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Biomedical subjects

H Magnussen

Publications and source records attributed to H Magnussen.

At least 145 records · Page 8Linked to original sources
PubMed1997

[Do patients with obstructive sleep apnea syndrome treated with nCPAP therapy lose weight?].

A simple therapy for obstructive sleep apnoea syndrome is weight reduction, which we always recommend before initiating and maintaining nCPAP-therapy. We documented the body weight of 123 patients (9 women, 114 men; age 53.8 +/- 10 years, initial apnoea-hypopnoea-index 40.7 +/- 22.6/hour) before and after 582 +/- 391 days nCPAP-therapy. Absolute and relative (Broca Index: weight [kg]/[height [cm] -100] x 100) body weight was 97.8 +/- 19.4 kg resp. 128.3 +/- 24.3 units before and 97.3 +/- 18.2 kg resp. 127.8 +/- 23.5 units during therapy (not significant). Body weight changes ranged from +22 to -26 kg. Only a subgroup of patients with a Broca index between 100-119 exhibited a significant weight change from 86.8 +/- 10.4 to 88.5 +/- 10.4 kg. We conclude that our recommendations to lose weight were unsuccessful in patients with obstructive sleep apnoea, although nCPAP-therapy generally improved well-being.

Adult↗
PubMed1997

[Extent of variations in minimal CPAP pressure requirements during a single night].

The frequency of apnoeic events during sleep depends on posture and sleep stage. This is due to a change of upper airway size and upper airway closing pressures during different postures and sleep stages. The extent of the change of the necessary "splinting" pressure during nasal CPAP therapy for obstructive sleep apnoea is unknown. We titrated during CPAP therapy the minimal effective pressure, depending on sleep stage and posture. The necessary pressure fluctuated, depending on the patient, between 3 and 10 mbar. The highest pressure was not solely achieved during supine position and REM; some patients needed higher pressures under other circumstances.

Adult↗
PubMed1996

Reproducibility of airway response to inhaled bradykinin and effect of the neurokinin receptor antagonist FK-224 in asthmatic subjects.

OBJECTIVE: Inhaled neurokinins have been shown to induce bronchoconstriction in asthmatic subjects. We have investigated the effect of a neurokinin receptor antagonist, FK-224, on bradykinin (BK)-induced bronchoconstriction, and have compared its effect with the spontaneous variability of BK responsiveness. METHODS: Thirteen subjects with mild extrinsic bronchial asthma participated in the study. Four BK inhalation challenge tests (Study Days 2 to 5) were performed over a period of several weeks. On Study Days 4 and 5 subjects inhaled either 2 mg FK-224 or placebo 30 min before the BK challenge. RESULTS: The geometric mean PC20FEV1 of BK was 0.04, 0.06, and 0.10 mg.ml-1 on the first and second BK challenge and after placebo. Mean PC20FEV1 after FK-224 was 0.20 mg.ml-1 and was not different from placebo, whereas there was a significant effect in PC15FEV1. The mean shift in PC20FEV1 after FK-224 vs placebo was 1.0 doubling concentrations. The mean changes in BK responsiveness on the second BK challenge and placebo days compared to the first BK challenge were 0.6 and 1.3 doubling concentrations. We observed a significant fall in FEV1 after inhalation of saline plus ethanol, which was the diluent for BK (mean decrease 4.2%). CONCLUSION: The data demonstrate that inhalation of 2 mg FK-224 is only marginally effective against BK-induced bronchoconstriction in mild asthmatic subjects and that its effect is similar to the variability in BK responsiveness assessed over several weeks.

Administration, Inhalation↗
PubMed1996

Eosinophil VLA-4 binding to fibronectin augments bronchial narrowing through 5-lipoxygenase activation.

We examined the effect of ligation of human eosinophils activated by platelet-activating factor (PAF) to soluble human fibronectin (FN) on the augmented contractile response of human bronchial explants. Styrene microplate wells were FN-coated and eosinophils were allowed to adhere in the presence of 1) buffer control, 2) 20 micrograms/ml monoclonal antibody (HP2/1) to the alpha 4 beta 1 ligand (VLA-4) on the eosinophils, 3) 20 micrograms/ml anti-CD18 R15.7, 4) 20 micrograms/ml anti-CD16 3G8, or 5) 10(-6) M A63162, a 5-lipoxygenase inhibitor. Sixty minutes later, treated cells were activated with either buffer or 10(-6) M PAF. Airway luminal diameter was assessed by computerized videomicrometry as a function of pixel number, and activation of eosinophils was confirmed by measurement of leukotriene C4 (LTC4) secretion. Ligation with FN caused an increase in PAF-stimulated LTC4 secretion from 276 +/- 75.6 pg/10(6) cell at baseline to 606 +/- 90.2 pg/10(6) cell (P < 0.01). This corresponded to augmented luminal narrowing of human bronchial explants from 25.3 +/- 9.39% (PAF activation alone) to 42.9 +/- 8.0% (PAF-activated eosinophils + FN) (P < 0.01). Both augmented airway luminal narrowing and increased LTC4 secretion caused by PAF-activated cells after FN ligation were blocked completely by anti-VLA-4 MAb (P < 0.05 vs. control). Pretreatment with 10(-6) MA63162 inhibited completely the PAF-stimulated LTC4 secretion to baseline level ( P < 0.001). Inhibition of 5-lipoxygenase similarly blocked luminal narrowing caused by eosinophils stimulated by PAF by > 95% (P < 0.001). We demonstrate that the binding of human eosinophils to the matrix protein FN causes augmented secretion of LTC4 which, in turn, causes augmented luminal narrowing of explanted human bronchi in vitro. We also demonstrate that the augmented activity is blocked selectively by pretreatment with specific monoclonal antibody against VLA-4 and blockade of eosinophil 5-lipoxygenase inhibits both LTC4 secretion and airway narrowing after PAF-stimulation.

Acetamides↗
PubMed1996

Assessment of mycobacterial DNA in cells and tissues of mycobacterial and sarcoid lesions.

In this study we applied a polymerase chain reaction (PCR) assay for the detection and species-specific identification of mycobacteria to samples from patients with sarcoidosis and mycobacterial infections and from control patients. The PCR-technique is based on the amplification of mycobacterial DNA coding for 16S rRNA, which is present in all mycobacterial species, and on the additional sequencing of the PCR fragment to determine the species. Mycobacterial DNA could be detected in lung tissues and bronchoalveolar lavage cells from cases of tuberculosis and infections with atypical mycobacteria. On the other hand, mycobacterial DNA was amplified only in lung tissue from one patient with sarcoidosis. Twenty-three samples from patients with sarcoidosis were negative for mycobacterial DNA. From our results we conclude that the granulomatous lesions in sarcoidosis may not be due to mycobacterial infections.

Base Sequence↗
PubMed1996

The effect of ozone exposure on allergen responsiveness in subjects with asthma or rhinitis.

The aim of this study was to determine whether ozone enhances bronchial responsiveness to allergens in subjects with allergic asthma, or facilitates a bronchial response in subjects with allergic rhinitis. Twenty-four subjects with mild stable allergic asthma, 12 subjects with allergic rhinitis without asthma, and 10 healthy subjects participated in the study. Subjects breathed 250 ppb ozone or filtered air (FA) for 3 h of intermittent exercise. Airway responsiveness to methacholine was determined 1 h before and after exposures, and allergen responsiveness 3 h after exposures. We determined the concentration of methacholine (PC20FEV1) and the dose of allergen (PD20FEV1) producing a 20% fall in FEV1. In the subjects with asthma, FEV1 decreased by 12.5 +/- 2.2% (mean +/- SEM; p = 0.0001), PC20FEV1 of methacholine by 0.91 +/- 0.19 doubling concentrations (p = 0.0001) and PD20FEV1 of allergen by 1.74 +/- 0.25 doubling doses (p < 0.0001) after ozone compared with FA. The changes in lung function, methacholine, and allergen responsiveness did not correlate with each other. In the subjects with rhinitis, mean FEV1 decreased by 7.8% and 1.3% when ozone or FA, respectively, were followed by allergen inhalation (p = 0.035). Therefore, our data suggest that short-term exposure to ozone can increase bronchial allergen responsiveness in subjects with mild allergic asthma or rhinitis.

Adult↗
PubMed1996

Prevalence of respiratory symptoms, bronchial hyperresponsiveness and atopy among adults: west and east Germany.

The prevalence of respiratory symptoms, atopic sensitization and bronchial hyperresponsiveness was compared in a random sample of adults, 20-44 yrs of age, in two cities in West and East Germany, Hamburg and Erfurt, respectively. There were much higher levels of outdoor air pollution due to sulphur dioxide and suspended particulates in Erfurt, and major differences in living conditions during the last 40 yrs. Within the European Respiratory Health Survey, a short questionnaire was answered by 3,156 (80% response rate) subjects in Hamburg and 3,272 (74%) in Erfurt. A subset of responders to the short questionnaire completed a long questionnaire, spirometry, methacholine or bronchodilator test, skin test, and total and specific immunoglobulin E (IgE) measurements, with a total number of 1,159 participants in Hamburg and 731 in Erfurt. Six out of 8 questions on respiratory symptoms and diagnoses were answered in the affirmative more frequently in Hamburg than in Erfurt. In Hamburg, mean forced expiratory volume in one second (FEV1)% of predicted was 105 vs 107% in Erfurt (p < 0.0001), and bronchial hyperresponsiveness was more frequently observed in Hamburg than in Erfurt (25 vs 19%; p < 0.05). Atopic sensitization was more prevalent in Hamburg than in Erfurt regarding the results of skin tests against grass pollen (24 vs 19%; p < 0.05), birch pollen (19 vs 8%; p < 0.0005), cat (10 vs 2%; p < 0.0005), and Dermatophagoides pteronyssinus (14 vs 10%; p < 0.05). This was reflected by the prevalences of positive specific IgE values, which were higher in Hamburg than in Erfurt for grass (26 vs 20%; p < 0.05), birch (20 vs 10%; p < 0.0005) and cat (12 vs 8%; p < 0.05). In Hamburg, compared to Erfurt, there was: a lower mean number of siblings (p < 0.005); a higher degree of childhood and current exposure to environmental tobacco smoke (p < 0.005); and a higher frequency of fitted carpets and reported mould or mildew inside the house (p < 0.005). Therefore, these data may support the hypothesis that childhood factors and exposure to indoor allergens and irritants may have been more relevant for the development of asthma and atopy than the potential long-term exposure to high concentrations of sulphur dioxide and particulate matter.

Adult↗
PubMed1996

[Oral testing for sulfite asthma].

AIM OF THE STUDY: Patients with asthma may develop bronchoconstriction after ingestion of sulfites. We studied the sensitivity and specificity of an oral provocation challenge with metabisulfite to detect a sulfite-sensitive asthma. METHODS: We performed an oral dose-response metabisulfite challenge in 44 patients with a history of sulfite-sensitive asthma, 27 patients with asthma but without a history of sulfite sensitivity, and 8 control subjects without asthma. Metabisulfite was administered in capsules in a single-blind manner. Airway response was assessed by FEV decline, measured 30' after each dose. RESULTS: Thirty-nine percent of patients with a history of sulfite-sensitive asthma demonstrated a significant bronchoconstriction after ingestion of metabisulfite, whereas patients without an appropriate history and control subjects did not respond to the challenge. CONCLUSIONS: The oral metabisulfite challenge exhibits a high specificity (100%) but low sensitivity of about 40%. Nonetheless, taking into account the uncertainties in the patients' history of sulfite-sensitive asthma, the oral metabisulfite challenge as performed by us is a useful method for the diagnosis of sulfite sensitive asthma.

Administration, Oral↗
PubMed1996

[Incidence of resistance and risk factors for resistance in Mycobacterium tuberculosis. A retrospective study of 1,055 patients of a specialty hospital 1984 to 1993].

For the past decade, there have been no data on the time course of drug-resistant tuberculosis and on risk factors for drug resistance in former West Germany. We reviewed the medical records of all patients with positive cultures for Mycobacterium tuberculosis from 1984 until 1993 in a hospital near Hamburg. Drug-susceptibility testing was performed for isoniazid, rifampicin, ethambutol, and streptomycin, using the modified proportion method. Of 1,055 patient, 9.6% had isolates resistant to one or more drugs. Of the isolates, 5.8% showed resistance to isoniazid or rifampicin and 1.8% to both isoniazid and rifampicin. There was no significant change of the resistance rate during the study period. Twenty six percent of 89 patients from South America, Africa or Asia had isolates resistant to one or more drugs, compared with 7.6% of 799 patients born in Germany (odds ratio (OR) 4.2; 95% confidence interval (95% CI) 2.5-7.3). Among patients born in Germany, 32% of 101 patients with a history of prior antituberculosis drug therapy had resistant organisms, versus 4.2% of 698 patients without prior therapy (OR 10.7; 95% CI 6.1-18.7). Resistance orates for 35 patients, who had been treated within the last 5 yrs, and for 65 patients, who had been treated more than 5 yrs ago, were 57 and 17%, respectively (OR 6.6; 95% CI 2.9-16.6). Our results suggest that there is no increase in the proportion of drug-resistant tuberculosis in our hospital, and that patients with a recent history of antituberculosis drug therapy and patients from South America, Africa, or Asia are at high risk for drug resistance.

Adult↗
PubMed1996

[Tachyphylaxis of airway response to inhaled bradykinin over several days].

Tachyphylaxis of airway responses has been described for a variety of pharmacological stimuli. A decrease in airway responsiveness to inhaled bradykinin has been reported when challenges were repeated within intervals of 60 minutes. Especially within the framework of drug studies, it is important to know whether tachyphylaxis persist over days. The aim of our study was to assess the occurrence of tachyphylaxis to inhaled bradykinin within several days. Thirteen patients with mild extrinsic bronchial asthma were included into the study. We performed two bradykinin inhalation challenges separated by an interval of three days and determined the provocative concentrations of bradykinin (PC20FEV1) which produced a 20% fall in FEV1. Geometric mean of PC20FEV1 was 0.033 mg/mL in the first and 0.105 mg/mL in the second challenge. These values were significantly different (p < 0.05). Our data demonstrate that tachyphylaxis of the airway response to bradykinin persists over a time period of three days.

Aerosols↗