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Biomedical subjects

G Bochenek

Publications and source records attributed to G Bochenek.

12 recordsLinked to original sources
PubMed2001

Safety of a specific COX-2 inhibitor in aspirin-induced asthma.

In a subset of patients with asthma, aspirin and several other non-steroidal anti-inflammatory drugs (NSAID) that inhibit simultaneously cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) precipitate dangerous asthmatic attacks. We tested the hypothesis that in patients with aspirin-induced asthma the attacks are triggered by inhibition of COX-1 and not COX-2. In twelve asthmatic patients (seven men, five women, average age 39 years) oral aspirin challenge precipitated symptoms of bronchial obstruction with fall in FEV1 > 20%, and a rise in urinary leukotriene E4 (LTE4) excretion; also in five patients the stable metabolite of PGD2, 9alpha11betaPGF2, increased in urine. The patients then entered a double-blind, placebo-controlled, cross-over study in which they received either placebo or rofecoxib in increasing doses 1.5-25.0 mg for 5 consecutive days, separated by a 1-week wash-out period. No patient on rofecoxib developed dyspnoea or fall in FEV1 > 20%; mean urinary LTE4 and 9alpha11betaPGF2 urinary levels, measured on each study day for 6 h post-dosing, remained unchanged. Two patients on placebo experienced moderate dyspnoea without alterations in urinary metabolites excretion. At least 2 weeks after completion of the study, all patients received on an open basis 25 mg rofecoxib without any adverse effects. NSAID that inhibit COX-1, but not COX-2, trigger asthmatic attacks in patients with asthma and aspirin intolerance. Rofecoxib can be administered to patients with aspirin-induced asthma.

Adult↗
PubMed2001

[A case of tracheal adenoid cystic carcinoma in a young woman].

A case of an adenoid cystic carcinoma of trachea is presented. A 30-year-old non-smoking woman with strong inspiratory dyspnea at rest was admitted to the Dept. of Pulmonary Diseases. At auscultation a respiratory murmur was more silent at right lung and stridor over trachea was heard. CT scan revealed tumor at the bifurcation of the trachea. Bronchoscopy was made and biopsy established the diagnosis: adenoid cystic carcinoma. The tumor was partially removed with rigid bronchoscope and radiotherapy was started. Clinical improvement occurred; in control CT scan tumor vanished. The trachea cancers are rare. Symptoms often mimic asthma or chronic bronchitis. Thus in every patient with chronic cough and dyspnea bronchoscopy should be made. A treatment of choice is primary resection and postoperative radiotherapy.

Adult↗
PubMed1998

Benefits from adding the 5-lipoxygenase inhibitor zileuton to conventional therapy in aspirin-intolerant asthmatics.

From bronchoprovocation studies and investigations of the acute effects of drugs that inhibit leukotrienes (LT), the hypothesis has emerged that leukotrienes are important mediators of airway obstruction and other symptoms in aspirin-intolerant asthma (AIA). However, it has yet not been shown if subjects with AIA respond favorably to clinical treatment with leukotriene inhibitors. Therefore, in a double-blind placebo-controlled crossover study, we examined the effects of 6 wk of treatment with the leukotriene-pathway inhibitor zileuton (600 mg, four times daily) in 40 patients with well-characterized AIA. The treatment was added to existing therapy, which included medium to high doses of inhaled (average daily dose 1,030 microg of beclomethasone or budesonide) or oral glucocorticosteroids (4 to 25 mg/d) for all but one of the patients. On top of this treated baseline, there were no significant effects of adding placebo, indicating that their asthma was kept relatively stable. However, there was an acute and chronic improvement in pulmonary function after treatment with zileuton, expressed both as increased FEV1 from baseline compared with placebo, and higher morning and evening peak expiratory flow rate (PEFR) values on zileuton treatment compared with placebo. The improvements occurred despite lower use of rescue bronchodilator with zileuton. Zileuton also diminished nasal dysfunction, which is one of the cardinal signs of AIA. There was a remarkable return of smell, less rhinorrhea, and a trend for less stuffiness and higher nasal inspiratory flow during treatment with zileuton. Zileuton caused a small but distinct reduction of bronchial hyperresponsiveness to histamine and inhibited aspirin-induced bronchoconstriction. Zileuton inhibited urinary excretion of LTE4 but did not change airway reactivity to inhaled LTD4, supporting that zileuton specifically inhibited leukotriene biosynthesis. The findings indicate that leukotrienes are important mediators of persistent airway obstruction and chronic nasal dysfunction in AIA. The study also suggests that addition of a leukotriene pathway inhibitor such as zileuton may bring about greater control of asthma than what is achieved by treatment with medium to high doses of glucocorticosteroids alone.

Adrenergic beta-Agonists↗
PubMed1997

Aspirin-induced asthma and HLA-DRB1 and HLA-DPB1 genotypes.

BACKGROUND: Aspirin-induced asthma (AIA) affects one in 10 individuals with adult-onset asthma. It is not known if aspirin sensitivity is due to immune mechanisms or to interference with biochemical pathways. OBJECTIVE: The study aimed to test for possible involvement of the genes of the Major Histocompatibility Complex (MHC) in AIA. METHODS: HLA-DPB1 and HLA-DRB1 genotyping was carried out by DNA methods in 59 patients with positive challenge tests for AIA and in 48 normal and 57 asthmatic controls. RESULTS: The DPB1*0301 frequency was increased in AIA patients when compared with normal controls (19.5% vs 5.2%, Odds Ratio = 4.4, 95% Confidence Interval (CI) 1.6-12.1, P = 0.002), and compared with asthmatic controls (4.4%, OR = 5.3, 95% CI = 1.9-14.4, P = 0.0001). The frequency of DPB1*0401 in AIA subjects was decreased when compared with normal controls (28.8% vs 49.0%, OR = 0.42, 95% CI = 0.24-0.74, P = 0.003) and asthmatic controls (45.6%, OR = 0.48, 95% CI = 0.28-0.83, P = 0.008). The results remained significant when corrected for multiple comparisons. There were no significant HLA-DRB1 associations with AIA. CONCLUSION: The presence of an HLA association suggests that immune recognition of an unknown antigen may be part of the aetiology of AIA.

Adult↗
PubMed1996

The atopy trait in hypersensitivity to nonsteroidal anti-inflammatory drugs.

The prevalence of atopy was evaluated in two groups of subjects with hypersensitivity to nonsteroidal anti-inflammatory drugs (NSAID): 1) 78 patients with aspirin-induced asthma (AIA) confirmed by oral or bronchial provocation challenges 2) 42 subjects with hypersensitivity to pyrazolone drugs (case history and positive skin tests to noramidopyrine/aminophenazone) who tolerated aspirin well. Fifty sex- and age-matched persons from an unselected general population, with no hypersensitivity to NSAID, formed the control group. Atopy was estimated from the results of the following clinical and biologic parameters: 1) personal and family history of atopic diseases 2) skin prick tests with 16 aeroallergens 3) serum levels of specific IgE to five aeroallergens 4) total serum IgE level. Different definitions of atopy were used, consisting of constellations of two or three of the above-mentioned features. The results of the study revealed that the prevalence of atopy varied according to the criteria used for its definition. Irrespective of the definition used, a similar distribution of atopy was observed in both groups of patients with hypersensitivity to NSAID. Atopy was more frequent in either group of patients with intolerance of NSAID than in the control group. Thus, atopy is related to adverse drug reactions to NSAID.

Adult↗
PubMed1995

Treatment of steroid-dependent bronchial asthma with cyclosporin.

The treatment of chronic severe asthma is unsatisfactory for many patients. The aim of the study was to determine the effects of treatment of steroid-dependent asthma with cyclosporin. We performed a double-blind, placebo-controlled, randomized, parallel group trial on the effect of cyclosporin on pulmonary function, asthma severity and tapering of prednisone in 34 steroid-dependent asthmatics (mean oral prednisone dose: 16 mg.day-1). The study consisted of: 1) baseline period (12 weeks); 2) experimental period divided into two parts: Part I (12 weeks) cyclosporin or placebo treatment; Part II (22 weeks) cyclosporin or placebo treatment and oral prednisone reduction; and 3) follow-up observation (8 weeks). Asthma symptoms score, pulmonary function tests (daily peak expiratory flow (PEF) and bi-weekly forced vital capacity (FVC), forced expiratory volume in one second (FEV1) and maximal mid-expiratory flow (MEF50), biochemical profile and blood cyclosporin levels were monitored throughout the study. Following cyclosporin administration, a slight beneficial effect on some subjective parameters of asthma severity was observed. At the same time, no beneficial effect on pulmonary function was noted. The time trends analysis of mean daily prednisone doses between the treatment groups revealed a statistically significant difference indicating that, during prednisone reduction, cyclosporin seemed to be slightly more efficient than placebo in reducing the requirement for systemic corticosteroid, even though the steroid reduction was accompanied by slight impairment of some pulmonary function. However, there was no significant difference in the final dose reduction between the treatment groups. These data and the known toxicity of the drug suggest a limited place for cyclosporin treatment in steroid-dependent bronchial asthma.

Adult↗
PubMed1991

[Lipoproteins (A) after a history of myocardial infarction, arteriosclerosis obliterans, hypertension and hyperlipidemia].

Serum lipoprotein(a) concentration in men with hypertension, arteriosclerosis obliterans, hypercholesterolemia and after myocardial infarction was measured using Laurell's immunoelectrophoresis. Lp(a) distribution and mean serum concentrations did not differ significantly from the controls, with the exception of a group of premature myocardial infarction (age below 45), in which high values were more frequent.

Adult↗