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Biomedical subjects

D Giannini

Publications and source records attributed to D Giannini.

At least 55 records · Page 3Linked to original sources
PubMed1998

Leukocyte counts in hypertonic saline-induced sputum in subjects with occupational asthma.

We measured markers of eosinophilic inflammation in the blood and in the sputum induced by hypertonic saline (HS) inhalation of 24 subjects with occupational asthma who were still exposed to high molecular weight compounds (HMWCs, n = 8) or to low molecular weight compounds (LMWCs, n = 16); all subjects were symptomatic and showed bronchial hyperresponsiveness to methacholine at the time of study. Sputum cell counts were also measured in 14 normal subjects and in 24 subjects with non-occupational asthma with asthma severity similar to that of occupational asthmatics. Both occupational and non-occupational asthmatic subjects showed higher neutrophil percentages in HS-induced sputum than normal subjects, asthmatics with LMWC-induced asthma showing the highest values. Eosinophil percentages in HS-induced sputum were higher in non-occupational asthmatics and in asthmatics with HMWC-induced asthma than in normal subjects and in subjects with occupational asthma due to LMWCs. No difference in bronchial responsiveness, peak expiratory flow variability and serum eosinophil cationic protein (ECP) levels were observed among the different asthma groups. Although sputum eosinophil percentages significantly correlated with blood eosinophil percentages, sputum allowed the detection of a higher number of subjects with eosinophilic inflammation than blood. Serum ECP levels were normal in most asthmatic subjects. A significant correlation between sputum eosinophil percentages and bronchial hyperresponsiveness to HS was observed. Despite a similar degree of functional abnormalities, subjects with asthma due to LMWCs and still exposed to the occupational sensitizer showed a lower degree of eosinophilic inflammation and a higher degree of neutrophilic inflammation in the airways than subjects with occupational asthma due to HMWCs or non-occupational asthmatics. Furthermore, sputum eosinophil counts detect, better than blood indices, the degree of airway inflammation in both occupational and non-occupational asthma.

Adult↗
PubMed1998

Comparison between eosinophilic markers in induced sputum and blood in asthmatic patients.

BACKGROUND: The usefulness and safety of the analysis of blood inflammatory markers in asthma are widely recognized. Recently, the analysis of induced sputum has been proposed as a safe, non-invasive tool in the study of airway inflammation in asthma. OBJECTIVE: Our aim was to test whether sputum analysis is more useful than blood analysis in the evaluation of airway inflammation in untreated and treated asthmatic patients. METHODS: Twelve untreated patients with mild to moderate asthma underwent a methacholine challenge test, sputum induction and blood sampling. A group of 14 normal subjects was also evaluated for baseline comparison. The same evaluation was repeated after 3 months of budesonide treatment. Before and after treatment, we tested the relationship of eosinophilic markers in induced sputum and blood with clinical and functional data. We also compared eosinophilic markers in induced sputum with the same markers in blood. RESULTS: Untreated patients showed a significant relationship between sputum eosinophils and symptom score, and between sputum eosinophilic cationic protein and symptom score, FEV1 and PD20FEV1. No relationship between blood eosinophilic markers and clinical or functional data was observed. In budesonide-treated patients, both sputum and blood eosinophils were significantly lower than in untreated patients, but eosinophil decrease was greater in sputum than in blood. Sputum eosinophilic proteins were also significantly lower in treated patients, whereas serum eosinophilic proteins were low at baseline and remained unchanged after treatment. Sputum eosinophilic markers were lower in normal subjects than in both untreated and treated patients, while blood eosinophils, but not serum eosinophilic cationic protein, were lower in normals than in untreated patients. CONCLUSIONS: The analysis of induced sputum is more useful than the analysis of blood in the evaluation of asthma severity and of the effect of glucocorticoid treatment in patients with mild to moderate asthma.

Adolescent↗
PubMed1997

Blood markers of early and late airway responses to allergen in asthmatic subjects. Relationship with functional findings.

We evaluated the relationship between blood markers of mast-cell (plasma histamine and serum level of heat-stable neutrophil chemotactic activity [NCA]) and eosinophil (serum eosinophil cationic protein [ECP]) activation during early airway response (EAR) and late airway response (LAR) to allergen inhalation in 24 asthmatic subjects. After EAR, 14 subjects showed significant LAR (FEV1 fall: > or = 25%), while 10 subjects showed equivocal LAR (FEV1 fall: 15-20%). A significant increase from baseline value was observed in plasma histamine and in serum NCA during both EAR and LAR, while serum ECP significantly increased only during LAR. The sensitivity of different markers to detect significant FEV1 fall during EAR and LAR was low, except for NCA. Changes in blood mediators were similar in both groups with significant and equivocal LAR. There was a significant relationship between the increase in NCA during EAR and the severity of LAR. Stepwise regression between changes in different blood markers showed a significant relationship between histamine increase during EAR and ECP increase during LAR. Thus, serum NCA is a more sensitive marker of EAR and LAR than plasma histamine and serum ECP, and its increase during EAR seems predictive of the severity of the subsequent LAR.

Adolescent↗
PubMed1997

Relationship between serum heat-stable neutrophil chemotactic activity during early airway reaction to allergen and the pattern of airway response (early versus late reactions) in asthmatic subjects.

In order to evaluate the relationship between allergen-induced heat-stable neutrophil chemotactic activity (HS-NCA) release during early asthmatic reaction (EAR) and the presence of a late asthmatic reaction (LAR), serum HS-NCA was measured at three serum dilutions (1:5, 1:40, 1:200) during EAR induced by allergen in 26 atopic asthmatics, 13 with isolated EAR and 13 with EAR followed by LAR. HS-NCA was measured using a 48-well microchamber with 5-micron-pore-size nitrocellulose filters, using isolated neutrophils from healthy donors and the leading front technique. Subjects with LAR developed EAR after inhalation of a lower dose of allergen than subjects with isolated EAR. Increase in serum HS-NCA during EAR was significantly higher in subjects with isolated EAR than in subjects with EAR plus LAR at the 1:5 dilution, while it was significantly higher in subjects with EAR plus LAR than in the subjects with isolated EAR at the 1:200 dilution; the 1:40 dilution gave similar results in both groups. Changes in serum HS-NCA during EAR significantly correlated with the maximum decrease in forced expiratory volume in 1 s (FEV1) during LAR: a higher decrease in FEV1 during LAR was associated with a lower increase in HS-NCA at the 1:5 dilution (Spearman's rho = 0.43, rho = 0.03), and with a higher increase in NCA at the 1:200 dilution (Spearman's p = -0.46, p = 0.02). These results can be explained by the 'high-dose-inhibition' phenomenon. Assuming that HS-NCA is associated with mast cell degranulation in the airways after allergen challenge, these findings demonstrate that higher mast cell activation during EAR is present in subjects with a subsequent LAR than in subjects with isolated EAR.

Adolescent↗
PubMed1997

Comparison between peak expiratory flow and forced expiratory volume in one second (FEV1) during bronchoconstriction induced by different stimuli.

To evaluate the sensitivity of peak expiratory flow (PEF), obtained by portable peak flow meter, in detecting mild changes in airway caliber as assessed by forced expiratory volume in 1 sec (FEV1), we studied 184 subjects who underwent different bronchial challenge tests for suspected bronchial asthma. We measured FEV1 and PEF during bronchoconstriction induced by different stimuli: allergen, methacholine, toluene diisocyanate vapors, exercise, or distilled water inhalation; a total of 186 tests were examined. Before and at different times after challenge, FEV1 was measured, and immediately after, PEF was obtained by Mini-Wright or Assess Peak Flow Meter; each time FEV1 and PEF were taken as the best of three satisfactory tracings. The median FEV1 change from baseline value of all steps in the different challenge tests was 7.5% (range: 0-66%). The correlation coefficients between FEV1 and PEF percent changes in different challenge tests were low (Spearman's p: 0.27-0.69), with high scattering of the data. The concordance between classes of percent changes in FEV1 and PEF was also low (Cohen's weighted kappa: 0.28-0.42). In subjects with a FEV1 fall > 15% after challenge, the median PEF change after bronchoconstriction was lower than the corresponding FEV1 change [17% (0-52) vs. 27% (17-66)]. When different cutoff limits of PEF percent change were considered, the sensitivity of PEF to detect a significant change in FEV1 (15 or 20% change) during bronchoconstriction was low; specificity was in general higher than sensitivity. We conclude that PEF and FEV1 changes are poorly related during mild bronchoconstriction induced by different stimuli. The low sensitivity of PEF to detect mild changes in airway caliber may represent a limit in the use of PEF in the day-to-day monitoring of asthma.

Allergens↗
PubMed1996

Anxiety-induced failure in erectile response to intracorporeal prostaglandin-E1 in non-organic male impotence: a new diagnostic approach.

Intracavernous injection (ICI) of prostaglandin-E1 (PGE1) is used widely as the first diagnostic test in the study of erectile dysfunction. However, a lack of full erection after a maximal dose is frequent. As well as vascular incompetence, this may be due to stress-induced changes, related to the ICI procedure. The aim of this study was to investigate the influence of emotional disturbances on erectile response to ICI in impotent patients. Initially, 24 young men with non-organic impotence (age 34.6 +/- 1.5 years; mean +/- SEM) were selected and randomized single-blind to pharmacoerection with PGE1 alone (20 micrograms/mL) or a mixture (cocktail) containing 20 micrograms PGE1 plus an alpha-adrenergic receptor blocker, phentolamine (Phe, 0.5 mg/mL). Additional studies were also performed double-blind on 10 men with non-organic impotence (age 37.6 +/- 1.2 years) utilizing higher PGE1 dosages for ICI (25 micrograms/mL alone or in combination with Phe, 0.5 mg/mL). After a 7-day interval, all subjects were crossed-over to receive the alternative treatment. The presence of emotional disturbances was assessed in all patients by the administration of rapid tests (Stai-X1 and Stai-X1r for state-anxiety before and after ICI, respectively; Stai-X2 for trait-anxiety; Zung-test for depression) at the first and at the remaining (Stai-X1 and Stai-X1r) ICI sessions. ICI with 20 and 25 micrograms/mL PGE1 led to a comparable percentage of patients who reported a valid-for-intromission (VFI) erection (63 and 60%, respectively). In contrast, use of the cocktails significantly increased the percentage of subjects with a VFI (87 and 90% of the total number of patients tested, respectively; p < 0.05). Moreover, a strong inverse correlation between state-anxiety scores (Stai-X1) and the erectile response to ICI with 20 and 25 micrograms PGE1 was found (r = -0.69, p < 0.001); such a correlation was not present in patients who underwent ICI with the cocktails. Two cases of prolonged erection occurred (one after 20 micrograms PGE1 and the other after 20 micrograms PGE1 plus Phe) which were reversed promptly by the intracavernous injection of metharaminol. It is concluded that the lack of a full erectile response after ICI with PGE1 can be related to the presence of a high 'state-anxiety' in the patients. In such patients, a VFI erectile response can be induced by the administration of a cocktail test-dose.

Adrenergic alpha-Antagonists↗
PubMed1996

Comparison of inhaled salmeterol and individually dose-titrated slow-release theophylline in patients with reversible airway obstruction. European Study Group.

The aim of this study was to compare the clinical efficacy of salmeterol versus theophylline in the treatment of moderate-to-severe asthma. One hundred and eighty nine asthmatic patients (forced expiratory volume in one second (FEV1) or peak expiratory flow (PEF) >50% of predicted) were randomized to receive either salmeterol dry powder, 50 microg b.i.d. via a Diskhaler (n=92) or dose-titrated slow-release theophylline capsules ("Theo-Dur") b.i.d. (n=97), in a double-blind, double-dummy, parallel group study for 4 weeks. Patients had previously been titrated with theophylline to a serum theophylline level of 10-20 microg x mL-1. The median percentage of nights with no asthma symptoms rose from 14% in both groups at baseline to 71% with salmeterol and to 46% with theophylline (p=0.044). There was also a significant increase for salmeterol in the median percentage of nights with no rescue salbutamol use (from 36 to 86%) compared with theophylline (from 71 to 78%; p=0.002). The mean morning PEF increased from 337 L x min-1 in the salmeterol group and 332 L x min-1 in the theophylline group to 372 and 357 L x min-1, respectively. No significant difference between the two treatments was observed for PEF, symptoms or additional salbutamol medication during the day. The incidence of gastrointestinal symptoms (gastric irritation, nausea and vomiting) was greater among patients receiving theophylline (11%) than with salmeterol (3%). These findings suggest that inhaled salmeterol is more effective in relieving symptoms of asthma, and better tolerated than theophylline in patients with moderate-to-severe asthma.

Administration, Inhalation↗
PubMed1996

Effect of short-term NO2 exposure on induced sputum in normal, asthmatic and COPD subjects.

The aim of this study was to assess the effects of short-term exposure to low levels of nitrogen dioxide (NO2) on airway inflammation. We studied seven normal, eight mild asthmatic and seven chronic obstructive pulmonary disease (COPD) subjects. All subjects were exposed to air or to 0.3 parts per million (ppm) NO2 for 1 h, with moderate intermittent exercise, on different days and in random order. Before and 2 h after exposure, symptom score and results of pulmonary function tests (PFTs) were assessed. All subjects performed nasal lavage and hypertonic saline (HS) inhalation to collect sputum 2 h after both exposures. Asthmatic subjects had a higher percentage of eosinophils than normal and COPD subjects in HS-induced sputum after air (asthmatics: median 13 (range 0.4-37)%; normals: 0 (range 0-2)%; COPD 1.8 (range 0.1-19)%), whilst COPD patients showed a higher percentage of neutrophils than the two others groups. No significant differences in PFT values or percentages of inflammatory cells were observed in nasal lavage and in HS-induced sputum in normal, asthmatic and COPD subjects after NO2 exposure compared to air exposure, except for a mild decrease in forced expiratory volume in one second (FEV1) 2 h after NO2 exposure in COPD patients. Symptom score showed a mild increase after NO2 exposure both in normal subjects and in COPD patients. We conclude that short-term exposure to 0.3 ppm nitrogen dioxide does not induce an early detectable acute inflammation in proximal airways of normal subjects or of patients with asthma or chronic obstructive pulmonary disease.

Administration, Inhalation↗
PubMed1996

Tolerance to the protective effect of salmeterol on allergen challenge.

Long-term treatment with inhaled beta 2-agonists may be associated with a deterioration in asthma control, potentially due to tolerance. Regular use of short-acting beta 2-agonists has been shown to induce tolerance to allergen or adenosine 5'-monophosphate challenge. The aim of the study was to detect the efficacy of a single dose and a short-term treatment with salmeterol, a long-acting beta 2-agonist, to protect against early asthmatic reaction (EAR) to allergen. Eight subjects with mild allergic asthma underwent two treatment periods in which subjects performed an allergen challenge (specific bronchial provocation test) protected by a single dose (50 micrograms) of salmeterol (Salm-1) followed by a second specific bronchial provocation test after regular treatment with salmeterol for 1 week (Salm-2), or a single dose of placebo (Plac-1) and regular treatment (1 week) with placebo (Plac-2). Each subject performed both treatments in a randomized order. Each time allergen challenge was performed 1 h after last drug inhalation and it was stopped when the same provocative dose of allergen of a previous screening allergen challenge was achieved. The maximum decrease in FEV1 and area under curve in the first hour after allergen inhalation were significantly lower in Salm-1 (max delta FEV1 %, median [range]: 4%[0 to 9]) with respect to Salm-2, Plac-1, Plac-2 (24%[13 to 38], 31%[19 to 50], 30%[6 to 44], respectively, p < 0.001); there was no difference among Salm-2, Plac-1 and Plac-2. In Salm-1, all subjects were protected against EAR, whereas in Salm-2 only 2 subjects showed a partial protection. In conclusion the protective effect of a single dose of salmeterol against allergen-induced EAR was lost after regular treatment with salmeterol for 1 week. The clinical relevance of this mechanism remains to be elucidated.

Adolescent↗
PubMed1996

[Adrenal adenoma or hyperplasia? Problems of differential diagnosis in an unusual case of primary hyperaldosteronism].

Although primary hyperaldosteronism is an uncommon cause of hypertension, it is the most common form of renin-independent hypermineralocorticoidism. The plasma aldosterone concentration and PRA with orthostatic test and saline infusion test are very useful aids to make a diagnosis. In this case the inconsistency between hormonal data and morphologic images (TC and NMR) led us to a dilemma: it was a question of adrenal adenoma or hyperplasia? Because it was impossible to dose the 18-OH-corticosterone, we had to perform a iodocholesterol scintigraphy NP 59. To distinguish an hyperplasia as cause of this kind of hyperaldosteronism made us able to define a therapeutic program useful to hypertension control.

18-Hydroxycorticosterone↗
PubMed1996

Comparison between hypertonic and isotonic saline-induced sputum in the evaluation of airway inflammation in subjects with moderate asthma.

BACKGROUND: Hypertonic saline-induced sputum has recently been used for the evaluation of airway inflammation in asthma. OBJECTIVE: To assess the effect of hypertonicity on airway inflammation. METHODS: We compared the inflammatory cell composition of hypertonic saline-induced sputum with that of isotonic saline-induced sputum in 21 asthmatic subjects and, at baseline and 30 min after each sputum induction, we measured bronchial hyper-responsiveness to methacholine as an indirect marker to detect increased airway inflammation. On two different days, the patients inhaled hypertonic saline (3-5% NaCl) or isotonic saline (0.9% NaCl) for 30 min via an ultrasonic nebulizer, while monitoring FEV1. Sputum was collected for inflammatory cell analysis. RESULTS: There was no difference in inflammatory cell percentages obtained with the two methods. Eosinophils were > 1% in 20 subjects after hypertonic saline and in 16 subjects after isotonic saline, but this difference was not statistically significant. Intraclass correlation coefficients for sputum inflammatory cells obtained with the two methods were +0.642 for eosinophils, +0.644 for neutrophils, +0.544 for lymphocytes and +0.505 for macrophages. Hypertonic saline induced bronchoconstruction in a significantly greater number of subjects than isotonic saline. Also, hypertonic saline increased bronchial responsiveness to methacholine, while isotonic saline did not. CONCLUSION: We conclude that hypertonicity does not affect sputum cell composition, suggesting that inflammatory cells in hypertonic saline-induced sputum are probably preexisting and not acutely recruited in the airways by the hypertonic stimulus. However, the bronchoconstriction and the increase in bronchial hyper-responsiveness after hypertonic saline inhalation may imply the release of inflammatory mediators. This fact must be considered in the evaluation of soluble markers of inflammation in hypertonic saline-induced sputum.

Adolescent↗
PubMed1995

Oral slow-release theophylline does not prevent early and late asthmatic response to allergen in sensitized subjects.

In order to assess whether treatment with oral slow-release theophylline prevents early (EAR) and/or late (LAR) airway responses to allergen, we treated six asthmatic subjects with either placebo or oral theophylline (350 mg b.i.d.) for one week before specific bronchial provocation test (sBPT) with allergen, in a double-blind, cross-over, placebo-controlled study. All subjects had previously shown both EAR and LAR to allergen sBPT. On the day of sBPT, serum theophylline concentration was > 9 micrograms.ml-1 in all subjects treated with theophylline except one (mean 9.8 +/- 2.6 micrograms.ml-1). The total dose (TD) of inhaled allergen, and the provocative dose of allergen causing a 15% fall in forced expiratory volume in one second (PD15FEV1) during sBPT was mildly but significantly lower during theophylline-sBPT than during placebo-sBPT. Theophylline treatment reduced EAR (maximum FEV1 fall from baseline: 26.3 +/- 6.7 vs 32.2 +/- 9.5% after placebo treatment) but not LAR (19.5 +/- 6.5 vs 26.3 +/- 6.1%). A significant protection of LAR (a reduction in FEV1 fall after theophylline treatment 50% more than after placebo treatment) was observed in only 2 out of 6 subjects. Area under the curve was not significantly different after the two treatments. There was no relationship between serum theophylline levels and the degree of protection on EAR or LAR. The decrease in PD15FEV1 methacholine observed at the end of LAR was similar in the two treatments.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1994

Postallergen inhaled budesonide reduces late asthmatic response and inhibits the associated increase of airway responsiveness to methacholine in asthmatics.

To determine whether inhaled budesonide given after allergen inhalation challenge inhibits the late asthmatic response (LAR) and/or the associated increase of airway responsiveness to methacholine, we performed a double-blind randomized cross-over study in 12 adult asthmatics (eight male, four female; mean age, 20.3 yr; range, 18 to 29 yr) sensitized to Dermatophagoides pteronyssinus (DP) previously shown to develop early and late asthmatic response to allergen challenge with DP. On different days each subject was randomized to receive budesonide 800 micrograms by Turbuhaler or placebo, given three times; (1) after allergen inhalation, after the onset of LAR, when FEV1 had fallen by > or = 15%; (2) 2 h later; (3) 4 h later. Airway responsiveness to methacholine was measured before allergen challenge at 8 to 10 h from allergen inhalation and 24 h after the allergen inhalation. Inhaled budesonide significantly reduced the LAR induced by allergen (maximal % fall in FEV1, delta FEV1%: -23 +/- 6% with budesonide versus -38 +/- 9% with placebo; p < 0.001) and inhibited the associated increase of airway responsiveness (geometric mean of PD20FEV1 methacholine: 0.047 mg after budesonide versus 0.033 mg after placebo at 8 to 10 h, p < 0.05; 0.119 mg after budesonide versus 0.062 mg after placebo at 24 h, p < 0.01). These results suggest that inhaled budesonide may not only prevent but also reduce the late asthmatic response induced by allergen and that it might also be considered in the treatment of exacerbation of asthma.

Administration, Inhalation↗
PubMed1994

Prognosis of occupational asthma.

Several studies on the prognosis of occupational asthma have shown that a significant proportion of patients continue to experience asthmatic symptoms and nonspecific bronchial hyperresponsiveness after cessation of work. The determinants of this unfavourable prognosis of asthma are: long duration of exposure before the onset of asthma; long duration of symptoms before diagnosis; baseline airway obstruction; dual response after specific challenge test; and the persistence of markers of airway inflammation in bronchoalveolar lavage fluid and bronchial biopsy. The relevance of immunological markers in the outcome of occupational asthma has not yet been assessed. Further occupational exposure in sensitized subjects leads to persistence and sometimes to progressive deterioration of asthma, irrespective of the reduction of exposure to the specific sensitizer, and only the use of particular protective devices effectively prevents the progression of the disease. A long-term follow-up study of toluene diisocyanate (TDI)-induced asthma showed that the improvement in bronchial hyperresponsiveness to methacholine occurred in a small percentage of subjects and only a long time after work cessation. Bronchial sensitivity to TDI may disappear, but non-specific bronchial hyperresponsiveness often persists unchanged, suggesting a permanent deregulation of airway tone. Steroid treatment significantly reduces nonspecific bronchial hyperresponsiveness only when started immediately after diagnosis.

Adult↗
PubMed1994

Peak expiratory flow monitoring in diagnosis and management of occupational asthma.

The role of peak expiratory flow (PEF) monitoring in the diagnosis of occupational asthma has recently been assessed by several studies, which agree that this procedure should always be used to confirm the relationship between symptoms and occupational exposure. Some specific issues should be satisfied: a minimum number of four PEF measurements in a day; several weeks of monitoring in and out of work; and the presence of specific patterns of PEF changes. The sensitivity and specificity of PEF monitoring to detect occupational asthma, in comparison with the specific challenge test in the laboratory (the "gold standard") have been shown to be fairly high, although many authors believe that PEF monitoring cannot substitute for the specific challenge test. Limitations include: the low sensitivity of PEF to detect mild changes in airway calibre with respect to forced expiratory volume in one second (FEV1); the blunting effect of pharmacological treatment; the episodic and irregular exposure to the sensitizer in the workplace; and the compliance and honesty of the subject. Further studies are required to select the best indices of daily and day-to-day variability to be used in the evaluation of PEF changes between work and out-of-work periods.

Asthma↗
PubMed1993

Duration of preventive effect of inhaled salbutamol on early airway response to allergen in asthmatic subjects.

Salbutamol is known to effectively prevent early asthmatic response (EAR) after specific bronchial provocation test (sBPT) in asthmatic subjects, but the time-course of this protection is not known. In this study the effects of 200 micrograms salbutamol inhaled 2 h before sBPT were compared with 200 micrograms salbutamol inhaled 10 min before sBPT in eight asthmatic subjects sensitized to Phleum pratensis (PP) or Dermatophagoides pteronyssinus (DP). All subjects showed an EAR (% decrease in FEV1 from baseline value: 30.4 +/- 11%) in a preliminary sBPT performed with cumulated doses of extracts of PP or DP titrated in biological units (BU). Each subject performed, on two different days, in a random, double-blind, cross-over study, two puffs of placebo 2 h before sBPT and two puffs of salbutamol 10 min before sBPT (treatment A) or two puffs of salbutamol 2 h before sBPT and two puffs of placebo 10 min before sBPT (treatment B). Baseline FEV1 were similar in both tests. In treatment B, 10 min, 1 h and 2 h after salbutamol inhalation, FEV1 increased significantly with respect to placebo inhalation in treatment A. Ten minutes after salbutamol inhalation in treatment A, FEV1 became similar to that obtained 2 h after salbutamol inhalation and 10 min after placebo in treatment B. Allergen inhalation induced an EAR in only one out of eight subjects after treatment A, and five of the eight subjects after treatment B.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗