Extra-esophageal manifestations of gastro-esophageal reflux disease, continued. flammation is caused by gastroesophageal reflux, on the assumption that pepsin originates only in the stomach.8 A therapeutic trial with a proton pump inhibitor (PPI), twice-daily, for 4-8 weeks in patients who have GERD and reflux laryngitis syndrome, and observation of their symptomatic response, is a reasonable approach. If symptoms improve, the therapy may need to be prolonged for an additional 2 to 3 months to allow healing of laryngeal inflammation, after which the dose of PPI should be tapered to the minimum level of acid suppression needed to maintain their response.9-11 Upper endoscopy and 24-hour esophageal pH and/or impedance monitoring should be reserved for patients in whom GERD is still suspected because of persistent symptoms despite appropriate therapy.10 Reflux cough syndrome Chronic cough (a cough lasting for more than 8 weeks) is a frequent symptom in patients suffering from GERD. Gastric refluxate may trigger a chronic cough either directly, by irritating the upper airway or, indirectly, by stimulating an esophago-bronchial reflex. Chronic cough in the general population is caused by many conditions, other than GERD; in a patient who is a non-smoker and has a normal chest X-ray, the four most important causes of a chronic cough are GERD, postnasal drip syndrome, asthma and angiotensin converting enzyme (ACE) inhibitors. There are certain characteristics which may suggest that a cough is caused by GER: these include day-time cough, cough in upright position, cough during phonation, cough during eating or cough when rising from bed. It is worth noting that GERD may induce a cough which can, then, increase intra-abdominal pressure, thereby inducing further reflux which may aggravate the cough still more. A systematic approach should be followed for patients with chronic cough. Common causes, such as medication (ACE inhibitors), postnasal drip and asthma must be excluded. In patients who have concomitant heartburn and/or regurgitation or those with high degree of suspicion for GERD, an empiric trial of a PPI, twice-daily, for 1 to 2 months is a reasonable approach. Upper endoscopy and 24-hour esophageal pH and/or impedance monitoring should be reserved for patients in whom GERD is still suspected and for whom treatment does not eliminate cough.10 A lack of response to empiric PPI trial may be an indicator that cough is not caused by GERD, and other causes of chronic cough should be sought. Reflux asthma syndrome Epidemiological studies suggest an association between bronchial asthma and GERD. Not only is there an association between the two conditions but each of two conditions or their treatment can aggravate the other. Whilst GERD can induce bronchial asthma by a vagally-mediated reflex or by a micro-aspiration-induced reflux mechanism, as discussed above, bronchial asthma, itself, can enhance reflux by creating a negative intra-thoracic pressure; in addition, medications (e.g. theophylline, beta-2 adrenergic agonists) used to treat bronchial asthma can cause relaxation of the lower esophageal sphincter (LES). Both GERD and bronchial asthma are common in the community and they may, also, co-exist independent of each other. How, then, does a clinician establish that asthma in a given patient is caused by GERD? Patients with bronchial asthma whose symptoms are worse after meals, or those who do not respond to traditional asthma medications should be suspected of having GERD. Patients who have heartburn and regurgitation before the onset of asthma symptoms may also be suspected of having reflux-induced asthma symptoms.1-3 As for patients with reflux-induced laryngitis, the yield of diagnostic tests such as upper endoscopy or 24-hour pH metry is not very encouraging. Furthermore, the response in the outcome parameters of bronchial asthma with treatment of GERD is not uniform. A Cochrane review of GERD treatment for patients with bronchial asthma found only minimal improvement of asthma symptoms following treatment for GERD.12 A recent, controlled trial in asthmatics has, however, suggested that there is therapeutic benefit from PPIs in a sub-group of asthmatics who have both nocturnal respiratory and GER symptoms.13 Therefore, the current recommendation in patients with asthma (with or without concomitant heartburn or regurgitation) is similar to those for patients with chronic cough and laryngitis; that is, an initial empirical trial of twice-daily PPI therapy for 2-3 months. 2,3,14 In those responsive to therapy for both heartburn and/or asthma symptoms, the PPI should be tapered to the minimal dose necessary to control symptoms.2,3,11 In unresponsive patients, testing for reflux by pH testing and/or impedance-pH monitoring may be considered to confirm the continued reflux of acid or non-acid material which might still be responsible for the patients’ asthma symptoms. Reflux-induced chest pain Non-cardiac chest pain (NCCP) is a recurring, angina-like, retrosternal chest pain in patients in whom cardiac evaluation is within normal limits. Clinically, cardiac chest pain and chest pain of esophageal origin often present with similar symptoms (often described as burning, pressure-like, sub-sternal or occurring with exercise) and the symptoms may improve with similar treatments (i.e., nitroglycerin); thus, it may be difficult for a clinician to differentiate chest pain of esophageal origin from that of cardiac origin. Pain that is post-prandial, continues for hours, is retrosternal without radiation and is relieved with antacids, and pain that disturbs sleep makes the diagnosis of GER-related chest pain more likely. Obviously, classic reflux symptoms such as heartburn and regurgitation, in the absence of cardiac disease, make the diagnosis more likely. In fact, the symptoms of GERD are found in majority of patients with chest pain due to GERD.15 Furthermore, NCCPis reported in one third of patients who are frequent refluxers compared to only 7.9% of patients reporting no GERD symptoms.16 Direct contact of the esophageal mucosa with gastro-duodenal contents, such as acid, pepsin or bile, leads to stimulation of the vagus nerve which, in turn, most likely causes chest pain. NCCP can also be caused by other esophageal disorders such as nutcracker esophagus or diffuse esophageal spasm; thus, for patients with persistent NCCP despite appropriate GERD therapy, esophageal motility studies should be considered.17 World Digestive Health Day WDHD May 29, 2015 WGO HANDBOOK HEARTBURN: A GLOBAL PERSPECTIVE 22
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