Alpha-ketoglutarate stabilizes redox homeostasis and improves arterial elasticity in aged mice.

The objective of this study was to evaluate the effect of α-ketoglutarate on redox state parameters and arterial elasticity in elderly mice. Mice in the control group were fed with standard diet, while the experimental animals received the diet supplemented either with calcium (Ca-AKG) or sodium salt of α-ketoglutarate (Na-AKG). The experimental animals were divided into 4 groups with 10 individuals in each: control I (12 months old), control II (2 months old), experimental group I fed with Ca-AKG (12 months old) and experimental group II fed with Na-AKG (12 months old). Mice treated with Ca-AKG as well as the control II animals demonstrated significantly higher level of total antioxidant status (TAS), comparing to the control I animals and those treated with Ca-AKG. Thiobarbituric acid reactive substances (TBARS) level in blood plasma was found significantly lower in young and Ca-AKG treated mice. TBARS liver concentration was significantly different in each examined group. The study also demonstrates the decrease in TBARS level in Ca-AKG treated animals. Treatment with Na-AKG significantly increased glutathione peroxidase activity and decreased the activity of superoxide dismutase. The presented results suggest that Ca-AKG protects the organism against the free radicals related elderly processes. The study presents also the effect of Ca-AKG treatment on arterial elastic characteristics in elderly mice. The beneficial effect of Ca-AKG on ageing organisms was confirmed via redox state stabilization and blood vessel elasticity improvement.

[Usefulness of the eosinophil count in induced sputum of asthmatic patients]. / Uzytecznosc badania eozynofilów w indukowanej plwocinie w astmie oskrzelowej.

Chronic mucosal inflammation is referred to as the primary cause of asthma. Treatment in the first place aims to prevent and reverse the above disease. It is possible to measure the inflammation relatively noninvasively and reliably by making use of induced sputum cell counts. The differential cell count points to the existence and sort of the inflammation (eosinophilic or neutrophilic) and the total cell count--to the intensity. Sputum eosinophilia responds to treatment with corticosteroid, while there is increasing evidence that an isolated neutrophilia does not. Clinical judgement of airway inflammation is further complicated due to the various types of inflammation and their inconsistent correlation with the clinical features. Hence, reliable measurement of induced sputum cell counts may be useful to guide treatment in clinical practice. Therefore, it should be considered how to make it more available.

[Pseudomonas aerogunosa pneumonia in patients treated at the Hospital for Chest Diseases]. / Zapalenia pluc wywolane przez paleczke ropy blekitnej u chorych leczonych w Szpitalu Chorób Pluc.

Retrospective analysis of pneumonia caused by Pseudomonas aeruginosa was made in 66 patients, treated in hospital. Nosocomial pneumonia was diagnosed in 11 (17%) patients. In 51 patients coexisting lung diseases were present: mainly COPD and bronchiectasis. Strains of Pseudomonas aeruginosa were susceptible mostly to imipenem, meropenem, aztreonam, ticarcillin-clavulanic acid, ceftazidime, ciprofloxacin, amikacin, piperacillin-tazobactam, netilmicin. Duration of treatment in hospital was very long--59% were treated over 30 days. Combined antibacterial therapy was applied in 35 (53%) patients and monotherapy, often with different antibiotics--in 31 (47%) patients. Treatment was successful in 45 (68%) patients. In 9 patients the results of treatment was not successful: mainly because of empyema in 7 pts. Twelve (18%) patients (with coexisting COPD--6 and lung cancer--6) died. We can support current recommendations for treatment of Pseudomonas aeruginosa infection with combination of aminoglycosides or fluoroquinolones plus one of remaining antipseudomonal antibiotics. Treatment failures occurred mainly in patients with severe coexisting diseases and/or empyema.

[Pet allergens in a house-dust and elimination procedures against them]. / Alergeny zwierzece zawarte w kurzu domowym oraz sposoby ich eliminacji.

The paper presents a group of allergens carried by the most popular home-kept animals (furred animals). Ubiquitous presence of these allergens (at schools and in public places) is caused by their specific characteristics different from those of house-dust-mites. It is stressed that the serum albumines coming from such animals can be the cause of allergic symptoms in the respiratory tract of patients suffering from bronchial asthma. The trials carried out so far have confirmed the reduction of the animal allergens' amount in different indoor environments when several ways of their elimination were applied. However only few clinical trials have been made to estimate the improvement of ventilation parameters, bronchodilatators requirement and the symptom intensification in bronchial asthma cases, after employing some of the recommended methods often in the continuing presence of the animal at home. Education and encouraging bronchial asthma patients and their families to get rid of animals from their homes and acquiting them with various reservoirs of animal allergens as well as the allergens' distribution and translocation should become the basis of therapeutic management in that group of patients.

A six week double blind, placebo controlled, crossover study of the effect of misoprostol in the treatment of aspirin sensitive asthma.

BACKGROUND: Prostaglandins of the E series and misoprostol (a stable analogue of prostaglandin E(1)) prevent bronchoconstriction following aspirin ingestion or inhalation in subjects with aspirin sensitive asthma. A study was undertaken to investigate the influence of misoprostol on the course of aspirin induced asthma. METHODS: A double blind, crossover, randomised, placebo controlled study was performed in 17 patients with aspirin sensitive asthma (13 women) aged 26-68 years. All subjects had aspirin sensitivity confirmed by means of oral aspirin or inhaled lysine aspirin challenge. Misoprostol (Cytotec, Searle, 800 or 1600 microg daily according to individual tolerance) or placebo were administered over a period of six weeks. Morning and evening peak expiratory flow rate (PEFR), beta(2) agonist use, asthma and rhinitis severity scores, and defaecation score were measured daily. At the beginning and end of each treatment period spirometric tests were performed and blood was taken for eosinophil count. Eight subjects took misoprostol at a dose of 800 microg and nine subjects at a dose of 1600 microg daily. RESULTS: No differences were seen in asthma control between misoprostol and placebo except for the rhinorrhoea score which was lower on misoprostol during the period of the study. CONCLUSION: Misoprostol in a daily dose of 800 or 1600 microg does not significantly improve asthma control in subjects with aspirin sensitive asthma.

[The clinical course of bronchial asthma from childhood to adult age]. / Przebieg kliniczny atopowej astmy oskrzelowej od dziecinstwa do wieku doroslego.

The aim of the study was to establish improvement and deterioration rate adolescence and in age over 20 years (young adults) in comparison with clinical course of asthma in those persons before adolescence. The study group consisted of 93 persons whose asthma started in childhood (mean age 4.50 +/- 2.93). In all of the patients atopy was confirmed by positive skin prick tests with common aeroallergens. The clinical course of asthma was evaluated by means of a questionnaire and the patients were grouped according to asthma severity (Global Initiative for Asthma 1995). In young adults (mean age 23.38 +/- 3.2) in comparison with the clinical course of asthma in childhood (mean age 8.9 +/- 2.2) there was improvement in 58.1% (including 20% persons without symptoms), no change in asthma severity in 25.8% and worsening in 17.2% patients (irrespective of the group they had been initially classified into). There is a correlation between FEV1 before puberty and FEV1 in the adulthood. Among the investigated factors probably influencing the course of asthma, atopic dermatitis persisting after puberty occurred significantly more frequently in severe asthma. There is no correlation between improvement/deterioration of asthma and gender, atopy in family, smoking, pets in home and coexisting atopic diseases.

[Cough, bronchoconstriction and bronchial hyperreactivity in relation to treatment with angiotensin-converting enzyme]. / Kaszel, obturacja i nadreaktywnosc oskrzeli podczas stosowania inhibitorów konwertazy angiotensyny.

In the paper available information concerning the influence of treatment with angiotensin converting enzyme inhibitors (ACE-I) on cough, bronchial hyperreactivity and bronchoconstriction are reviewed. Cough occurs in 0.7% to 19% of patients treated with angiotensin converting enzyme inhibitors according to various reports. In the mechanism of angiotensin converting enzyme inhibitor-induced cough accumulation of bradykinin and substance P due to decreased degradation of this mediators caused by ACE-I may be involved. Part of tussive effect may be mediated via prostaglandins and histamine. In a few studies symptoms of airway obstruction and asthma worsening in relation to treatment with this drugs was reported. However, majority of reports suggest safety in taking ACE-I by patients with asthma. The only effective method to relieve angiotensin converting enzyme-induced cough is a drug withdrawal. The change of drugs within the whole class of ACE-I does not bring effect.

[Pleural needle biopsy in the diagnostic standards of pleural diseases in the past and today]. / Biopsja iglowa oplucnej w standardzie diagnostyki chorób oplucnej wczoraj i dzis.

Pleural needle biopsy (PNB) maintained its value in spite of introduction of videothoracoscopy. Diagnostic possibilities of PNB using Abrams needle were evaluated during 1989-1998 in 114 patients aged 17-82 years. In histological examinations of the biopsy specimens were diagnosed: neoplasms--in 47 (41%) patients, tuberculosis--in 10 (9%) and chronic nonspecific pleuritis--in remaining 57 patients. Data from further course of the disease confirmed diagnosis of neoplasms and tuberculosis. Complication of PNB was encountered only in 1 patient (pneumothorax). Among 47 patients with malignant infiltration of the pleura in the biopsy specimen only in 20 (42%) neoplastic cells were demonstrated in cytologic examination of the pleural fluid. PNB remains still useful in the diagnosis of causes of pleural diseases. Specificity of this method can be enhanced by more precise localization of the pleural lesions using imaging technics (USG, CT, MRI). PNB should be more widely performed in the diagnosis of pleural diseases of unknown etiology particularly when videothoracoscopy is not feasible.

[Comparison of the influence of celiprolol, metoprolol and atenolol on pulmonary ventilation in patients with asthma]. / Porównanie wplywu Celiprololu, Metoprololu i Atenololu na wentylacje pluc u chorych na astme oskrzelowa.

Usage of beta-blocking agents in patients with bronchial asthma is restricted due to their ability to precipitate bronchospasm. Celiprolol beta1-selective beta-blocker with associated beta2-agonist activity gives brand new possibilities of treatment with beta-blockers in asthmatics. The aim of the study was to compare the pulmonary effects of single dose of celiprolol (200 mg), atenololol (25 mg), metoprolol (50 mg) and placebo. Ten stable asthmatic patients, aged 21-60 years (mean age 44.1 yrs.) were studied. During four separate visits with 3 days wash-out period physical examination, ECG recordings were done and lung function tests (FEV1, FVC, FEF25-75), blood pressure, heart rate and saturation were recorded. All parameters were measured again after 45, 90, 150 and 210 minutes from the beginning of the visit. On the contrary to metoprolol and atenolol single dose of celiprolol and placebo did not significantly affect respiratory functions (FVC--area under curve). There was significant decrease of FEV1 calculated as area under curve (AUC) after application of metoprolol in comparison to celiprolol. There were no significant changes in FEV1 after use of atenolol and celiprolol. Celiprolol ian dose 200 mg can be safely used in asthmatic patients.

[Relationship between the clinical course of bronchial asthma from childhood to adulthood (deterioration/improvement), bronchial hyperreactivity and incidence of house dust mite allergens in households of persons treated for atopic bronchial asthma as children]. / Zaleznosc miedzy przebiegiem klinicznym astmy oskrzelowej od dziecinstwa do wieku doroslego (poprawy/pogorszenia) oraz nadreaktywnoscia oskrzeli, a wystepowaniem alergenów roztoczy kurzu domowego w mieszkaniach osób leczonych w dziecinstwie z powodu astmy oskrzelowej atopowej.

The aim of the study was to determine the impact of the exposition to house dust mite allergens or its lack on clinical state of asthma in young adults treated in their childhood for atopic bronchial asthma. The concentration of house mite allergen was studied with the method of Acarex test (detection of guanine--excretory product of house dust mites) in the flats of 55 persons treated for atopic asthma before adolescence. There was significant difference (p < 0.006) between the clinical course of asthma (improvement) in persons living in flats free of house dust mite allergens and those living in flats infested with mites. House dust mite allergens were present significantly more frequently in flats of persons with a low histamine threshold (19 of 20 examined flats) than in flats of persons with a high histamine threshold or without hyperreactivity to histamine (6 of 20 examined flats).

[Staphylococcal pneumonia--analysis of material from patients treated at the Hospital for Lung Diseases in the years 1981-1994]. / Gronkowcowe zapalenia pluc--analiza materialu chorych leczonych w Szpitalu Chorób Pluc w latach 1981-1994.

Retrospective analysis of staphylococcal pneumonia was made in 182 patients, aged 18-88 years /61% more than 60 years old/ treated in hospital in years 1981-1994. Majority of these patients had various concomitant diseases, mostly chronic bronchitis and lung cancer. Strains of Staphylococcus aureus were sensitive mainly to amoxycillin--clavulanic acid, roxitromycin, amikacin, netilmicin, clindamycin, cefamandol, chloramphenicol, rifampicin and resistant mostly to penicillin /90% of strains/, ampicillin, tetracyclines. In many cases initial antibacterial treatment was inadequate in relation to sensitivity pattern of staphylococci--hence many changes of antibiotics were observed in the course of the therapy. Newer antistaphylococcal drugs were applied only in the last years of the study. Despite these therapeutical drawback outcome of staphylococcal pneumonia was good in 85% of patients; 14% of patients died /mainly as a consequence of comorbidities/. Successful therapy of staphylococcal pneumonia requires early recognition of possibility of infection due to Staphylococcus aureus and adjustment of drugs to probable or actual sensitivity of these pathogens.

The influence of misoprostol (synthetic analogue of prostaglandin E1) on aspirin-induced bronchoconstriction in aspirin-sensitive asthma.

It is believed that aspirin (ASA) and other nonsteroidal anti-inflammatory drugs elicit dyspnea in ASA-sensitive asthmatics by blocking cyclooxygenase. It is unclear whether this bronchospasm is due to the shunting of arachidonic acid into the lipoxygenase pathway or to the removal of a cyclooxygenase product which prevents bronchospasm. Diminished tissue concentration of PGE may cause bronchoconstriction. PGE also modulates mast cells, decreasing the release of anaphylaxis mediators. The authors investigated the influence of a synthetic analogue of PGE1-misoprostol (Cytotec, Searle)-on post-aspirin bronchoconstriction in seven ASA-sensitive asthmatics. On the first day, the effect of a placebo was studied. On the second day, the bronchodilatory effect of misoprostol (Cytotec, Searle) alone was examined. After a few days, a predetermined threshold dose of ASA was administered. Seven days later, at least 400 micrograms of misoprostol +200 micrograms 2 h later, together with a predetermined ASA dose, were administered. In all but one patient, the protective influence of misoprostol on ASA-induced bronchoconstriction was observed. The maximum drop in FEV1 (forced expiratory volume in one second) in % after ASA in each of the patients was 40, 25, 24, 33, 47 and 54, and after ASA with misoprostol 10, 9, 4, (+8), 10, (+2) and 45, respectively. Misoprostol given together with ASA attenuated aspirin-induced bronchoconstriction, reaching statistical significance at 3 and 3.5 h. It also diminished extrapulmonary symptoms.

[Pleural needle biopsy in diagnosis of pleural effusion]. / Biopsja oplucnej w rozpoznawaniu przyczyn wysieku oplucnej.

Diagnostic reliability of percutaneous parietal pleural biopsy with use of the Abrams needle technique performed over a period 1989-1994 was assessed in 37 patients with pleural effusion of unknown etiology, aged 24-82 years. Adequate diagnostic specimens were obtained in 33 patients. Histopathological diagnosis established neoplasma (39,4%), tuberculosis (9.1%) and chronic nonspecific pleuritis (51,5%). No complications of the procedure were encountered. Pleural needle biopsy should be more widely applied as a basic method in the diagnosis of pleural effusions of unknown etiology.

[A case of premature emphysema with hereditary alpha-1-antiproteinase deficiency]. / Przypadek przedwczesnej rozedmy pluc uwarunkowanej wrodzonym niedoborem alfa-I-antyproteinazy.

A case of alpha-I-antiproteinase (AIPI) hereditary deficiency (serum concentration 34 mg%, determined by NOR-Partigen Assay F-my Behringer) in 41 years old patient with premature emphysema, confirmed by phenotyping (isoelectrofocusing in polyacrylamide gel) phenotype PiZ is presented. Lung function tests showed considerable decrease (FEV1 = 1,2 l., i.e. 34% pred., FEF50% = 0.55 l., i.e. 12% pred., diffusing capacity DLCO = 12.8 ml/min/mmHg, i.e. 43% pred.). Computed tomography revealed huge emphysematous bullae mainly in supradiaphragmatic parts of the lungs. The authors discuss the difficulties in diagnosing homozygotes with A1P1 deficiency. They suggest screening of severe hereditary deficiency in persons with emphysema in age interval 30-55 years. The presented case of premature emphysema and AIPI deficiency (confirmed by phenotyping variant Z) is the first in the polish literature.

The value of C1 esterase inhibitor in patients with aspirin-sensitive urticaria.

The aim of the study was to evaluate the concentration and activity of C1 esterase inhibitor (C1 INH) in patients with aspirin-sensitive urticaria. C1 INH deficiency is the basis of hereditary angioneurotic edema. The study was performed on 32 subjects with aspirin-sensitive urticaria. The value of C1 INH in examined patients was the same as in the control group. There seems to be no coexistence of aspirin-sensitive urticaria and C1 esterase inhibitor deficiency.

[Psychogenic pseudo-asthmatic syndrome]. / Psychogenny zespól pseudoastmatyczny.

The authors present a case of a 42-year-old patient treated for severe attacks of dyspnoea and wheezing of 12 years duration. She was hospitalized 8 times in medical or pneumonology wards and underwent treatment in a sanatorium 6 times. Since 5 years she has been periodically and recently permanently on oral glucocorticosteroids. Dyspnoea was accompanied by diffuse wheezing and prolongs expiration. It was also observed that her mode of respiration during an attack consisted in forced expiration at small air volumes in the lungs. Theatrical behaviour of the patient was striking. Bronchial challenge with acetylcholine and metacholine was negative. Bronchoscopy revealed profound intussusception of the membraneous part of the trachea and bronchi. Psychiatric diagnosis confirmed hysterical personality. The demonstrated case proves that the value of bronchial challenge is difficult to overestimate in diagnosing asthma. It concerns not only cases where symptoms are scanty but also patients with the so-called troublesome treatment-resistant asthma.

[The influence of misoprostol on post-aspirin bronchoconstriction in patients with aspirin sensitive asthma]. / Wplyw misoprostolu na poaspirynowe zwezenie oskrzeli chorych na astme z nadwrazliwoscia na aspiryne.

It is believed that aspirin (ASA) and other nonsteroidal antiinflammatory drugs elicit dysponea in ASA sensitive asthmatics by blocking the cyclooxygenase. It is unclear whether this bronchospasm is due to shunting of arachidonic acid into the lipooxygenase pathway or removal of cyclooxygenase product which prevent bronchospasm. Diminished tissue concentration of PGE may cause bronchoconstriction. PGE play also modulatory function to mast call decreasing the release of mediators of anaphylaxis. There are some evidences concerning the mast cell degranulation in postaspirin reaction in ASA sensitive asthmatics. The authors investigated the influence of synthetic analogue of PGE1--misoprostol (Cototec, Searle) on the postaspirin bronchoconstriction in seven ASA sensitive asthmatics aged 33-62. Aspirin threshold doses ranged from 10 to 150 mg. Postaspirin bronchoconstriction begun usually within 1-2 hrs after digestion of ASA and 200 micrograms were additionally given 2 h later. Seven days later misoprostol (400 micrograms) was administered together with previously determined dose of ASA. One the other day the bronchodilating effect of misoprostol alone was examined. In all but one patients we observed the protective influence of misoprostol on ASA induced bronchoconstriction. Max. fall in FEV1 in % after ASA in each of the patients was 40, 25, 24, 33, 47 and 54, and after ASA with misoprostol, respectively 10, 9, 4, (+8), 10, (+2) and 45. Misoprostol given together with ASA attenuated aspirin-induced bronchoconstriction reaching statistical significance at 3 and 3.5 h, and also diminished extrapulmonary symptoms. The authors discuss the possible mechanism of protective influence of misoprostol.

[Bronchial asthma caused by exposure to ash wood dust]. / Astma oskrzelowa wywolana ekspozycja na pyl drewna jesionowego.

A 42-year-old man reported attacks of dyspnoea on non-professional exposure to ash wood dust. The skin prick tests with common allergens and ash pollen were positive. Inhalation of ash wood dust (challenge test) elicited a very strong, immediate bronchospastic reaction, associated with profuse watery rhinorrhea, conjunctival congestion and lacrimation. The symptoms did not occurred after inhalation of pine wood dust. A positive skin (prick test) reaction to ash wood extract was documented. When the patient remained unexposed to ash wood dust the dyspnoea subsided and 4-fold decrease in bronchial reactivity to histamine-PC20 increase from 0.53 mg/ml to 2.1 mg/ml (according to Cockroft) was observed. The authors conclude that the immediate bronchial reaction to inhaled ash wood dust and the immediate skin positive response to ash wood extract were due to IgE-allergen reaction. This is the second case of hypersensitivity to ash wood dust reported in the literature.

[Psychogenic laryngeal dysfunction--pseudo-asthmatic syndrome]. / Psychogenne zaburzenia motoryki krtani--zespól pseudoastmatyczny.

Laryngeal dysfunction occurs as periodical narrowing or closing of the glottis which does not depend on respiratory phase. Mechanism of this disorder is unknown. It is believed that it is caused by psychological factors or disturbed neural transmission from the respiratory tract. It results in disfunction of vocal cords and presents as episodes of airways obstruction misdiagnosed as asthma attacks. Authors present five cases mostly treated as severe bronchial asthma in which disfunction of vocal cords has been diagnosed on confirmed. In most of observed patients the psychological factor connected with family conflicts were the most probably background of the illness.

Aspirin-induced neutrophil chemotactic activity (NCA) in patients with aspirin-sensitive urticaria after desensitization to the drug.

The increase in neutrophil chemotactic activity (NCA) is related to mast cell degranulation. This study was performed in 10 patients in whom aspirin-induced urticaria was connected with increased NCA. A state of tolerance to aspirin (ASA) was achieved by administering incremental doses of acetylsalicylic acid. In none of the examined patients was an increase in NCA observed after 600 mg of ASA given after desensitization. The authors conclude that in patients with ASA-induced urticaria, mast cell degranulation does not occur after ASA desensitization.