[Pneumonia caused by Legionnaire's disease?].
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Biomedical subjects
Publications and source records attributed to B Piotrowska.
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Studies of bronchial asthma pathogenesis, conducted over many years, have shown that inflammatory process plays a major role in the development of this disease. Glucocorticosteroids are agents with strongest antiinflammatory activity and together with beta 2-agonists are thought of as firstline therapy in the treatment of bronchial asthma. New inhaled glucocorticosteroids are preparations with small systemic activity, despite the fact, that some of them are more lipophyllic than the others, despite the differences in solubility, affinity to lung tissue, different serum concentrations and affinity to receptors. Even with the tremendous progress in increasing efficacy and lowering side effects of inhaled glucocorticosteroids, no ideal preparation was found so far, however the antiinflammatory activity was increased and the dose lowered, which means increasing clinical efficacy and lowering the systemic effects. Only in the future we can hope for developing an ideal preparation of inhaled glucocorticosteroid with common specificity towards lung tissue and direct influence on the target cell, and maybe even on a specific gene.
The therapy with immunoglobulin have been used since many years, although its clinical efficacy still is uncertain. The aim of this study was to compare the clinical course of severe pneumonia and concentration of immunoglobulin in patients admitted to the intensive care units (ICU). The patients were treated either with antibiotics only or with antibiotics and Gamma-Venin P. Investigates group consisted of 30 patients with severe pneumonia. 15 of them (group A) were treated with antibiotics only, and another 15 (group B) with antibiotics and Gamma-Venin P. Immunoglobulins were administrated intravenously in the maximum single dose 3.0 g/kg. The serum concentration of immunoglobulin were measured before and every second day after beginning of the treatment. 27 patients completed the study due to protocol (14 patients in group A and 13 patients in group B). Only two patients revealed sings of intolerance of Gamma-Venin P during the first infusion of immunoglobulin. The clinical course of pneumonia and duration of treatment in ICU were similar in both groups. Statistically significant differences in concentration of immunoglobulins in patients treated without immunoglobulin infusion in comparison with patients with Gamma-Venin P were not found. We conclude, that infusion of immunoglobulins did not improve the clinical course of the severe pneumonia.
Platelet-activating factor (PAF), proposed as an important inflammatory mediator in asthma, reproduces several of the features of asthma, such as microvascular leakage, mucus secretion, bronchoconstriction, and possibly increased airway responsiveness. Modipafant (UK-80,067) is the (+)-enantiomer of UK-74,505, a potent and specific PAF antagonist. We have assessed the effect of modipafant over 28 d in adult subjects with moderately severe asthma in a placebo-controlled parallel group study. A total of 218 patients with asthma were enrolled into the single-blind run-in, of whom 120 (93 males and 27 females, mean age 41.0 yr) entered the double-blind treatment phase after demonstrating symptomatic asthma in the final week of the single-blind run-in phase. Patients could take up to 1600 micrograms inhaled corticosteroid and an inhaled beta 2 agonist as rescue medication. A total of 59 patients with asthma took modipafant (one 50 mg capsule twice daily), and 61 took matched placebo. There was no significant difference between placebo and modipafant in diurnal variation in PEF, morning and evening PEF, clinic FEV1, rescue bronchodilator usage, symptom score, or airway responsiveness. We previously showed that the racemate UK-74,505 had no effect on antigen challenge, and this study shows that the active (+)-enantiomer modipafant has no effect in chronic asthma. This suggests that PAF is not an important mediator in asthma.
We studied 21 subjects with clinically stable atopic asthma. Our aim was to evaluate the relationship between the changes of the nonspecific bronchial responsiveness and spirometry, PEF- and laboratory parameters during 6 weeks observations. The spirometry values (FEV1%VC, MEF50), measurements of the provocative concentration of histamine causing a 20% fall in FEV1 (PC20H, according to Cockcroft) and analysis of blood eosinophil count and total IgE titre were performed twice, at 6 week interval. The studied patients recorded daily their symptoms and the number of puffs of betamimetics. They also measured daily their morning and evening PEF. We found any statistically significant changes during the study in evaluated parameters (t-Test). There was a degree of correlation between the symptom score and the use of bronchodilators. At the same time there were no trends in PC20H and the symptoms score, B2-agonist use, bronchial obstruction (FEV1%VC, MEF50) or mean amplitude of PEF. We conclude, that in the clinical assessment of asthma nonspecific bronchial responsiveness seems to be an independent variable.
UNLABELLED: In atopic asthmatics we have found, that 2 weeks of regular inhalative salbutamol monotherapy (200 mcg/qid) enhances BHR to histamine. Aim of this study was to evaluate the effect of this kind of ST on BHR in asthmatics under concomitant treatment with inhalative corticosteroids. We studied three group of patients: group 1--nonsymptomatic untreated asthmatics (n = 7); group 2--asthmatics under 2.42 +/- 1.3 years of continuous therapy with beclomethasone dipropionate (bdp, n = 8); group 3--in which bdp (200 mcg bid) was started at the same time as ST (n = 6). Spirometry and BHR challenge with histamine were performed before and after 2 weeks of ST. During the study the patients registered their PEF-values and asthma symptoms. RESULTS: 1) we observed any effect of ST on symptoms score, PEF--variability or spirometry values in none of the groups, 2) in the group 1 ST increases BHR (PC20H from 0.939 +/- 0.577 to 0.387 +/- 0.337; Wilcoxon p < 0.025; 3) ST evoked no significant change in BHR in the groups 2 and 3.
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Fifty-one fish meal factory workers in four Polish harbour cities were investigated. They had been employed in the fish meal factory for 1--33 years and 10.7 years on average. All but seven of these were smokers. The investigation consisted of respiratory symptoms questionnaire, chest X-ray, physical examination, respiratory function assessment, intradermal skin tests to ten fish genera, total serum IgE and serum precipitins to fish antigen assessment. Chronic bronchitis was diagnosed in 29 investigated patients. In 12 (23%) of the patients, according to their case history or to skin tests, allergy to fish was suspected, but was confirmed by elevated serum IgE levels in only two of these. In no cases were serum precipitins against fish antigen found. In six patients, either obstructive or restrictive changes were diagnosed according to conventional spirometry, but by MEF50% VC in 17 subjects (33%) slight airways obstruction was diagnosed and can be regarded as the result of the habit of smoking. According to the performed investigation, only two workers presented a full clinical and immunological picture of allergy to fish. From the practical point of view, this type of professional activity is less dangerous than might be theoretically expected.
The causes for an abnormal five-hour tetracosactrin test in 14 out of 75 patients (18.5% of the entire group), treated continuously with triamcinolone acetonide long-term (mean 3.2 years) for asthma or related syndromes, were investigated. The average daily dosage, duration of treatment and age of the patients were analyzed. Statistical analysis indicated that the risk of adrenocortical suppression was increased by the patient's age and the average patients under the age of 50, receiving less than 1.2 mg triamcinolone acetonide daily, only rarely develop adrenocortical functional impairment.
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