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Nasal response to allergen challenge in patients with immediate asthmatic reaction
Abstract
Ten patients with bronchial asthma and allergy to house-dust mite (HDM) and ten normal, nonatopic control subjects underwent a bronchial challenge with flour. Before and 24 h after the allergen provocation with flour, the levels of eosinophil cationic protein (ECP) and myeloperoxidase (MPO) were determined in the serum and nasal lavage fluid. All allergics showed an isolated immediate asthmatic reaction (IAR). After the flour challenge only in asthmatic patients the increase was detected in the mean values of: 1/eosinophils (mean value before 16.7 x 10(3)/mm3; mean after; 10 min 132.9 x 10(3)/ml; 3 hr 183.6 x 10(3)/mm3; 24 h 110.6 x 103/mm3, p < 0.05), 2/basophils (mean before 1.2 x 10(3)/mm3; mean after: 10 min 5.3 x 10(3)/ml; 3 h s 14.1 x 10(3)/mm3 24 h was 18.3/mm3, p < 0.05), 3/neutrophils (mean before 9.2 x 10(3)/mm3; mean after 24 h 18.2 x 10(3)/mm3, p < 0.05) in the nasal lavage fluid. In contrast to a group of normal subjects, asthmatics were found to have higher postchallenge levels of ECP and MPO in the nasal secretions as compared with the prechallenge levels (ECP-mean 3.85 ug/l compared with 32.17 ug/l p < 0.05; MPO-mean 120.02 ug/l compared with 1313.2 ug/l, p < 0.05). The authors did not find any significant difference between pre- and postchallenge levels of ECP and MPO in the serum of asthmatics and controls. The higher levels of MPO as well as higher count of neutrophils observed in asthmatic patients 24 h after allergen challenge support the neutrophil involvement in the allergic inflammation. Our results indicate that both neutrophils and eosinophils take part in allergic reaction in the mucosa.
... Asthma and rhinitis are characterized by similar pathophysiological mechanisms and are often observed in the same patients [12,13]. Previous studies have shown eosinophilic inflammation in the airways of rhinitic patients without asthma as well as eosinophilic infiltration of the nasal mucosa of asthmatic patients without rhinitis [14][15][16]. Furthermore, there is evidence of a cross-talk between nasal and bronchial mucosa after nasal allergen provocation, with an overexpression of adhesion molecules in both nasal and bronchial mucosa in rhinitic patients [17]. ...
... A number of investigators emphasized the unique importance of ECP levels in assessing the extent of the body's reaction to pathological effect of the allergen. Pałczynski et al. achieved a manyfold increase in ECP levels from 3.85 mg/L to 32.17 mg/L in a group of patients with a history of allergy; this change was statistically significant [20]. The findings were consistent with those by Lopez et al., who reported significantly higher ECP levels in 65% of the study population (P < 0.05) [17], and Bernardinii et al., who achieved significantly higher ECP levels in nasal lavage (P < 0.05) at hour 24 of the study [21]. ...
The Purpose of the study was to assess the inflammatory response of the nasal mucosa based on nitric oxide concentration in exhaled breath and the level of inflammatory markers tryptase/eosinophil cation protein (ECP) in the nasal lavage fluid obtained via a nasal lavage collection device of our design. Material: The study group included 60 subjects: 30 patients diagnosed with an allergy to common environmental allergens (dust mites/grasses) and 30 healthy controls. The Method used in the study was NAPT, monitored via measuring nasal nitric oxide (nNO), and tryptase/ECP in nasal lavage fluid. Results: The early phase of the allergic reaction involved a drop in nNO with a simultaneous increase in nasal lavage tryptase levels (2.23 μg/L in the allergic rhinitis subgroup), which significantly differentiated between the allergic rhinitis and healthy groups. The late phase of reaction showed a significant increase in nNO and nasal lavage ECP levels (three-fold higher in the allergic rhinitis group than in healthy individuals). Conclusion: NAPT affects the nasal mucosa locally by initiating a series of symptoms characteristic for the early and late phases of the allergic reaction resulting from inflammatory marker secretion.
... Asthma and rhinitis are characterized by similar pathophysiological mechanisms and are often observed in the same patients [12,13]. Previous studies have shown eosinophilic inflammation in the airways of rhinitic patients without asthma as well as eosinophilic infiltration of the nasal mucosa of asthmatic patients without rhinitis [14][15][16]. Furthermore, there is evidence of a cross-talk between nasal and bronchial mucosa after nasal allergen provocation, with an overexpression of adhesion molecules in both nasal and bronchial mucosa in rhinitic patients [17]. ...
The site and distribution of inflammation in the airways of asthmatic patients has been largely investigated. Inflammatory cells are distributed in both large and small airways in asthma. It has been demonstrated that distal lung inflammation in asthma may significantly contribute to the pathophysiology of the disease. The upper airways have also been implicated in the overall asthmatic inflammation. Although it is now accepted that lung inflammation is not restricted to the intrapulmonary airways in asthma, little is known about cell distribution in the other lung compartments and their relation to the intrapulmonary airways.
We aimed to map the inflammatory process in fatal asthma (FA), from the upper airways to the lung parenchyma.
Eosinophil, neutrophil, mast cell and lymphocyte content were determined in nasal mucosa, the trachea, intrapulmonary airways and parenchyma (peribronchiolar and distal) of 20 patients with FA and 10 controls.
Eosinophil content was higher in all studied areas in FA compared with controls (P<0.02). Mast cell content was higher in the outer area of larger airways, small membranous bronchioles and in peribronchiolar parenchyma of FA compared with controls (P<0.04). CD3+, CD4+and CD20+cells showed increased content in FA intrapulmonary airways compared with controls (P<0.05). There was a positive correlation between CD4+cell content in nasal mucosa and larger airways in asthmatics. Increased neutrophil content was observed only in peribronchiolar parenchyma of FA (P=0.028).
Eosinophils present a widespread distribution within the respiratory tract in FA, from the nasal mucosa to the distal lung. The outer wall of small membranous bronchioles is the main site of inflammatory changes in FA. There is a localized distribution of alveolar inflammation at the peribronchiolar region for mast cells and neutrophils. Our findings provide further evidence of the importance of the lung periphery in the pathophysiology of FA.
Background
Reports on the studies conducted in Western Europe and North America revealed that from 2.8 to 16.9% of the health care personnel were allergic to latex. No respective data are available from Eastern European countries.MethodsA postal questionnaire inquiring about the history of latex-induced allergic reactions was distributed among 3,750 nurses. The participation rate was 77.3%. To verify the results of the survey, in randomly selected nurses, skin prick tests with latex and tropical fruit allergens, evaluation of total IgE, and specific anti-latex IgE, skin and nasal provocation with latex were performed.ResultsAllergic symptoms in the workplace were reported by 1,016 subjects (35%); out of this group 847 (29.2%) persons associated the symptoms with latex exposure. The group of cases with self-reported latex allergy revealed a significantly increased frequency of history of atopy, allergy to β-lactam antibiotics and tropical fruits. Allergy to latex was confirmed in 33.3% of randomly selected nurses with a positive history of occupational allergy. It was found that 18.6% of nurses working at hospital wards were allergic to latex. The 95%CI was estimated to be 13.5–23.6%.Conclusions
Latex allergy is an important health problem among nurses in Poland. Atopy, allergy to >-lactam antibiotics and tropical fruits, are the risk factors for latex allergy. Am. J. Ind. Med. 35:413–419, 1999. © 1999 Wiley-Liss, Inc.
Respiratory function and immunological status were studied in 40 cocoa and 53 flour processing workers employed as packers in a confectionry industry and in 65 unexposed control workers in the same industry. A high prevalence of chronic respiratory symptoms was recorded in exposed workers, varying from 5.0% to 30.0% in cocoa workers and from 5.7% to 28.3% in flour workers. Occupational asthma was diagnosed in 2 (5%) of the cocoa workers and in 3 (5.7%) of the flour workers. None of the control workers suffered from occupational asthma. The prevalence of almost all chronic respiratory symptoms was significantly greater in cocoa and flour workers than in control workers. There was also a high prevalence of acute symptoms that developed during the work shift, being highest for cough (cocoa: 57.5%; flour: 50.9%) and eye irritation (cocoa: 50.0%; flour: 54.7%). Significant across-shift reductions of ventilatory capacity were recorded in exposed workers, being largest for flow rates at 50% and the last 25% of the vital capacity on maximum expiratory flow-volume (MEFV) curves (FEF50, FEF75). The prevalence of positive skin tests for cocoa (60.2%) was significantly higher than the prevalence of positive skin tests for flour (25.8%) among the 93 exposed workers (p < 0.05). Control workers had significantly lower prevalences of positive skin tests to cocoa (4.6%) and flour (12.3%) than exposed workers (p < 0.01). Increased total serum IgE levels were found in 17.5% of cocoa and in 18.7% of flour workers; none of the control workers had increased IgE levels. Bronchoprovocation testing demonstrated significant decreases in lung function following inhalation of cocoa dust extract and flour dust in workers with respiratory symptoms and large across-shift reductions in lung function. Dust concentrations in the working environment were higher than those recommended by Croatian standards. These data suggest that workers employed in the processing of cocoa and flour may be at a high risk for the development of allergic sensitization and respiratory impairment. Am. J. Ind. Med. 33:24–32, 1998 © 1998 Wiley-Liss, Inc.
The objective of this study was the evaluation of the usefulness of the nasal challenge test in the diagnosis of allergic respiratory diseases in subjects occupationally exposed to flour. A single-blind, placebo controlled study was conducted in 100 subjects with occupational atopic asthma with rhinitis. The control groups consisted of 20 atopic subjects not sensitized to investigated allergens and 20 healthy subjects. A 'nasal pool' technique was used to evaluate the changes of the cellular response and protein level in nasal washings after topical provocation with allergen or placebo. The concentrations of eosinophil cationic protein and mast cell-derived tryptase in nasal fluid were evaluated in 60 cases. There were significant increases in eosinophil and basophils number, albumin/total protein ratio, eosinophil cationic protein and tryptase levels in occupationally sensitized patients challenged with specific allergens. There were neither severe bronchial reactions or an increase of bronchial hyperreactivity in occupationally sensitized patients after the nasal provocation with flour. The nasal challenge test appears to be a very useful and safe tool for diagnosing occupational allergy.
Reports on the studies conducted in Western Europe and North America revealed that from 2.8 to 16.9% of the health care personnel were allergic to latex. No respective data are available from Eastern European countries.
A postal questionnaire inquiring about the history of latex-induced allergic reactions was distributed among 3,750 nurses. The participation rate was 77.3%. To verify the results of the survey, in randomly selected nurses, skin prick tests with latex and tropical fruit allergens, evaluation of total IgE, and specific anti-latex IgE, skin and nasal provocation with latex were performed.
Allergic symptoms in the workplace were reported by 1,016 subjects (35%); out of this group 847 (29.2%) persons associated the symptoms with latex exposure. The group of cases with self-reported latex allergy revealed a significantly increased frequency of history of atopy, allergy to beta-lactam antibiotics and tropical fruits. Allergy to latex was confirmed in 33.3% of randomly selected nurses with a positive history of occupational allergy. It was found that 18.6% of nurses working at hospital wards were allergic to latex. The 95% CI was estimated to be 13.5-23.6%.
Latex allergy is an important health problem among nurses in Poland. Atopy, allergy to beta-lactam antibiotics and tropical fruits, are the risk factors for latex allergy.
Treatment options for allergic rhinitis include antihistamines, decongestants, anticholinergics, cromolyn sodium and corticosteroids. As the nose is a small organ, comprising less than 1% of total body mass and surface area, it seems logical to confine treatment of rhinitis to the diseased organ.
To evaluate the effects of therapy with intranasal fluticasone propionate (FP), both on subjective symptoms and pathophysiological mechanisms, in rhinitis patients during pollen season when the patients were symptomatic.
We used a double-blind, placebo (PLA)-controlled, randomized, double dummy, parallel group study of the effect of 6 weeks treatment. The double-blind comparison was made between the following three treatments: FP aqueous nasal spray, 200 microg taken once daily, levocabastine (LEV) nasal spray, 200 microg taken twice daily and PLA nasal spray. Clinical evaluation and the levels of cells and mediators in nasal washing were performed before and after treatments. Twenty-four patients (11 men and 13 women, aged 17-50 years, mean age 30.1 +/- 8.5) with strictly seasonal allergic rhinitis to Parietaria entered the study. Clinical evaluation and the levels of inflammatory cells (eosinophils and activated eosinophils, i.e. EG2+) and their mediators (tryptase, eosinophil cationic protein, eosinophil protein X and neutrophil myeloperoxidase) in nasal-lavage were performed before and after treatments.
Treatment with FP significantly increased, with respect to placebo, the percentage of days without sneezing (P < 0. 001), nasal blockage (P < 0.001), rhinorrhea (P < 0.001), nasal itching (P < 0.001). Furthermore, treatment with FP showed additional benefits with respect to LEV. The percentage of days without nasal blockage was significantly higher in the FP group that in the placebo group (P = 0.018). The same applied to rhinorrhea (P = 0.009). The percentages of days without sneezing and itching were instead not significantly different between the two groups. As expected, no significant differences were observed in baseline medians of the rhinitis symptom scores as well as in mean values of all mediators and eosinophils in nasal lavages of the various groups under study. After treatment the mean of subjective symptoms as well as all values in nasal lavage level fell significantly only in the FP group, whereas no significant changes were observed either in LEV or PLA groups. Accordingly, significant differences were observed at the end of the treatments between the values of fluticasone group vs LEV and PLA group values. Significant correlations between these values and symptom scores were found, according with literature data suggesting a pathogenetic role for these mediators and eosinophils in rhinitis.
FP (200 microg once daily) affords a significant degree of improvement in rhinitis control during pollen season, as measured by subjective and objective parameters, compared with LEV (200 microg twice daily) and PLA. The therapeutic benefits of intranasal FP are reflected in, and may be caused by, the decrease in nasal inflammatory cells.
The three forms of IgE receptor: the heterotrimeric high-affinity receptor for IgE (FcepsilonRI), the low-affinity receptor for IgE (FcepsilonRII/CD23) and the Mac-2/IgE-binding protein (epsilonBP), have previously been found on human neutrophils. We have previously shown that specific allergens are able to activate functional responses by neutrophils from allergic patients sensitized to those allergens. Neutrophils are present in the sites of allergic inflammation. The primary (azurophilic) granules of neutrophils contain a variety of enzymes that might potentiate inflammation, such as myeloperoxidase (MPO). It is not known whether specific allergens are able to elicit MPO release by neutrophils from allergic patients.
Neutrophils were challenged in vitro with the specific allergen that produced clinical symptoms in asthmatic patients. Also, the cells were challenged with allergens that the patients were not sensitive to. Neutrophils from normal subjects were also challenged with allergens.
The in vitro challenge of neutrophils with allergens that the patients were sensitive to elicited a release of MPO by these cells. The in vitro activation of neutrophils was highly allergen-specific, in such a way that allergens other than those accounting for clinical symptoms did not evoke MPO release, and allergens were ineffective on neutrophils from healthy donors.
An IgE-dependent mechanism might promote MPO release by neutrophils at allergic sites.
Corticosteroids are considered to be particularly effective in reducing nasal congestion and are therefore recommended as first-line treatment in allergic rhinitis patients with moderate to severe and/or persistent symptoms.
We compared the clinical efficacy of fluticasone propionate aqueous nasal spray (FPANS) 200 microg given once daily, administered in mono-therapy or combined therapy with a H1 receptor antagonist (cetirizine, CTZ) or with a leukotriene antagonist (montelukast, MSK), and the combined therapy of CTZ plus MSK in the treatment of patients affected by allergic rhinitis to Parietaria during natural pollen exposure. In addition, we examined the effect of the treatment on eosinophil counts and eosinophil cationic protein (ECP) in nasal lavage performed at beginning of season, during season and at the end of the season.
One hundred patients aged 12-50 years (mean+/-SD 31.8+/-9.6) with a history of moderate to severe Parietaria pollen-induced seasonal allergic rhinitis were selected. A randomized, double-blind, double dummy, placebo (PLA)-controlled, parallel-group study design was used. Patients were treated FPANS 200 microg once daily (n=20) or with FPANS 200 microg once daily, plus CTZ (10 mg) in the morning (n=20), or with FPANS 200 microg once daily, plus MSK (10 mg) in the evening (n=20) or with CTZ (10 mg) in the morning plus MSK in the evening (n=20) or matched PLA (n=20). Assessment of efficacy was based on scores of daily nasal symptoms and on eosinophil counts and ECP in nasal lavage.
All treatments showed significant differences (P<0.001) compared with PLA in terms of total symptom, rhinorrhea, sneezing and nasal itching scores. Concerning nasal congestion on waking and daily only the groups treated with FPANS in mono-therapy or in combined therapy showed significant differences compared with PLA. Comparing the group treated with FPANS alone and the groups treated with FPANS plus CTZ, we found significant differences for total symptom score (P=0.04) and for nasal itching (P=0.003). The comparison between FPANS plus CTZ and FPANS plus MSK showed significant difference for nasal itching (P=0.003). Finally, there were significant differences between the group treated with FPANS and the group treated with CTZ plus MSK for total symptom score (P=0.009), for nasal congestion on waking (P<0.001) and nasal congestion daily (P<0.001). Also the comparisons between the group treated with FPANS plus CTZ and the group treated with CTZ plus MSK demonstrated significant differences (P<0.001) for total symptom, for nasal congestion on waking and for nasal congestion on daily, for rhinorrhea (P=0.04) and for nasal itching (P=0.003) scores. Concerning the comparison between the group treated with FPANS plus MSK and the group treated with CTZ plus MSK we found significant differences for total symptom score (P=0.005), for nasal congestion on waking (P<0.001) and for nasal congestion on daily (P<0.001). No other differences were observed between the groups. Concerning blood eosinophil counts, significant differences were found between the treatments with FPANS in mono-therapy or in combined therapy with PLA group during and at the end of the season (P=0.0003 and P<0.0001, respectively). Concerning eosinophils and ECP in nasal lavage, all treatments showed significant differences (P<0.001) compared with PLA. Besides, there were significant differences (P<0.001) between the groups treated with FPANS alone or in combined therapy and the group treated with CTZ plus MSK.
The results of this comparative study demonstrate that FPANS is highly effective for treating patients affected by allergic rhinitis, with efficacy exceeding that of CTZ plus MSK in combined therapy. In addition, the regular combined therapy of FPANS plus CTZ or plus MSK would not seem to offer substantial advantage with respect to FPANS in mono-therapy in patients affected by seasonal allergic rhinitis.
Allergen-specific conjunctival challenge is a fruitful and complete tool in evaluating pathophysiological phenomena of allergic inflammation. After challenge, a significant neutrophil infiltrate occurred in allergic subjects. The primary (azurophilic) granules of neutrophils contain a variety of enzymes that might potentiate inflammation, such as myeloperoxidase (MPO). It is not known whether allergen-specific conjunctival challenge (ASCC) is able to elicit MPO release. We also investigated the possible role of immunotherapy (IT) in the release of MPO.
The groups studied included Dactylis glomerata-sensitive adult atopic patients suffering from seasonal allergic rhinoconjunctivitis, and healthy adult nonatopic volunteer controls. One group of allergic patients received no specific hyposensitization (not-IT allergic group). A second group of allergic patients had been immunotherapy-treated with Dactylis glomerata extract for the preceding three years and continued to receive a maintenance dose within the highest potency of the extract (IT-allergic group). ASCC with Dactylis glomerata was performed outside the pollen season in all subjects. Myeloperoxidase was assayed by MPO-enzyme immunoassay method.
Thirty minutes after challenge, myeloperoxidase levels in the non-immunotherapy allergic patients were significantly higher compared than in the healthy group (p<0.001). The levels of myeloperoxidase released in the immunotherapy allergic group were significantly lower than those in the nonimmunotherapy allergic group (p<0.001) and higher than those in nonallergic subjects (p<0.001).
These results indicate that after ASCC there is a release of MPO. Our study suggests that immunotherapy actively modifies the release of MPO after ASCC.
Hyperreactivity to environmental factors is objectively expressed as respiratory, cutaneous and gastrointestinal disease. Approaching the diagnosis of an occupational disorder, a practical distinction was made between toxicity and allergy. The study of occupational allergic disease included particular procedures that led to standardized models and concepts. The contribution to the improvement of medical knowledge is reviewed according to selected experiences. The diagnostic aspects of asthma, rhinitis, dermatitis and urticaria are considered as regards to methodology of assessment of the occupational etiology with attention to demonstrative examples, which are worthwhile for the general medicine, too. Basic steps of risk agent identification, exposure assessment, threshold dose response measurement, allergen challenges and interaction are the original contribution of the occupational medicine to the diagnosis of allergic disorder. The clinical picture of asthma was clarified by the results of the specific bronchial provocation test, proving the important role of di-isocyanates and metal salts. Occupational rhinitis showed to be connected to asthma with predictive aspects in bakers' disease. Occupational dermatitis was linked to the development of experimental patch tests. Occupational urticaria included the concept of airborne contact allergy or nickel interactive food and occupational sensitivity. Occupational allergic diseases are emerging as a consequence of low environmental exposure, but they were remarkably studied in the past either for pathogenesis or for diagnostic procedures. Methods and acquisition are available also for the general medicine when an individual's specific reactivity is under investigation.
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