[Balance of proteinases and antiproteinases and smoking tobacco]. / Równowaga proteazowo-antyproteazowa a palenie tytoniu.

Smoking tobacco can induce formation of inflammable state in respiratory tract and cause lungs damage. Experimental investigations affirm, that the exposure to tobacco smoke causes growth of penetrability of blood-vessels, which favors the enlarged migration of inflammable cells. The growth of exposure to reactive forms of oxygen and concentration changes of cellular antioxidants enzymes, leads to disorders in balance of proteinases and antiproteinases and oxidative stress. As the years go, the disorders mentioned above can lead to deterioration of ventilating efficiency of lungs, and consequently to pronouncement chronic obstructive pulmonary disease (COPD), which becomes serious problem on a world scale.

Periprocedural soluble P- and E-selectin levels fail as predictors of clinical restenosis in patients treated with elective coronary stenting.

An increasing amount of basic scientific data indicates that adhesion molecules may be involved in the pathogenesis of vessel re-narrowing in patients undergoing coronary angioplasty. Furthermore, inflammation is suggested to be a pivotal mechanism linking atherosclerosis and restenosis. The aim of this study was to assess if periprocedural evaluation of soluble P-selectin (sP-selectin) and E-selectin (sE-selectin) possesses any additive value in the restenosis prediction to C-reactive protein (CRP) measurement. One hundred and nine stable angina patients were consecutively enrolled into the prospective cohort study. All participants were treated with single vessel coronary bare metal stenting. sP-selectin, sE-selectin and CRP were measured in peripheral venous blood samples collected before and 6, 24 h and 1 month after the procedure. Clinical follow-up visits were held 7 days(*), 1(*), 3, 6(*), and 12 months ((*)with an exercise test) after stenting. Any symptoms of restenosis were verified angiographically. Clinical restenosis occurred in 18 subjects. Concentrations of sP-selectin and sE-selectin did not differ between patients with and without clinical restenosis at any measuring point. In the latter group a decrease in sP-selectin and sE-selectin levels was observed 6 h after stenting. These findings when considered in all of the investigated subjects had no impact on the subsequent incidence of restenosis. An inflammatory response assessed as an increase in CRP level with the peak values at 24 h was noted in the whole population. However, it was significantly more pronounced in the restenosis group. Application of the Cox's proportional hazard model revealed a high CRP level 24 h after stenting and the history of coronary angioplasty concerning a nontarget lesion to be the only independent predictors of clinical restenosis. To conclude, the periprocedural evaluation of sP-selectin and sE-selectin in peripheral venous blood in patients undergoing elective coronary stenting provides no prognostic information in terms of clinical restenosis prediction, and the magnitude of the systemic inflammatory response triggered by coronary angioplasty assessed as an increase in CRP level and the history of coronary angioplasty concerning nontarget stenosis remain independent predictors of lesion re-narrowing.

[Alternations of bronchial smooth muscle and effect of therapy on remodeling in asthma]. / Udzial miesniówki gladkiej w przebudowie oskrzeli oraz wplyw terapii na remodeling w astmie.

Alternations in airway wall architecture, particularly increased smooth muscle mass are associated with pathogenesis of asthma. Muscle fiber hyperplasia and hypertrophy is a major contributor to the increase in smooth muscle mass. Airway smooth muscle was traditionally considered to have only contractile and proliferative functions and has little attention with regard to its ability to express and release inflammatory mediators. Airway smooth muscle cells have been shown to release cytokines such as: GM-CSF, IL-11, IL-6, IL-1, IL-5, IL-8, PGs and NO. Airway remodeling has been shown to respond to some degree anti-inflammatory therapy. Several study results indicate that steroid can positively influence progressive airflow limitation. Combined use of a beta2-agonist and steroid can reduced the remodeling progression.

[Remodeling of the basement membrane and airway epithelium in patients with asthma]. / Przebudowa blony podstawnej oraz zmiany w nablonku oskrzelowym w astmie oskrzelowej.

Chronic inflammation is recognized as a primary factor in the development of asthma, and its role in the induction of the remodeling of the airways has recently been emphasized. Changes in airway structure such as thickening of the airway wall are common findings in cases of asthma. Thickening of the epithelial reticular basement membrane has been reported to show a positive correlation with airway hyperresponsiveness, the frequency of asthma attacks, and the numbers of fibroblasts and myofibroblasts that lie external and adjacent to it. Studies on the pathology of asthma showed changes of airway epithelium. The most common of these changes are squamous cell metaplasia, goblet cell hyperplasia and damage and shedding of airway surface epithelium.

Combined periprocedural evaluation of CRP and TNF-alpha enhances the prediction of clinical restenosis and major adverse cardiac events in patients undergoing percutaneous coronary interventions.

To assess the value of serial C-reactive protein (CRP), serum amyloid A (SAA), tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) evaluation in the risk stratification in patients undergoing percutaneous coronary intervention. The study was designed as a prospective cohort trial with a 1-year follow-up. Eighty patients (70 with stable angina, 10 with unstable angina) were enrolled. Blood samples were collected before the procedure and after 6 and 24 h, and 1 month. Clinical follow-up visits were performed (*with exercise test) 7 days* and 1*, 3, 6* and 12 months after the procedure. Any symptoms of restenosis were verified angiographically. Multivariate logistic regression analysis identified increased preprocedural TNF-alpha and CRP levels and elevated CRP concentrations evaluated 24 h after the procedure as significant predictors of both clinical restenosis and major adverse cardiac events (MACE), while high SAA values at 24 h accurately predicted clinical restenosis. Patients, who were in the highest tertile of, either, baseline TNF-alpha and/or baseline CRP/CRP at 24 h, were more prone to develop restenosis and MACE than stratified only on the basis of a single marker. Our data indicate that combined analysis of CRP and TNF-alpha might be an effective approach to the clinical restenosis and MACE prediction. Additionally, long-term outcome is markedly influenced by the periprocedural activation of inflammation.

[Eosinophil apoptosis and asthma]. / Apoptoza eozynofilów w astmie oskrzelowej.

Eosinophils play an important role in airway inflammation in asthma. Eosinophils are believed through the release of their mediators to develop the irreversible structural airway changes. Dysregulation of apoptosis can lead to pathological accumulation of eosinophils in bronchial tissue. Apoptosis (programmed cell death) leads to the characteristic morphologic changes including reduction of the cellular volume, blebbing of the membrane, condensation of the nuclear chromatin, DNA laddering, mitochondrial dysregulation and finally to apoptotic bodies. Apoptosis can be induced by oncogenes, specific ligands and some cytokines. On the other hand IL-5, IL-3 and GM-CSF (granulocyte-macrophage-colony stimulating factor) dramatically increase the life span of eosinophils. Glucocorticoids promote eosinophil apoptosis and totally reverse the delayed death cased by beta2-agonists.

[Role of neurotrophin and neuropeptides in bronchial asthma]. / Rola neurotrofiny i neuropeptydów w patogenezie astmy oskrzelowej.

Asthma represents a chronic inflammatory process of the airways. The neurothrophin (NGF) and neuropeptides such as substance P (SP), neurokinin A (NKA), and calcitonin gene-related peptide (CGRP) play important role in stimulation of airways inflammation in asthmatics. NGF stimulates the differentiation and the migration of mast cells to bronchi epithelium. Furthermore, NGF stimulates mast cell degranulation and mediator upregulation and release. It also influences activity of basophils, eosinophils, neurophils, macrophages and T-cells. In addition, its important role in releasing of hyperresponsiveness has been proved. Neuropeptides such as CGRP and SP stimulate migration and degranulation of eosinophils and influence on airway responsiveness in asthmatics. This review article discusses the neuropeptides and NGF actions and mechanisms in the pathogenesis of asthma.

Selenium supplementation on plasma glutathione peroxidase activity in patients with end-stage chronic renal failure.

Patients with chronic renal failure (CRF) usually have a lower than healthy level of selenium (Se) in whole blood and plasma. Plasma glutathione peroxidase (GSH-Px) is synthesized mostly in the kidney. In CRF patients, activity of this enzyme is significantly reduced and its reduction increases with the progress of the disease. The aim of the study was to evaluate the effect of Se supplementation to CRF patients at various stages of the disease on Se concentration in blood components and on plasma GSHPx activity. The study group comprised 53 CRF patients at various stages of the disease supplemented with Se (200 microg/d for 3 mo as Se-enriched yeast, containing about 70% L-selenomethionine [SeMet]). The control group consisted of 20 healthy subjects. The Se concentration in blood components was measured spectrofluorometrically with 2,3-diaminonaphthalene as a complexing reagent. GSH-Px activity in red cell hemolysates and plasma was assayed by the coupled method with tert-butyl hydroperoxide as a substrate. The Se concentration in whole blood and plasma of CRF patients is significantly lower as compared with healthy subjects, but similar at all stages of the disease. In the patients' plasma, total protein and albumin levels are also significantly lower than in healthy subjects. Plasma GSH-Px activity in patients is extremely low, and contrary to Se concentration, it decreases linearly with the increasing stage of the illness. Se-supplied patients show an increased Se concentration in all blood components and at all disease stages, whereas plasma GSH-Px activity is enhanced only at the incipient stage of the disease. Se supply has no effect on plasma GSHPx activity in uremic patients at the end stage of the disease. Total plasma protein and albumin levels did not change after Se supplementation. Our data seem to show that in patients with CRF lower total protein and albumin levels in plasma may be the chief cause of the low blood and plasma Se concentrations. GSH-Px activity decreases along with the kidney impairment. At the end stage of the disease, Se supplementation in the form of Se-enriched yeast has no effect on the increase in plasma GSH-Px activity.

[Influence of physical effort on concentration of lactic acid and acid-base equilibrium in patients with mild and moderate bronchial asthma]. / Wplyw wysilku fizycznego na stezenie kwasu mlekowego i równowage kwasowo-zasadowa u chorych na astme oskrzelowa lekka i umiarkowana.

PURPOSE: Estimate influences of standard physical exercise on lactic acid concentration and acid-base equilibrium in patients with mild and moderate bronchial asthma compared with healthy trained persons and do not ones. MATERIAL AND METHODS: In 47 asthmatic patients and 20 healthy persons: 1) bronchial reactivity was investigated; 2) at rest and 1, 5 and 10 min after 8 min exercise (PWC85%max, bicycle ergometer): FEV1, lactic acid concentration (LAC), pH, pO2, pCO2 and HCO3 (in capillary blood) were investigated. Among asthmatic patients: 1) 21 experienced exercise-induced asthma (EIA), 2) 20 reacted to histamine in concentration of 0.125 mg/ml/3', 3) 6 reacted to histamine in concentration of 0.25 mg/ml/3'. In healthy persons, without EIA and reaction to histamine, were: 12 who did not train, and 8 athletes. RESULTS: After exercise LAC increased in all groups (p<0.05); the increase was significantly higher in patients and persons who did not train, then athletes, and did not normalised, in opposite to athletes, however in persons who did not train was significantly lower then in asthmatics. pH and pCO2 did not change significantly in all examined persons, but HCO3 decreased significantly in patients with bronchial hyperactivity and in persons who did not train. Significant increase of pO2 appeared only in healthy persons. CONCLUSION: Physical effort caused significant greater metabolic changes in asthmatic patients then in healthy persons, especially athletes

[Quality of life in patients with chronic obstructive pulmonary disease before and after the treatment with prednisone]. / Jakosc zycia chorych na przewlekla obturacyjna chorobe pluc przed i po leczeniu prednizonem.

OBJECTIVE: To evaluate quality of life (QOL) and correlation between QOL and lung ventilation in chronic obstructive pulmonary disease (COPD) patients before and after the treatment with prednisone. MATERIAL AND METHODS: 75 patients with COPD were enrolled in the open study (mean 57,76 years of age; 32 smokers, reversible obstruction <15%). Before and after the treatment with prednisone (encorton, Polfa Pabianice) in patients with COPD: 1) IC, VC, FEV1, PEF, MEF75, MEF50, MEF25, FEV1%VC (Lung-Test 500 MES), and 2) QOL questionnaire were studied. The treatment with prednisone was as follows: 1) 30 mg/d - 14 days, 2) 20 mg/d - 14 days, 3) 15 mg/d - 7 days, 4) 10 mg/d- 7 days. At the same time formoterol and i theophylline were continued with COPD patient in stable doses as before enrolment. RESULTS: In patients with COPD after the treatment with prednisone statistical significant increase quality of life (QOL) was obtained. The improvement of QOL questionnaire scores was accompanied by the improvement of the lung function and relationship between them after the treatment with prednisone was statistical significant better then before treatment. CONCLUSIONS: In patients with COPD after the treatment with prednisone: the significant improvement QOL and lung function were found; the significant higher correlation between QOL and lung function then before treatment was determined.

[Bronchial asthma and menopause]. / Astma oskrzelowa a menopauza.

The existing literature suggests that asthmatic women suffer from an increase in asthma symptoms just before and during menstruation. Many investigators speculated that estrogen and progesterone plays a modulating role in asthma features. Estradiol administration was associated with improvement in symptoms, dyspnea index scores, pulmonary function, and decrease in corticosteroid requirement. It is established that estrogen deficiency plays an important role in the pathogenesis of post-menopausal osteoporosis particularly in women with steroid-dependent asthma. This article provides an overview of the mechanisms of beneficial effects of in estrogen and progesterone therapy in asthmatic post- menopausal women.

[Usefulness of antibiotics in the treatment of bronchial asthma]. / Przydatnosc antybiotykoterapii w kontrolowaniu astmy oskrzelowej.

The efficacy and safety of antibiotics in the treatment of asthma are not unequivocal. Among various antibiotics, macrolides play the main role in the therapy of bronchial asthma. Macrolides are useful in the treatment of asthma not only because of their antimicrobial activity. The mechanism of action of macrolides in improving asthma and reducing airway responsiveness is evaluated especially due to their activity in non-infectious asthma. Macrolides may not only enhance the host defense system through increased cytokine synthesis, but also exhibit anti-inflammatory activity mediated by anti-inflammatory cytokines. The steroid-sparing effect of macrolide antibiotics has been postulated to contribute to their beneficial actions in the treatment of asthma. Macrolides may be useful in the treatment of patients with steroid-dependent asthma, probably because they inhibit eosinophilic inflammation. It has also been suggested that the effect of macrolides on bronchial hyperresponsiveness is mediated by their inhibitory action on superoxide production and chemotaxis of polymorphonuclear neutrophils and the mixed lymphocyte reactions. In spite of these suggestions, the mechanism of action of macrolides in asthmatic syndrome is not clear. Only well-designed and conducted clinical studies are capable of assessing the efficacy and safety of immunosuppressive macrolides in the treatment of asthma.

[Role of fibroblasts in bronchial asthma]. / Rola fibroblastów w astmie oskrzelowej.

The major role of fibroblasts is maintaining integrity, solidity and form of lung tissue. This is achieved by producing a vest variety of extracellular matrix (ECM) components such as collagen, laminin, fibronectin, hyaluronic acid and proteoglycans. Remodeling in the airways as seen in asthma is largely a result of altered fibroblast behavior. Fibroblasts produces a variety of inflammatory cytokines, chemokines and surface molecules which are able to activate and attract that stimulate inflammatory reactions. This paper presents a review of the fibroblast behavior and their interaction in the ongoing inflammatory and remodeling processes of the airway in asthma. Further we discuss the influence of glucocorticoids and long-acting beta 2-agonists on fibroblast in relation to their beneficial clinical effects in asthma therapy.

[Risk factors and pathogenesis of occupational asthma]. / Czynniki ryzyka i patogeneza zawodowej astmy oskrzelowej.

Workplace exposure may be an important cause of both new-onset occupational asthma and exacerbations of preexisting disease. In the paper, the risk factors and mechanisms of occupational asthma development are discussed.

[Thalidomide--a new prospective therapy in rheumatology and transplantation]. / Talidomid--nowe mozliwosci terapeutyczne w reumatologii i transplantologii.

This review article discusses the thalidomide therapy of diseases such as systemic sclerosis, rheumatoid arthritis, Behçet syndrome, lupus erythematosus disseminatus and graft-versus-host disease. The main mechanism of action of thalidomide in these diseases is probably based on the suppression of tumor necrosis factor-alpha and the modulation of interleukins.