Nonspecific Bronchial Hyperreactivity Research Articles

Feather or synthetic? That is the question

Feather or synthetic? That is the question

Asthma-like symptoms, atopy, and bronchial responsiveness in furniture workers.

OBJECTIVES: To study the role of individual and occupational risk factors for asthma in furniture workers. METHODS: 296 workers were examined (258 men, 38 women) with a questionnaire of respiratory...

Do genetics play a role in the pathogenesis of asthma?

Asthma is a phenotypically heterogeneous disorder associated with intermittent respiratory symptoms, bronchial hyperresponsiveness (BHR), and reversible airflow obstruction. 1, 2 Most individuals with asthma have evidence of BHR and atopy, with elevated total serum IgE, allergen-specific IgE, or skin-test reactivity to common allergens. At present, it is not clear whether asthma, BHR, and atopy are clinical manifestations of the same underlying primary defect or whether they share common pathways with distinct primary molecular origins. A genetic component to asthma has long been suggested by studies demonstrating increased prevalences of asthma among first-degree relatives of asthmatic subjects and greater concordance rates among monozygotic compared with dizygotic twins. 3-7 Such “clustering” in families is consistent with a genetic cause but may also reflect the effects of shared environmental exposures. Thus familial clustering does not prove a genetic cause. Although segregation analyses in populations of asthmatic families have suggested the likelihood of a major

The combined influence of immunotherapy and mite allergen reduction on bronchial hyperresponsiveness in mite-sensitive asthmatic children.

Encasings for mattresses, blankets and pillows in combination with mite allergen reduction on the floor have proved effective in reducing bronchial hyperreactivity of mite-allergic children. We studied the effect of combining the use of encasings with specific immunotherapy in comparison to the use of encasings alone (control group). Twenty mite-allergic children (Skin Prick Test, RAST, mean age 10 years) with asthma and high domestic mite allergen exposure ( > 2 microg Der p 1 + f 1/g mattress dust) were included in our study. The concentration of these major allergens as well as specific and nonspecific bronchial hyperreactivity (PC20 FEV1 histamine) were assessed before, 6 months after and 1 year after start of treatment. All children received elongated polytetrafluorethylene (ePTFE; Goretex/Intervent Allergy Bedding System) encasings. A subgroup of eight children were treated additionally by specific immunotherapy with a partially purified mite extract (ALK Scherax) and a maximum dose of 100000 SQ-U Der p + f. Initially both groups were comparable with respect to the parameters assessed. In 80% of children, encasings reduced Der p 1 and Der f 1 concentrations on the mattress to below 3% of the initial values (P < 0.01). The median reduction was 99%. PC20 FEV1 histamine increased from 0.4 to 1.4 mg/dl (median) in the combined group with immunotherapy and encasings (P < 0.05) and remained essentially unchanged in the control group. PC20 FEV1 Der p did not increase significantly in either group. Specific immunotherapy with allergen extracts is an effective adjunct to encasings. Encasings, a key factor for reducing Der p 1 and Der f 1 on the mattress, should be used in combination with other avoidance measures (e.g. removal of carpets) in order to improve allergen-induced bronchial hyperreactivity.

The Nonspecific Bronchial Hyper-reactivity during Refractory Period Following Exercise in Exercise-Induced Asthma

The Nonspecific Bronchial Hyper-reactivity during Refractory Period Following Exercise in Exercise-Induced Asthma

Circulating levels of soluble interleukin-6 receptor in patients with bronchial asthma.

In the search for markers of airway inflammation, we investigated the role of soluble interleukin-6 receptor (sIL-6R) in patients with bronchial asthma. Serum levels of sIL-6R were measured in 20 patients with stable asthma and in 18 healthy control subjects by means of a sandwich enzyme-linked immunosorbent assay. Such levels were also evaluated during a spontaneous attack of asthma (n = 10) as well as that after allergen inhalation (n = 7). Results were compared with those observed during the stable state and after the inhalation of methacholine. Serum levels of sIL-6R in asthmatic patients (132 +/- 31 ng/ml) significantly exceeded those of control subjects (111 +/- 16 ng/ml) (p < 0.05). These levels showed no correlation with such clinical variables as nonspecific bronchial hyperreactivity, atopic status, or serum concentration of IgE. Serum sIL-6R levels observed during an asthmatic attack versus those during the stable state (4 wk later) differed significantly. After a severe attack of asthma, such levels were significantly elevated on the second and third days, but not on Day 5. After challenge, circulating levels of sIL-6R were significantly increased 24 h after the inhalation of allergen but not of methacholine. Results suggest that serum levels of sIL-6R are increased in patients with asthma and are further increased during a spontaneous attack or that provoked by the inhalation of allergen. Thus, serum sIL-6R may reflect inflammation of the airway. Further studies are indicated to determine the clinical significance and the application of serum levels of sIL-6R in evaluating asthmatic patients.

Non-specific airway hyperresponsiveness in mono-sensitive Sicilian patients with allergic rhinitis. Its relationship to total serum IgE levels and blood eosinophils during and out of the pollen season.

Initial attempts to evaluate the association between allergic rhinitis and non-specific bronchial responsiveness has produced conflicting results. In fact, some studies showed a strong correlation and other failed to find an association. However, little is known about the effect of natural specific allergen exposure on the bronchial reactivity of mono-sensitive patients with rhinitis in the southern Mediterranean area, in relation to skin reactivity to allergens, total serum IgE levels and blood eosinophils. The significance of the association between allergic rhinitis, and abnormal airway responsiveness with regard to the pathogenesis of asthma is unclear. For this reason, we have studied non-specific bronchial hyperreactivity, in patients with seasonal allergic rhinitis, with reference to the responsible allergen. The aim of the study was to correlate the responsiveness to bronchoprovocation with methacholine in subjects a with allergic rhinitis during and out of the pollen season with total serum IgE and blood eosinophils. Fourty-nine non-smoking patients with clinical diagnosis of allergic rhinitis and mono-sensitive skin-prick tests to pollen allergens were enrolled in the study. Twenty patients suffered from seasonal rhinitis to Parietaria pollen, 15 patients to Gramineae pollen and 14 patients to Olea pollen. In all patients lung function measurements (assessed as response to methacholine), total serum IgE and blood eosinophil counts were measured during and out of the pollen season. During pollen season, 16 out of 49 rhinitis patients demonstrated values of bronchial responsiveness measured as response to inhaled methacholine in the asthmatic range whereas out of the pollen season only eight patients were in the asthmatic range. By analysing the results with reference to the responsible allergen, during the pollen season 15 out of 16 patients were Parietaria-sensitive and out of the pollen season seven out of eight patients. Finally, in Parietaria-sensitive rhinitis bronchial responsiveness significantly correlated, during and out of the pollen season, with total serum IgE and with blood eosinophil counts. Our results are consistent with the hypothesis that Parietaria is more important than Olea and Gramineae as a risk for developing non-specific bronchial hyperresponsiveness. On the whole, present observations provide further evidence that there is an interrelationship of allergen kind, total serum IgE, eosinophil and bronchial hyperresponsiveness suggesting that they may play a role in the development of bronchial asthma in rhinitis patients.

High prevalence of mollusc shell hypersensitivity pneumonitis in nacre factory workers

Following the discovery of hypersensitivity pneumonitis caused by the inhalation of mollusc shell dust in two workers from a nacre-button factory, the health status of 26 workers employed in sawing mollusc shells was investigated. The evaluation included the administration of two questionnaires and radiological, functional and immunological assessments of all workers at the outset and 1 year later, when hygienic and therapeutic measures had been taken. Six workers, in whom specific inhalation challenge test was positive, were diagnosed with mollusc shell hypersensitivity pneumonitis, thus yielding a prevalence of 23%. Evidence of diffuse lung disease and systemic symptoms was found in these patients. Nonspecific bronchial hyperreactivity was also found more frequently in patients with mollusc shell hypersensitivity pneumonitis. Specific immunoglobulin G (IgG) level and specific skin testing failed to differentiate patients with mollusc shell hypersensitivity pneumonitis from other exposed workers; whereas, nonspecific skin testing, which was impaired in the patients, did differentiate. Bronchoalveolar lavage and transbronchial biopsy performed in patients with mollusc shell hypersensitivity pneumonitis were consistent with the disease. Removal from an environment containing mollusc shell dust was followed by regression of clinical, radiological and functional changes. The clinical picture of the 20 workers who did not present mollusc shell hypersensitivity pneumonitis remained unchanged, but functional decline was observed despite improvement in the environmental conditions of the factory. This report describes the first series of patients with mollusc shell hypersensitivity pneumonitis studied, and underlines the importance of careful follow-up of workers occupationally-exposed to mollusc shell dust.

Role of tachykinins and neutral endopeptidase in toluene diisocyanate-induced bronchial hyperresponsiveness in guinea pigs

The role of tachykinins in toluene diisocyanate (TDI)-induced non-specific bronchial hyperreactivity (NSBH) in guinea pigs was investigated, and it was determined whether or not the activity of airway neutral endopeptidase (NEP) was inhibited in conditions where a bronchial hyperreactivity to acetylcholine (ACh) was observed. Exposures to 3 ppm TDI for 1 h, or to 0.029 ppm for 8 weeks caused a significant bronchial hyperreactivity to ACh. The depletion of tachykinins by a pretreatment with capsaicin (140 mg/kg) eliminated the TDI-induced airway hyperresponsiveness in both patterns of exposure to TDI. Capsaicin treatment had no effect on the response to ACh in guinea-pigs exposed to air (controls). Bronchial NEP activity determined by histoenzymology was significantly less 4 and 24 h after the end of a 1-h exposure to 3 ppm TDI than after exposure to air. Bronchial NEP activity evaluated 24 h after the end of a 48-h exposure to 0.116 ppm TDI, or a 1-week exposure to 0.050 ppm TDI was not significantly different from those of controls exposed to air, whereas in the same conditions of exposure a NSBH is observed in guinea-pigs. These data suggest that tachykinins released from C-fibers upon acute or repeated exposures to high or low concentrations of TDI, respectively, play an essential role in the observed bronchial hyperreactivity, and that the inhibition of NEP by TDI cannot completely account for the observed airway hyperreactivity.

Asthma and rhinitis in wooding workers.

We present some cases of rhinitis and asthma in wooding workers exposed to hard or soft woods. The specific provocation test confirmed the diagnosis of rhinitis in three patients and of asthma in four. Rhinitis was caused by oak, beech, and pine, while asthma was caused by obeche, chestnut, acacia, and iroko. Occupational exposure to the specific wood, before onset of symptoms (symptom latency) was shorter for patients with asthma. All seven patients with respiratory symptoms were nonsmokers; three were atopics and four, all with asthma, had nonspecific bronchial hyperreactivity. Twenty-four hours after the test, PD20FEV1 had decreased in two cases with rhinitis and two with asthma, although the data did not reach statistical significance (Wilcoxon matched-pairs test: NS). After the SBPT, blood eosinophils increased in two cases with rhinitis and three with asthma, and the data were at the limit of statistical significance (P = 0.046). The study confirms that not only hard essences, but also soft woods can cause respiratory symptoms, although the pathogenetic mechanisms are still unclear. A specific provocation test is still the best and sometimes only means of diagnosing wood asthma; standardized protocols with repeated measurements of nonspecific airway responsiveness and of eosinophils in the blood may be helpful for a better understanding of the pathogenetic mechanism and predisposing factors.

Accelerated cell‐mediated broncho‐obstructive reaction to inhaled stepronin: a case report

We describe the case of a 20-year-old man who developed an obstructive bronchial reaction accompanied by a maculopapular facial rash 8 h after an aerosol treatment with the mucolytic drug stepronin. The results of intradermal and patch testing with stepronin, together with those of bronchial challenge and histologic findings in patch-tested skin, indicate that the patient's reaction involved an accelerated cell-mediated mechanism of hypersensitivity. Bronchial challenges with methacholine demonstrated a transient increase in nonspecific bronchial hyperreactivity.

Gas Trapping as a Predictor of Positive Methacholine Challenge in Patients With Normal Spirometry Results

Methacholine challenge studies are often conducted to diagnose asthma in patients with mild or intermittent respiratory symptoms when screening spirometry results are normal. We hypothesized that in patients with increased nonspecific bronchial hyperreactivity (NSB-HR), gas trapping might be present and that this information could be a factor in clinical decision making. To assess the relationship between gas trapping and NSBHR, we conducted a retrospective chart review of 500 patients who had undergone pulmonary function testing, including lung volume measurement and methacholine challenge. Measurements of airflow, lung volumes, and methacholine PC20 values were compiled and analyzed. FRC was determined by body plethysmography (FRCB) and by helium dilution (FRC-He). FRCB-FRC-He, RV (percent of predicted) RV/TLC, and RV/TLC (percent of predicted) were used as measures of gas trapping. RV% and RV/TLC% were the best predictors of a PC20 < or = 8 mg/mL. In the subset of 169 patients who had FEV1/FVC > or = 90% of pred, an RV/TLC% value of 125% of predicted or greater had a positive predictive value of 62.5% and a negative predictive value of 62.0%. RV/TLC% was the only measure of gas trapping that was associated with a PC20 < or = 8 mg/mL (p < 0.05). Linear regression revealed no correlation between any measure of gas trapping and quantified PC20 value (< or = 16 mg/mL). These results suggest that patients with a normal FEV1/FVC who show gas trapping have an increased likelihood of a positive methacholine challenge study. Furthermore, in these patients, RV/TLC (percent of predicted) is the best predictor of a positive methacholine challenge and this parameter may be useful in raising the clinical suspicion of asthma in the large population of patients presenting with respiratory symptoms and normal flow rates.

Occupational asthma and related respiratory disorders

Occupational rhinitis is a common but generally underreported entity. Although it may occur alone, it is frequently associated with occupational asthma. Occupational asthma may have one of several presentations that are difficult to distinguish from non-work conditions. The respiratory tract acts as the final common pathway for all inhaled environmental pollutants, whether encountered in the home or at work. More than 200 chemicals have been incriminated as a cause of work-related asthma. It is said that about 2% of the 10 million Americans who have asthma acquired it as a result of some chemical irritant or immunogen in their work environment. A number of predisposing factors facilitate the development of work-related asthma. These include industrial conditions, climatic factors, atopic predisposition, smoking, recreational drug use, viral infection, nonspecific bronchial hyperreactivity, and a variety of miscellaneous factors. Pathogenetically, occupational asthma may be immunologic or nonimmunologic in nature. The immunologic variants involve sensitization to a variety of large-molecular-weight constituents. The major nonimmune variant is referred to as inflammatory bronchoconstriction or reactive airways dysfunction syndrome (RADS). There are well-defined criteria for the diagnosis of immunologic and nonimmunologic asthma. The several clinical variations of occupational asthma can be difficult to distinguish from nonindustrial disorders. The most common presentation in practice involves the worker with preexistent asthma who has been adversely affected by work exposures. Occasionally these industrial exposures precipitate permanent impairment. It is clear, however, that occupational asthma is not a single, simple, or homogeneous entity, even when a single specific causal factor can be identified in the workplace. Therefore the physician must be aware of the patient's entire medical history and the precise occupational exposures and must have convincing physiologic evidence that demonstrates a cause-and-effect relationship before making a definitive diagnosis of work-related asthma. Once the diagnosis is established, the worker should be removed from the workplace. If the diagnosis is made in a timely fashion, the patient should experience a significant improvement. The major factor in determining a poor prognosis in occupational asthma is the duration of exposure before the diagnosis is established. Prevention of the disorder is the best therapeutic intervention.

Lack of Significant Bronchial Reactivity to Inhaled Normal Saline in Subjects with a Positive Methacholine Challenge Test

Patients with symptoms suggestive of asthma often have normal resting pulmonary function. In these patients, a determination of airway responsiveness by bronchial challenge is useful in demonstrating bronchial hyperreactivity (BHR), a defining feature of asthma. In the methacholine (Mch) challenge, it is recommended that following a baseline measurement of FEV1, the patient inhale the normal saline (NS) diluent and FEV1 be repeated to assess for nonspecific BHR to NS. It is also recommended that post-NS inhalation FEV1 should be used as the control value from which decrement in FEV1 is compared following Mch challenge. Mch testing was performed in 44 patients with symptoms suggestive of asthma (cough, chest tightness, dyspnea) and normal resting pulmonary function. Baseline spirometry was obtained and repeated after inhalation of NS and after five breaths each of Mch at the following concentrations: 0.025 mg/ml, 0.25 mg/ml, 2.5 mg/ml, 10 mg/ml, and 25 mg/ml. The procedure was terminated when FEV1 decreased to at least 80% of the post-NS value or if the maximal concentration of Mch had been reached. The post-NS FEV1 value was > or = 91% of the pre-NS value in all the subjects range 91-105%). Using the post-NS FEV1 as the recommended control value, 20 patients (45%) had a positive Mch challenge and 24 patients (55%) had a negative Mch challenge. Had we used the pre-NS FEV1 as a control value, only 2 patients would have been reclassified, and when these 2 cases are carefully examined, there would have been no significant change in the clinical interpretation of the MCh test.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of Zatebradine, a Novel 'Sinus Node Inhibitor', on Pulmonary Function Compared to Placebo

Summary: Zatebradine, a member of a novel class of drugs called 'sinus node inhibitors', is a specific heart rate lowering drug suitable for the treatment of stable angina pectoris. Animal studies showed that relatively high intravenous doses of zatebradine contracted guinea-pig airways by a histamine-like mechanism. Therefore, the objective of the present study was to assess the bronchopulmonary effects in asthmatic patients who showed a moderate to severe bronchial hyperreactivity towards histamine (PC 20 FEV 1 ≤1 mg/ml). Moreover, it had to be established to what extent the bronchial responsiveness to inhaled salbutamol was retained and whether pulmonary effects were related to the severity of bronchial hyperreactivity. By means of a double-blind cross-over design, single oral doses of zatebradine (10 mg) or placebo were administered on two occasions with a washout phase of at least 3 days. Sixteen patients, four female and 12 male, with stable mild to moderate bronchial asthma (FEV 1 less than 80% predicted) were selected. Their mean age was 54 years and the mean FEV 1 was 1.831 (59% predicted). They showed a mean improvement in FEV 1 of 27% 15 min after inhaling 200 μg salbutamol; the mean PC 20 was 0.35 mg/ml. Following test drug intake, the respiratory and cardiac effects were assessed at regular time intervals up to 6 h after administration. In comparison to placebo, zatebradine induced small, but significant ( P<0.05), mean falls of 128 ml and 168 ml in FEV 1 at 3 h and 6 h after drug intake. A large inter-individual variation in response was noted. In two of the 16 patients a deterioration by more than 20% was observed 6 h after zatebradine intake: 21% and 38% below pre-dose FEV 1 (at 3 h the values were +2% and -14%, respectively). Analysis of the FVC data confirmed the FEV 1 findings. No significant differences were found between zatebradine and placebo for the pulmonary parameters PEF and SG AW. Compared to that on the placebo test day the salbutamol dose-response curve determined 6 h after zatebradine intake did not show a parallel shift to the right; the response to salbutamol was fully retained. No correlation was identified between PC 20 and the FEV 1 response observed in the individual patients. One patient reported severe visual disturbances and vomiting, which occurred rather late following zatebradine intake. On both test days no influence on blood pressure was observed, while zatebradine induced a small, but significant, decrease in heart rate at 3 h post-dosing. It is concluded that zatebradine has the potential to cause a deterioration of pulmonary function in asthmatic patients, regardless of the severity of their non-specific bronchial hyperreactivity towards histamine. However, the mean small decrease in pulmonary function as observed in the present study population did fully respond to treatment with a β 2-agonist. Also the patient who showed a deterioration in FEV 1 of 38% following drug intake did fully respond to salbutamol.

The skin as a model to study the pathogenesis of IgE-mediated acute and late-phase responses

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Peak flow variation in childhood asthma: A three-year analysis

Measuring peak expiratory flow (PEF) variation has been suggested as a indicator of asthma disease severity and also of nonspecific bronchial hyperreactivity. To test these assumptions, we examined the relationships between PEF variation, methacholine reactivity, symptom scores, and medication requirements in 74 children with tightly controlled allergic asthma. The level of mean diurnal variation (MDV) for the group was 7.1%, which is generally regarded as normal. We found statistically significant correlations between MDV and both methacholine reactivity ( r = 0.43, p = 0.0001) and symptom scores ( r = 0.28, p = 0.016). These asthma variables were analyzed longitudinally in 33 children who were followed up at 6-month intervals for at least 36 months. Visit-to-visit changes in MDV were generally not reflective of changes in other variables. However, group levels of MDV gradually decreased over time, especially in children with initial MDV of more than 8%. This reduction in group MDV coincided with similar reductions in group medication requirements and methacholine reactivity. We conclude that children with moderately severe asthma that is tightly controlled may have normal levels of PEF variation. The correlation between PEF variation and other asthma variables is statistically significant but too weak to be useful in the treatment of individual patients. In contrast, measurement of MDV may be a useful indicator of disease severity in group studies of asthma.

Monoclonal antibody–standardized cat extract immunotherapy: Risk-benefit effects from a double-blind placebo study

Twenty-eight patients (14 in an active treatment group and 14 in a placebo group) with rhinoconjunctivitis and asthma caused by cat hypersensitivity took part in a placebo-controlled, randomized, double-blind study to evaluate the risk-benefit quotient of the maintenance dose corresponding to 13.2 μg Fel d I antigen. The cat extract was biologically standardized and quantified with monoclonal antibodies (100 biological units: 33 μg of Fel d I antigen, 650 μg of albumin, and 99 μg of Fel d Bd/K30 antigen). After 1 year of treatment, the systemic reactions to cat extract immunotherapy were mild and infrequent. Improvement was observed in the active treatment group in comparison with the placebo group in the medication-symptoms score ( p < 0.001); in skin prick test ( p < 0.001), conjunctival provocation test ( p < 0.001), and allergen bronchoprovocation test ( p < 0.05) results, and in nonspecific bronchial hyperreactivity measured with methacholine, which was not statistically significant. This study demonstrates the favorable risk-benefit quotient of the dose of 13.2 μg of Fel d I antigen, which may serve as a future reference in defining the optimum dose and appropriate proportion of antigens that should be administered in cat extract immunotherapy. (J A LLERGY C LIN I MMUNOL 1994;93:556-66.)

Respiratory symptoms and bronchial reactivity among pig and dairy farmers.

This study assessed the prevalence of respiratory manifestations among French pig and dairy farmers and determined the relationship between bronchial reactivity and respiratory manifestations. The pig farmers included 102 men working more than half-time inside swine confinement buildings. There were 51 male dairy farmers and 81 male referents. The demographic characteristics of the three groups were similar except for more smokers among the referents. Each subject completed a standardized questionnaire. Pulmonary function tests were performed before and after a methacholine challenge (cumulative doses 80, 240, and 560 micrograms). Airborne dust, ammonia, and carbon dioxide were measured inside 28 swine confinement buildings. The pig farmers were exposed to a total dust level of 2.41 mg.m-3. The respirable particle concentration was low. The pig and dairy farmers had a significantly higher prevalence of cough and morning phlegm than the referents. Before the methacholine challenge, the dairy farmers had nonsignificantly lower mean lung function values than the other groups. Among the subjects with no history of asthma, nonspecific bronchial hyperreactivity was significantly higher among the pig and dairy farmers than among the referents. There was a fall in the forced expiratory volume in 1 s (FEV 1.0) that was greater than 10% in 6.7% of the referents, 17.9% of the swine workers, and 35.6% of the dairy farmers. This result was unchanged after adjustment for the initial FEV1.0. The prevalence of respiratory symptoms was significantly higher among the pig farmers without base-line lung function impairment. However, both the pig and the dairy farmers had increased bronchial reactivity.

From allergen sources to reduction of allergen exposure

Allergen exposure plays a major role in the development of sensitization, inflammation and symptomatic asthma. The development of new means of detecting allergens has enabled the evaluation of the effect of a reduction in allergen exposure to be better assessed. In order to prevent allergen exposure it is necessary to determine the allergen sources and reservoirs to which avoidance measures should be directed. The allergen sources and reservoirs of mite, cat, dog, cockroach, rodent, mould and pollen allergens are briefly reviewed. The relationships between allergen exposure, sensitization, nonspecific bronchial hyperreactivity and asthma symptoms are discussed. Recognition of the risks, environmental control, and reduction in allergen loads should be among the objectives of asthma management.