Can mild bronchospasm reduce gastroesophageal reflux?

During attacks of asthma, changes in the transdiaphragmatic pressure gradient may impair the antireflux barrier and provoke gastroesophageal reflux (GER). If GER triggers asthma and asthma causes GER, a vicious circle could arise with an increase in the severity of asthma symptoms. The aim of this investigation was to determine whether postprandial reflux in asthmatics with GER disease is increased during histamine-induced bronchospasm and also if theophylline increases GER during provoked episodes of bronchospasm. Ten patients with chronic asthma and pathologic GER were challenged with either histamine or saline in randomized order with and without their regular dose of oral slow-release theophylline. FEV1 was recorded at regular intervals during the hour of provocation, and acid reflux (pH less than 4) was monitored by antimony pH electrodes in the esophagus. GER was not more pronounced during the provoked bronchospasm period irrespective of theophylline treatment or not. It seems unlikely that mild bronchospasm provokes reflux in patients with asthma and GER. It would appear that mild bronchospasm is rather protective against gastroesophageal reflux.     

The association of gastroesophageal reflux with bronchial asthma. Can asthma also trigger reflux?

BACKGROUND/AIMS: The frequency of gastroesophageal reflux (GER) among asthmatic patients was found to range from 34% to 89% at different locations. The aims of this study have been to determine the frequency of GER in patients with asthma in the Saudi environment, to ascertain the main mechanism whereby GER triggers asthma, and to seek any evidence whether asthma can also trigger GER. METHODOLOGY: Fifty asthmatic patients were consecutively recruited as they reported to King Fahd Hospital of the University (KFHU), Al-Khobar, Saudi Arabia, in the period from February 2000 to February 2001; their mean age +/- SD was 38.0 +/- 9.8 years. Twenty-two subjects without asthma or GER served as controls; their mean age +/- SD was 29.4 +/- 8.6. Both groups were subjected to a questionnaire, esophageal manometry, dual probe ambulatory 24-hour pH monitoring, and pulmonary function tests. RESULTS: Among the asthmatic group 22 patients (44%) had GER. Accordingly, the asthmatic patients were divided into two groups: asthmatic with GER (n=22), and asthmatic without GER (n=28). Hoarseness of voice and nocturnal symptoms were found to be significant predictors for the presence of GER in asthmatics. Manometry revealed that asthmatic patients with GER had higher gastric pressure (11.4 +/- 4.0 mmHg vs. 8.4 +/- 2.8 mmHg; p=0.006) and lower resting pressure at the lower esophageal sphincter (LES) (21.2 +/- 8.7 mmHg vs. 28.2 +/- 9.3 mmHg; p=0.013) when compared with controls, both factors favoring the occurrence of reflux. With regard to pH data, acid reflux occurred both at the distal and proximal esophagus but the percent total acid exposure time was about 7 times longer at the distal than at the proximal esophagus (5.80 vs. 0.9). In addition, gastric pressure was positively and significantly correlated with distal esophageal acid exposure time and the DeMeester score, negatively correlated with spirometric parameters in asthmatic patients, as well as found to be a significant predictor of the severity of asthma (p=0.006). CONCLUSIONS: Forty-four percent of the sample of asthmatic patients reporting to KFHU had GER. Since distal esophageal total acid exposure time was nearly 7 times longer than at the proximal esophagus, the main mechanism for GER triggering asthma is the vagally mediated reflex initiated by acid in the distal esophagus. In addition, the positive correlation of increased gastric pressure with the distal esophageal acid exposure time and the DeMeester score, its negative correlation with spirometric parameters and being a significant predictor of asthma severity suggest that severe asthma may trigger or aggravate GER.     

Asthme et reflux gastro-œsophagien

Asthma and gastroesophageal reflux (GER) frequently coexist in patients. GER is usually considered to be potential trigger for asthma symptoms. This hypothesis is based more on pathophysiological considerations than on clinical data. Indeed, experimental data show that acid perfusion of the lower esophagus in humans induces increased bronchial hyperreactivity, and various mechanisms have been proposed to explain this observation. Recent studies also demonstrate that, in patients with asthma, obstruction induced by non-specific bronchial challenge increases the number of reflux episodes. This suggests that asthma by itself might be responsible for GER. Despite these facts, a review of published reports claiming to demonstrate the clinical effectiveness of medical or surgical treatment of GER on asthma symptoms yields inconsistent results. Nevertheless, it appears that a few asthmatic patients do benefit clinically and/or have improved lung function when treated for GER. However, the criteria for patient selection and, especially, the anti-reflux treatment modalities (choice and dose of medication and the duration of treatment) need to be more clearly defined through additional studies.     

Gastric Asthma: An Unrecognized Disease with an Unsuspected Frequency

Bronchial asthma is a disease that has been recognized for centuries, which is influenced mainly by genetic and environmental factors. The current interest of bronchial asthma is focused to ascertain the causes and the mechanisms that induce bronchoconstriction. Recently, abnormalities of the esophageal and gastric tracts have become important related areas for research. In predisposed individuals, these abnormalities can trigger or worsen the particular syndrome better known as “gastric asthma.” In bronchial asthma the disorder of gastroesophageal reflux (GER) occurs more often than would be expected by chance. The neurogenic mechanism is considered to be the main cause of bronchoconstriction. The diagnosis of gastric asthma is particularly difficult and it should be considered also when GER is less evident or not recognized. In asthmatic patients the recognition of gastric abnormalities is very relevant for therapeutic problems also when GER is in a subclinical stage. In fact, many drugs used in the treatment of bronchial asthma can promote or enhance GER and subsequently they can worsen the symptoms of gastric asthma.     

Cellular events in the bronchi in mild asthma and after bronchial provocation

We have undertaken detailed cellular and ultrastructural examination of bronchial biopsies and bronchial lavage fluid from allergic asthmatic patients in order to determine the nature and degree of the inflammatory processes in mild allergic asthma. Eight atopic asthmatic patients (mean PC20 histamine, 0.90 mg/ml) and four nonasthmatic control subjects underwent fiberoptic bronchoscopy. All asthmatic subjects were clinically stable for 2 wk prior to bronchoscopy and required either no treatment or inhaled albuterol alone. A single 50-ml bronchial wash was undertaken, followed by endobronchial biopsy of subcarinae. These procedures were repeated in the asthmatic subjects 18 h after bronchial provocation with allergen or methacholine. Subsequently, all subjects underwent bronchial reactivity testing with inhaled histamine. The clinical and physiologic data were not revealed to the pathologist interpreting the specimens. The asthmatic subjects shed a significantly greater number of epithelial cells into the lavage fluid than did the nonasthmatic subjects (7.23 versus 1.48 x 10(4)/ml, p = 0.048). There was a statistically significant inverse correlation between the lavage epithelial cell count and bronchial reactivity (rho = -0.64, p = 0.03). In the asthmatic subjects, but not in the control subjects, there was extensive deposition of collagen beneath the epithelial basement membrane, mast cell degranulation, and mucosal infiltration by eosinophils, which exhibited morphologic evidence of activation. Eosinophils, monocytes, and platelets were found in contact with the vascular endothelium, with emigration of eosinophils and monocytes in the asthmatic subjects. These changes were found irrespective of bronchial challenge with allergen. We conclude that allergic asthma is accompanied by extensive inflammatory changes in the airways, even in mild clinical and subclinical disease.     

24-h esophageal pH testing in asthmatics: respiratory symptom correlation with esophageal acid events

BACKGROUND: Gastroesophageal reflux (GER) may be a trigger for asthma and may be clinically silent. Twenty-four-hour esophageal pH testing accurately diagnoses GER in asthmatics. There are no reports correlating respiratory symptoms with esophageal acid events. This study examines the prevalence and severity of GER in asthmatics with and without reflux symptoms and examines respiratory symptom correlation with esophageal acid. METHODS: All esophageal manometry and 24-h esophageal pH tests performed were reviewed in asthmatics who met entrance criteria from July 1, 1989, through November 1, 1994. GER was present if esophageal pH tests were abnormal. Results of esophageal tests were compared for asthmatics with reflux symptoms and GER and asthmatics without reflux symptoms and GER. Respiratory symptoms correlated with esophageal acid events if the esophageal pH was < 4 simultaneously with the respiratory event or within 5 min before its onset. RESULTS: Of 199 asthmatics who qualified for analysis, 164 (82%) had reflux symptoms. The results of 24-h esophageal pH tests were abnormal in 118 of 164 asthmatics with reflux symptoms (72%), compared with 10 of 35 asthmatics without reflux symptoms (29%). Among asthmatics with GER, 119 of 151 respiratory symptoms (78.8%) were associated with esophageal acid. Seventy-six of 84 reported coughs (90.5%) were associated with esophageal acid. Theophylline did not alter esophageal parameters. CONCLUSIONS: There is a strong correlation between esophageal acid events and respiratory symptoms in asthmatics with GER. Respiratory symptom correlation with esophageal acid events further supports that GER may be a trigger for asthma.     

Effects of esophageal acid perfusion on cough responsiveness in patients with bronchial asthma

STUDY OBJECTIVES: The effect of gastroesophageal reflux (GER) on cough responsiveness in patients with bronchial asthma has yet to be studied in significant detail. The purpose of this study was to assess the effect of distal esophageal acid perfusion on cough responsiveness in patients with bronchial asthma. PATIENTS AND INTERVENTIONS: In seven patients with mild persistent bronchial asthma (mean +/- SD age, 57.7 +/- 3.7 years; four women and three men), esophageal pH was monitored by a pH meter and cough responsiveness was evaluated by single-breath aerosol inhalation of capsaicin with increasing dosage from 0.30 to 9.84 nmol. Simultaneously, esophageal perfusion was performed through an esophageal tube filled with either saline solution or 0.1 N hydrochloric acid (HCl), the order of which was selected at random, in 1-week intervals. Results were expressed as the lowest concentration of capsaicin eliciting three coughs (PD3). Spirometry was also performed during esophageal pH monitoring. RESULTS: A significant decrease in the geometric mean of log PD3 was observed during distal esophageal HCl perfusion (0.45 +/- 0.04 nmol) compared with that of the saline solution perfusion (0.04 +/- 0.06 nmol) [p < 0.01]. However, no significant changes were observed either in FVC, FEV1, or peak expiratory flow during the periods of the saline solution or HCl perfusion. CONCLUSION: The present data demonstrate that an increase in cough responsiveness may be induced when HCl stimulates the distal portion of esophagus in patients with bronchial asthma, suggesting that the GER would be one of the important factors that influence asthmatic status.     

Bronchial hyperresponsiveness is a common feature in patients with chronic urticaria.

BACKGROUND: Chronic urticaria (CU) is a skin disorder characterized by long-lasting release of histamine, and sometimes leukotrienes, from both mast cells and basophils. Although both these substances are potent inductors of contraction of airway smooth muscle, pulmonary function and airway hyperresponsiveness have not been systematically investigated in patients with CU. OBJECTIVE: To assess pulmonary function and airway hyperresponsiveness in patients with CU. METHODS: Twenty-six clinically well-characterized adult patients with CU (M/F 8/18; mean age 47 years) underwent pulmonary function tests and methacholine provocation during a phase of moderate activity of their disease. Twenty-six adult asthmatic patients submitted to methacholine provocation were used as controls. RESULTS: Two patients (8%) had overt asthma on baseline pulmonary function tests. Twenty (77%) patients with a normal baseline pulmonary function showed significant bronchial hyperresponsiveness on methacholine provocation. Altogether, 22/26 (85%) patients had asthma or abnormal bronchial reactivity. Airway hyperresponsiveness was not associated with gender, disease duration, intolerance to NSAID, positive autologous serum skin test or respiratory allergy. On average, asthmatic controls showed a much severer airway hyperresponsiveness than urticaria patients (p < 0.01). CONCLUSION: Patients with CU frequently show bronchial hyperresponsiveness. Prospective studies are needed to assess whether they are at risk for bronchial asthma.     

Intraesophageal perfusion of acid increases the bronchomotor response to methacholine and to isocapnic hyperventilation in asthmatic subjects

Gastroesophageal reflux (GER) has been shown to be more frequent in people with asthma, but the mechanism by which it might aggravate asthmatic symptoms remains unclear. We compared the effects on maximal expiratory flow at 50% of VC (MEF50) of esophageal perfusion of hydrochloric acid (HCl) and of normal saline (NaCl) in 12 asthmatic subjects chosen at random. In all subjects, HCl perfusion did not change MEF50 but potentiated the bronchoconstriction induced by isocapnic hyperventilation of dry air (maximal decrease in MEF50 = 44 +/- 7% with HCl versus 22 +/- 5% with NaCl; p less than 0.001) or methacholine (provocative dose producing a 20% decrease in FEV1 = 349 +/- 99 micrograms with HCl versus 496 +/- 119 micrograms with NaCl; p less than 0.01). Seven of the asthmatic subjects were found to have GER on esophageal pH monitoring. In these subjects, HCl alone decreased MEF50 slightly but significantly (-17.5 +/- 5.5%; p less than 0.05), possibly reflecting the higher degree of basal bronchial hyperreactivity observed in this group. Thus, perfusion of acid into the distal esophagus caused slight but significant bronchoconstriction in asthmatic subjects with GER and increased the bronchoconstriction produced by isocapnic hyperventilation and by methacholine in asthmatic subjects without regard for the presence of GER.     

Enhanced IgE-dependent basophil histamine release and airway reactivity in asthma

IgE-dependent basophil histamine release does not necessarily correlate with the amount of cell-bound IgE, thus it has been suggested that basophil "releasability" is an important, but yet undefined, factor in this secretory process. Because mast cell, and possibly basophilic leukocyte, mediator release contributes to airway reactivity, any enhancement of this secretory process would favor asthma provocation. To evaluate IgE-dependent basophil histamine releasability in asthma, suspensions of leukocytes were isolated from patients with an allergic and nonallergic component to their airway disease and stimulated with concanavalin A (Con A) (0.03 to 10.0 micrograms/ml) and anti-IgE (10 to 1,000 ng/ml). Basophil histamine release to Con A and anti-IgE was significantly greater in both allergic and nonallergic asthmatic patients when compared with normal subjects. In contrast, basophil histamine release to the calcium ionophore A23187 was similar in leukocytes from normal subjects and asthmatic patients, suggesting the observed abnormality in secretion may be limited to an IgE-dependent process. To further determine if basophil histamine releasability in asthma correlated to measures of airway reactivity, bronchial provocation with histamine was performed. An inverse correlation was found between the provocative dose of inhaled histamine required to produce a 20% decrease, PD20, in the FEV1 and the leukocyte histamine release to Con A (p less than 0.05) and anti-IgE (p less than 0.05). Thus, we have new evidence that enhanced IgE-dependent release of leukocyte histamine correlates with airway reactivity in asthma. The mechanism of basophil releasability and its relationship to the pathogenesis of airway reactivity in asthma have yet to be established.     

Gastroesophageal reflux and bronchial responsiveness: correlation and the effect of fundoplication

BACKGROUND: A causal relationship between gastroesophageal reflux (GER) and asthma has been suggested. Should this be the case, one could expect treatment of GER to diminish bronchial sensitivity. There has been a lack of trials evaluating the efficacy of antireflux surgery on airway reactivity. OBJECTIVES: To investigate the correlation between GER and bronchial responsiveness, and to determine the efficacy of Nissen fundoplication on bronchial responsiveness and pulmonary function. METHODS: A methacholine inhalation challenge was performed on 15 consecutive GER patients preoperatively and approximately 5 months after Nissen fundoplication. Airway responsiveness was quantified with a dose-response slope (DRS), calculated by dividing the decrease in FEV(1) (%) with the dose of methacholine administered (micromoles). RESULTS: A positive correlation between the severity of distal esophageal reflux and bronchial responsiveness was found (r = 0.83, p < 0.001). There was an improvement in FEV(1) after fundoplication (p = 0.03). All 3 asthmatic patients participating in the study presented with bronchial hyperresponsiveness (BHR) which improved clearly in all of these patients after fundoplication. This resulted in an apparent trend for DRS to improve when the entire study population was considered (p = 0.12). CONCLUSIONS: According to the current study there seems to be a positive correlation between the severity of distal esophageal reflux and bronchial responsiveness. These data suggest that operative treatment of GER may ameliorate BHR in asthmatic patients. Moreover, the results of the present study suggest that fundoplication may improve pulmonary function in patients with GER.     

Determination of airway hyper-reactivity in asthmatic children: a comparison among exercise, nebulized water, and histamine challenge

An easy and accurate method of assessing bronchial hyper-reactivity could be of great value in identifying and classifying the degree of severity of asthma in children. The sensitivity and specificity of three methods of provocation, ie, histamine, nebulized water, and exercise, were compared in 20 asthmatic and 20 control children between ages 5 and 13 years. Three clinical categories of severity ranging from slight (Group 1) through moderate (Group 2) to severe asthma (Group 3) were identified. The three methods were compared in each subgroup for detecting a tendency to bronchospasm. An inverse correlation (-0.57) was found between the histamine dose and clinical degree of severity, whereas distilled water and exercise proved to be too insensitive for identifying Group 1 asthmatics. Histamine challenge in children is a safe and sensitive technique for identifying asthma and for monitoring the severity of the disease during follow-up.     

Gastroesophageal reflux in asthmatics: A double-blind, placebo-controlled crossover study with omeprazole

STUDY OBJECTIVES: To investigate the prevalence of gastroesophageal reflux (GER) among patients with asthma and to determine the effect of omeprazole on the outcome of asthma in patients with GER. DESIGN: A double-blind, placebo-controlled crossover study. SETTING: Asthmatic patients who attended the pulmonary outpatient clinic of Turku University Central Hospital, Finland. PATIENTS: One hundred seven asthmatic patients. INTERVENTIONS: The patients who were found to have GER in ambulatory esophageal pH monitoring were randomized to receive either omeprazole, 40 mg qd, or placebo for 8 weeks. After a 2-week washout period, the patients were crossed over to the other treatment. Spirometry was performed at baseline and immediately after both treatment periods. Peak expiratory values, use of sympathomimetics, and pulmonary and gastric symptoms were recorded daily in a diary. RESULTS: Pathologic GER was found in 53% of the asthmatic patients. One third of these patients had no typical reflux symptoms. Daytime pulmonary symptoms did not improve significantly (p = 0.14), but a reduction in nighttime asthma symptoms (p = 0.04) was found during omeprazole treatment. In the patients with intrinsic asthma, there was a decline in [corrected] FEV(1) values (p = 0.049). Based on symptom scores, 35% of the patients were regarded as responders to 8-week omeprazole treatment. The reflux (time [percent] of pH < 4) was found to be more severe (p = 0. 002) in the responders. CONCLUSIONS: There is a high prevalence of GER in the asthmatic population. This reflux is often clinically "silent." After an 8-week omeprazole treatment, there was a reduction in nocturnal asthma symptoms, whereas daytime asthma outcome did not improve. There seems to be a subgroup of asthma patients who benefit from excessive antireflux therapy.     

Gastroesophageal reflux disorders and asthma

Gastroesophageal reflux (GERD) may trigger asthma. Approximately 77% of asthmatic people experience reflux symptoms, although GERD may be clinically silent in some. Esophagitis is found in 43% of asthmatic people, and 82% have abnormal esophageal acid contact times on esophageal pH testing. Clearly, GERD is prevalent in asthmatic people. Pathophysiologic mechanisms of acid-induced bronchoconstriction include a vagally mediated reflex and microaspiration. Whether these airway responses are clinically significant is the subject of some debate. Interestingly, peak expiratory flow rates and specific airway resistance alterations persist despite esophageal acid clearance. Preliminary evidence shows that substance P, an inflammatory mediator that causes airway edema, is released with esophageal acid. Although therapeutic studies are limited by their small population sizes and study design, up to 70% of asthmatic people have asthma improvement with antireflux therapy. Possible predictors of asthma response include patients with symptomatic esophageal regurgitation; abnormal proximal esophageal acid exposure; and, in surgical studies, those with normal esophageal motility and asthma response with medical therapy. Future research will further define the association between asthma and gastroesophageal reflux.     

Abnormal acid reflux in asthmatic patients in a region with low GERD prevalence

Background A high prevalence of gastroesophageal reflux disease (GERD) in asthmatic patients has been reported from North America and Europe. However, only a few data from Asia are available. This study evaluated the incidence of abnormal gastroesophageal reflux (GER) in asthmatic patients in Taiwan.Methods Fifty-six consecutive ambulatory patients with clinically stable asthma (41 men and 15 women; age, 57.7 ± 12.4 years; range, 24 to 74 years) were evaluated prospectively. All patients underwent esophagogastroduodenoscopy, esophageal manometry, and 24-h esophageal pH monitoring.Results Twenty-nine patients (51.8%) had abnormal GER, as defined by 24-h esophageal pH monitoring. There were 42 patients without endoscopic evidence of esophagitis, 10 patients with Los Angeles (LA) grade A esophagitis, and 4 patients with LA grade B esophagitis. The esophageal motility function studies revealed 21 patients with normal esophageal motility, 23 patients with ineffective esophageal motility (IEM), and 12 patients with nonspecific esophageal motility disorders other than IEM. Although the lower esophageal sphincter (LES) basal pressure was higher in the patients without GER, the difference was not statistically significant.Conclusions Abnormal GER seems to be a clinically significant problem in asthmatic patients in Taiwan. The most common esophageal motility dysfunction is IEM. However, the status of Helicobacter pylori infection plays no role in abnormal GER.     

The potential role of gastroesophageal reflux in asthma

Gastroesophageal reflux disease (GERD) afflicts approximately 20% of adults in the United States on a weekly basis and 40% on a monthly basis, and is also a trigger for asthma. The prevalence of GERD is higher in asthmatics compared to control groups, with 77% of asthma patients having reflux symptoms and 82% of asthmatics having abnormal esophageal acid contact times on 24-hour esophageal pH testing. Esophageal acid elicits respiratory responses including decreases in airflow, oxygen saturation, and increases in respiratory resistance, minute ventilation, and respiratory rate. Mechanisms of esophageal acid-induced bronchoconstriction include a vagally-mediated reflex, heightened bronchial reactivity, and microaspiration. Esophageal acid also produces airway neurogenic inflammatory responses with the release of substance P, tachykinins, nitric oxide, and other cytokines. Predisposing factors to GERD development in asthmatics include autonomic dysregulation, an increased pressure gradient between the thorax and the abdomen, a high prevalence of hiatal hernia, and altered crural diaphragm function. Theophylline may also potentiate GERD. Therapy of GERD improves asthma outcome. In combined studies examining 326 medically treated asthma patients, asthma symptoms improved in 69% of patients. Surgical therapy trials in 417 asthma patients show asthma symptoms improved in 79%. Management strategies for GERD in asthmatics with reflux symptoms include utilizing an empiric trial of a proton pump inhibitor for three months while measuring asthma outcomes. Since GERD may be clinically 'silent' in asthma patients, consider 24-hour esophageal pH testing in severe asthma patients who do not have GERD symptoms. Future research will develop the association between asthma and GERD.     

Cold air as a bronchial provocation technique. Reproducibility and comparison with histamine and methacholine inhalation

Bronchial provocation testing with cold air was carried out on 36 asthmatic and 13 normal subjects in order to assess the reproducibility and clinical relevance of the technique as a test of airways reactivity. Sixteen subjects underwent repeat testing after an interval of two to three weeks. Using a least squares linear regression analysis, the technique was highly reproducible, with a correlation of r = 0.93 (p less than 0.001). The 21 asthmatic subjects who had exercise-provoked symptoms required a significantly lower level of ventilation of cold air to produce a 35 percent drop in specific airways conductance (PD35) than did those who had no exercise-induced asthma (33.9 L min-1 vs 45.8 L min-1; p less than 0.02). Subjects requiring no regular treatment for their asthma had a geometric mean PD35 of 62.6 L min-1, significantly higher than those requiring inhaled therapy (44.9 L min-1; p less than 0.005). Subjects requiring oral in addition to inhaled treatment had the lowest PD35 (23.6 L min-1; p less than 0.02). Atopic status did not appear to influence the response. There was a strong correlation between the PD35 to cold air and to histamine (r = 0.92; p less than 0.001) and between the PD35 to cold air and to methacholine (r = 0.86; p less than 0.001). The three techniques of assessing bronchial reactivity were equally successful in separating the normal and asthmatic groups. The results indicate that cold air provocation may be reliably and reproducibly used to assess bronchial reactivity. The use of a naturally-occurring stimulus of asthma in all subjects has great potential as an investigational technique.     

支气管哮喘患者与胃食管返流的症状相关性

目的　探讨胃食管返流 (GER)与成人中、重度支气管哮喘的症状相关性 ,了解 2 4h食管pH监测对哮喘合并GER的诊断价值及抗返流治疗对合并GER的哮喘患者症状的影响。方法　对 2 6例常规治疗后仍有顽固性咳嗽等症状的成人哮喘患者进行 2 4h食管pH监测 ,严格记录监测期间患者出现的各种症状 ,每小时记录 1次呼气峰流速 (PEF)。筛选出适当病例分组抗返流治疗并观察疗效。结果　 2 6例中有 15例DeMeester总积分≥ 14 72 ,2例虽DeMeester总积分 <14 72 ,但咳嗽与返流的症状相关概率 (SAP)≥ 95 % ,共筛选出 17例。将 17例患者随机分为治疗组 (9例 )和对照组 (8例 )。经抗返流治疗后 ,治疗组咳嗽、胸闷和胸骨后烧灼感等症状均较对照组有明显改善 ,2 4hPEF波动率治疗前 [(3 8± 8) % ]、后 [(16± 3 ) % ]比较差异有显著性 (P <0 0 5 )。结论　 (1)中、重度支气管哮喘患者具有较高的GER发生率 (5 8% )。 (2 ) 2 4h食管pH监测有助于了解哮喘患者的症状与GER的相关性。 (3 )对于有GER并与哮喘症状密切相关的患者 ,抗返流治疗可显著地改善其症状及PEF波动率     

Reflux gastro-œsophagien et manifestations respiratoires de l'enfant

Symptoms related to gastro-oesophageal reflux (GER) are more prevalent during asthma (approximately 75%) than in controls. A correlation is found between GER and respiratory symptoms and inhaler use. But GER may also occurr with out oesophageal symptoms. An increased oesophageal acid contact time is a common finding in patients with asthma, with a prevalence of 80%. Among the physiopathologic mechanisms involved, are a vagally mediated reflux, a higher bronchial reactivity and microaspirations. The phenomenon may involve the release of mediators, such as substance P, resulting in airway oedema. The best antireflux therapy is the use of proton pump inhibitors (PPIs), which may improve asthma symptoms in 70% of patients. Some indicators of a positive asthma response are the presence of regurgitations, of proximal acid reflux or of oesophagitis healing with therapy, of respiratory symptoms associated with reflux and of nocturnal asthma. In patient with potential GER triggered asthma, a correct handling relies on a 3-month trial of high-dose PPI, with a correct monitoring of asthma outcome.     

Fiberoptic bronchoscopy in bronchial asthma. A word of caution.

Three instances of intense laryngospasm and bronchospasm occurred as a result of fiberoptic bronchoscopic examination in three patients with quiescent bronchial asthma. The indications for the procedure were hemoptysis in one patient and lobar collapse in two. It is likely that vagally mediated reflex laryngospasm and bronchoconstriction occur when irritant receptors are mechanically stimulated by the bronchoscope. Therefore, in the asthmatic population with its increased airway reactivity, indications for fiberoptic bronchoscopy should be absolute, and the procedure should be performed under optimal conditions. A rationale for minimizing the risk of this procedure in patients with bronchial asthma is discussed.