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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastroesophageal reflux is often overlooked as both a cause and a complication of respiratory disease in children. The manifestations may be protean and may bear little clinical relationship to the gastrointestinal tract. However, a high index of suspicion for its potential role in unexplained respiratory symptoms may yield large benefits for the physician and patient alike.
J Asthma 1995
PMID:Respiratory manifestations of gastroesophageal reflux in children. 775 56

Asthma is increasing in prevalence and morbidity worldwide. Worsening of asthma symptoms during sleep and following exercise is an important component of this morbidity. Better recognition and management of nocturnal asthma and exercise-induced broncho-constriction should lead to improved outcomes. Measures to alleviate nocturnal asthma include elimination of exposure to allergens, use of measures to control contributing factors (rhinitis, sinusitis, gastroesophageal reflux, sleep apnea), maximization of the dosage of daytime asthma medications, and appropriately timed use of medications such as a long-acting inhaled beta 2 agonist, a once-daily sustained-release theophylline product, and an oral corticosteroid. Bronchoconstriction after exercise can be decreased by physical conditioning, warm-up exercises, wearing of a face mask in cold weather, postponement of exercise until at least 2 hours after a meal, and pretreatment with an inhaled beta agonist. Pretreatment with inhaled cromolyn sodium (Intal), nedocromil sodium (Tilade), or ipratropium bromide (Atrovent) may be added if necessary.
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PMID:Nocturnal asthma and exercise-induced bronchospasm. Why they occur and how they can be managed. 777 48

Asthma and gastro-oesophageal reflux commonly occur together but the association in any individual may or may not be causal. Aspiration of gastric acid into the trachea has been demonstrated in some patients with asthma with concomitant falls in lung function, while acid in the lower oesophagus can exacerbate asthma by a vagal reflex following stimulation of lower oesophageal receptors. Conversely, asthma can lead to worsening reflux both through the use of smooth muscle relaxing anti-asthma medication and by the mechanical effects of hyperinflation reducing lower oesophageal sphincter pressures. The effects on asthma following treatment of reflux has been anecdotally reported to be successful in some individuals, particularly those with severe reflux, but surgery should be reserved for individuals only after failure of medical treatment and should be aimed at improving reflux symptoms rather than improving asthma control.
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PMID:Oesophageal reflux and asthma. 879 71

When infants with recurrent wheezing have a clinical course inconsistent with asthma, an extensive list of alternative diagnoses needs to be considered. Anatomic malformations, such as congenital heart disease, laryngotracheomalacia, and diaphragmatic hernia, should be considered for immediate medical stabilization and early surgical correction. Life-threatening infections such as bacterial epiglottitis, retropharyngeal cellulitis, and viral myocarditis require prompt intervention. A careful history and physical examination reveal important diagnostic clues that, in this case, prompted a directed evaluation to rule out common masqueraders of asthma such as foreign body aspiration, cystic fibrosis, gastroesophageal reflux, viral pneumonitis, or pulmonary tuberculosis. On occasion, such a search is unrevealing and a diagnostic challenge remains. In those situations, judicious use of modern technology to scrutinize anatomic (high-resolution computed tomography) and functional (infant pulmonary function tests) pathology, and justifiable invasive procedures such as bronchoscopy and lung biopsy, uncover the true diagnosis, allowing for optimal management.
Ann Allergy Asthma Immunol 1997 May
PMID:A wheezy infant unresponsive to bronchodilators. 916 57

Various practice parameters have emphasized a step-wise approach to the treatment of asthma utilizing high doses of inhaled corticosteroids, i.e., 2000 ug per day for the most difficult-to-manage asthmatic patient, along with maximum bronchodilator therapy. The use of such vigorous therapy presupposes that various triggers that perpetuate asthma have been considered and hopefully eliminated or diminished, such as occupational incitants, gastroesophageal reflux, and concomitant medication such as beta blockers and perhaps difficult-to-recognize allergen stimulation. As new therapies emerge, their role in the treatment of a severe subgroup of the population remains uncategorized and will only be clarified with personal experience and appropriate double-blind studies. For example, there are data to support the concept that salmeterol plus moderate dose aerosol corticosteroids is superior to high dose corticosteroid aerosols. Theoretically, the use of anti-leukotrienes for a patient with aspirin idiosyncrasy may be superior to other combinations as would be conjectured from aspirin challenge data. Lidocaine has recently been employed in severe asthmatics, and preliminary data suggest benefit. The purpose of this review is to summarize some of our knowledge regarding medications that are either steroid-sparing or that might be useful in a subgroup of asthmatic patients with severe asthma.
Allergy Asthma Proc
PMID:Treatment of the unusually difficult asthmatic patient. 919 41

To evaluate the incidence of abnormal gastroesophageal reflux in patients with bronchial asthma and the influence of drug therapy on the gastroesophageal reflux, we investigated the gastroesophageal reflux patterns using an ambulatory 24-hour esophageal monitoring in 25 healthy volunteers and 58 asthmatics. All the patients were stable conditions at the time of the study. Bronchodilator therapy was continued, if necessary along with steroid inhalation and xanthines. Compared with healthy volunteers, the asthmatics had significantly greater esophageal acid exposure time, more frequent reflux episode, and longer single reflux time. About 70% of asthmatics had abnormal gastroesophageal reflux. Asthma medications were not associated with the incidence of abnormal gastroesophageal reflux. However, asthmatics receiving beta(2)-stimulants therapy (n = 27) had significantly greater esophageal reflux exposure time than those not receiving (n = 31). Our study suggested that most asthmatics have abnormal gastroesophageal reflux unrelated to asthma attack or asthma medications and that beta(2)-stimulants used in asthmatics may worsen gastroesophageal reflux.
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PMID:[A study of gastroesophageal reflux by 24-hour esophageal pH monitoring in patients with bronchial asthma]. 928 40

Extraesophageal manifestations of gastroesophageal reflux disease (GERD) include chronic cough, asthma and 'acid' laryngitis. The response to medical and/or surgical therapy of these conditions is highly variable and often delayed. Of patients with GERD-related symptoms, those with extraesophageal manifestations are some of the most difficult to treat. Histamine antagonists, proton pump inhibitors and antireflux surgery have all been used to treat GERD-related asthma with variable results. Asthma patients who do not respond to high-dose acid suppression may be refractory to all forms of therapy. GERD is the third most common cause of chronic cough, and therapeutic results with acid suppression and antireflux surgery are variable. Posterior laryngitis presents as chronic hoarseness and has been shown to resolve clinically and histologically with acid suppression therapy or antireflux surgery. Results are variable, and controlled trials are lacking.
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PMID:Treatment of extraesophageal manifestations of gastroesophageal reflux disease. 934 89

Asthma has a tendency to destabilize at night in patients that are diurnaly active and try to sleep at night. As asthma worsens, the expression of this disease seems to increase at night. Additionally, nocturnal asthmatics have increased airway hyperresponsiveness and likely more active inflammation at night as compared with the daytime. Although the cause of nocturnal asthma cannot be completely explained, there do appear to be a variety of internal body circadian rhythms that play a role in this disease. Also, noncircadian rhythmic influences such as sleep, supine posture, snoring, and gastroesophageal reflux cannot be dismissed. Directing therapy, perhaps in unique ways, may be essential for the control of nocturnal asthma. Patients on inhaled corticosteroid therapy or nonsteroidal anti-inflammatory agents often persist in asthmatic disease expression at night. Long-acting bronchodilator therapy, either by inhalation or with sustained-release tablets, is often added to inhaled anti-inflammatory therapy for more complete 24-hour disease control. Using existing therapies but employing chronotherapeutic strategies is likely to improve the overall asthma management. By focusing on nocturnal asthma, we may be able to improve our understanding of this disease and more effectively control it over each 24-hour period.
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PMID:Nocturnal asthma: physiologic determinants and current therapeutic approaches. 936 15

The relationship between gastroesophageal reflux (GER) and asthma remains controversial. Asthma symptoms worsen with GER, but are not consistently related to changes in lung function. The purpose of this study was to determine whether acid perfusion (AP) of the esophagus alters ventilation and causes respiratory symptoms. Nonasthmatic patients with normal lung function and esophageal disease (16 females and nine males, FEV1 %predicted = 99+/-9.6), underwent a Bernstein test after motility testing. Airflow, rib cage (Vrc), and abdominal (Vab) tidal volumes, esophageal (Pes) and gastric (Pga) pressure, and surface (Es) and esophageal (Edi) diaphragm electromyographic (EMG) signals were measured. Throat, swallowing, chest, and stomach discomfort and respiratory sensation were estimated with the Borg scale. Minute ventilation (VE) increased during AP and declined during recovery with saline perfusion of the esophagus (7.1+/-1.5 to 8.5+/-2.4 to 7.3+/-2.1 L/min; n = 25; p = 0.0002). Respiratory rate (RR) went from 13.6+/-2.6 to 15.8+/-3.4 to 15.3+/-3.1 breaths/min (n = 25; p = 0.0002) during AP. VE was greater in the Bernstein-positive patients during AP. Tidal volume (VT), Vrc, Vab, Pes, Pga, Es, and Edi did not change during AP. Chest discomfort (D) correlated with ventilation (VE = 0.7 + 0.8 D; r = 0.67; p < 0.001) and respiratory effort sensation (B) (B = 0.2 + 0.4 VE; r = 0.70; p < 0.001) during AP. AP did not inhibit diaphragm activity. Increased VE may explain the paradox of GER worsening respiratory symptoms without changing lung function.
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PMID:The effects of acid perfusion of the esophagus on ventilation and respiratory sensation. 956 19

Asthma is usually easy to manage, but approximately 5% of patients are not controlled even on high doses of inhaled corticosteroids. It is important to assess these patients carefully in order to identify whether there are any correctable factors that may contribute to their poor control. It is critical to make a diagnosis of asthma and to exclude other airway diseases, particularly chronic obstructive pulmonary disease (COPD), and vocal cord dysfunction ("pseudo-asthma"). Poor adherence to therapy, particularly inhaled corticosteroids, is a common reason for a poor response. There may be unidentified exacerbating factors, including unrecognized allergens, occupational sensitizers, dietary additives, drugs, gastro-oesophageal reflux, upper airway disease, or other systemic diseases, that need to be identified and avoided or treated. Psychological factors may be important in some patients, but it is difficult to know whether these are causal or secondary to troublesome disease. Some patients have instability of their asthma, with resistant nocturnal asthma, premenstrual exacerbations or chaotic and unpredictable instability (brittle asthma). A few patients are completely resistant to corticosteroids, but more patients are relatively resistant and require relatively high doses of corticosteroids to control their symptoms (steroid-dependent). Some patients develop progressive loss of lung function, as in patients with COPD. Management of patients with difficult asthma should be supervised by a respiratory specialist and should involve careful assessment to confirm a diagnosis of asthma, identification and treatment of exacerbating factors, particularly allergens, and recording of peak expiratory flow patterns. A period of hospital admission may be the best way to assess and manage these patients. Treatment involves optimizing corticosteroids therapy, assessing additional controllers such as long-acting inhaled or subcutaneous beta2-agonists or subcutaneous, theophylline and antileukotrienes. In some patients, the use of immunosuppressive treatments may reduce steroid requirements, although these treatments are rarely effective and have side-effects. In the future, the nonsteroid anti-inflammatory treatments now in development may be useful in these patients.
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PMID:Difficult asthma. 986 23


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