Increased frequency of bronchial hyperresponsiveness in patients with inflammatory bowel disease

Although bronchopulmonary manifestations are rare in inflammatory bowel diseases (IBD), subclinical abnormalities have been described in up to 50% of cases. The pathophysiology of these abnormalities remains unknown. However, a latent inflammation of the bronchial mucosa secondary to the inflammation of the intestinal mucosa has been suggested. This subclinical inflammation may lead to increased bronchial responsiveness. We studied the bronchial responsiveness in 38 inflammatory bowel disease (IBD) patients, using the methacholine test. Bronchial hyperresponsiveness was defined by a PC₂₀M <16 mg/ml. Twenty-four healthy controls were also studied. There was no significant difference in baseline FEV₁ between IBD patients and controls. However, there was a significantly greater fall in FEV₁ in the IBD patients at the concentrations of methacholine tested. The frequency of bronchial hyperresponsiveness was significantly higher in the IBD population (45%) than in controls (17%; P <0.03). Atopy, defined by skin test, was more common in IBD patients (42%) than in controls (21%). Even when only nonatopic subjects were considered, the frequency of bronchial hyperresponsiveness was significantly higher in IBD patients (41%) than in controls (5%; P <0.02). Thus, subclinical bronchial hyperresponsiveness is common in IBD, and may be considered a further extraintestinal manifestation.     

Inhaled lysine acetylsalicylate (L-ASA) attenuates histamine-induced bronchoconstriction in asthma

When administered by inhalation, histamine provokes dose-related bronchoconstriction in asthmatic subjects mainly by a direct activation of histamine H1-receptors on airway smooth muscle. However, little is known of the change in airway responsiveness to histamine after cyclooxygenase blockade. The aim of the study was to investigate the effect of the potent cyclooxygenase inhibitor, lysine acetylsalicylate (L-ASA), administered by inhalation on histamine-induced bronchoconstriction in a group of 16 asthmatic subjects. The subjects studied attended the laboratory on four separate occasions to receive nebulized L-ASA (solution of 90 mg/ml) or matched placebo (glycine solution of 30 mg/ml) 15 min before bronchoprovocation tests with histamine and methacholine in a randomized, double-blind order. Changes in airway caliber were followed as forced expiratory volume in 1 s (FEV₁), and agonist responsiveness was expressed as the provocative concentration causing a 20% fall in FEV₁ from baseline (PC₂₀). Administration of both L-ASA and glycine solution caused a small but significant acute fall in FEV₁ from baseline, which returned to normal within 15 min. When compared to placebo, inhaled L-ASA reduced the airway responsiveness to histamine in 13 of the 16 subjects studied, the geometric mean (range) values for PC₂₀ histamine increasing significantly ( P < 0.001) from 1.72 (0.13–5.49) mg/ml to 3.31 (0.36–12.00) mg/ml after placebo and L-ASA, respectively. No significant change in airway responsiveness to methacholine was recorded after L-ASA. Acute administration of L-ASA by inhalation protects the asthmatic airways against histamine-induced bronchoconstriction, thus suggesting that endogenous prostaglandins may play a contributory role in the airways response to histamine in human asthma.     

Bronchial hyperresponsiveness in two populations of Australian schoolchildren. I. Relation to respiratory symptoms and diagnosed asthma

In order to explore the relationship between bronchial hyperresponsiveness (BHR) to inhaled histamine, respiratory symptoms and diagnosed asthma in children, we undertook a cross-sectional study of 2363 Australian schoolchildren aged 8–11 years. The methods used included a self-administered questionnaire to parents, which was shown to have a high degree of repeatability, and a histamine inhalation test to measure bronchial responsiveness (BR). The study showed that 17.9% of children had BHR, defined as a 20% fall in FEV₁ at a provoking dose of histamine (PD₂₀ FEV₁) of less than 7.8 μmol. The distribution of PD₂₀ FEV₁ appeared to be continuous. Most children with PD₂₀ FEV₁ values < 1.0μmol had symptoms of asthma. However, 6.7% of children had BHR without symptoms or a previous diagnosis of asthma and 5.6% had had a diagnosis of asthma but had no BHR. Although there was a good association between BHR and respiratory symptoms, questionnaire data of wheeze and diagnosed asthma do not reflect accurately the level of BHR in the community. We conclude that cross-sectional studies of BR to identify children with BHR probably do not reflect the prevalence of asthma in populations of children. However, the strong association between BHR and symptoms, particularly in children with severe and moderate BHR, suggests that measurements of BR in populations are useful for defining a group of children whose airways behave differently from those of the majority. Prospective studies are needed to define the level of BHR that is associated with important sequelae.     

Plasma histamine and bronchial reactivity in allergic asthma

Histamine is an important mediator of allergic inflammation and bronchial hyperresponsiveness (BHR), a hallmark of asthma. Studies on the relationship between plasma histamine and BHR in allergic asthmatic patients have yielded controversial results. We therefore measured plasma histamine and bronchial reactivity in 30 nonsmoker volunteers taking no medication. Eleven were normal subjects; 19 were stable, mildly allergic asthmatic patients. Venous blood was taken to measure blood cells and basal plasma histamine by radioimmunoassay. After blood sampling, all subjects underwent a measurement of PC₂₀M (concentration of methacholine causing a 20% fall in FEV₁). Mean plasma histamine levels were 0.21 ± 0.1 ng/ml and 0.44 ± 0.3 ng/ml in normal and asthmatic subjects, respectively (P<0.05). We found a significant increase of blood eosinophils and basophils in asthmatic patients, and a positive correlation between plasma histamine and circulating basophils. PC₂₀M was greater than 16 mg in normal volunteers, and mean PC₂₀M was 2.1 ± 2 mg/ml in asthmatic patients. PC₂₀M did not correlate with plasma histamine levels, but it did so negatively with blood eosinophils. The increased plasma histamine concentration in mildly atopic asthmatic patients might be a consequence of the high basophil releasability of atopies and the higher basophil counts in allergic asthma. Plasma histamine is thus unlikely to be a determinant of BHR in asthma.     

Recovery of FEV1 after histamine challenge in asthmatic children

Factors that influence the time necessary for complete recovery of FEV₁ after inhaling histamine were analysed in forty-five children with asthma. These included the initial bronchial obstruction (baseline FEV₁), the provocation dose of histamine producing a 20% fall in FEV₁ (PD₂₀) and the fall in FEV₁ after the histamine challenge. In addition it was also investigated whether a second challenge carried out after complete recovery of FEV₁ would produce a reproducible PD₂₀-histamine value. The time for complete recovery varied widely from 15 to more than 75 min. The time needed for complete recovery of FEV₁ after the histamine challenge seems to be mainly determined by the PD₂₀ value. The other factors such as initial bronchial obstruction and the fall in FEV₁ after the challenge showed no significant relationship with the recovery time. A second challenge with histamine resulted in a highly reproducible PD₂₀ value. The clinical implication of this study is that other tests can only be performed when FEV₁ has returned to 95% of baseline.     

Airway inflammation in asthma and chronic obstructive pulmonary disease with special emphasis on the antigen-presenting dendritic cell: influence of treatment with fluticasone propionate

Asthma is a chronic inflammatory disorder of the airways characterized by variable airflow limitation and airway hyperresponsiveness. The type of inflammatory response in asthma is compatible with a major contribution of professional antigen-presenting cells. The airways in chronic obstructive pulmonary disease (COPD) are also markedly inflamed; however, the predominant types of inflammatory cells and the main anatomical site of the lesion appear to differ from those in asthma. COPD is characterized by reduced maximum expiratory flow and slow forced emptying of the lungs. Steroids are the most prominent medication used in the treatment of asthma and COPD; however, the beneficial effect of steroid treatment in COPD is subject of debate. We investigated the efficacy of fluticasone propionate (FP) treatment in atopic asthmatics and in COPD patients with bronchial hyperreactivity who smoke. The effect of the treatment on bronchial hyperreactivity and indices of the methacholine dose–response curve were analysed, as well as indices of inflammation of the airway mucosa with special emphasis on the antigen presenting dendritic cell. Treatment of allergic asthmatic patients resulted in improvement of lung function (FEV₁), a decrease in bronchial hyperresponsiveness and a decrease of maximal airway narrowing. During the FP-treatment of COPD patients, FEV₁ remained stable, while FEV₁ deteriorated significantly in the placebo group. Therefore, steroid treatment may have a beneficial effect in COPD patients with bronchial hyperresponsiveness (BHR). Since immunohistochemical analysis of bronchial biopsy specimens from asthma and COPD patients show disease-specific aspects of inflammation, the anti-inflammatory effect of FP is obtained through modulation of different cell populations in asthma and COPD.     

Serum eosinophil cationic protein (ECP) as a marker of disease activity and treatment efficacy in seasonal asthma

This study was carried out to determine whether serum eosinophil cationic protein (ECP) represents a sensitive marker for disease activity in atopic asthmatic patients during the pollen season. The study, in double-blind fashion, was performed between February and June 1994. Two groups of 10 seasonal asthmatic patients randomly received two different treatments. The first group was treated with inhaled beclomethasone dipropionate (BDP) 500 μg bid; the second received a matched placebo (P). At the beginning and every month, blood samples for determination of ECP and eosinophil count were collected and lung function (FEV₁) and methacholine responsiveness (PD₂₀) were performed. Subjects recorded daily symptoms of asthma, salbutamol consumption, and peak expiratory flow (PEF) values. In the P group, all indices, except FEV₁, showed significant changes during the pollen season ( P < 0.001). In the BDP group, significant changes were detected for symptom score ( P < 0.01), salbutamol consumption ( P < 0.01), and eosinophil number ( P < 0.05). Between the two groups, significant differences for symptom score ( P < 0.001), salbutamol consumption ( P < 0.001), ECP levels ( P < 0.05), eosinophil count ( P < 0.02), PD₂₀ methacholine ( P < 0.02), and PEF values ( P < 0.01) were detected. Changes in serum ECP significantly correlated with changes in other parameters ( P < 0.001), except FEV₁. Our results provide evidence that serum ECP is a sensitive marker for monitoring of the disease activity in seasonal asthma. Furthermore, it may offer a useful tool for estimating treatment efficacy.     

Relationships between Responsiveness of the Bronchi to Acetylcholine and Cyclic AMP Response of Lymphocytes to Beta1- and Beta2-Adrenergic Receptor Stimulation in Patients with Asthma

Decreased response of beta-adrenergic receptor has been considered to he one of the causes of increased responsiveness of the bronchi in asthma. Since beta-adrenergic receptor has two subtypes, beta₁ and beta₂, and the bronchodilating effect of beta stimulants is mediated by beta₂-receptor, responsiveness of the bronchi is expected to correlate to the cyclic AMP response of lymphocytes to a beta₂-stimulant. Responsiveness of the bronchi was expressed as respiratory threshold to acetylcholine (RT-Ach), which was the minimal concentration of acetylcholine solution to cause an initial decrease of FEV₁ of more than 20% of the baseline value. Beta₁ and heta₂-responses were expressed as the increments of cyclic AMP content of 10⁶ lymphocytes incubated with norepinephrine (beta₁-stimulant) and salbutamol (beta₂-stimulant).
RT-Ach showed a significant correlation with the beta₂-cyclic AMP response of lymphocytes, but not with the beta₁ -response among patients with asthma. Sixteen symptomatic patients on continuous beta-stimulants showed lower RT-Ach value and diminished beta₂-receptor activity of lymphocytes compared with 14 patients in remission. These results suggest that selective beta₂-adrenergic blockade may he one of the causes of bronchial hypersensitivity in asthma, though it should be noted that in this study beta-adrenergic responses were examined in lymphocytes and were compared with the responsiveneness of the bronchi. Possible beta-receptor subsensitivity induced by administration of beta-stimulants is discussed.     

Comparison of four different measures of bronchial responsiveness in asthmatic children

Although several tests are available to assess the presence and severity of bronchial hyperresponsiveness (BHR), there is no agreement on the most appropriate stimulus. The most commonly used stimuli are methacholine, histamine, and exercise. Daily peak expiratory flow (PEF) variation has been reported to correlate with the severity of BHR, and in recent years this has been widely used because of its noninvasiveness and ease of performance. This study was carried out to determine the relationship among these four commonly used measures of bronchial responsiveness in asthmatic children. For this purpose, 12 asthmatic children of varying disease severity were recruited. Subjects underwent three challenges on 3 separate days in 1 week. During the week preceding the challenges (methacholine, histamine, and exercise), patients recorded PEF three times a day. All patients had PC₂₀ less than 8 mg/ml with methacholine and histamine. Patients with PC₂₀ greater than 3.5 mg/ml for both methacholine or histamine had negative exercise challenges. The strongest correlation was between histamine and methacholine ( r =0.95). Exercise-induced bronchospasm had substantial and significant correlation with the other three measures. No significant correlation was observed between PEF variability and histamine or methacholine. The varying degrees of relationships among the four commonly used measures suggests that each method yields information on different but related phenomena. More than one measure may be required to detect the different aspects of asthmatic bronchial responsiveness.     

High-dose inhaled steroids in the management of asthma A comparison of the effects of budesonide and beclomethasone dipropionate on pulmonary function, symptoms, bronchial responsiveness and the adrenal function

Svendsen UG, Frølund L, Heinig JH, Madsen F, Nielsen NH, Weeke B. High-dose inhaled steroids in the management of asthma. A comparison of the effects of budesonide and beclomethasone dipropionate on pulmonary function, symptoms, bronchial responsiveness and the adrenal function.
The efficacy of budesonide (800 μg b.d.) and beclomethasone dipropionate (750 μg b.d.) in controlling the symptoms of asthma, pulmonary function, bronchial responsiveness to histamine, and adrenal function, was assessed in a double-blind, double-dummy cross-over study of 36 adult chronic asthmatic patients. The patients, the majority of whom were assessed to be affected to a severe degree, were insufficiently controlled in their current regimen of inhaled steroids and/or inhaled and oral bronchodilators. A 2 weeks baseline period preceded 6 weeks of treatment with each of the study drugs. Both treatment groups showed improvements from baseline in clinical assessment of lung function carried out after the first 6 weeks of treatment. No significant differences were seen throughout the entire 12 weeks study, when comparing the effects of the treatments on FEV₁ FVC, PEF or the histamine PC₂₀. Asthma severity, symptom score and inhaled bronchodilator use showed the same results after both treatments. It is concluded that inhalations of budesonide and beclomethasone dipropionate in high doses are equally potent in the treatment of severe asthma. There is no significant influence on the adrenal function and no significant side effects during a period equal to that of the present study.     

Potentiating effect of spirometric maneuver on bronchial responsiveness to methacholine in asthmatic subjects--the role of deep inspiration and forced expiration

We previously reported that spirometric maneuver (SM) had potentiating effect on bronchial responsiveness (BR) in asthmatic subjects but not in normal subjects. SM consists of deep inspiration to TLC (DI) and forced expiration to RV (FE). In this study, we examined the effect of SM, DI and FE on BR in 9 asthmatic subjects. Provocative concentration of methacholine producing a 35% fall in respiratory conductance (PC35-Grs) was significantly (p less than 0.02 and p less than 0.025) decreased from 0.34 mg/ml (GSEM, 1.51) to 0.16 mg/ml (GSEM, 1.45) and 0.14 mg/ml (GSEM, 1.51) by SM and DI, respectively but it was not altered by FE. These findings indicate that potentiating effect of SM on BR which is characteristic of asthma may be due to DI effect.     

Occupational asthma and rhinitis caused by ash (Fraxinus excelsior) wood dust

An 18-year-old man who worked in a furniture factory reported rhinitis and asthma when he was exposed to ash wood dust. Monitoring of the patient's peak expiratory flow rate (PEFR) when off work and at work showed increased variations of PEFR at work. Basal PC₂₀ methacholine was 1.41 mg/ml. A bronchial provocation test (BPT) with a 1: 1000 w/v ash wood dust extract induced a dual asthmatic response with a 7.5-fold increase of nonspecific bronchial responsiveness. Intradermal testing with ash wood extract elicited a positive immediate response. IgE antibodies against ash wood were found in the patient's serum with a RAST value of 0.57 PRU/ml. Similar skin tests, BPT, and RAST with ash wood dust performed in control patients were all negative. All the studies performed suggest that our patient had occupational rhinitis and asthma caused by exposure to ash wood dust in which a type I immunologic mechanism was implicated.     

Impact of allergic rhinitis on asthma: effects on bronchial hyperreactivity

Background:  Remarkable relationship exists between upper and lower airways. Bronchial hyperreactivity (BHR) is a paramount feature of asthma and may be considered a strong risk factor for the onset of asthma in patients with allergic rhinitis.
Objective:  This study is aimed at evaluating the presence of BHR in a large group of patients with moderate-severe persistent allergic rhinitis alone, and at investigating possible risk factors related to severe BHR.
Methods:  Three hundred and forty-two patients with moderate-severe persistent allergic rhinitis were prospectively and consecutively evaluated. Clinical examination, skin prick test, spirometry and bronchial methacholine (MCH) test were performed in all patients.
Results:  Twenty-two (6.4%) patients had severe BHR, 74 (21.6%) patients had mild BHR and 192 (56.2%) had borderline BHR; 54 (15.8%) patients had a negative MCH test. The logistic regression analysis evidenced that trees and house dust mites sensitization (OR_Adj: 8.1), rhinitis duration > 5 years (OR_Adj: 5.4) and FEV₁ ≤ 86% of predicted (OR_Adj: 4.0) were significantly associated with severe BHR. The discriminative ability of this model is appreciably satisfactory, being the AUC = 0.90.
Conclusion:  This study highlights the close link between upper and lower airways and the role of some risk factors, such as tree and mite sensitization, > 5-year duration, and ≤ 86% FEV₁ values, as risk factors for severe BHR in patients with moderate-severe persistent allergic rhinitis alone. Therefore, BHR is frequently present in patients with chronic rhinitis and should be suspected in the presence of defined risk factors.     

Occupational asthma caused by chromium

Summary. We report four cases of occupational asthma caused by chromium salts, three of whom showed dual and one isolated early asthmatic responses on specific chromium bronchoprovocation test (BPT). All of them were ex–smokers. Two showed positive skin–prick tests to 10mg/ml of Cr₂(SO₄)₃, but negative results on patch testing. The remaining two showed positive results on patch testing with Cr₂(SO₄)₃. Three had airway hyperresponsiveness to methacholine on initial examination. Although initial methacholine airway challenge testing showed a negative result in the remaining patient, airway hyperresponsiveness developed transiently 24 h after an isolated immediate asthmatic reaction induced by chromium. Three patients were reassessed after complete avoidance of chromium. Two subjects showed marked improvement of their symptoms with significant increases of PC20 methacholine. We conclude that chromium induces occupational asthma in exposed workers. Further investigations are needed to clarify the pathogenetic mechanism.     

Peptide leukotrienes mediate acetaldehyde-induced bronchial hyper-responsiveness in guinea-pigs

Background We previously reported that inhaled acetaldehyde, a metabolite of ethanol atid a maiti factor in alcohol-induced asthma, causes bronchial hyper-responsiveness (BHR) in asthmatics. However, the mechanisms are unclear. Objective The purpose of this study was to investigate a role of a peptide leukotriene (LT) in acetaldehyde-induced BHR. Methods Effects of LT antagonists, ONO-1078 (O.l-l.Omg/kg) and ICI-198, 615 (0.03–0.3 mg/kg), on acetaldehyde-induced bronchoconstriction and BHR to inhaled methacho-line were examined using a modified Konzett-Rössler method in guinea pigs. Results Aeetaldehyde at 0.8mg/ml, which failed to induce significant changes in Pao (pressure at the airway opening), enhanced an increase in Pao induced by subsequent inhalations of ascending doses (50–200 μg/ml) of methacholine. suggesting a potentiating effect of acetaldehyde oti bronchial responsiveness. Although ONO-1078 had no inhibitory effect on bronchoconstriction caused by ascending doses (5.0–20 mg/ml) of acetaldehyde, ONO-1078 and ICI-198, 615 reduced the acetaldehyde-induced BHR. Conclusion Acetaldehyde causes BHR via LT release in guinea-pigs.     

A breathing filter exchanging heat and moisture prevents asthma induced by cold air

In order to devise a protective aid against bronchial obstruction induced by cold air, we have tested a breathing filter with heat and moisture exchanging properties. Nine asthma patients, who all had a history of cold-induced asthma, took part in exercise tests on an ergometer bicycle at a temperature of approximately −10deg;C, without and with a breathing filter. Without a breathing filter, the maximum reduction in FEV₁ was, on average, 36%. With the breathing filter, the maximum reduction in FEV₁ was, on average, 11%. The difference was clearly significant ( P < 0.001). A further five cold-sensitive asthmatics performed similar exercise tests at −10°C on three occasions: 1) without and 2) with a breathing filter as above, and 3) with two breathing filters connected in parallel: one for inspiration and the other for expiration. Thus, no heat-moisture exchange could take place. The fall in FEV₁ after provocation without a breathing filter and with parallel breathing filters was similar but attenuated when rebreathing took place through the breathing filter. The results confirm the theory that in cold/exercise-induced asthma, it is indeed the heat and or water loss from the airways that triggers airway narrowing, and that a heat and moisture exchanging filter has a considerable protective effect and can be of value in the treatment of asthma.     

Predictors of early- and late-phase reactions to bronchial allergen challenge

The influence of inhaled steroids and predictive factors on the response to bronchial allergen challenge (BCA) was evaluated in. 80 asthmatics allergic to Dermatophagoides pteronyssinus (Der p). All underwent BCA with Der p and measurement of early (EAR) and late asthmatic reaction (LAR). The cumulative dose of allergen producing 20% fall in FEV₁, in the EAR (PD₂₀) was calculated. Bronchial histamine provocation, conjunctival provocation test (CPT), and skin prick test with Der p extract were performed. Specific IgE to Der p in serum (RAST), blood eosinophil (EOS) count, serum eosinophil cationic protein, and eosinophil protein X were measured. Thirty patients (38%) were treated with inhaled steroids. All patients had at least a 20% fall in FEV₁ in EAR. Some 42% of nonsteroid- and 33% of steroid-treated patients had LAR with fall in peak flow of at least 20%. For patients not treated with steroid, 35% of variation in PD₂₀ was explained by RAST and histamine reactivity, and 53% of variation of observed PD₂₀ could be predicted. The baseline FEV₁, EOS, and EAR explained 28% of variation in LAR, and 28% of variation in observed LAR could be predicted. For patients treated with steroids, 38% of variation in PD₂₀ was explained by EOS and histamine reactivity, and only 18% of variation of observed PD₂₀ could be predicted. For patients treated with steroids, it was impossible to predict LAR. We conclude that to achieve a quantitative estimation of allergen-specific EAR and LAR, BCA cannot be replaced by the tests used in this study. Treatment with inhaled steroids modifies the response to BCA, making quantitative prediction of EAR less accurate and prediction of the magnitude of LAR impossible.     

Relationship between nasal and bronchial responsiveness in perennial allergic rhinitic patients with asthma

BACKGROUND: The nasal and bronchial mucosa present similarities and most patients with asthma also have rhinitis, suggesting the concept of 'one airway one disease'. Although many studies may suggest the relationship between nasal and bronchial responsiveness in patients with allergic rhinitis and asthma, few studies have been published which address this question directly. The aim of this study is to investigate whether the relationship between nonspecific nasal and bronchial responsiveness exists in perennial allergic rhinitic patients with asthma. METHODS: Fifty-one perennial allergic rhinitic patients with the definitive or suspected asthma underwent methacholine bronchial provocation tests and nasal histamine challenge tests. A slope of the absolute changes in nasal symptoms score/log concentrations of histamine was calculated by linear regression analysis. A ratio of the final absolute change in nasal symptoms score to the sum of all the doses of histamine given to the subject was also calculated. The degree of bronchial responsiveness to methacholine was categorized as positive bronchial hyperresponsiveness (BHR) if PC(20) (provocative concentration of methacholine resulting in 20% fall in FEV(1)) was <4 mg/ml, borderline BHR if PC(20) was >or=4 but 16 mg/ml. Another index of bronchial responsiveness (BRindex) was calculated as the log [(% decline in FEV(1)/log final methacholine concentration as mg/dl) + 10]. RESULTS: The geometric means of the slope (4.47 vs. 2.95, p < 0.05) and the ratio (1.68 vs. 0.54, p < 0.01) were higher in patients with positive BHR (n = 23) than in patients with negative BHR (n = 19), respectively. The geometric means of the slope (3.50) and the ratio (1.13) in patients with borderline BHR (n = 9) were between the two groups, respectively. In all patients, the log-slope (r = 0.48, p < 0.001) and the log-ratio (r = 0.51, p < 0.001) were correlated well with the BRindex, respectively. Even in allergic rhinitic patients with definitive asthma, the log-slope was correlated with the BRindex (r = 0.39, p < 0.05) or log-PC(20) (r = -0.36, p < 0.05). CONCLUSIONS: The nonspecific nasal responsiveness may be related to the nonspecific bronchial responsiveness in patients with allergic rhinitis and asthma, which may support the viewpoint that allergic rhinitis and asthma represent a continuum of inflammation involving one common airway.     

Standardized Allergen Provocation Test

Standardized bronchial allergen provocation with the same individual allergen dose was performed 3–9 times in 20 symptomless adult asthmatic patients at intervals of 1 week or more during 1/222 months in order to study variations in bronchial response. The immediate type reaction was recorded by monitoring FEV₁, FVC, PEFR and MEF_50% for 30–40 min after provocation. FEV₁ was highly significantly correlated to the other variables.
The coefficient of variation corresponding to maximum decrease in FEV, was 23%. All provocations were followed by a bronchial reaction within clinically acceptable limits. There was no indication of hypo- or hypersensitization.
It is concluded that although many different factors influence the bronchial response, careful standardization of the provocation procedure leads to a moderate variation in bronchia! response, making the allergen provocation test suitable for pathophysiological studies and clinical evaluation of anti–asthmatic drugs.     

Role of symptoms and lung function in determining asthma control in smokers with asthma

Background:  Cigarette smoking in asthma increases the severity and accelerates the decline in lung function. The relative role of symptoms and lung function in determining asthma control in smokers with asthma is not known.
Aim of the study:  The aim of this study was to compare asthma control in smokers vs never-smokers with asthma, using the validated Juniper asthma control questionnaire (ACQ), and assess if any difference was because of a particular symptom or the forced expiratory volume in one second (FEV₁) value.
Methods:  This was a cross-sectional study of 134 asthmatics (74 never-smokers and 60 smokers) with ≥15% reversibility in FEV₁ after salbutamol. All subjects completed the ACQ, recording FEV₁ and asthma symptoms (night awakening, morning symptoms, dyspnoea, wheeze, activity limitation and use of reliever inhaler).
Results:  Compared with the never-smokers, smokers with asthma had significantly worse median (IQR) total asthma control score [1.6 (1.1–2.3) vs 2.8 (1.7–3.4); ( P  < 0.0001)] and in each of the six individual symptom question scores ( P  < 0.001), but no difference in FEV₁ levels ( P  = 0.908).
Conclusion:  Asthma control is significantly worse in asthmatics who smoke compared with never-smokers, with all symptoms related to asthma control uniformly worse in smokers, independent of FEV₁.