Effect of oxolamine on cough sensitivity in COPD patients.
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Aged↗
Biomedical subjects
B B Ceyhan
Publications and source records attributed to B B Ceyhan.
Plasma adrenomedullin levels in asthmatic patients.
Adrenomedullin (ADM) is a newly discovered endogenous vasorelaxing peptide isolated from pheochromocytoma. Some experimental studies suggest that ADM plays a role in asthma. The purposes of the present study were to assess the plasma ADM levels in adults with mild to severe asthma and controls and to correlate those with the findings on lung function test results and other clinical indices. We recruited 16 mild, 10 moderate, and 11 severely asthmatic patients and 12 healthy controls. We measured the plasma concentrations of ADM in patients with asthma and in healthy subjects using RIA. We assessed FEV1, FEV1 predicted %, FEV1/FVC, symptom score, IgE, ECP, and morning and evening peak expiratory flow measurements. There was no significant difference between the asthmatic and the control group ADM levels, which were 26.3 +/- 24.2 pg/mL and 22.9 +/- 17.6 pg/mL, respectively. Furthermore, plasma ADM levels increased as the severity of the disease increased in asthmatic patients (20.7 +/- 14.4 pg/mL in mild, 25.2 +/- 24.3 pg/mL in moderate, and 35.5 +/- 33.6 pg/mL in severe asthmatics), although they did not result in any statistical significance. However, the plasma ADM levels correlated negatively with the FEV1 levels in the asthmatic group (p < 0.02, r = -0.37). Peripheral blood eosinophilia, IgE, and ECP levels did not correlate with plasma ADM levels. These results suggest that the measurement of ADM concentration in plasma will not be of diagnostic use in asthma, but may be a reflection of the severity of asthma.
Adrenomedullin↗
Effect of inhaled low molecular weight heparin on methacholine-induced bronchoconstriction.
OBJECTIVES: Recent studies have shown that inhaled standard heparin exhibits protection towards various bronchoconstrictor stimuli in asthma including methacholine. Low molecular weight heparins (LMWH) (4000-5000 daltons) have higher bioavailability than standard heparins (12,000-16,000 daltons). It is possible that the anti-asthmatic activity of heparin may be molecular weight-dependent. The purpose of the present investigation was to study the effect of LMWH on methacholine-induced bronchoconstriction and to compare the effect of LMWH with that of standard heparin. SUBJECTS: Fifteen subjects (7 male, 8 female, mean age: 33 +/- 13 years, range: 20-65) with mild asthma were studied. METHOD: Methacholine bronchial provocation tests were performed in a single-blind, crossover, randomized order and repeated 45 minutes after placebo or aerosolized standard heparin (1.000 U/kg) or aerosolized LMWH (Enoksaparin, Clexane, 0.8 mg/kg). RESULTS: There was no significant difference in baseline FEV1 values between study days. The standard heparin and enoksaparin inhibited bronchoconstriction induced by methacholine. The geometric mean log PD20 values after placebo, standard heparin, and enoksaparin were 0.24 +/- 0.57 (1.74) mg/ml, 0.79 +/- 0.59 (6.17 mg/ml), 0.76 +/- 0.57 (5.75 mg/ml), respectively (p < 0.0009). Three subjects in standard heparin group and two subjects in enoksaparin group showed increased hyperreactivity, the others showed decreased bronchial hyperreactivity. The degree of protection offered by standard heparin and enoksaparin did not show any statistical difference. CONCLUSIONS: These data suggest that both inhaled LMWH and inhaled standard heparin play inhibitory roles in methacholine-induced bronchoconstriction.
Administration, Inhalation↗
Effect of inhaled cyclosporin on the rat airway: histologic and bronchoalveolar lavage assessment.
Airway inflammation plays a pivotal role in asthma. Over the last 10 years, evidence has accumulated for the potential role of lymphocytes in airway inflammation. Since cyclosporin A (Cyc-A) can profoundly influence lymphocyte activation, it is appropriate to consider this drug as a novel antiasthmatic. The effect of inhalation of low doses of Cyc-A on airway inflammation remains unclear. The purpose of this study was to investigate the bronchoalveolar lavage (BAL), peripheral blood cell profiles, and lung biopsy specimens in Cyc-A-pretreated rats. Twenty-nine rats (8 controls, 10 ovalbumin sensitized, and 11 Cyc-A inhaling and ovalbumin sensitized) were included in the study. A commercial intravenous Cyc-A solution was given as a single dose of 20 mg/kg 1 h prior to inhalation of ovalbumin via nebulizer. The total number of BAL cells significantly increased in rats inhaling Cyc-A when compared with ovalbumin-sensitized rats (2.37 +/- 2.34 x 10(6)/ml and 1.01 +/- 0.49 x 10(6)/ml respectively, p < 0.05). There was a significant increase in the percentage of lymphocytes (14.5 +/- 8.5 versus 27.4 +/- 7.4%, p < 0.03), a nonsignificant increase in the percentage of eosinophils (0.8 +/- 1.0 versus 3.0 +/- 4.6%), and a significant decrease in the percentage of polymorphonuclear leukocytes (9.4 +/- 6.9 versus 3.4 +/- 3.8%, p < 0.01) and macrophages (75.4 +/- 5.1 versus 50.2 +/- 11.8%, p < 0.02) in BAL in the ovalbumin-sensitized group as compared with controls. Differential cell counts revealed a higher percentage of neutrophils and macrophages in the BAL of Cyc-A-pretreated rats than in that of the ovalbumin-sensitized group (26.3 +/- 26.8 versus 3.4 +/- 3.8%, p < 0.01 and 66.1 +/- 7.7 versus 50.2 +/- 11.8%, p < 0.02). There was a nonsignificant decrease of lymphocytes and eosinophils in the Cyc-A-pretreated group when compared with the ovalbumin-sensitized group (27.4 +/- 7.4 versus 21.1 +/- 12.4 and 3.0 +/- 4.6% versus 2.4 +/- 2.6%). The peripheral blood total white blood cell count decreased in the ovalbumin-sensitized and Cyc-A-pretreated groups as compared with the control group (2,520 +/- 1,098/mm3, 3,591 +/- 2,251/mm3, and 5,975 +/- 2,787/mm3, respectively, p < 0.01). In addition, peripheral eosinophilia was detected in the Cyc-A-pretreated group when compared with controls and the ovalbumin-sensitized group (6.9 +/- 4.7, 2.4 +/- 1.1, and 2.6 +/- 2.4%, respectively, p < 0.01). Light-microscopic examination of the airways revealed prominent eosinophilia in tracheal, bronchial, and bronchiolar sections in the ovalbumin-sensitized group: counts were 1.8 +/- 2.3/HPF, 10.3 +/- 11.4/HPF, 63.3 +/- 45.0/HPF, respectively. Cyc-A resulted in a decrease of the eosinophil counts/HPF to 0/HPF in trachea (p < 0.05), to 4.3 +/- 9.4/HPF in bronchi (p < 0.02), to 19.4 +/- 38.4 in bronchioles (p < 0.004). In conclusion, the present study supports the theory that locally administered inhaled low-dose Cyc-A is effective on inflammatory cells of sensitized airways and peripheral cells. It may therefore be useful in elucidating the inflammatory mechanisms involved in asthma.
Administration, Inhalation↗
Effect of inhaled heparin on adenosine-induced bronchial hyperreactivity.
Glycosaminoglycan heparin possesses multiple noncoagulant properties including antiinflammatory actions. We have previously shown that heparin attenuates the methacholine-induced bronchoconstriction in humans. In contrast to methacholine, a stimulus that induces airway constriction mainly by "direct" stimulation of airway smooth muscle cells, adenosine airway responsiveness reflects "indirectly" induced airway narrowing via inflammatory mediators or neural reflex mechanisms. Whether heparin modulates bronchial hyperreactivity induced by adenosine, is not well known. We investigated the effect of inhaled heparin on adenosine-induced bronchoconstriction and compared the inhibitory role of heparin on the adenosine challenge test with that on the methacholine challenge test. Fifteen subjects (7 males, 8 females) with mild asthma were included in the study. Bronchial provocation tests were performed in a single-blind, crossover, randomized order, and repeated 45 minutes after placebo or aerosolized heparin inhalation (1,000 U/kg). The heparin increased the geometric mean log methacholine PD20 value from 0.47 +/- 0.16 (2.95 mg/ml) to 0.96 +/- 0.10 (8.91 mg/ml), (P < 0.0009) in 15 patients and the geometric mean log adenosine PD20 values from 1.59 +/- 0.23 (38.9 mg/ml) to 1.98 +/- 0.14 (97.7 mg/ml) (NS) in 7 patients whose baseline adenosine PD20 levels were less than 200 mg/ml. The degree of protection by heparin against adenosine-induced bronchoconstriction was not correlated with that against methacholine-induced bronchoconstriction (r = 0.60, NS). The data suggest that inhaled heparin may have an inhibitory effect on the methacholine bronchial challenge, and thus, most likely directs its effect against smooth muscle. Heparin caused less attenuation of a challenge with adenosine and probably does not affect mast cell degranulation.
Adenosine↗
IL-8 in pleural effusion.
Interleukin-8 (IL-8) is a recently described potent chemotactic factor that may be involved in the pathogenesis of pleural effusions. To understand the actual mechanisms mediating the inflammatory response, changes in cellular components and IL-8 level in pleural fluid of different aetiologies were evaluated. Thirty-four patients (19 male, 15 female) with a mean age of 46 +/- 22 years (range 16-92) were included in the study. Of these, 13 had tuberculous pleural effusion, seven had empyema/parapneumonic pleural effusion, and 14 had malignant pleural effusion (seven adenocarcinoma, three ovarian carcinoma, two lymphoma, one chronic myeloid leukaemia, and one small cell carcinoma) with positive cytology. Differential cell counts in the pleural fluid were obtained using cytocentrifuge preparations. The concentrations of IL-8 in pleural fluid were measured by the ELISA method. Interleukin-8 was detected in all 34 pleural fluid samples. The serum IL-8 level was analysed only in the empyema/parapneumonic pleural effusion group. The mean IL-8 levels of tuberculous, empyema/parapneumonic, and malignant pleural effusions were 1420 +/- 1049 pg ml-1, 4737 +/- 2297 pg ml-1, and 1574 +/- 1079 pg ml-1, respectively. The IL-8 levels in the empyema/parapneumonic group were significantly raised over malignant and tuberculous groups (P < 0.02). The mean pleural fluid neutrophil counts in tuberculous, empyema/parapneumonic and malignant pleural effusions were 315 +/- 575 cells mm-3, 11,136 +/- 12,452 cells mm-3, and 635 +/- 847 cells mm-3, respectively (P < 0.003). There was a significant positive correlation between pleural IL-8 levels and neutrophil counts (r = 0.46, P < 0.006). The levels of IL-8 in paired samples of serum and pleural fluid in the empyema/parapneumonic effusion group were compared, and the concentration of IL-8 was higher in the pleural effusion than serum (means, 4737 +/- 2297 pg ml-1 and 130.0 +/- 62.5 pg ml-1, respectively, P < 0.03). There was a significant negative correlation between IL-8 concentrations in serum and pleural fluid (r = -0.80, P < 0.03). This data suggests that production of IL-8 in pleural effusion may play a key role in initiation and maintenance of inflammatory reactions, especially in empyema/parapneumonic pleural effusions. It may offer the basis for introduction of novel anti-inflammatory agents in treatment.
Adolescent↗
Analysis of pleural effusions using flow cytometry.
Flow cytometry allows a rapid and accurate analysis of the cells in serous fluids. The aim of this study was to evaluate the use of flow cytometric analysis in malignant pleural effusions. 26 patients (13 females, 13 males; mean age 52 +/- 19 years; range 16-82) were included in the study. 15 had malignant pleural effusions (7 adenocarcinoma, 2 lymphoma, 2 chronic myeloid leukemia, 1 ovarian carcinoma, 1 small cell lung carcinoma, 1 squamous cell lung carcinoma and empyema, and 1 malignant mesothelioma) with positive cytology. 2 had benign effusions associated with malignancy (1 squamous cell lung carcinoma and congestive heart failure, and 1 neuroblastoma and hypoproteinemia). 9 had benign effusions (3 tuberculosis, 1 congestive heart failure, 3 parapneumonic pleural effusion, 1 benign mesothelioma, and 1 pulmonary embolism). Flow cytometric analysis of pleural effusions revealed an increased DNA index in malignant effusions: 1.32 +/- 0.44 versus 0.88 +/- 0.23 in benign effusions (p < 0.04). The cell cycle distribution of cells such as G1/G0 and S in malignant effusions did not differ from that of benign pleural effusions; however G2+M increased significantly in malignant effusions (p < 0.03). Using analysis of mononuclear immunophenotyping, CD3+, CD4+, and CD8+ cells did not show any significant difference between the two groups. The lymphocyte activation marker CD38 was positive in 57.6 +/- 11.5% of malignant fluid cells and 38.5 +/- 6.2% of benign fluid cells (p < 0.04). The mean carcinoembryonic antigen levels in malignant and benign pleural effusions were 98.7 +/- 157.3 and 0.9 +/- 1.2 ng/ml, respectively (p < 0.03). In conclusion, the results of our study indicate that finding cells with an abnormal DNA content strongly supports the diagnosis of malignant pleural effusions. Additionally, mononuclear cell phenotypes have to be taken into consideration for malignant pleural effusions, particularly activated T cells. We recommend that flow cytometry should be performed if the cytology is equivocal.
Adolescent↗
Ofloxacin-induced vasculitis.
We describe a patient with hypersensitivity vasculitis due to ofloxacin therapy; the vasculitis was associated with elevated transaminase and IgA levels. Cyclophosphamide and intravenous pulse prednisolone resulted in clinical improvement.
Aged↗
Role of the adhesion molecule ICAM-1 in asthma.
Cells need to interact with one another for the inflammatory response to occur. The intercellular adhesion molecule-1 (ICAM-1), a member of the immunoglobulin supergene family, plays an important role in inflammation, and circulating ICAM-1 has been reported to be elevated in patients with some inflammatory disorders. To study the influence of asthma on circulating ICAM-1 levels, we measured concentrations of circulating ICAM-1 in patients with asthma. Fifteen patients (6 male, 9 female, mean age: 30 +/- 7 years) and 5 controls (2 male, 3 female, mean age: 25 +/- 6 years) were included in the study. Daily peak flow rates and symptom scores were monitored over a week in all patients and methacholine challenge tests were performed in 7 patients. The spirometric analysis of asthmatic patients demonstrated mean FEV1: 2.57 +/- 0.97 L (74.9 +/- 17.7% predicted), mean FEV1/FVC: 70.1 +/- 9.6%, mean bronchodilator response: 19.2 +/- 8.4%. The mean morning peak flow rate was 331.0 +/- 122.2 L/min, the mean evening peak flow rate 389.0 +/- 118.5 L/min, the mean peripheral eosinophil count 268 +/- 451/mm3, and the mean serum IgE level 327.4 +/- 238.2 IU/ml. The mean serum ICAM-1 levels of asthmatic patients and controls were 429 +/- 133 ng/ml and 405.0 +/- 81.0 ng/ml, respectively. There was no statistical difference between these levels. Furthermore, we could find no correlation between serum ICAM-1 levels and FEV1, serum IgE levels, peak flow rates, and symptom scores, or methacholine PD20 values in asthmatic patients. The results of this study suggest that serum ICAM-1 levels are not increased in asthmatic patients over controls and do not correlate with clinical asthma status.
Adult↗