Evaluation of the enhaled glucocorticosteroid effect on non-specific and specific bronchial reactivity with particular reference to the late inflammatory phase in atopic asthma patients. I. The effect of a single dose of budesonide R on specific and non-specific bronchial reactivity]

The effect of a single dose of 320 micrograms of budesonide R on specific and non-specific bronchial response was evaluated. The study was carried out on a group of 12 patients suffering from mild allergic asthma, sensitive to Dermatophagoides pteronyssinus (D. pteronyssinus). On the first day the bronchial provocation test (BPT) with metacholine was performed, and the next day the effect of a single dose of the drug studied on bronchial response to metacholine was evaluated. On the third day sBPT with D. pteronyssinus allergen was performed. The allergen challenge could induce an early (EAR) and a late asthmatic reaction (LAR). After the BPT with the allergen, a 42 days' run-out period was required to eliminate the effects of the allergen provocation on the results of the next tests. Before the evaluation of the effect of budesonide on the allergen challenge, the non-specific response to metacholine was checked again. The results indicate that a single dose of budesonide R does not affect non-specific and specific bronchial response.     

Bronchodilator response to salbutamol after spontaneous recovery from nonspecific bronchial provocation tests in asthma

Assessment of airway responsiveness by bronchoprovocation and bronchodilatation tests is important in the diagnostic work-up protocol of bronchial asthma and it would be convenient to undertake both tests on the same occasion. However, it is not known whether this can be done accurately. Therefore, this study evaluated the effect of a prior bronchial provocation test on the bronchodilator response to salbutamol after spontaneous recovery of the forced expiratory volume in one second (FEV1) in a group of asthmatic subjects. On two separate occasions at the same time of day, concentration-response studies with inhaled histamine or methacholine, or a sham challenge with normal saline were carried out in a blinded, randomized manner. Changes in airway calibre were followed as FEV1 and agonist responsiveness expressed as the provocative concentration causing a 20% fall in FEV1 (PC20). After either spontaneous recovery or a fixed-duration wait of 45 min (when appropriate), the subjects received 2x100 microg of salbutamol from a metered dose inhaler with a spacer. The bronchodilator response to salbutamol was expressed as a percentage of initial FEV1 (deltaFEV1% init). Bronchial challenge with both agonists failed to alter significantly the airway response to salbutamol, with the deltaFEV1% init mean value (range) being 16.9% (9.0-31.9) and 17.5% (11.6-31.2) on the sham and histamine/methacholine challenge day respectively. It was shown that the degree of bronchodilatation achieved after salbutamol 200 microg is not affected by prior bronchoprovocation testing when enough time is allowed for the airways to recover spontaneously to baseline forced expiratory volume in one second. Thus evaluation of airway responsiveness by both bronchial provocation tests and bronchodilator testing can be assessed reliably within a few hours in asthmatic patients.     

Relationship between serum immunoglobulin, inhalation bronchial challenges and skin tests in severe asthmatics

The relationship among inhalation bronchial challenge tests, skin tests, total serum immunoglobulin E, A, M, and G values were investigated. Positive correlation between the results of the inhalation bronchial challenges and IgG and negative correlation between the value of IgG and IgA were found but no other correlations.     

Increase in non-specific bronchial hyperresponsiveness without specific response to isocyanate in isocyanate-induced asthma: a pilot study

Increased non-specific bronchial hyperresponsiveness (BHR) has been reported after positive reaction to isocyanates in patients with isocyanate-sensitive asthma. The increased responsiveness may, however, also precede the asthma attack. We therefore compared non-specific BHR to a cholinergic agent before and after exposure to toluene-diisocyanate (TDI) that induced no asthma symptoms in 11 workers with isocyanate-related asthma. Patients were exposed for 3 consecutive days to progressively increasing doses of TDI (5, 10, and 20 ppb min-1 for 20 min) in an exposure chamber with continuous TDI monitoring. No immediate nor late asthmatic bronchial reaction was observed in any patient after any dose of TDI during or after challenge. A significant increase in non-specific BHR was noted 24 h after the last dose of TDI challenge, however. This increase was at least one doubling dose for seven of 11 patients. In conclusion, our study shows that, in patients with isocyanate-induced asthma, exposure to TDI induces a slight but significant increase in non-specific BHR in the absence of any immediate or late bronchial response to isocyanate. This result, which requires further confirmation, may justify a proposal to measure non-specific BHR, even after a negative specific inhalation test to TDI, as an additional diagnostic element for TDI-induced occupational asthma, to help lower the percentage of the undetected occupational asthma cases.     

Mental illness in the biological and adoptive families of adopted individuals who have become schizophrenic

Early asthmatic responses (EAR) of similar severity were produced by allergen inhalation challenges in nine asthmatic subjects. The severity of the airways allergic reaction was estimated by measuring the skin test weal size produced by the same dilution of allergen which caused the EAR. The non-specific bronchial reactivity was assessed by inhalation of incresing concentrations of histamine acid phosphate. Possible relationships between the severtiy of the airways allergic reaction, the level of non-specific bronchial hyper-reactivity and the pattern of asthmatic response were examined. There was a marked inverse correlation between the required severity of the airways allergic reaction and the non-specific bronchial reactivity (log10) of the individual (r = -0-96, P less than 0-001). The EAR was followed by a late asthmatic response (LAR) in five subjects. There was no evident correlation between the magnitude of the EAR and that of the LAR. In addition, no correlation was obtained between the pattern of response interms of EAR or LAR and the severity of the allergic reaction, or the level of non-specific bronchial reactivity. These results indicate that the allergic reaction and the non-specific bronchial reactivity are interrelated in the production of allergen-induced asthma. Thus a mild allergic reaction will induce and EAR in patients with markedly increased non-specific bronchial reactivity, whereas a severe allergic reaction is required to produce an EAR in those with only slightly increased non-specific reactivity. The lack of correlation between the occurrence of the LAR and the intensity of the airways allergic reaction, the non-specific bronchial reactivity and the intensity of the EAR indicates that other factors are involved in the development of LAR.     

Dezincing of zinc alloy coated steel scrap in hot caustic soda

Dezincing of zinc and zinc alloy coated industrial scrap could make a useful contribution to steel recycling. Earlier studies have demonstrated the possibility of dezincing hot dip galvanised steel scrap in hot caustic soda. The work is now extended to dezincing of zinc alloy coated steel, with the emphasis on galvannealed steel. The zinc dissolution rate of galvannealed steel turns out to be higher than that of hot dip galvanised steel. However, the residual zinc content is higher. This zinc is contained in a loosely bound film of black dust. Methods to remove the residual zinc can be found in mechanical treatments such as dezincing in a rotating drum.     

Comparison of bronchial challenge with ultrasonic nebulized distilled water and hypertonic saline in children with mild-to-moderate asthma

There is still controversy about the most suitable method to measure bronchial hyperresponsiveness in children. In epidemiological surveys, nonisotonic aerosols are being used increasingly for bronchial provocation testing. Our aim was to study the acceptability, safety and correlation between two published bronchial challenge tests. Two standardized protocols--the inhalation of hypertonic saline (HS) and ultrasonically-nebulized distilled water (UNDW)--were performed in 36 children: 19 patients with the clinical diagnosis of mild-to-moderate asthma (7-12 yrs of age), and 17 control subjects (8-18 yrs of age). HS challenge involved stepwise inhalation of 4.5% saline (for 0.5, 1, 2, 4 and 8 min), whereas challenge with UNDW was performed as a single step protocol with 10 min inhalation of cold UNDW. Asthma medication was withheld prior to challenge testing. Thirty five subjects completed both challenge tests (one asthmatic patient did not return after UNDW challenge) in random order within a 7 day time interval. For HS a > or = 15% reduction in forced expiratory volume in one second (FEV1) from baseline was considered a positive response, and for UNDW a > or = 10% decrease. In 13 of the 19 asthmatic patients, but in none of the controls, a positive response was observed for UNDW. Fifteen out of 18 patients and one control subject had a positive response to HS. Twelve out of 18 asthmatic children responded to both challenges, three responded only to HS and three had no response to either challenge. There was a negative correlation between log provocative dose causing a 15% reduction in FEV1 (PD15) after HS and the maximum fall in FEV1 after UNDW (rs = -0.63; p < 0.005). The HS challenge had a lower acceptability than challenge with UNDW due to the unpleasant salty taste of HS. However, this did not inhibit the completion of the tests in any subject. The results of this study suggest a good correlation between response to hypertonic saline and ultrasonically-nebulized distilled water in children with mild-to-moderate asthma. A multiple step protocol might be safer when applied in field studies involving children.     

Citric acid-induced cough thresholds in normal subjects, patients with bronchial asthma, and smokers

Several challenge procedures have been developed to characterize the cough reflex in patients with airway diseases. This study was performed to compare the interindividual range of cough sensitivity in asthmatic and normal subjects as well as smokers using an identical method. Sixteen normal subjects, 20 patients with mild bronchial asthma, 6 patients with moderate to severe bronchial asthma, 9 current smokers, and 7 occasional smokers were included. In all subjects, methacholine challenges and standardized citric acid challenges were performed. Sensitivity of the cough reflex was expressed as cough threshold, i.e., as concentration at which coughing occurred. Reproducibility was assessed in 23 subjects. Within a concentration range of 0.625-320.0 mg/ml, inhaled citric acid caused cough in all subjects. Geometric mean (range) cough threshold was 13 (2.5-160) in normal subjects, 14 (5-40) in patients with mild, and 32 (20-40) mg/ml in patients with moderate to severe asthma, 40 (20-80) in current smokers, and 119 (80-160) in occasional smokers. Cough thresholds were reproducible within one doubling concentration. In normal subjects and patients with mild bronchial asthma, thresholds were not significantly different from each other but lower than those of the other groups (p<0.05 each). Cough thresholds in smokers and patients with moderate to severe asthma did also not differ significantly and were lower than in occasional smokers (p<0.05). There was no significant correlation between cough threshold, baseline FEV subset1 , and methacholine responsiveness. Our data indicate that (1) subjects with mild asthma showed on average similar cough thresholds as normal subjects, (2) there was a large variation in cough thresholds within groups, (3) the reproducibility of cough thresholds was within one doubling concentration, (4) cough thresholds did not correlate with methacholine responsiveness or baseline airway tone. In view of the prevalence of cough as a symptom of bronchial asthma, it appears that the determination of citric acid-induced cough thresholds does not yield additional diagnostic information in these subjects.     

Both intravenous and inhaled lidocaine attenuate reflex bronchoconstriction but at different plasma concentrations

Intravenous lidocaine can attenuate bronchial hyperreactivity. However, lidocaine inhalation might yield the same or better results at higher airway and lower lidocaine plasma concentrations. Therefore, we tested in awake volunteers with bronchial hyperreactivity the effect of lidocaine on histamine-induced bronchoconstriction administered either intravenously or as an aerosol. After approval of the local ethics committee, 15 volunteers were enrolled in this placebo-controlled, double-blinded, randomized study. Volunteers were selected by showing a decrease in FEV1 greater than 20% of baseline (PC20) in response to histamine inhalation. On three different days the challenge was repeated after pretreatment with either intravenous lidocaine, inhaled lidocaine, or placebo. Blood samples for determination of lidocaine plasma concentration were drawn. Comparisons were made using the Friedman and Wilcoxon signed-rank tests. Baseline PC20 was 6.4 +/- 1.1 mg. ml-1. Both inhalation of lidocaine and intravenous administration significantly increased PC20 to 14.8 +/- 3.5 mg. ml-1 and 14.2 +/- 2. 5 mg. ml-1, respectively (p = 0.0007). Peak plasma lidocaine concentrations at the end of challenges were 0.7 +/- 0.1 microg. ml-1 (inhaled) and 2.2 +/- 0.1 microg. ml-1 (i.v.). However, 7 of 15 subjects showed an initial decrease of FEV1 greater than 5% following lidocaine inhalation. While both intravenous as well as inhaled lidocaine attenuate reflex bronchoconstriction significantly, lidocaine plasma concentrations are significantly lower after inhalation. However, the high incidence of initial bronchoconstriction to lidocaine inhalation may limit its use in patients with asthma and thus offers therapeutic advantages for intravenous lidocaine.     

Treatment of recurrent corneal erosion using phototherapeutic keratectomy with the excimer laser

Tachyphylaxis to methacholine has been reported in nonasthmatic subjects. In a recent study on the prevalence of airway hyperresponsiveness (AHR) and atopy, we performed duplicate methacholine inhalation tests at a 60-min interval, in subjects with symptomatic asthma (n = 33), asymptomatic AHR (AAHR) (n = 72) and in a group of normal subjects (n = 130); 135/235 subjects were atopic. All subjects had a respiratory questionnaire, allergy skin prick tests, blood eosinophil counts and determination of total serum IgE level. In asthmatic subjects, PC20 just failed to be significantly higher on a second methacholine challenge (p = 0.09); when they were stratified according to severity of AHR and use of inhaled corticosteroids, we observed a significant increase in PC20 on the second test in asthmatic subjects with mild AHR not using corticosteroids (p < 0.01). In normal controls, PC20 methacholine was slightly increased on rechallenge (p < 0.01) as it was in those with AAHR (p < 0.01). There was no relationship between the magnitude of the change in PC20 and age, sex, baseline airway responsiveness, percent fall in FEV1 on the first challenge, atopic score, blood eosinophil counts and serum IgE levels. In conclusion, tachyphylaxis to methacholine is observed in normal or mild asthmatic subjects not using inhaled corticosteroids and in subjects with AAHR; however, in most subjects this change is of a small magnitude.     

Occupational asthma due to latex in health care workers

Immediate hypersensitivity reactions ranging from mild urticaria to life threatening anaphylaxis after exposure to natural rubber latex have been reported frequently in health care workers while occupational asthma due to latex exposure is less well studied. The results of specific challenge tests and immunological tests in four health care workers with work related respiratory and skin disorders induced by the use of latex gloves are described. Occupational asthma was confirmed in three subjects by specific challenge tests. All had a positive skin test reaction to the latex extract; specific IgE antibodies were detected in only one subject. The fourth subject had a negative specific inhalation and skin test reaction to the latex extract. Peak expiratory flow monitoring at work and away from work showed a pattern consistent with work related asthma. These findings confirm that latex is a cause of occupational asthma in health care workers.     

Evaluation of the inhaled glucocorticosteroid effects on non specific bronchial reactivity with particular reference to the late inflammatory phase in atopic asthma patients. II. The effect of regular administration of budesonide R on specific and non-specific bronchial reactivity

The purpose of the study was to determine whether regular administration of budesonide R decreases inflammation, specific and non-specific bronchial hyperreactivity in allergic asthma patients. The studies were carried out on 16 patients suffering from mild to moderate allergic asthma, sensitive to D. pteronyssinus allergen. After performance of the specific and non-specific bronchial provocation tests, collection of blood samples for an ECP evaluation, the patients were regularly treated with budesonide R, 2 x 320 micrograms for a period of 8 weeks. At the end of the study the BPTs and blood collection were repeated. BPTs with methacholine and D. pteronyssinus were performed according to Ryan's method. After the allergen challenge, early (EAR) and late asthmatic reaction (LAR) were to be observed. After the therapy non-specific BHR to methacholine expressed as PC20FEV1 and specific BHR to allergen (PD20FEV1D. pteronyssinus) and serum ECP concentrations decreased significantly. Although after the treatment with budesonide R, the patients had to inhale much larger amounts of allergen, in order to induce EAR, the number of LAR did not change significantly. After treatment the LAR appeared about 1 hour later and the decrease in FEV1 was less than previously. We conclude that budesonide R decreases the intensity of the inflammation and BHR.     

Scorpion stings in Spain. Popular therapies, proverbs and pharmacopoeias]

There is evidence that bronchial responsiveness to allergen is quantitatively correlated with bronchial responsiveness to nonspecific stimuli in subjects with allergic asthma. This association has been questioned in occupational asthma due to low molecular weight substances. It was the aim of this study to assess the quantitative association of bronchial responsiveness to methacholine (MCh) and platinum salts (Pt), in the form of hexachloroplatinic acid, in workers with occupational asthma due to platinum salts. Fifty seven subjects with exposure to Pt, work-related asthma, and a positive bronchial challenge with Pt, underwent skin prick tests with Pt and bronchial challenge with MCh. Using the provocation concentration causing a > or = 50% fall in specific airway conductance (PC50sGaw(Pt)) as dependent variable, anamnestic data (period from first symptoms to removal, period between removal from exposure and diagnosis, and smoking), season of the investigation, skin prick tests with environmental allergens, total immunoglobulin E (IgE), skin reactivity to Pt (Pt concentration causing a 2 mm wheal), and PC50sGaw(MCh) were included as independent variables for regression analysis. Fifty two subjects (91%) showed a PC50sGaw(MCh) < 8 mg.mL-1 (geometric mean for all subjects 1.6 mg.mL-1). Responsiveness to Pt varied widely between subjects (geometric mean of PC50sGaw 9 x 10-5 mol.L-1, range 2 x 10-7 to 10-2 mol.L-1). There was no univariate correlation between bronchial responsiveness to MCh and Pt, but there was a correlation between skin reactivity to Pt and PC50sGaw(Pt) (r = 0.6). This association could not be improved by considering PC50sGaw(MCh), the period from first symptoms to removal, or the period between removal from exposure and diagnosis. The parameters that showed the highest (negative) associations with PC50sGaw(Pt) were skin reactivity to Pt and the period between removal from exposure and diagnosis (r = 0.65). We conclude that there is a moderate association between bronchial responsiveness to platinum salts and skin reactivity to platinum salts. However, there is no association between methacholine responsiveness and bronchial responsiveness to allergen in occupational asthma due to platinum salts.     

Airway responsiveness to hyperosmolar saline challenge in cystic fibrosis: a pilot study

Hyperosmolar aerosols are used to assess airway responsiveness in subjects with asthma. Using a 10% NaCl aerosol, we investigated airway responsiveness in 23 cystic fibrosis (CF) subjects (12 females, 11 males; 19.1 +/- 3.3 years) who had asthma-like symptoms. The pre-challenge predicted forced expiratory volume in 1 second (FEV1) was 74.7 +/- 21.5. The aerosol was generated by a MistO2gen 143A ultrasonic nebulizer and inhaled for 0.5, 1, 2, 4, 8, 8, and 8 minutes or part thereof. Spirometry was performed before and 1 minute after each inhalation period. The challenge was stopped when a > or = 20% fall from the baseline FEV1 was recorded, after the last inhalation period, or when requested by the subject. We recorded different responses to 10% NaCl among subjects. In 7, the FEV1 fell progressively throughout the challenge in a manner similar to asthmatics. By contrast, in 15 subjects the FEV1 was higher at the completion of challenge compared to during challenge, i.e., the fall in FEV1 was transient. In 7 of these subjects, the final FEV1 at the end of the challenge was higher than the pre-challenge FEV1. We conclude that inhaled 10% hyperosmolar saline causes either progressive and sustained or transient airway narrowing during challenge in the majority of CF subjects. The cause of the transient airway narrowing requires further investigation.     

The effect of inhaling a dry powder of sodium chloride on the airways of asthmatic subjects

Wet aerosols of 4.5% sodium chloride (NaCl) are often used to assess the bronchial responsiveness associated with asthma. We questioned whether dry NaCl could be used as an alternative. Dry powder NaCl was inhaled from capsules containing either 5, 10, 20 or 40 mg to a cumulative dose of 635 mg. The powder was delivered via an Inhalator or Halermatic. The airway sensitivity to the dry and wet NaCl was compared in 24 patients with asthma aged 19-39 yrs. All subjects responded to both preparations and the geometric mean (95% confidence intervals) for the provocative dose of NaCl causing forced expiratory volume in one second (FEV1) to fall 20% from baseline (PD[20,NaCl]) for dry NaCl was 103 mg (68-157) versus 172 mg (102-292), p<0.03 for the wet NaCl. The response to dry NaCl was reproducible and on repeat challenge the PD20 was 108 mg (75-153). The mean maximum fall in FEV1 was approximately 25% on each of the two test days. Spontaneous recovery occurred within 60 min after challenge with dry NaCl and within 5 min after bronchodilator. There were no serious side-effects requiring medical attention, however some patients coughed on inhalation of the 40 mg dose and three gagged. Arterial oxygen saturation remained within normal limits. We conclude that a suitably prepared dry powder of sodium chloride could potentially replace wet sodium chloride to assess bronchial responsiveness in patients with asthma, but further studies are required to establish the long-term stability of the dry powder preparation.     

Evaluation of the Brusini glaucoma staging system for follow-up in glaucoma

There is evidence that bronchial responsiveness to allergen is quantitatively correlated with bronchial responsiveness to nonspecific stimuli in subjects with allergic asthma. This association has been questioned in occupational asthma due to low molecular weight substances. It was the aim of this study to assess the quantitative association of bronchial responsiveness to methacholine (MCH) and platinum salts (Pt), in the form of hexachloroplatinic acid, in workers with occupational asthma due to Pt salts. Fifty-seven subjects with exposure to Pt, work-related asthma, and a positive bronchial challenge with Pt underwent skin prick test with Pt and bronchial challenge with MCH. Using the provocation concentration causing a > or = 50% fall in specific airway conductance (PC50sGaw(Pt)) as a dependent variable, anamnestic data (period from first symptoms to removal, period between removal from exposure and diagnosis, and smoking), season of the investigation, skin prick tests with environmental allergens, total immunoglobulin E (IgE), skin reactivity to Pt (Pt concentration causing a 2 mm wheal), and PC50sGaw(MCH) were included as independent variables for regression analysis. Fifty-two subjects (91%) showed a PC50sGaw(MCH) < 8 mg.mL-1 (geometric mean for all subjects 1.6 mg.mL-1). Responsiveness to Pt varied widely between subjects (geometric mean of PC50sGaw(Pt) 9 x 10(-5) mol.L-1, range 2 x 10(-7) to 10(-2) mol.L-1). There was no univariate correlation between bronchial responsiveness to MCH and Pt, but there was a correlation between skin reactivity to Pt and PC50sGaw(Pt) (r = 0.6). This association could not be improved by considering PC50sGaw(MCH), the period from first symptoms to removal, or the period between removal from exposure and diagnosis. The parameters that showed the highest (negative) associations with PC50sGaw(Pt) were skin reactivity to Pt and the period between removal from exposure and diagnosis (r = 0.65). We conclude that there is a moderate association between bronchial responsiveness to platinum salts and skin reactivity to platinum salts. However, there is no association between methacholine responsiveness and bronchial responsiveness to allergen in occupational asthma due to platinum salts.     

Apheresis platelets: emerging issues related to donor platelet count, apheresis platelet yield, and platelet transfusion dose

The prevalence of atopic dermatitis and other allergic diseases is increasing in industrialized countries. Today we know that atopy is conditioned genetically, but the development of the atopic phenotype requires environmental factors. It is believed that the genetic factors have not changed and that the increased prevalence is due to the increase in exposure to allergenic and non-specific environmental factors. The potential for sensitization is greater in the early years of life, so it is necessary to reduce harmful environmental exposure at these ages. Atopic clinical manifestations develop sequentially, in many cases beginning with atopic dermatitis in the early months of life. We know that children with atopic dermatitis present non-specific bronchial hyperreactivity (58 to 82%), which is a risk factor for the later development of asthma. The presence of specific bronchial hyperreactivity for mites in atopic dermatitis with mite sensitization also has been described, and it has been demonstrated that signs of eczema can develop or become exacerbated by airway exposure during bronchial challenge tests. The evolution from atopic dermatitis to asthma is a possibility that must be kept in mind. Patients should be followed-up and study of hyperreactivity and sensitization to allergens should be carried out in order to prevent the development of clinical symptoms. Prevention should include pneumoallergens, food allergens, and non-specific environmental risk factors, such as parental smoking (particularly mothers), pollution inside and outside the home, etc. Prevention is particularly important in children at risk of allergy, as determined by a family history among first-degree relatives, as well as the presence of atopic dermatitis, particularly of early onset, because these patient are most at risk of developing bronchial asthma in later years. At present, pharmacological prevention is being studied, without overlooking environmental prevention, in children at high risk of atopic disease for the purpose of preventing chronic inflammations that will condition their future as adults. In our daily clinical experience, atopic dermatitis is responsible for 8% of visits to a pediatric allergology unit. We emphasize that 62.5% of our patients with dermatitis are referred when they already have bronchial asthma, which represents an important delay in diagnosis with respect to the onset of symptoms.     

Induction of atopic dermatitis by inhalation of house dust mite

BACKGROUND: The pathogenetic role of house dust mite in atopic dermatitis remains controversial. Recent studies have shown that intensive epicutaneous contact of house dust mite allergen with premanipulated skin may induce dermatitis. It is, however, uncertain whether such conditions are met during natural contact with house dust mite. In the past, allergen inhalation has been suggested to induce exacerbation of atopic dermatitis. The aim of this study was to investigate whether dermatitis could be induced in patients with atopic dermatitis by inhalation of house dust mite. METHODS: Twenty patients with atopic dermatitis underwent bronchial provocations with house dust mite. Challenge tests were performed with four concentrations of a standardized house dust mite extract in a double-blind, randomized, placebo-controlled fashion. Spirometry was performed, and FEV1 was measured before and after each challenge dose. Changes in severity or localization of itching or erythema were recorded. RESULTS: In nine of 20 patients with atopic dermatitis bronchial challenge with house dust mite induced unequivocal skin symptoms after 1.5 to 17 hours. Pruritic erythematous lesions on noninvolved sites together with exacerbations of existing lesions were seen in three patients. Three patients had an exacerbation only, and three other patients had new lesions only. In eight of nine patients with house dust mite inhalation-induced dermatitis, skin symptoms were preceded by an early bronchial reaction. All patients with house dust mite-induced dermatitis had a history of asthma, and as a group they had a higher mean blood total IgE level compared with the "negative skin responders." One patient had pruritic erythema on the placebo challenge day, without a preceding bronchoconstrictive reaction. The number of patients who had a skin response on the house dust mite challenge day was significantly higher than the number of patients who had a skin response on the placebo day (p = 0.011 [Prescott's test]). CONCLUSIONS: The respiratory route may be relevant in the induction and exacerbation of dermatitis in a subset of patients with atopic dermatitis who have early bronchial reactions after house dust mite inhalation, a history of asthma, and an elevated blood total IgE level. Furthermore, these findings suggest a possible causal relationship between bronchial reactions and skin reactions.     

Assessing the effect of deep inhalation on airway calibre: a novel approach to lung function in bronchial asthma and COPD

Bronchoconstriction in bronchial asthma and chronic obstructive pulmonary disease (COPD) may be due to decreased airway calibre and/or to the inability of the airways to distend after a deep inhalation (DI). The purpose of this review is to discuss the physiological and clinical relevance of this latter mechanism. During induced constriction, DI shows remarkable bronchodilatation in normal subjects, but a blunted or null effect in asthmatics. In contrast, during spontaneous bronchospasm DI tends to decrease airway calibre. From a functional point of view, airway inflammation, remodelling, and peripheral bronchoconstriction could prevent airway smooth muscle from stretching. Therapeutic intervention improving lung function may change the response to DI. For example, bronchodilators allow expiratory airflow before DI to increase more than after DI, because of decreased bronchial hysteresis. This suggest that bronchodilation might be systematically underestimated from parameters derived from maximal expiratory manoeuvres. Inhaled corticosteroids tend to increase the dilator effect of DI, likely due to decreased bronchial and peribronchial oedema. In conclusion, measuring the effects of deep inhalation on lung function is an easy and simple test able to evaluate the structural changes occurring in the airways and to monitor the effectiveness of therapy.