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Biomedical subjects

P Clementsen

Publications and source records attributed to P Clementsen.

At least 37 records · Page 2Linked to original sources
PubMed1992

Increased myelosuppression during cytostatic treatment and pleural effusion in patients with small cell lung cancer.

30 patients with small cell lung cancer (SCLC) and malignant pleural effusion were compared with 30 matched patients with SCLC but without pleural effusion. In the 30 with pleural effusion, white blood cell and platelet counts fell significantly after initial chemotherapy, necessitating dose reduction. Of the patients with pleural effusion, 16 developed severe (WHO grade IV) leukopenia, 7 had severe thrombocytopenia, and 2 patients died of infection. Accordingly, exhaustive aspiration of radiologically verified pleural effusion before starting chemotherapy in patients with SCLC is recommended.

Adult↗
PubMed1991

Bacteria-induced histamine release from human bronchoalveolar cells and blood leukocytes.

Histamine release induced by Staphylococcus aureus was examined in cells obtained by bronchoalveolar lavage (BAL) in non-atopic individuals. Approximately half of the individuals responded with mediator release to the bacterium, and the release was found to be time- and concentration dependent. No difference was found between the patients who responded and those who did not respond in regard to age, sex, smoker/non-smoker, % recovery of BAL-fluid, total cell count, differential cell counts, histamine content per mast cell, or diagnoses. Also stimulation of the BAL-cells with the calcium-ionophore A23187 resulted in histamine release. S. aureus-induced histamine release from basophils was examined in leukocyte suspensions obtained from the same individuals, and in all experiments release was found. The dose-response curves were similar to those obtained with BAL cells. The bacteria-induced mediator release from superficially lying cells in the airways epithelium might be of importance for the precipitation or exacerbation of bronchial asthma in respiratory tract infections.

Adult↗
PubMed1991

Virus, bacteria and lipopolysaccharide increase basophil cell response to histamine releasing stimulators and calcium. Examination of allergic and normal individuals.

Histamine release from human basophil leukocytes from allergic patients or controls was induced by specific antigens, anti-IgE or calcium ionophore A23187. Influenza A virus, S. aureus and lipopolysaccharide from S. typhimurium increased the maximum release of histamine and caused a shift to the left of the dose-response curves showing increased cell sensitivity and lowering of the threshold to these stimuli. The mechanism of action was elucidated by examining the mediator release as a function of increasing extracellular concentration of calcium. In these experiments the dose-response curves were changed by the microorganisms and lipopolysaccharide as before. This indicates that the microorganisms and lipopolysaccharide change the basophil cell response to IgE-dependent and non-immunological stimuli by causing a change in the subcellular handling of calcium.

Adult↗
PubMed1990

Carbohydrates inhibit the potentiating effect of bacteria, endotoxin and virus on basophil histamine release.

Histamine release caused by calcium ionophore A23187 and anti-IgE was examined in leukocyte suspensions from 8 healthy individuals. Staphylococcus aureus, lipopolysaccharide (LPS) from Salmonella typhimurium and influenza A virus were found to enhance the histamine release but did not release histamine per se. The potentiation of mediator release depends on a non-transient signal since the potentiating effect was also obtained by preincubation of the cells with LPS followed by wash-out and stimulation of the cells with anti-IgE. The potentiation was abolished or reduced by galactose, N-acetyl-glucosamine, alpha-methyl-D-glucoside, alpha-methyl-D-mannoside, N-acetylneuraminic acid and lactose, but not by glucose. These findings indicate that the enhancement of mediator release by bacteria, endotoxin, and virus depends on a sugar-mediated reaction.

Basophils↗
PubMed1990

Haemophilus influenzae potentiates basophil histamine release possibly by its endotoxins.

Haemophilus influenzae and its extracellular products (EP) did not release histamine in leukocyte suspensions from normal individuals. However, the EP were found to enhance basophil histamine release triggered by anti-IgE and by the calcium ionophore A23187. Experiments with EP indicate that it is the content of endotoxins which is responsible for the potentiating effect. Removal of endotoxin from the EP thus completely abolished the potentiating effect, whereas inactivation of its protease and proteins by heat-treatment or by proteinase K did not change the potentiation. A reinforcement of mediator release by the extracellular products of H. influenzae might play a pathophysiological role in chronic obstructive pulmonary disease.

Basophils↗
PubMed1990

Virus enhances IgE- and non-IgE-dependent histamine release induced by bacteria and other stimulators.

Histamine release from human basophil leukocytes was triggered by Staph. aureus, Salmonella enteritidis, non-haemolytic streptococci, or E. coli. Influenza A virus was found to enhance the mediator release and the effect was caused by synergism, since the virus did not induce release of histamine per se. This potentiating effect of the virus was seen both when the bacteria-induced histamine release was IgE-dependent (i.e. patient sensitized to the bacterium) and when the bacterium caused mediator release by a non-immunological mechanism independent of IgE (putative sugar-lectin mediated). Histamine release induced by anti-IgE and calcium ionophore or agarose-beads was also enhanced in the presence of the virus. These findings indicate that influenza A virus potentiates both IgE- and non-IgE-mediated histamine release induced by bacteria and other stimulators.

Bacterial Infections↗
PubMed1990

Endotoxin from Haemophilus influenzae enhances IgE-mediated and non-immunological histamine release.

Haemophilus influenza and its extracellular products (EP) did not release histamine from basophil leukocytes in cell suspensions from normal individuals, patients with chronic bronchitis or patients allergic to either house dust mite, grass pollen, cat dander or to their own bacteria. However, the EP was found to enhance their basophil histamine release. IgE-mediated histamine release was examined by stimulation of the cells with anti-IgE or the specific allergens, and non-immunological histamine release by stimulating the cells with the calcium ionophore A23187 or Staphylococcus aureus. In all the experiments EP caused a significant increase in the histamine release. When H. influenzae endotoxins were removed from the EP, the potentiating effect of EP was completely abolished, whereas heating (80 degrees C, 30 min) or treatment of EP with proteinase did not influence the potentiating effect. These results indicate that H. influenzae endotoxin potentiates histamine release caused by IgE-mediated reactions or by non-immunological mechanisms.

Adult↗
PubMed1990

Bacteria and endotoxin enhance basophil histamine release and potentiation is abolished by carbohydrates.

Histamine release caused by anti-IgE, specific antigens and calcium ionophore A23187 was examined in leukocyte suspensions from healthy individuals and patients allergic to house dust mite and birch pollen. Staphylococcus aureus and LPS from Salmonella typhimurium were found to cause a synergistic enhancement of the release. The potentiation of mediator release by the bacteria and the endotoxin depends on a binding to the basophilocyte, followed by a non-transient event, since the potentiating effect persists after preincubation of the cells with the LPS followed by washout and leaving the cells for 30 min at 37 degrees C before stimulation with anti-IgE. The potentiation was abolished or reduced by galactose (10(-7) and 10(-6) M) and N-acetylglucosamine (10(-6) and 10(-5) M), acting by a binding to the basophil cell membrane, demonstrated by the persistence of effect after preincubation and washout of unbound sugar.

Adult↗
PubMed1990

Influenza A virus potentiates bacteria-induced histamine release. Examination of normal individuals and patients allergic to bacteria.

Influenza A virus was found to enhance basophil histamine release induced by Escherichia coli, Salmonella enteritidis, Staphylococcus aureus, Streptococcus pneumoniae and Streptococcus sanguis, but did not per se release histamine. This potentiating effect of the virus was seen both when the bacteria-induced mediator release was IgE-dependent (i.e. patient allergic to bacterium) and when the bacterium caused histamine release by a non-immunological mechanism independent of IgE (putative sugar-lectin mediated). Also histamine release induced by other immunological and non-immunological stimuli, such as anti-IgE, calcium ionophore or agarose beads was enhanced in the presence of the virus. The potentiating effect of the virus on bacteria-induced mediator release might be of importance for the conversion from latent to manifest asthma in upper respiratory tract infections.

Adult↗
PubMed1990

Influenza A virus enhances basophil histamine release and the enhancement is abolished by carbohydrates.

Basophil histamine release was studied in leukocyte suspensions from normal individuals and from patients allergic to house dust mite or birch pollen. Mediator release caused by IgE-mediated reactions was examined by stimulating the cells with anti-IgE or specific antigens, and the calcium ionophore A23187 was used for a non-immunological histamine release. In all experiments influenza A virus caused a synergic enhancement of the mediator release and the potentiation was abolished by galactose (10(-7) to 10(-6) M) and by 10(-6) to 10(-5) M of N-acetylglucosamine, alpha-methyl-D-glucoside, alpha-methyl-D-mannoside, N-acetylneuraminic acid and lactose, but not by glucose. Wash-out experiments show that the sugars prevent the aggravation of mediator release by a binding of sugar to the basophil cell membrane, thereby causing a blockade of binding sites responsible for the potentiating effect of virus.

Adult↗
PubMed1990

PEEP-masks in patients with severe obstructive pulmonary disease: a negative report.

Positive pressure during expiration by face masks applied by the patient has gained wide acceptance in the treatment of chronic bronchitis, but the efficacy is still unproven. The effect of 6 months of treatment with PEEP-masks (positive end-expiratory pressure) was therefore studied in 47 patients with severe irreversible obstructive pulmonary disease (forced expiratory volume in one second (FEV1) about 1 l), and mucus hypersecretion. Patients were double-blindly randomized to at least 45 min daily treatment with PEEP-masks with either 10 or 0 cm water pressure. After 6 months of treatment, no statistical difference was found between the two groups in change of median values (month 6 - month 0) of FEV1, forced vital capacity (FVC), arterial oxygen tension (PaO2), amount of sputum or dyspnoea. Median values of arterial carbon dioxide tension (PaCO2) decreased significantly (0.03 kPa) in the placebo group. Cough intensity and dyspnoea during walking on staircases improved significantly in the placebo group. No difference among groups was found in number of days bedridden, hospitalized, number of exacerbations or antibiotic consumption. We conclude, that the use of PEEP-masks in these patients is without clinical documentation and cannot be recommended.

Adult↗
PubMed1989

Influenza A virus enhances IgE-mediated histamine release from human basophil leukocytes. Examination of the effect of viral neuraminidase and haemagglutinin.

Histamine release caused by anti-IgE was examined in leukocyte suspensions from 10 healthy individuals. Influenza A virus was found to enhance the histamine release but did not release histamine per se. When monoclonal antibodies directed against the viral neuraminidase were included in the samples, the potentiating effect of the virus was completely abolished. The same occurred using a neuraminidase inhibitor. However, monoclonal antibodies directed against the viral haemagglutinin also abolished the potentiation. A binding of virus to the basophil cell surface by haemagglutinin therefore seems to be necessary for the viral neuraminidase to cause potentiation of mediator release.

Antibodies, Anti-Idiotypic↗
PubMed1989

Staphylococcus aureus and influenza A virus stimulate human bronchoalveolar cells to release histamine and leukotrienes.

Mediator release was examined from superficially lying cells in the airway epithelium obtained by bronchoalveolar lavage (BAL) in 13 non-atopic individuals. The BAL-cells were incubated (20 min, 37 degrees C) with Staphylococcus (Staph.) aureus or with human influenza A virus Staph. aureus was found to release histamine from cells from 7 of the 13 individuals and influenza A virus in 3 of 5 persons. Furthermore, Staph, aureus stimulated the BAL-cells to release leukotriene B4 in 7 of 11 subjects, whereas no release was found by influenza A virus in 7 examined persons. When cells from 4 persons were stimulated with Staph. aureus no release of leukotriene C4 was found. The mediator release caused by bacteria and virus might be of importance for the exacerbation of bronchial asthma in upper respiratory tract infections, since histamine is assumed to increase the epithelial permeability with entrance of allergens and other insulting particles, and leukotriene B4 facilitates airway inflammation.

Adult↗
PubMed1989

Bartter's syndrome--treatment with potassium, spironolactone and ACE-inhibitor.

The treatment of Bartter's syndrome is fraught with difficulties, and there is no consensus concerning the pathogenetic mechanisms involved. Potassium depletion with hypokaliaemia is a dominant feature of the syndrome. In this case history, a 42-year-old woman suffering from Bartter's syndrome did not improve on several therapeutic trials. An impressive progress was noted, however, after intensive potassium repletion with subsequent potassium/spironolactone/ACE-inhibitor treatment. After 24 months her condition was unchanged with normal and stable Se-potassium concentration.

Adult↗