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					ADVANCE for Physician Assistants Issue Date: 1/1/2000 ACID REINS Does GERD Cause Some Asthma or Just Contribute? BY SULTAN S. AHMED, PA-C, MBBS, AND CYRIL BLAVO, DO, MPH, TM In 1892, Sir William Osler, the Canadian physician and scholar who is often called the most influential physician in history, described the risk of asthma in a patient with an overfilled stomach. Since then, researchers have performed many studies to attempt to establish a correlation or causation between asthma and gastroesophageal reflux disease (GERD). But now more than 100 years after Osler's observation, the causal link between GERD and asthma still is controversial. So what is the association between the two conditions, and how does that link affect treatment? Overview of Asthma Asthma is a chronic, reversible, reactive airway disease characterized by inflammatory changes in the lungs, airway hyper-responsiveness and partial airway obstruction.1 It manifests clinically in a variety of ways, including coughing, wheezing, chest retractions and shortness of breath. Symptoms of asthma may occur sporadically, seasonally or perennially. A family history of atopy is usually present. Response to inhaled allergens or to other environmental triggers such as viral respiratory infections, house dust mites, occupational chemicals, weather changes, food additives, chemical preservatives, cigarette smoke, pet dander, emotions or exercise is the basis for its pathogenesis.1 The asthmatic response results in the release of inflammatory mediators, which cause changes in the bronchioles such as smooth-muscle contraction, increased vascular permeability, pulmonary vasodilation, increased mucus secretion and edema of the airways. Asthma may be classified as mild intermittent, mild persistent, moderate persistent or severe persistent.2 This classification serves as a framework for therapeutic guidelines that are based on pulmonary function tests and symptom presentation. A comprehensive approach to managing asthma is important and should include elimination or control of triggers of the asthmatic response, the routine use of peak flow meters to objectively measure pulmonary function and the use of topical modalities (such as metered-dose inhalers with spacer devices and nebulizers) whenever appropriate to administer medications. Allergen immunotherapy may be considered when practical. Medications used in the asthma treatment include:2 * short-acting oral or inhaled bronchodilators (e.g., albuterol, pirbuterol, terbutaline, bitolterol), long-acting beta-agonists (e.g., salmeterol), * oral corticosteroids (e.g., prednisone, prednisolone, methylprednisolone),

* methyl xanthines (e.g., aminophylline, theophylline), * cromolyn sodium, nedocromil sodium, * inhaled corticosteroids of varying dosage intensities (e.g., beclomethasone, budesonide, triamcinolone, flunisolide and fluticasone), * anticholinergic agents (e.g., ipratropium bromide) and * leukotriene inhibitors (e.g., montelukast, zafirlukast, zileuton). The goals of asthma therapy are to resolve or significantly improve respiratory symptoms using the most effective medications with the fewest side effects, to enhance the activities of daily living, to decrease the number of days missed from school or work and to decrease the number of hospital visits. Strong emphasis is placed on patient education, anticipatory guidance and regular follow-up care. Overview of GERD Gastroesophageal reflux disease (GERD) is a result of abnormal exposure of the esophageal mucosa to gastric content, which causes symptoms such as heartburn, regurgitation, substernal pain, hoarseness and at times coughing. Factors contributing to gastroesophageal reflux include ingesting fatty foods, caffeine, alcohol and chocolate, as well as obesity, pregnancy and the presence of hiatal hernia.3 The lower esophageal sphincter (LES) serves as an intermittent mechanical barrier to retrograde passage of gastric content into the esophagus. It is influenced by neuromuscular and humoral factors. The esophageal mucosa, with the help of peristalsis, gravity, its intrinsic buffering mechanism and mucosal integrity, is normally protected from the damage that results from extensive exposure to acid reflux. Prolonged or frequently low resting LES tone, impaired esophageal motility, decreased gastric emptying and diminished esophageal mucosal resistance to acid and pepsin contribute to the erosive esophagitis that sometimes develops in GERD.4 Serious complications from GERD include esophageal strictures, Barrett's esophagus and esophageal adenocarcinoma. The gold standard for evaluation of patients presenting with signs and symptoms of GERD is ambulatory esophageal pH monitoring.5 The pH probe measures frequency, severity and duration of acid reflux into the esophagus. It is a highly sensitive and specific test. Upper gastrointestinal barium studies may be performed to confirm suspicion of gastroesophageal reflux.4 Although this technique is sensitive to anatomical abnormalities associated with reflux, it has a rather low sensitivity for the detection of abnormalities of the esophageal mucosa. Gastroesophageal scintiscan, which uses less radiation, is a suitable

alternative.3 Upper gastrointestinal endoscopy is indicated when esophagitis is suspected. Histologic studies of biopsy specimen may reveal inflammatory changes in the esophageal mucosa.4 When endoscopy fails to confirm GERD, in spite of apparent signs and symptoms of reflux, the Bernstein test, a stimulation of symptoms of GERD through the dripping of exogenous acid into the lower esophagus, may be performed.4 Management of GERD consists of dietary and lifestyle changes, weight control and appropriate medications. Medications used to treat gastroesophageal reflux include:3 * antacids, * histamine antagonists (e.g., ranitidine, cimetidine, famotidine, nizatidine), * prokinetic agents (e.g., metoclopramide, bethanechol, cisapride) and * proton-pump inhibitors (e.g., omeprazole, lansoprazole). Surgical intervention (e.g., Nissen fundoplication, laparoscopic fundoplication) may be indicated with failure of medical therapy or in the presence of serious complications such as severe bleeding and strictures.6 Coexistence of Asthma, GERD Evidence of the coexistence of asthma and GERD has been extensively documented.5 A cross-sectional study of 109 patients with asthma revealed symptoms of gastroesophageal reflux in 77% of the patients, in contrast to 52% and 48% in two control groups of 135 persons.7 Sontag and colleagues reported complaints of heartburn in 72% of 189 asthma patients studied at a veteran's hospital.8 In another study involving more than 100,000 veterans, patients with significant esophageal disease had a higher incidence of asthma than did patients without esophageal disease.9 And, an esophageal pH study of 104 asthma patients demonstrated abnormal esophageal acid contact times in 82% of the subjects.8 In a 1999 study by Harding and colleagues, 82% of 199 asthma patients reported reflux symptoms, while 72% of the patients showed evidence of abnormal esophageal acid contact times.5 Esophageal mucosal inflammation was noted in 43% of 186 asthma patients in another study.10 And according to one group of authors, the prevalence of GERD in patients with asthma is reportedly between 33% and 89%.11 What's the Association? The relationship between asthma and GERD has been explored in many studies over the last few decades.5 Studies that suggest GERD is a contributing factor in the pathogenesis of asthma also propose two probable mechanisms: either vagal-mediated bronchospasm11 or microaspiration

of gastric contents into the lungs.13

Wright and colleagues performed esophageal acid infusion in 136 patients with asthma and observed a resultant decrease in air inflow and oxygen saturation.14 A vagolytic dose of atropine administered to each of these patients resulted in ablation of the responses, implying a vagal-mediated response. A study that monitored tracheal and esophageal pH simultaneously revealed a significant decrease in peak expiratory flow when both esophageal and tracheal acid were present, compared with the presence of esophageal acid alone.13 While tracheal aspiration of esophageal content has been associated with decreased pulmonary function in some asthma patients, evidence of a vagal-mediated reflex bronchospasm is more compelling. Improvement of asthma symptoms has been demonstrated when coexisting GERD is appropriately treated, either medically15 or surgically.6 In a double-blind, placebo-controlled crossover study of 15 patients with coexisting asthma and GERD whose reflux symptoms were treated with omeprazole, 29% reported improvement in their asthma symptoms. Studies on antireflux surgery for asthma patients have generally reported better outcomes than in patients who are treated medically. In one study, Nissen fundoplication performed on 50 asthma patients with severe GERD resulted in complete resolution of asthma symptoms in 26% of the patients, a significant improvement in 36% of the patients and moderate improvement in 16% of the patients.6 The rest of the patients experienced no change in their symptoms. Put simply: There is sufficient evidence to seriously consider an association between gastroesophageal reflux and chronic respiratory symptoms in some cases of asthma. A Cause-Effect Relationship? Failure to induce a significant change in pulmonary function after esophageal acid perfusion has, however, been demonstrated in a number of studies.15 Ekstrom and Tibbling16 performed peak expiratory flow (PEF) measurements on 42 asthma patients with gastroesophageal reflux, and they found no statistically significant difference in PEF in either the presence or absence of spontaneous reflux. A critical review of 18 published studies addressed the effects of spontaneous and simulated gastroesophageal reflux on pulmonary function in asthma patients.15 Although the results of the studies were conflicting, the review authors concluded that acid perfusion has minimal effect on pulmonary function of patients with asthma. These studies suggest that coexistence of asthma and GERD does not necessarily imply causation.

GERD in Childhood Asthma The relationship of gastroesophageal reflux and nocturnal wheezing has been well-documented in children with reactive airway disease using esophageal pH monitoring during sleep.17 In a controlled study of children with cough and wheezing in which both proximal and distal intra-esophageal pH were recorded, respiratory symptoms induced by reflux appeared to occur via a vagal-mediated reflex mechanism rather than by aspiration of gastric reflux.18 Predictors of GERD-Induced Asthma While the causal link between GERD and asthma remains controversial, and the presence of gastroesophageal reflux in asthma patients is often subclinical, GERD-induced asthma should be considered in the following situations: * when asthma presents for the first time in adulthood; * when symptoms of asthma occur after meals, while lying down or during exercise; * when symptoms of asthma appear worse at night; * in cases of nonallergic asthma; * if symptoms of asthma do not improve after prolonged medical therapy; and * when asthma symptoms resolve after treatment of coexisting GERD. Investigation for the presence of gastroesophageal reflux would be indicated in such cases, and appropriate anti-reflux therapy instituted.

References 1. Lemanske RF Jr, Busse WW. Asthma. JAMA. 1997;278:1855-1873. 2. National Asthma Education and Prevention Program. Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma. Bethesda, Md: National Institutes of Health; 1997. Publication 97-4051. 3. Hillemeier AC. Gastroesophageal reflux. Diagnostic and therapeutic approaches. Pediatr Clin North Am. 1996;43:197-212.

4. DeVault KR, Castell DO. Guidelines for the diagnosis and treatment of gastroesophageal reflux disease. Practice Parameters Committee of the American College of Gastroenterology. Arch Intern Med. 1995;155:2165-2173. 5. Harding SM, Guzzo MR, Richter JE. 24-h esophageal pH testing in asthmatics: respiratory symptom correlation with esophageal acid events. Chest. 1999:115:654-659. 6. Perrin-Fayolle M, Gormand F, Braillon G, et al. Long-term results of surgical treatment for gastroesophageal reflux in asthmatic patients. Chest. 1989;96:40-45. 7. Field SK, Underwood M, Brant R, Cowie RL. Prevalence of gastroesophageal reflux symptoms in asthma. Chest. 1996;109:316-322. 8. Sontag SJ, O'Connell S, Khandelwal S, et al. Most asthmatics have gastroesophageal reflux with or without bronchodilator therapy. Gastroenterology. 1990;99:613-620. 9. el-Serag HB, Sonnenberg A. Comorbid occurrence of laryngeal or pulmonary disease with esophagitis in United States military veterans. Gastroenterology. 1997;113:755-760. 10. Sontag SJ, Schnell TG, Miller TQ, et al. Prevalence of oesophagitis in asthmatics. Gut. 1992;33:872-876. 11. Harding SM, Richter JE. The role of gastroesophageal reflux in chronic cough and asthma. Chest. 1997;111:1389-1402. 12. Lodi U, Harding SM, Coghlan HC, Guzzo MR, Walker LH. Autonomic regulation in asthmatics with gastroesophageal reflux. Chest. 1997;111:65-70. 13. Jack CIA, Calverley PMA, Donnelly RJ, et al. Simultaneous tracheal and oesophageal pH measurements in asthmatic patients with gastro-oesophageal reflux. Thorax. 1995;50:201-204. 14. Wright RA, Miller SA, Corsello BF. Acid-induced esophagobronchial-cardiac reflexes in humans. Gastroenterology. 1990;99:71-73. 15. Field SK. A critical review of the studies of the effects of simulated or real gastroesophageal reflux on pulmonary function in asthmatic adults. Chest. 1999;115:848-856. 16. Ekstrom T, Tibbling L. Gastro-oesophageal reflux and triggering of bronchial asthma: a negative report. Eur J Respir Dis. 1987;71:177-180. 17. Martin ME, Grunstein MM, Larsen GL. The relationship of gastroesophageal reflux to nocturnal wheezing in children with asthma. Ann Allergy. 1982;49:318-322. 18. Cucchiara S, Santamaria F, Minella R, et al. Simultaneous prolonged recordings of proximal

and distal intraesophageal pH in children with gastroesophageal reflux disease and respiratory symptoms. Am J Gastroenterol. 1995;90:1791-1796. Sultan S. Ahmed is an assistant professor and the continuing medical education chair at the physician assistant program at Nova Southeastern University in Fort Lauderdale, Fla. Cyril Blavo is chairman of the pediatrics department and associate director of the public health program at Nova Southeastern University's College of Osteopathic Medicine in Fort Lauderdale, Fla. ADVANCE for Physician Assistants 1/1/2000

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