Biomedical subjects
Publications and source records attributed to I Grzelewska-Rzymowska.
The paper deals with urticaria/angioedema type of sensitivity to aspirin and other nonsteroidal antiinflammatory drugs. The clinical, alergological studies and usefulness of the available diagnostic methods are presented. The pathomechanism of bronchospastic and urticarial type of sensitivity to aspirin is also discussed.
The authors present the pathomechanism of allergic diseases and the role of adhesion molecules in this process. The antiallergic and antiinflammatory activities of selective antagonists of H1 receptors are presented.
The study was performed in 19 patients with stable mild/moderate asthma aged from 16 to 66. Nonspecific airway hyperresponsiveness (AH) to histamine was measured according to Cockcroft's et al. method and expresses as PC20H in mg/ml. The study was controlled by inhalation of PBS. The histamine or PBS challenges were performed three times at 45 min. intervals on the third day in case when the stability of AH on two preceding days was observed. The geometric means of PC20H (xg PC20H) during the consecutive three days did not change. They were 0.97, 0.92, 0.87 mg/ml (p > 0.05) respectively. Three times histamine challenges performed on the same day induced the decrease of AH (xg PC20H increased from 1.48 to 6.55 mg/ml) in 5 patients. In 4 other subjects the increase of AH was observed (xg PC20H decreased from 1.14 to 0.20 mg/ml). In 10 subjects the three times histamine challenges performed on the same day had no influence on AH to histamine.
The study was performed in 11 patients suffering from stable mild and moderate atopic asthma. Bronchial allergen challenges were performed according to Chai et al method. Airway hyperreactivity-AH (PC20H in mg/ml) was determined in each study day before subthreshold allergen inhalation dose, meaning the dose which did not induce asthmatic responses. Then FEV1 was measured in 2, 5, 15, 30 i 60 min. after allergen provocation throughout 4 to 9 consecutive days. A significant increase of PC20H was observed in 8 patients (xg PC20H in whole group decreased from 0.93 to 0.35 mg/ml after allergen challenges). The authors conclude that allergen inhalation challenge without asthmatic bronchial responses can cause an increase AH.
Seasonal bronchial asthma causally connected with the exposure to pollen allergens is a chronic, eosinophilic mucosal inflammation of airway. This inflammation is the basis for the development of nonspecific bronchial hyperreactivity which is the most typical but mutable feature of asthma. Bronchial hyperreactivity often determines asthma intensity and the need of asthma treatment. The nonspecific bronchial hyperreactivity over two consecutive years was evaluated in 11 patients (2 women and 9 men) with seasonal bronchial asthma, sensitized to grass, remaining under the conditions of natural allergen exposure and out of this period. Bronchial reactivity to histamine was measured by Cockcroft's at all method. So called histamine threshold (PC20H) in mg/ml was assessed. The values of ventilatory parameters (FVC, FEV1) and asthma symptom scores were also measured. It was showed that nonspecific bronchial hyperreactivity significantly increased in subjects with seasonal bronchial asthma during natural pollen exposure. PC20H in two studies performed during this period decreased 3 and 6 times when compared to preseasonal values. The majority part of patients (80%) has the increased bronchial reactivity to histamine also beyond the of grass season when clinical symptoms of asthma and rhinitis are not observed. This postseasonal hyperreactivity could be the effect of the chronic inflammation process persisted from the period of natural allergen exposure. Continuous subthreshold, which means asymptomatic exposure to perennial allergens to which most of patients are sensitized, could be another reason of this hyperreastivity. The possibility of exposure to the activity of seasonal allergens the whole year in persons with asthma can not omitted, as the presence of pollens in the sample of the house dust in patient's flat is observed during the yield of pollen season. Nonspecific bronchial hyperreactivity in individual patients is fluctuated, which probably is not dependent on the intensity of natural allergen exposure.
The efficacy of nedocromil sodium (NED) (8mg twice daily) in controlling the clinical symptoms of asthma (score symptoms), the pulmonary parameters (FEV1, FVC) and bronchial hyperreactivity to histamine was assessed. The study was performed in double-blind, cross-over and placebo-controlled way in 16 patients suffering from nonatopic, stable, moderate asthma treated with beclomethasone dipropionate (from 400 micrograms to 800 micrograms). NED and placebo were administered in a randomized way with 8-week wash-out period. Bronchial reactivity to histamine, was measured as the amount of histamine causing a 20% fall in FEV1 (PC20H in mg/ml). Treatment with NED did not change asthma symptom scores, FVC and FEV1. Decreased usage of beta 2-agonist was observed. NED did not influence bronchial hyperreactivity to histamine (xg PC20H was respectively 0.09 and 0.11 mg/ml after placebo and 0.06 and 0.08 after NED). The authors conclude that studies with NED in nonatopic asthmatics should be continued, but the dosage of the drug ought to be bigger and the time of treatment ought to be longer.
The aim of the study was to evaluate the effect of 28-days antiinflammatory treatment with nedocromil sodium (Ned.sod.) (Tilade-8 mg/24 hours) on nonspecific bronchial hyperreactivity (PC20H in mg/ml) and spontaneous HRF activity production by mononuclear blood cells in patients with nonatopic bronchial asthma treated with beclomethasone dipropionate. The correlation between PC20H and HRF was also examined. The study was performed in 10 subjects with mild and moderate chronic, stable asthma in a double-blind, placebo-controlled way. Placebo and Ned. sod were given through 4 weeks in a randomized way with 8 weeks wash-out period. It was shown that Ned. sod. did not influence clinical asthma symptom scores, ventilatory parameters and PC20H. No changes in the spontaneous production of HRF activity were observed. The correlation between HRF activity and PC20H assessed 4 times was not significant. The authors conclude that studies with Ned. sod. in nonatopic asthma should be continued, but the dosage of the drug ought to be bigger and the time of treatment should to be longer.
Nedocromil sodium (NS- Tilade) is an effective therapeutic agent against asthma and has been shown to exhibit antiinflammatory activity in vitro. The aim of this study was to assess the effect of NS on the serum neutrophil (NCA) and eosinophil (ECA) chemotactic activity and mononuclear cells-derived histamine releasing factor (HRF) activity in 14 patients with seasonal allergic asthma. The chemotactic activities, HRF and bronchial reactivity to histamine (PC20H in mg/ml) were determined before the grass-pollen season and at the end of the 14-day placebo treatment and 21-day NS treatment during the pollen-season. NCA and ECA were assessed using of the Boyden chamber methods. Blood samples for mononuclear cells culture were collected during the trial. The supernatants were assayed for HRF activity with basophils from a single donor. The NCA index was unaltered during the trial. There was a significant (p < 0.05) increase in the ECA after the NS treatment period (ECA index--2.5) compared with out of season and after placebo treatment (ECA index, 1.88 and 1.82). HRF activity increased after placebo compared with out of season (HRF % activity--38.62 before season, 47.61 after placebo p < 0.05) but NS did not revealed the further effect on HRF activity (49.81 p > 0.05). During placebo the significant decrease in PC20H from 1.81 mg/ml to 0.54 mg/ml (p < 0.05) was observed. NS did not have the effect on nonspecific bronchial reactivity--PC20H--0.74 mg/ml (p > 0.05). The correlation between PC20H and spontaneous production of HRF activity was not found. The results indicate that NS has some effect on inflammatory process which takes place in seasonal asthmatic patients during the natural allergic exposure.
60 patients aged 16 to 46 years with seasonal allergic rhinitis were selected for study. Daily symptom scores of seasonal allergic rhinitis and nonspecific bronchial hyperresponsiveness to histamine (PC20H in mg/ml) before, during the pollen season and after 3 weeks of treatment with loratadine, beclomethasone dipropionate were evaluated. The control group received oxymetazoline. Nonspecific bronchial hyperresponsiveness for 11 patients (18.3%) before the seasons was observed. At the beginning of the season frequency of nonspecific bronchial hyperresponsiveness increased to 26.3% and to 36.8% after 3-week treatment course. Bronchial hyperresponsiveness was not related to any of the way of treatment. The patients treated with beclomethasone dipropionate and oxymetazoline showed significant relief of nasal symptoms. The patients without bronchial hyperresponsiveness showed lower value of symptom scores.
The study was performed in 8 patients suffering from mild asthma. Bronchial allergen challenges with Dermatophagoides pretonyssinus were performed according to Chai et al method. Nonspecific bronchial reactivity to histamine (PC20H in mg/ml) were determined before the allergen challenge and in 90 min. and 24 hrs. after allergen provocation. Blood samples for mononuclear cells culture were collected before the trial and after the allergen challenge in 15, 90 min. and 8 and 24 hrs. The supernatants were assayed for HRF activity with basophils from a single donor. The significant increase of PC20H was observed xgPC20H in mg/ml 0.43 before allergen challenge and 0.08 and 0.125 after allergen provocation. Blood samples did not reveal any significant changes in HRF % activity--mean and SD before challenge test 47.7 16.2 and 49.9 15.0 in 15 min, 53.3 19.0 in 90 min, 56.6 15.8 in 8 hr, 52.5 20.4 in 24 hr after allergen provocation. The correlation between postallergen, nonspecific bronchial reactivity and spontaneous production of HRF activity was not found. The authors discuss the role of HRF in pathogenesis of nonspecific bronchial reactivity of asthmatic patients.
Bronchial hyperresponsiveness is the characteristic feature of bronchial asthma. Inhalation of allergen can cause dual asthmatic response--early and late reaction. Thirteen patients with mild and moderate asthma underwent bronchial allergen challenge. Non-specific bronchial reactivity was measured before, 90 minutes, on the 2nd, 7th, 14th day after provocation. Peak Expiratory Flow was measured every hour during 12 hours after challenge to search for late phase reaction. Increased bronchial reactivity was discovered as early as 90 minutes after challenge, it was still observed on the 2nd and 7th but not on the 14th day after allergen provocation. No relationship was found between appearance of late asthmatic reaction and increased bronchial reactivity.
The aim of this study was to assess the duration of Loratadine effect on histamine H1 receptor in the airway. Six patients with mild or moderate asthma were examined. Bronchial reactivity to histamine was measured according to Cockcroft. The significant blockade of histamine H1 receptors in airway was observed from the 2nd day when 10 mg of Lo was given daily. The maximal protection with 10 mg doses was observed after 3-4 days. After another 5-6 days without Loratadine bronchial responsiveness return to the initial values. Single dose of 30 mg Loratadine given better protection against histamine bronchoconstriction than 10 mg given for 5 days. This effect was observed as early as 60 minutes after administration of Loratadine.
Nedocromil sodium is a non-steroidal prophylactic agent for the management of asthma. We assessed the effect of inhaled of nedocromil sodium 8 mg/24 h in a double blind, placebo controlled study in 14 patients suffering from seasonal (grass-pollen) asthma. Symptom scores for dyspnoe, cough, rhinitis and airway responsiveness to histamine (PC20H) according to Cockcroft et al were estimated before the grass-pollen season and at the end of 14-day placebo treatment and 21-day nedocromil sodium treatment. During placebo period the significant decrease in PC20H from 1.81 mg/ml to 0.54 mg/ml (p < 0.01) was observed. Nedocromil sodium did not have the effect on nonspecific bronchial responsiveness, PC20 - 0.74 mg/ml (p = 0.25). Subjective global assessment scores were significantly better with nedocromil sodium (31.15 mean 2.23) than with placebo (10.5 mean 0.7) p < 0.05.
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.
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The aim of the study was to evaluate concentration and activity of C1 esterase inhibitor (C1 INH) in patients with aspirin-sensitive urticaria. Deficiency of C1 INH is the basis for hereditary angioneurotic oedema. The study was performed in 32 subjects with aspirin-sensitive urticaria. The value of C1 INH in examined patients was the same as in control group. It seems there is no coexistence of aspirin-sensitive urticaria and C1 esterase inhibitor deficiency.
The increase in neutrophil chemotactic activity (NCA) is related to degranulation of mast cells. The study included 10 patients in whom aspirin-induced urticaria was related to NCA increase. Tolerance state to ASA was achieved by administering this drug in incremental doses. In none of the examined patients after 600 mg of ASA given during induced tolerance state, the increase of NCA was observed. The authors conclude that in patients with ASA-urticaria, after ASA desensitization, mast cells degranulation does not occur.
In the paper clinical characteristics of patients with aspirin-induced urticaria were performed. The group of 71 patients, 49 women (69%) and 22 men (31%), mean age of sensitivity symptoms demonstration--32.5 years, underwent allergological, laryngological and histamine dihydrochloride inhalatory tests. Nasal polyps were found in 2 persons (2.8%), atopic diseases in 23 persons (32.3%) and at least one feature of atopy in 37 persons (51.9%). 49 subjects (69%) suffered from urticaria which was not associated with ingestion of aspirin. In 22 patients urticaria developed solely due to aspirin. Urticaria not associated with aspirin had been presents for 2 weeks to 30 years before the onset of sensitivity to aspirin. The authors conclude that aspirin-sensitive urticaria results from concomitance of two different phenomena in one person, i.e. sensitivity to aspirin and urticaria not associated with ingestion of the drug.