Biomedical subjects

H Matthys

Publications and source records attributed to H Matthys.

At least 37 records · Page 2Linked to original sources

PubMed1990

[The value of bronchoalveolar lavage in the diagnosis of interstitial lung diseases].

Bronchoalveoläre lavage (BAL) allows microscopic, cytologic and immunocytologic diagnosis of alveolar and interstitial lung disease. The indications for BAL depend on chest X-rays, signs and symptoms and lung function tests, e.g., spirometry or whole-body plethysmography, CO-diffusion capacity and blood gases during exercise. Supporting laboratory parameters are angiotensin converting enzyme, antinuclear antibodies and serum precipitins. Pulmonary parenchymal pathology documented on chest X-rays or by high-resolution computed tomography of the chest allows selective investigation of the involved areas. Different typical patterns with predominantly neutrophils or lymphocytes and their subsets or the presence of malignant cells or Pneumocystis carinii in the BAL fluid allowed the diagnosis in 115 patients. If possible, histological confirmation should be achieved by transbronchial biopsy. When indications are carefully applied and are based on the history as well as the clinical signs and symptoms, BAL is an efficient diagnostic tool in interstitial lung disease, which can be performed in out-patients even if transbronchial biopsy is done.

Alveolitis, Extrinsic Allergic↗

PubMed1990

[Procollagen-III-peptide in bronchoalveolar lavage fluid as an index of fibrosis in sarcoidosis and idiopathic lung fibrosis?].

In order to answer the question whether in sarcoidosis and idiopathic pulmonary fibrosis there is a relationship between the activity of alveolitis (T4/T8 ratio in sarcoidosis, number of granulocytes in idiopathic pulmonary fibrosis) and the activity of connective tissue formation (type III procollagen peptide in the BAL fluid) BAL was performed in 12 healthy subjects, 33 patients with type II sarcoidosis, and 26 patients with idiopathic pulmonary fibrosis. In the unconcentrated BAL fluid of the healthy subjects, P3P was not measurable. On the basis of the T4/T8 ratio and P3P in type II sarcoidosis, three groups of patients with possibly different risks of progression were found: 1) T4/T8 normal and P3P not or only mildly elevated, 2) T4/T8 elevated and P3P normal or only mildly elevated, 3) T4/T8 elevated and P3P greatly increased. In patients with idiopathic pulmonary fibrosis, the concentration of P3P correlated significantly with the number of granulocytes and the clinical activity parameters. On the basis of these results, we conclude that P3P levels in the BAL fluid, as a direct measure of connective tissue neogenesis, may be a valuable addition to cellular and immunocytological BAL findings.

Bronchoalveolar Lavage Fluid↗

PubMed1990

[Discriminatory value of bronchoalveolar lavage parameters in differential diagnosis--exogenous allergic alveolitis, sarcoidosis and patients with healthy lungs].

For this study, the results of 487 BAL investigations involving 126 patients with sarcoidosis, 34 patients with exogenous-allergic alveolitis, 18 subjects with healthy lungs, and 309 patients with other pulmonary disorders, were analysed. The diagnoses had been established independently of the BAL results. After elimination of interdependent variables, the discriminatory usefulness of the BAL parameters: total number of cells, relative percentage of lymphocytes, natural killer cells, and T4/T8 ratio, was analysed with the aid of ROC curves and the Wilcoxon test. The ROC curves permit a rapid overview of the differential significance of the various BAL variables, and identify the relationship between sensitivity and specificity.

Alveolitis, Extrinsic Allergic↗

PubMed1990

[Degranulation of human eosinophilic granulocytes by the platelet activating factor].

Incubation of purified human eosinophil granulocytes (greater than 93%) with the platelet activating factor (PAF), led at concentrations of 1 pM to 10 microM, to a non-cytotoxic and dose-dependent liberation of proteins both from the "small" and the "specific" granules. The mean EC50 for this PAF-induced effect was 1.47 nM (n = 9), with a maximum at 100 nM PAF. The degranulating effect of PAF can be inhibited competitively by the specific PAF-receptor antagonist, WEB 2086 (KB between 12 and 13 nM), and is Ca2(+)-dependent.

Cell Degranulation↗

PubMed1990

[Cytologic and immunocytologic findings in bronchoalveolar lavage as a contribution to the differential diagnosis of chronic lung hemorrhage].

In the present paper, the results of cytological and immunocytological investigations of the broncho-alveolar lavage fluid obtained from 13 patients with pulmonary haemorrhage were studied for their differential-diagnostic usefulness. Five patients each were suffering from idiopathic pulmonary haemosiderosis (IPH) and the Goodpasture syndrome (GPS), one patient had a Wegener's granulomatosis, and two patients presented with vasculitis (VA) which was not amenable to further histological characterization. Parameters that proved particularly suitable for differentiation were the total cell count, the number of haemosiderin-positive macrophages, the extent of the expression of the transferrin receptor (OKT 9) on the macrophages, and the relationship of OKT 4 and OKT 8-positive lymphocytes.

Anti-Glomerular Basement Membrane Disease↗

PubMed1990

[Detection of the activation of alveolar lymphocytes in alveolar proteinosis].

In 7 patients with pulmonary alveolar proteinosis, differential cytology and lymphocyte subsets in BAL fluid were investigated. The study showed that pulmonary alveolar proteinosis is another disorder characterized by a lymphocytic alveolitis and activation of T-lymphocytes (expression of HLA-DR antigens and IL-2 receptors). Our data indicate that immunological mechanisms involving T-cell activation may contribute to be pathogenesis of pulmonary alveolar proteinosis.

Adult↗

PubMed1990

[Surfactant phospholipids in bronchoalveolar lavage fluid in smokers with healthy lungs and non-smokers].

The surfactant phospholipids were determined in the BA1 fluid of 9 smokers and 9 non-smokers with no disease of the lungs. The total phospholipid content was reduced significantly in smokers to 10 +/- 6 nmol/ml as compared with 24 +/- 10 nmol/ml in the non-smokers (p less than 0.02). The composition of major phospholipid fractions (phosphatidyl-choline and phosphatidyl-ethanolamine) did not differ between the two groups. Possible reasons for this reduction of surfactant in smokers are discussed.

Bronchoalveolar Lavage Fluid↗

PubMed1990

[Systemic autoimmune diseases of the lung of unknown etiology].

Explore the source record for details and available documents.

Autoantibodies↗

PubMed1989

[Methodologic study for measuring oronasal airflow using thermistors].

In an attempt to simplify the diagnostic work-up of sleep apnea syndrome, a method has long been sought that would permit the recording of apnea on an ambulatory basis. To this end, we have since developed a face mask and special electronics capable of recording expiration and inspiration via thermistors. We made use of a respirator and a ventilation mannikin in order to simulate respiratory activities in the patient. Since the heat given off during respiration is influenced by a variety of factors, we investigated the following parameters: room temperature (12, 17 and 22 degrees) respiratory rate (15, 18, 21, breaths per minute), maximum airflows (0.5 and 0.6 l/sec) and tidal volume (TV 0.3, 0.5, 0.7 l). Erroneous recording of apneic episodes was observed only with changes from complete mouth to nose breathing; otherwise, the apneic episodes were correctly recognized and counted. TV following an apneic phase must exceed at least TV/2 in order to be recorded as a breath. With a set duration of apnea of more than 30 seconds, apnea is considered to be terminated only by a breath of more than 60% of the last amplitude preceding the apneic phase. Changes in the respiratory rate and maximum airflow, or a change between 12 an 22 degrees within the mask has no effect on the recording of apneic phases. We conclude, therefore, that devices for the automatic detection of apnea should be calibrated by simulated respiratory activities, and specified accordingly.

Humans↗

PubMed1989

[Pulmonary hypertension. Clinical picture and therapy].

Pulmonary hypertension occurs frequently in patients with chronic lung disease and contributes to morbidity and mortality. The most common symptoms are dyspnea, fatigue, chest pain, and syncope; sudden death can occur. Signs of pulmonary hypertension include prominent a-waves in the jugular venous pulse, a prominent P2 and murmur of tricuspid regurgitation. Introduced in 1964, cardiac catheterization is still required for the clinical assessment. Many patients reveal a vasoconstrictive component in their lung vessels that is potentially reversible therapeutically. Accurate noninvasive diagnostic methods and an understanding of the mechanisms causing pulmonary hypertension are necessary, as is appropriate therapy based upon the results.

Humans↗

PubMed1989

[Classification and diagnosis of pulmonary hypertension].

An increase in wedge pressure distinguishes right heart strain due to pulmonary congestion from cor pulmonale with normal pulmonary capillary pressure. Pulmonary hypertension might be due to exogenous hypoxia, obstructive sleep apnea, acute and chronic airway obstruction, diseases of the lung parenchyma, and vascular bed impairment of the thoracopulmonary mechanics, including neurogenic and muscular disorders, cardiac insufficiency of the left heart, and valvular diseases.

Diagnosis, Differential↗

PubMed1989

Is hyperreactivity correlated with the degree of airway inflammation.

10 patients with a history of bronchial asthma showed in the symptom-free interval a clear negative correlation between bronchial hyperreactivity and airway inflammation measured by mc. 10 normal subjects without any history of asthma and no signs of airway inflammation showed unimpaired mc-measurements, and the same degree of hyperreactivity as the symptom-free asthmatics.

Adolescent↗

PubMed1988