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H Matthys

Publications and source records attributed to H Matthys.

At least 73 records · Page 4Linked to original sources
PubMed1996

"Open-word" questions: an effective tool in gauging education of patients with COPD.

For evaluation of the success of patient education in patients suffering from chronic obstructive pulmonary disease (COPD), multiple-choice tests are commonly used. Using these tests, however, only passive knowledge can be examined. We attempted to evaluate, with the help of "open-word" questions and keywords, as used in examinations of students of arts, the active knowledge achieved by 12 patients who had been participants in one of our indepth courses of patient education. The results of this "open-word" test were compared with the results of multiple-choice tests with 91 participants. The average results of the "open-word" tests, with 36% correct answers, were remarkably worse than those of the multiple-choice tests with 80% correct answers. In our opinion, this allows the conclusion that the active knowledge attained in the patient-education courses is clearly lower than the passive knowledge achieved, and that, on the other hand, multiple-choice tests cannot be considered as the exclusive method to evaluate the success of patient education because their questions may quite often prove to be too easy.

Female↗
PubMed1996

Inflammatory determinants of asthma severity: mediator and cellular changes in bronchoalveolar lavage fluid of patients with severe asthma.

Cellular and mediator profiles in bronchoalveolar lavage have not been compared systematically between patients with asthma of different severities, mainly because the patients with more severe asthma have an increased need for antiinflammatory medication. Information is limited to comparisons of allergic and intrinsic asthma, which can be distinguished clinically. When patients from these two groups with similar degrees of bronchial hyperresponsiveness were compared, both groups showed increased numbers of activated T-helper lymphocytes; those in the allergic group expressed the IL-2 receptor (CD25+), whereas in patients with intrinsic asthma there was also an increased number of T-suppressor cells with the activation markers CD25, class II histocompatibility antigen, and very late activation antigen-I, as well as T-helper cells class II histocompatibility antigen and very late activation antigen-I. This pattern is compatible with a more chronic T-cell activation in patients with intrinsic asthma. In patients with allergic asthma the cytokine pattern is compatible with a pure TH2 response (elevated IL-4 and IL-5); however, intrinsic asthma is characterized by elevated IL-5 and IL-2 but not IL-4. Our own findings show similar concentrations of IL-1, IL-8, and granulocyte-macrophage colony-stimulating factor in bronchoalveolar lavage fluid of patients with allergic and intrinsic asthma, whereas IL-6 and interferon-gamma tended to be higher in patients with intrinsic asthma. There are probably fundamental differences in the pathogenesis of allergic and intrinsic asthma. These findings suggest that asthma does not depend on the presence of IgE or IL-4, although both may contribute to the pathogenesis of atopic asthma. The only common pathway in the different presentations of asthma that has been related to clinical symptoms appears to be IL-5-mediated activation of eosinophils; therapies aimed at this mechanism may be promising.

Asthma↗
PubMed1995

[Pulmonary emphysema--lung transplantation].

The most frequent form of lung emphysema leading to respiratory failure is the tobacco bronchitis-induced type of emphysema the so called chronic obstructive pulmonary (lung) disease (COPD). Histologically the centrilobular or centriacinar emphysema is believed to develop due to elastase and oxidant overload with concomitant antiprotease deficiency. The alpha1-antitrypsin deficiency is a rare genetic defect leading also in non-smoking patients to early death due to panlobular or panacinar emphysema. The functional pattern of both emphysema types shows irreversible lung overinflation with severe mainly expiratory bronchial obstruction with various degrees of pulmonary hypertension alpha1-proteinaseNinhibitor deficiency emphysema is prophylactically treated with prolastine and if hypoxia (PaO2 > 55 mm/Hg) is present with long term oxygen therapy. If hypercapnia develops O2 Therapy is combined with non invasive pressure supported ventilation. Volume reducing surgery may precede. In nonsmoking emphysema patients long term oxygen therapy and later unilateral lung transplantation improves quality of life as well as life expectancy.

Adult↗
PubMed1995

[Immunopathogenesis of allergic bronchial asthma. Detection of activated CD25-CD4 lymphocytes and release of cytokines in the bronchoalveolar space following segmental allergen challenge].

The aim of this study was to investigate the fundamental processes underlying the inflammatory response to allergen in mild non-symptomatic asthmatics, using a new model entailing endobronchial segmental provocation. Ten asymptomatic asthmatic volunteers (8 male, 2 female; mean age 28.2 [24-41] years) were challenged employing the segmental allergen provocation technique. 250 PNU in 5 ml 0.9% NaCl solution of either birch (n = 8) or grass (n = 2) pollen were instilled into one segment. As control, only the solvent was instilled into a segment of the contralateral lung. Bronchoalveolar lavage (BAL) with 100 ml prewarmed saline was performed 10 min and 18 h after allergen provocation. The cellular distribution and activation state in BAL fluid and peripheral blood was analysed by immunofluorescence and flow cytometry. The concentration of various cytokines was determined in the BAL fluid using ELISA and bioassays. In blood, segmental allergen provocation led to an increase both in numbers of neutrophils (3833 cells/microliters vs 6830 cells/microliters; P < 0.005) and activated IL-2R expressing (CD25+) CD4+ T cells (3.6% vs 4.8% of all CD4+ lymphocytes; P < 0.05). No change was observed in eosinophils and other leukocytes and lymphocyte subsets. In contrast, a significant 30-fold increase in eosinophils (0.39 x 10(6) vs 11.5 x 10(6) cells/100 ml; P < 0.01) and a twofold increase in CD25+ CD4+ T cells (P < 0.05) were found in BAL samples 18 h after segmental allergen challenge, when compared to the control segment. Analysis of the cytokine profile revealed significantly increased levels of several cytokines. Allergen challenge of extrinsic asthmatic subjects causes differentiation of activated CD25+ CD4+ lymphocytes which may contribute to the pathogenesis of the asthmatic inflammation through the release of various cytokines.

Adult↗
PubMed1995

Immunocytochemical characterization of malignant mesothelioma and carcinoma metastatic to the pleura: IOB3--a new tumor marker.

We have tried to find a reliable panel of markers that would allow distinction between mesotheliomas and carcinomas metastatic to the pleura. In a prospective study, we evaluated 54 pleural effusions: In 27 of the patients, a diagnosis of histologically proven metastatic carcinoma was subsequently established, 7 patients had biopsy-proven malignant mesotheliomas and 20 had benign, reactive effusions whose benign etiologies were established by more than 2 years clinical follow-up. The MAb (monoclonal antibody) IOB3 proved to be diagnostic for carcinomas in all 27 cases (100%), whereas CEA (carcinoembryonic antigen) expression was found in only 22 out of 27 (81%). None of the malignant mesotheliomas, nor benign reactive mesothelial cells reacted with these two markers. All carcinomas, as well as one malignant mesothelioma, reacted with the MAb HEA125. Antibodies against 12 single cytokeratins, vimentin, and EMA (epithelial membrane antigen) were not helpful in the differentiation between malignant mesotheliomas and malignant carcinomatous pleural effusions. We conclude that adding the antibody IOB3 to the CEA assay should allow a reliable differentiation between these two entities.

Adult↗
PubMed1995

T cells and cytokines in bronchoalveolar lavage fluid after segmental allergen provocation in atopic asthma.

Increasing evidence suggests a role for activated T cells and cytokines in the regulation of eosinophilic inflammation in asthma. In this study, we investigated the distribution of leukocytes, lymphocytes, their activation state, and the cytokine profile in BAL from 10 atopic asthmatics with positive skin prick tests and elevated specific IgE levels to birch or grass pollen. Using segmental allergen challenge, 250 PNU of the appropriate allergen or saline were instilled into different segments, which were lavaged 10 min (10 min) and 18 h (18 h) after allergen challenge or 18 h after saline challenge (C). In peripheral blood the number of neutrophils and activated IL-2R+/CD4+ T cells increased significantly 18 h after allergen provocation; there was no change in eosinophils, other leukocytes, or lymphocyte subsets. In contrast, numbers of eosinophils, neutrophils, and IL-2R+/CD4+ T cells increased significantly in BAL samples at 18 h. The numbers of neutrophils and eosinophils were not significantly different in the lavage performed at 10 min and at C. Analysis of cytokines in concentrated BAL fluid revealed significantly increased levels of IL-5, IL-2, IL-1, TNF-alpha, IL-6, IL-8, and GM-CSF, but not of IL-4 and IFN-gamma at 18 h compared with those at C and at 10 min. The correlation between IL-5 levels, eosinophil numbers, and activated T cells supports a role for T-cell-derived IL-5 in causing tissue eosinophilia in allergic asthma.

Adult↗
PubMed1995

[Nasal BiPAP (bilevel positive airway pressure) respiration with controlled respiratory mode in neuromuscular diseases and severe kyphoscoliosis].

The BiPAP-System is a useful ventilatory support for patients with severe sleep apnea and need for high inspiratory pressure. Using the BiPAP as a full ventilatory support is new due to the recent addition of a timed control modus and individual control of inspiratory time. We used the new BiPAP ST-System in one young men with Duchenne-disease, one man with heredo ataxia (Friedreich), one women with spinal muscular atrophy, one man with central sleep apnea due to brainstem infarction as well as two women and one men with severe kyphoscoliosis. All patients had a significant hypoventilation and hypoxemia at night, which was documented by polysomnography. Mechanical ventilation at night with nasal BiPAP increased the baseline oxygen saturation (SaO2) by an average of 11.9% in all seven patients. The frequency of desaturations below 90% diminished by an average of 81%. The lowest SaO2 measured increased by 28% in all seven patients combined. Rhinitis due to the dryness of the inspired air were noticed in only two patients. Two other patients needed adaptation to the customized mask. The nasal BiPAP-System using the T-mode is a useful device to support ventilation at night and thus it could replace ventilatory support by the IPPV-mode in many patients.

Adult↗
PubMed1995

Lectin binding sites and immunocytochemical characterization of normal pleural mesothelium.

20 specimens of normal pleural mesothelium were investigated with six lectins using isolated cells and tissue specimens as well as two different fixation techniques (glutaraldehyde and formaldehyde) and 10 monoclonal antibodies (MAb) on cytologic preparations only. Lectin binding sites for ConA, WGA, and PNA were present in all cases, whereas binding sites for the lectins HPA, SBA, and UEA-I could never be found. There was no staining difference with the two preparation and fixation techniques proving that they may be used to compare directly histologic and cytologic studies. Ten of fourteen histologic specimens were positive for the blood group antigen Lewis(y), three of them were positive for the antigen Lewis(b), all fourteen specimens were negative for Lewis(a) and Lewis(x). In all cases, mesothelial cells expressed ICAM1 and pancytokeratin. The antibodies against EMA, CEA, CD24, CD15, CD20, CD5, and HEA125 showed no reaction in mesothelial cells. Because HPA, UEA-I, SBA as well as CEA and HEA125 react in a high percentage with adenocarcinomas, non reactive cells of pleural effusions negative with these markers may be confidentially considered to be mesothelial in origin.

ABO Blood-Group System↗
PubMed1994

Cellular and immunological markers of allergic and intrinsic bronchial asthma.

Based on a growing body of evidence, allergic as well as intrinsic bronchial asthma have recently been defined as chronic persistent inflammatory disorders. Agreement has been reached that asthma can no longer be equated with bronchospasm only, and that the absence of reversibility of airflow obstruction does not exclude bronchial asthma. Bronchial hyperreactivity, on the other hand, although common to the vast majority of asthmatics, is not specific for bronchial asthma and provocation tests to measure bronchial hyperreactivity are not suited for routine monitoring of bronchial asthma. The clinical features of asthma are related to cellular as well as to soluble parameters of bronchial inflammation. Therefore, means of assessing and monitoring asthmatic inflammation have been investigated. Since eosinophils, T lymphocytes, mast cells, macrophages, neutrophils, epithelial cells, and structural cells, as well as various proinflammatory mediators and proteins, have been implicated in the pathogenesis of bronchial asthma, it has been anticipated that several of these cells or mediators might be either diagnostic of bronchial asthma or could serve as markers to monitor the underlying bronchial inflammation. Currently there is no diagnostic marker of bronchial asthma, which, on its own, either confirms or excludes bronchial asthma with appropriate sensitivity and specificity. Clinically the most reliable feature of bronchial asthma that seems to be related closely to the symptomatology still is the presence of eosinophils in peripheral blood, and especially in sputum. Eosinophil-derived products, particularly eosinophil granule proteins, have been investigated as markers of eosinophil participation in the pathogenesis of asthma and, comparable to eosinophil numbers themselves, are possible predictors of impending exacerbations of allergic, as well as intrinsic bronchial asthma. However, clinically their precise value in diagnosing and monitoring of bronchial asthma has not been documented convincingly and requires further investigation. Increasing data suggest that the regulation of eosinophilia is largely conveyed by interleukin-5 (IL-5) released from activated T-helper lymphocytes and possibly other cells. Therefore, T-lymphocyte activation, and especially assessment of systemic and local IL-5 levels, might be of diagnostic value and possibly useful in monitoring of inflammation in bronchial asthma in the future. A possible role and future applications for other markers of inflammation not related to eosinophils in monitoring or diagnosing bronchial asthma need to be established.

Adult↗
PubMed1994

Pulmonary function, activated T cells, peripheral blood eosinophilia, and serum activity for eosinophil survival in vitro: a longitudinal study in bronchial asthma.

A close correlation among the number of activated, peripheral blood T helper cells, eosinophilia, and airflow obstruction has been reported in patients with asthma. To test these cross-sectional data we performed a prospective, longitudinal study investigating the relationships among T-cell activation in peripheral blood, eosinophilia, forced expiratory volume in 1 second (FEV1), and serum activity toward eosinophil survival in 20 individuals with asthma over a period of 21 days after admission to a clinic located 1560 m above sea level. During the study, maintenance treatment with inhaled beta 2-agonists and theophylline was unchanged. Five patients had also been taking inhaled corticosteroids, and this was also not changed during the study period. According to the changes in pulmonary function observed at the end of the study, patients were divided into three groups: twelve patients whose pulmonary function improved by more than 10% from baseline (group I), four patients whose pulmonary function deteriorated by more than 10% from baseline necessitating therapeutic intervention (group II), and four patients with no change in FEV1 (< 10% from baseline) (group III). Activation of T cells as determined by interleukin-2 receptor expression, number of eosinophils, and serum activity toward eosinophil survival in vitro declined in group I; whereas FEV1 increased. The decrease in FEV1 in group II was associated with an increase in interleukin-2 receptor-positive T cells, number of eosinophils, and serum activity. In group III FEV1, interleukin-2 receptor expression on T cells, the number of peripheral blood eosinophils, and the measured serum activity for eosinophil survival in vitro did not change significantly from baseline.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Theophylline vs. budesonide in the treatment of mild-to-moderate bronchial asthma.

Eight patients with mild extrinsic asthma participated in a double-blind randomized intraindividual cross-over study involving 6 weeks' treatment with twice daily oral theophylline (2 x 1 capsules = 800 mg/day Cronasma 400) and 6 weeks' treatment with twice daily inhaled budesonide (2 x 2 puffs = 0.8 mg/day Pulmicort) with nebuhaler administered in the morning and in the evening before eating. Lung function and carbachol provocation measured with the whole-body box method were performed at the beginning and after 6 weeks of treatment. Mucociliary clearance (MC) assessed with a scintillation camera and bronchoalveolar lavage (BAL) were both performed after 6 weeks of treatment. All patients documented daily peak flows in the morning and in the evening. [table: see text] Additional use of beta 2-agonists at night and during the day was not different for theophylline (0.10 +/- 0.39 and 1.16 +/- 2.87 puffs) and budesonide (0.11 +/- 0.45 and 1.97 +/- 3.02 puffs). MC (32 +/- 15% under theophylline and 33 +/- 14% after budesonide), carbachol provocation and lung function data at the end of both treatment periods were the same as well as BAL data. Two patients needed a reduction of the theophylline dose due to nausea. This study documents the equipotency of theophylline (mean blood level 11.9 +/- 4.6 mg/l) and budesonide (2 x 2 puffs = 0.8 mg/day) in patients with mild-to-moderate asthma.

Administration, Inhalation↗
PubMed1994

Modulatory role of protein kinase C on the signal transduction pathway utilized by platelet-activating factor in eosinophil activation.

To determine the role of protein kinase C (PKC) in the signal transduction in eosinophil pathways, we have assessed the effects of the phorbol ester phorbol 12-acetate 13-myristate (PMA) on guinea pig peritoneal eosinophils challenged with platelet-activating factor (PAF). Pretreatment with PMA completely inhibited the PAF-induced release of eosinophil peroxidase (EPO) and superoxide anions and the rise in intracellular Ca2+ concentration ([Ca2+]i), with IC50s of 2 to 10 nM. This inhibition was reversed when the cells were preincubated with the PKC inhibitor staurosporine for 5 min before the addition of PMA. Staurosporine also inhibited PAF-induced EPO release but not the rise in [Ca2+]i. The inactive ester 4 alpha-phorbol 12,13-didecanoate had no inhibitory effect on eosinophil activation. Finally, PMA inhibited the binding of the PAF antagonist [3H]WEB 2086 to intact eosinophils. Taken together, these data suggest that PKC may have a physiologic role in regulating PAF-induced eosinophil responses through expression of PAF receptors on the cell surface.

Alkaloids↗