proteinase inhibitor by alveolar macrophages from healthy smokers requires the presence of myeloperoxidase.

The aim of this work was to study the ability of human alveolar macrophages (AM) of 10 healthy smokers to inactivate alpha 1-proteinase inhibitor (alpha 1PI). Purified alpha 1PI was incubated for 45 min, with human alveolar macrophages before and after stimulation by phorbol myristate acetate (PMA) or opsonized zymosan. As a positive control, the same experiments were performed in parallel with blood human neutrophils (PMN). Results are expressed as percentage of inactivation of alpha 1PI as evaluated from its inhibitory activity against porcine pancreatic elastase. A strong correlation (r = 0.99) was shown when inhibitory activity of alpha 1PI was evaluated against porcine pancreatic elastase or human neutrophil elastase. Unstimulated AM (1.57 +/- 0.9%) as well as stimulated AM (PMA: 1 +/- 0.4%; zymosan: 3 +/- 0.6%) were unable to inactivate alpha 1PI. Gel electrophoresis of alpha 1PI demonstrated that AM before or after stimulation induced a slight proteolysis of alpha 1PI, whereas both cleaved and complexed alpha 1PI were found when alpha 1PI was incubated with activated PMN. Both unstimulated (22 +/- 2.6%) and activated PMN (PMA: 91.7 +/- 4.7%; zymosan: 90 +/- 5.5%) were responsible for a significant inactivation of alpha 1PI. Catalase, in contrast to superoxide dismutase, was responsible for a near complete protection of alpha 1PI inactivation by PMN. To better determine the role of PMN secretory products, especially myeloperoxidase (MPO), we also investigated the effect of zymosan-activated PMN supernatants or of purified MPO on the alpha 1PI-AM reaction. MPO assay in PMN supernatants demonstrated that activated neutrophils released significant amounts of MPO (16.8 +/- 4.1 U/ml), whereas MPO was undetectable in activated AM supernatants.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Metastatic prostatic adenocarcinoma-diagnosed by bronchoalveolar lavage and tumour marker determination.

We report a patient who presented with a diffuse interstitial lung disease in whom clinical and radiologic investigation led to the suspicion of lymphangitis carcinomatosa. Bronchoalveolar lavage (BAL) was performed and revealed the presence of prostatic specific antigen (PSA) positive cells. A prostatic needle aspiration confirmed the diagnosis of adenocarcinoma. This case demonstrates the value of tumour marker determination in BAL.

Adenocarcinoma↗