Search PubMed⌕ Search

Biomedical subjects

J Orehek

Publications and source records attributed to J Orehek.

At least 19 recordsLinked to original sources
PubMed1994

Tumor necrosis factor-alpha levels and weight loss in chronic obstructive pulmonary disease.

Unexplained weight loss is common in chronic obstructive pulmonary disease (COPD). Blood levels of tumor necrosis factor-alpha (TNF-alpha), a cytokine causing cachexia in laboratory animals, are elevated in various human diseases associated with weight loss. We therefore prospectively measured TNF-alpha serum levels (immunoradiometric assay) in patients with clinically stable COPD (n = 30; all male; mean age, 65 yr) whose weight was less (Group I; n = 16) or more (Group II; n = 14) than the lower limit of normal taken from Metropolitan Life Insurance Company tables. The patients had no cause known to elevate TNF-alpha serum levels; notably, they were not infected. Group I patients had unintentionally lost weight during the previous year, whereas the weight of Group II patients had not changed during the same period. The two groups had similar chronic airflow obstruction and arterial blood gas impairment; hyperinflation and reduction in diffusing capacity were more pronounced in Group I, but differences were not significant. TNF-alpha serum levels (pg/ml; mean [SD]) were significantly higher in Group I than in Group II (70.2 [100.0] versus 6.7 [6.4]; p < 0.001). Group II TNF-alpha serum levels did not differ significantly from those of healthy subjects (7.8 [3.9]), whereas those of Group I were significantly higher (p < 0.001). Because renal function was in the normal range, we conclude that increased TNF-alpha production--and not decreased TNF-alpha clearance--is a likely cause of weight loss in patients with COPD.

Aged↗
PubMed1993

Left lung asthma.

The chest radiograph of a woman with acute asthma showed signs of obstructive emphysema of the left lung. Fiberoptic bronchoscopy excluded obstruction of a large bronchus. The signs disappeared after antiasthmatic treatment, suggesting that they were caused by airway closure. In usual asthma, airway closure affects both lungs; the reason for the unilateral predominance we observed is unknown.

Acute Disease↗
PubMed1990

Manufacturer's information insert and subjective theophylline side-effects.

In Western Europe medicine packages contain an insert prepared by the manufacturer which enumerates the drug side-effects. We investigated the influence of this insert on alleged theophylline side-effects. Forty literate adult asthmatics were randomly allocated into two groups (n = 20 each): theophylline packages contained the manufacturer's insert in group A but not in group B. Theophylline was prescribed (10 mg.kg-1 body weight qd) for one week. During this period the patients filled a diary grading 13 different symptoms from 0 to 3; 5 of these symptoms were listed on the insert as theophylline side-effects. On the eighth day the patients were interviewed and theophylline blood levels measured. Theophylline side-effects were significantly more marked in group A than in group B, whereas the other symptoms were of similar magnitude. Eight patients prematurely stopped their treatment in group A vs 3 in group B, because of alleged intolerance. Theophylline blood levels did not differ significantly in the two groups; neither did they in the subgroup which stopped treatment and in the one which complied to prescription. We conclude that side-effects were suggested to the patients by the insert and/or that the insert increased their awareness of side-effects, with a subsequent detrimental influence upon compliance to therapy.

Adult↗
PubMed1988

Attenuation of hyperventilation-induced bronchospasm by terfenadine: a new antihistamine.

The effect of terfenadine, a selective H1-receptor antagonist devoid of central nervous system side effects, was evaluated on hyperventilation-induced bronchospasm in 11 adult subjects with asthma in a double-blind, placebo-controlled, crossover study. Increases in specific airway resistance (SRaw) were induced by isocapnic hyperventilation with dry air on two occasions, 7 days apart. Before the tests, the subjects received oral terfenadine (120 mg, twice daily) or placebo for 3 days with the last dose administered 3 hours before the test. Baseline SRaw and spirometric values (vital capacity and FEV1) were similar for the two tests. Terfenadine yielded a significant (p less than 0.001) parallel shift to the right of the stimulus (hyperventilation)-response (SRaw) curve; 100% increases in SRaw occurred at ventilation rates of 44 L/min after placebo treatment and 64 L/min after terfenadine treatment. These data suggest that histamine release plays a role in hyperventilation-induced bronchospasm despite the fact that increase in plasma histamine has not been found in this situation, in contrast to exercise-induced bronchospasm.

Adolescent↗
PubMed1988

Treatment of brain metastases of lung cancer with high doses of etoposide (VP16-213). Cooperative study from the Groupe Franais Pneumo-Cancérologie.

To study the efficacy of etoposide in brain metastases of lung carcinoma, etoposide was given during 3 consecutive days. The total dose of 1500 mg/m2 was divided into six 1 h perfusions delivered over 3 days to 19 patients having squamous (7), large cell (3), small cell (5) or adenocarcinoma (4). Response to chemotherapy was assessed by means of computerized tomography (CT) before and 15-30 days after the last course of chemotherapy (course interval = 28 days, maximum of four courses). Severe myelotoxicity was observed in nine patients with seven patient deaths resulting from infection. Efficacy could be evaluated in 13 patients. Failure was observed in seven cases. An objective response was observed in six patients (4/14 NSCLC and 2/5 SCLC), two patients having a complete regression. Average survival time was 10 weeks.

Adenocarcinoma↗
PubMed1988

Cholinergic responsiveness of respiratory and vascular tissues in two different rat strains.

The airway and systemic arterial smooth muscle responsiveness to cholinergic agents of two strains of rats, Rat Albino (RA) and Brown Norway (BN), was compared in vivo and in vitro. In vivo, we measured the doses of carbachol that induced a 100% increase in lung resistance (PD100 RL), a 50% decrease in dynamic lung compliance (PD50 Cdyn), and the value of systolic blood pressure at the carbachol dose of 10 micrograms (Pa 10 micrograms). In vitro airway smooth muscle and systemic arterial smooth muscle responsiveness was assessed by measuring the maximal response to acetylcholine, the slope of the linear portion of the dose-response curve, and the negative logarithm of the molar concentration of acetylcholine producing 50% of the maximal response (pD2). PD100 and PD50 were about four times greater in BN rats than in RA rats. In contrast, Pa 10 micrograms was 1.5 lower in the BN rats. These differences persisted after bivagotomy. Tracheal pD2 was 25% greater in the RA than in the BN strain. The mean dose-response curve of parenchymal strips of RA rats was situated upward and to the left of the BN curve, but the reverse was observed for aortic smooth muscle dose-response curves. Thus 1) airway smooth muscle responsiveness to cholinergic agents is greater in RA strain than in BN, but the reverse is true for systemic arterial smooth muscle responsiveness; and 2) these differences are not due to factors extrinsic to the smooth muscle, since they occurred in vitro and may depend on different densities of muscarinic receptors.

Acetylcholine↗
PubMed1988

Attenuation of bronchofiberscopy-induced cough by an inhaled beta 2-adrenergic agonist, fenoterol.

We investigated the antitussive effect of fenoterol in 40 patients (34 males) undergoing bronchofiberscopy for diagnostic purposes. The patients were randomly allocated into two groups, one receiving two puffs (400 micrograms) of fenoterol and the other two puffs of placebo, from a metered-dose inhaler in a double-blind fashion. The following procedure was used: premedication with 0.5 mg atropine sulfate and 100 mg hydroxyzine administered intramuscularly; 50 min later, aerosol administration; 10 min after aerosol administration, a standardized topical anesthesia was performed. As soon as the bronchofiberscope had entered the trachea, sounds were recorded for a 5-min period, while the tracheobronchial tree was systematically inspected. Additional lidocaine (2% solution, 2 ml boluses) was injected into the airways if troublesome cough occurred. The two groups did not differ significantly in terms of age, sex ratio, and smoking history. In contrast, both the number of coughs and the volume (ml) of additional lidocaine were significantly smaller in the fenoterol group than in the placebo group: m +/- SEM: 35.0 +/- 5.5 versus 51.6 +/- 6.5, p less than 0.01 and 1.9 +/- 0.5 versus 3.3 +/- 0.4, p less than 0.01, respectively. Thus, fenoterol exhibits antitussive properties and can usefully be administered before bronchofiberscopy.

Administration, Inhalation↗
PubMed1988

[Medical history of severe respiratory insufficiency].

To evaluate retrospectively health care in severe chronic respiratory failure, we interviewed 38 patients, admitted for the first time to a pulmonary intensive care unit for an acute episode. A standardised questionnaire was devoted to establishing if the patients were aware of chronic respiratory disease prior to admission, if they had visited a general practitioner or a chest clinic, and had undergone a lung function evaluation. Six patients were unaware of any respiratory disease prior to the acute episode. Six others realised they had suffered from a respiratory disease, but had failed to visit a physician. Among the remaining 26 patients, two-thirds had visited a chest physician. Fourteen of them had undergone spirometry and arterial blood gas measurements. One third had visited a general practitioner but spirometry was performed in only 3 and arterial blood gas analysis in only 1. Thus, chronic respiratory failure is sometimes ignored, and most of the time diagnosed with delay and inadequately evaluated.

Adult↗
PubMed1987

Different bronchoconstrictor effects of carbachol boluses inhaled near residual volume or total lung capacity.

The purpose of this study was to determine if the lung volume at which aerosol inhalation begins (LVi) influences airway responses to bronchoconstrictor agents. We compared the effects of carbachol boluses (25, 50 and 100 ml), inhaled at high and low LVi (averaging 72.2 and 15.8% of vital capacity, respectively) on specific airway resistance (SRaw). In order to eliminate the possible influence of airway obstruction on aerosol distribution and deposition, we selected 5 asthmatic subjects with normal respiratory function (spirometry, SRaw, nitrogen washout and closing volume); furthermore, non-cumulative dose-response curves were obtained (i.e. the patients inhaled only one dose of carbachol on a given test day). Inhaling carbachol at low LVi yielded a significantly (p less than 0.01) larger degree of bronchoconstriction. Differences in bronchial responses were probably due to differences in the amount of particles deposited in the airways and/or to their distribution. These data suggest that LVi should be controlled for quantified inhalation provocation tests.

Adult↗
PubMed1987

Asthma without airway hyperresponsiveness to carbachol.

Generally, asthma is closely associated with hyperresponsiveness to bronchoconstrictor agents. However, we have observed three patients who initially had symptoms of asthma but no hyperresponsiveness. Responsiveness to carbachol was assessed by specific airway resistance (SRaw) measurement after bronchodilatators had been discontinued. The carbachol challenge was repeated 6-18 months later. Initially, no change in SRaw was observed after inhalation of 3 mg carbachol (cumulated dose). On the second occasion, carbachol responsiveness increased into the asthmatic range while the baseline values of SRaw were not different. Since we have used the SRaw measurement, the bronchodilatator effect of maximal inspiration is not the explanation for the failure to demonstrate hyperresponsiveness. These observations suggest that airway hyperresponsiveness is not a necessary condition for induction of asthma and symptoms of asthma may precede the appearance of airway hyperresponsiveness.

Adolescent↗