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Gastroesophageal reflux

Gastroesophageal Reflux Disease (GERD; or GORD when spelling oesophageal, the BE form) is defined as chronic symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus. . more...

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This is commonly due to transient or permanent changes in the barrier between the esophagus and the stomach. This can be due to incompetence of the lower esophageal sphincter (LES), transient LES relaxation, or association with a hiatal hernia. Gastric regurgitation is an extension of this process with retrograde flow into the pharynx or mouth.


Heartburn is the symptom of acid in the esophagus, characterized by a burning discomfort behind the breastbone (sternum). Findings in GERD include esophagitis (reflux esophagitis) – inflammatory changes in the esophageal lining (mucosa) – strictures, difficulty swallowing (dysphagia), and chronic chest pain. Patients may have only one of those findings. Atypical symptoms of GERD include cough, hoarseness, changes of the voice, chronic ear ache, or sinusitis. Complicatons of GERD include stricture formation, Barrett's esophagus, esophageal ulcers and possibly even lead to esophageal cancer.

Occasional heartburn is common but does not necessarily mean one has GERD. Patients that have heartburn symptoms more than once a week are at risk of developing GERD. A hiatal hernia is usually asymptomatic, but the presence of a hiatal hernia is a risk factor for development of GERD.


The most prominent symptom of GERD is heartburn, the sensation of burning pain in the chest coming upward towards the mouth caused by reflux of acidic contents from the stomach to the esophagus.

Patients with GERD also tend to get the feeling of a sour or salty taste at the back of their throats due to regurgitation. This can sometimes happen even if the pain of heartburn is absent.

Less common symptoms:

  • Chest pain without any of the above
  • Dysphagia (difficulty swallowing)
  • Halitosis (bad breath)
  • Regurgitation (vomit-like taste in the mouth)
  • Repeated throat clearing
  • Water brash (the sensation of a large amount of non-acid liquid due to sudden hypersecretion of saliva)


  • Strictures or scarring of esophagus (especially young children).
  • Barrett's esophagus (sometimes referred to as Barrett's Disease)
  • Esophageal cancer

Important Warning symptoms:

  • Trouble swallowing Dysphagia requires immediate medical attention
  • Vomiting blood or partially-digested blood (looks like coffee grounds) requires immediate medical attention as does digested blood in the stools.

GERD in Children

GERD is commonly overlooked in infants and children. Symptoms may vary from typical adult symptoms. GERD in children may cause repeated vomiting, effortless spitting up, coughing, and other respiratory problems. Inconsolable crying, failure to gain adequate weight, refusing food and bad breath are also common. Children may have one symptom or many - no single symptom is universally present in all children with GERD.


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Gastroesophageal reflux as an asthma trigger: acid stress
From CHEST, 11/1/04 by Susan M. Harding

Since Sir William Osier recognized that gastroesophageal reflux (GER) is a potential asthma trigger more than a century ago, multiple investigations have shown a potential interaction between the esophagus and the lung. Despite this, there are still many unanswered questions as to how these two organs interact. To substantiate this interaction and to begin to examine causality, three criteria should be met. First, GER prevalence should be higher in asthmatic patients than in control subjects. Second, GER should alter airway reactivity and inflammatory markers. And third, GER therapy should improve asthma outcomes. So where do we stand concerning acid stress? (1,2)

GER symptom prevalence is higher in asthmatic patients compared to control subjects. Field et al (3) examined 109 asthmatic patients and 135 control subjects in two control groups, finding that heartburn was present in 77% of asthmatic patients compared to 48% of control subjects. Furthermore, 41% of asthmatic patients noted reflux-associated respiratory symptoms, and 28% of them utilized inhalers while experiencing GER symptoms. So, not only do asthmatic patients have a higher prevalence of GER symptoms than control subjects, they also associate GER symptoms with asthma symptoms. Our laboratory noted (4) that of 151 respiratory symptoms reported in 199 asthmatic patients during 24-h esophageal pH testing, 79% of respiratory symptoms were temporally related to esophageal acid.

In this issue of CHEST (see page 1490), Kiljander and Laitinen provide further insight into GER prevalence in asthmatic patients. In randomly selected asthmatic patients undergoing 24-h esophageal pH testing, 36% of asthmatic patients had abnormal esophageal acid contact times and 25% of asthmatic patients with abnormal esophageal acid contact times were flee of typical GER symptoms including heartburn. Furthermore, heartburn was not always associated with abnormal esophageal acid contact times. So, should esophageal pH testing be performed in asthmatic patients to identify GER in clinical practice? My answer is, no! Although esophageal pH testing is considered to be the "gold standard" for identifying GER, it has a sensitivity and specificity of approximately 90% and is not a perfect test. (5) Day-to-day esophageal acid contact times vary with activity and diet. Recently, a wireless esophageal pH system has been developed that allows monitoring up to 48 h without the use of an intranasal catheter, so that patients are less likely to alter their daily activities and/or diet. (6) Also, a non-acid refluxate, undetectable with pH monitoring, may have an impact. Currently, minimal data exist on nonacid reflux and its effect on the lung. Nonacid GER can be measured by esophageal impedance monitoring, which was not performed in this study. (7) Despite these issues, Drs. Kiljander and Laitinen verify for us again that the prevalence of GER is indeed high in asthmatic patients.

So, why is GER so prevalent in asthmatic patients? Predisposing factors include an increased pressure gradient between the thorax and abdomen, leading to more frequent reflux episodes. Asthmatic patients with GER also have a higher prevalence of hiatal hernia (64%) compared to control subjects (19%), predisposing them to GER development. (1) Finally, asthma medications may potentiate GER. For instance, theophylline increases gastric acid secretion and decreases lower esophageal sphincter pressure, inhaled [[beta].sub.2]-adrenergic agonists decrease lower esophageal sphincter pressure in a dose-dependent manner, and oral corticosteroids increase esophageal acid contact times. (1,8)

If GER is an important asthma trigger, then mechanisms should explain how GER alters airway reactivity and inflammatory markers. The potential mechanisms include a vagally mediated reflex, a local axonal reflex, heightened bronchial reactivity, and microaspiration. (1) Furthermore, neurogenic inflammation appears to play a key role in esophageal acid-induced bronchoeonstriction. Elegant morphologic studies identified a direct connection between the esophagus and the lung with nitric oxide-containing neurons. In animal models, esophageal afferent nerve stimulation results in action potentials and tachykinin release (substance P and neurokinin-A) in the lung. (8) Aspiration may damage the airway epithelium, resulting in the release of cytokines and adhesion molecules leading to neurogenic inflammation and the initiation of other inflammatory pathways. (9) These mechanisms are dependent on the activation of capsaicin-sensitive sensory nerves, with the subsequent release of tachykinins that, in conjunction with kinins, nitric oxide, oxygen radicals, and proteases, modulate diverse aspects of airway inflammation. (2) Thus, excessive acidification leading to "acid stress" has many potential adverse effects on the lung.

So, with this in mind, does antireflux therapy improve asthma outcomes? Previous trials have shown that antireflux therapy improves asthma symptoms in approximately 70% of asthmatic patients with GER. (10,11) However, these trials had major design flaws, including small patient populations, inadequate asthma outcome analyses, and the use of a placebo crossover design in many of the proton pump inhibitor trials. Another important finding is that pulmonary function improvement does not always follow asthma symptom improvement. (10,11) The Cochrane Airways Group Registry (12) examined randomized controlled trials of children and adults who had been treated with medical or surgical antireflux therapy, identifying 328 subjects and finding that seven of nine studies had at least one significantly improved asthma outcome. There are hints in large cohort studies that GER may impact asthma. GER was noted to be a risk factor for asthma hospitalization in asthmatic patients over the age of 19. (13) Also, in a retrospective cross-sectional analysis of 10,959 asthmatic patients, (14) GER was predictive for higher numbers of oral steroid bursts and asthma hospitalizations. So GER may be an important asthma trigger in selected asthmatic patients, however, a definitive outcomes study has not been published to date.

A problem with our current state of knowledge is that we do not know which asthmatic patients would benefit from GER therapy. Many asthmatic patients have GER without GER actually being a trigger of their asthma. Potential predictors of asthma response include the presence of regurgitation, nocturnal asthma, nonallergic asthma, difficult-to-control asthma, a history of reflux-associated respiratory symptoms, and a high body mass index. (1) These predictors have not been validated in larger studies, so currently it is up to the clinician to determine whether GER is indeed a trigger of their individual patient's asthma. A 3-month empiric trial of aggressive acid suppression utilizing a proton pump inhibitor could be used to identify these asthmatic patients. (1) Hopefully, future investigations will allow clinicians to target those asthmatic patients who have acid stress.


(1) Harding SM. Gastroesophageal reflux and asthma: insight into the association. J Allergy Clin Immunol 1999; 104:251-259

(2) Ricciardolo FL, Gaston B, Hunt J. Acid stress in the pathology of asthma. J Allergy Clin Immunol 2004; 113:610-619

(3) Field SK, Underwood H, Brant R, et al. Prevalence of gastroesophageal reflux symptoms in asthma. Chest 1996; 1009:316-322

(4) Harding SM, Guzzo MR, Richter JE. 24-h esophageal pH testing in asthmatics: respiratory symptoms correlation with esophageal acid events. Chest 1999; 115:654-659

(5) Kahrilas PJ, Quigley EM. Clinical esophageal pH recording: a technical review for practice guideline development. Gastroenterology 1996; 110:1982-1996

(6) Pandolfino JE, Richter JE, Ours T, et al. Ambulatory esophageal pH monitoring using a wireless system. Am J Gastroenterol 2003; 98:740-749

(7) Shay S, Tutuian R, Sifrim D, et al. Twenty-four hour ambulatory simultaneous impedance and pH monitoring: a multicenter report of normal values from 60 healthy volunteers. Am J Gastroenterol 2004; 99:1037-1043

(8) Harding SM. Recent clinical investigations of asthma and gastroesophageal reflux. Am J Med 2003; 115(suppl):39S-44S

(9) Stein MR. Advances in the approach to gastroesophageal reflux (GER) and asthma. J Asthma 1999; 35:309-314

(10) Field SK, Sutherland LR. Does medical antirefux therapy improve asthma in asthmatics with gastroesophageal reflux? Chest 1998; 114:275-283

(11) Field SK, Gelfand GA, McFadden SD. The effects of surgery on asthmatics with gastroesophageal reflux. Chest 1999; 116:766-774

(12) Gibson PG, Henry RL, Coughlan JL. The effect of treatment for gastro-oesophageal reflux on asthma in adults and children. Cochrane Database Syst Rev (database online) Issue 2, 2002

(13) Diette GB, Krishnan JA, Dominici F, et al. Asthma in older patients: factors associated with hospitalization. Arch Intern Med 2002; 121:8-10

(14) Shireman TI, Heaton PC, Gay WE, et al. Relationship between asthma drug therapy patterns and healthcare utilization. Ann Pharmacother 2002; 36:557-564

Susan M. Harding, MD, FCCP

Birmingham, AL

Dr. Harding is Associate Professor of Medicine, the Division of Pulmonary, Allergy & Critical Care Medicine, University of Alabama at Birmingham.

This research was-funded by National Institutes of Health National Heart, Lung, and Blood Institute grant RO1 HL75614-01. Dr. Harding has been a Consultant to and has received Clinical Trial Funding from AstraZeneca LP.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail:

Correspondence to: Susan M. Harding, MD, FCCP, Division of Pulmonary, Allergy & Critical Care Medicine, 1900 University Blvd, THT Rm 215, University of Alabama at Birmingham, Birmingham, AL 35294; e-mail:

COPYRIGHT 2004 American College of Chest Physicians
COPYRIGHT 2004 Gale Group

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