Chocolate, Mint and Tea for your Stomach
Buried deep within an article in American Family Physician is a note of some of the foods that can decrease the lower esophageal sphincter, thereby reducing gastroesophageal reflux. Among the listed foods are carminitives, such as peppermint and spearmint, and chocolate. One of the drugs listed as having this effect is theophylline, a caffeine related alkaloid in found in tea.
Prokinetic therapy for gastroesophageal reflux disease. (includes patient information sheet)
From:
American Family Physician
Date:
September 1, 1995
Author:
Robinson, Malcolm
Prokinetic drugs theoretically have the ability to correct the pathophysiologic abnormalities of gastrointestinal motility that lead to gastroesophageal reflux disease. However, the prokinetic agents bethanechol and metoclopramide have been associated with central nervous system and other side effects, as well as uncertain efficacy. In addition, erythromycin seems unsuitable for use as an oral prokinetic agent. A recently introduced prokinetic agent, cisapride, has a minimum incidence of side effects and is effective in the treatment of reflux symptoms, but trials in the United States have not confirmed the symptomatic improvement or healing of erosive esophagitis that has been demonstrated in studies abroad. An expanded role may unfold for cisapride and additional new prokinetic drugs as primary therapy for reflux in some patients, as adjunctive treatment with an antisecretory agent, or as maintenance treatment for a subset of patients with gastroesophageal reflux. Therapy tailored to individual pathophysiology is appropriate and may offer cost savings and improved clinical outcome.
The recent introduction of cisapride (Propulsid), a gastrointestinal prokinetic drug approved by the U.S. Food and Drug Administration for the relief of nocturnal heartburn, has generated renewed interest in the role of this class of agents in the treatment of gastroesophageal reflux disease. Before the availability of cisapride, prokinetic agents were seldom used as primary therapy for patients with gastrointestinal reflux. This article reviews the reasons for the increase in usage, evaluates the efficacy and safety of prokinetic drugs and reassesses their role in the treatment of gastrointestinal reflux disease.
Excessive exposure of the esophageal mucosa to injurious gastric contents causes the diverse symptoms and complications of gastroesophageal reflux disease. Although acid and pepsin are important direct causes of mucosal damage, many factors may determine the duration and frequency of esophageal acid contact. It is becoming increasingly clear that gastroesophageal reflux, a multifactorial disease, is primarily a motility disorder.(1)(2) The lower esophageal sphincter–the smooth muscle that is the chief barrier against reflux–may relax inappropriately or exhibit low basal pressure. Absent or diminished peristaltic contractions can impair the clearance of esophageal acid, while delayed gastric emptying can increase gastric volume and impair the tone of the lower esophageal sphincter.
The rationale for prokinetic therapy is to correct some or all of the defects in gastrointestinal neuromuscular activity that promote reflux by affecting neurotransmitter release at the level of the central or enteric nervous system. The mechanisms by which prokinetic drugs exert their effects on gastrointestinal smooth muscle are not completely understood, but each agent seems to have a unique pharmacologic impact that accounts for variations in clinical efficacy and safety.
Bethanechol
Bethanechol (Myotonachol, Urecholine), a cholinergic agonist, increases pressure of the lower esophageal sphincter and the amplitude of esophageal peristaltic contractions, but it may not coordinate gastrointestinal motility or gastric emptying.(3) Prolonged pH monitoring in patients taking bethanechol indicates improvement in esophageal acid exposure. Subcutaneous administration of bethanechol increases salivary flow, which would be expected to improve esophageal acid clearance, although oral administration does not appear to have the same effect.
In a few small clinical trials, bethanechol in dosages of 25 mg four times daily for eight weeks variably but significantly improved symptoms of gastrointestinal reflux when compared with placebo.(4)(5) In a six-week study requiring intensive adjunctive use of antacids, bethanechol, 25 mg four times daily, and cimetidine (Tagamet), 300 mg four times daily, produced comparable rates of symptomatic improvement and complete healing of esophagitis with a severity of grade 2 or higher.(6) Nevertheless, clinical experience suggests a 10 to 15 percent incidence of abdominal cramping, blurred vision, fatigue and other bothersome cholinergic symptoms.(7) Despite scattered reports supporting its use, bethanechol has not been widely accepted for the treatment of reflux disease.
Metoclopramide
Metoclopramide (Reglan) stimulates gastrointestinal smooth muscle by a number of mechanisms. In addition to inhibiting dopamine receptors, this para-aminobenzoic acid derivative may enhance the release of acetylcholine from intramural nerve cells.(3)(8) Metoclopramide produces dose-dependent increases in lower esophageal sphincter pressure, accelerates gastric emptying and coordinates gastrointestinal motor activity. It does not appear to affect esophageal contractions.
In two placebo-controlled trials, metoclopramide, 10 mg four times daily, improved reflux symptoms significantly.(9)(10) In another study, an eight-week trial of metoclopramide, 10 mg four times a day, in combination with cimetidine, 1,200 mg per day, was more effective in healing esophagitis than cimetidine alone.(11) However, other reports suggest that endoscopic healing is not improved with metoclopramide, either in combination with cimetidine(12) or in single-agent regimens, compared with placebo or cimetidine.(9)
Metoclopramide inhibits dopamine receptors in the central nervous system and peripherally. Hyperprolactinemia related to metoclopramide therapy leads to galactorrhea in some patients and can disrupt normal menstrual function. Antidopaminergic side effects include neurologic and psychotropic reactions (such as lethargy) and extrapyramidal motor effects similar to those commonly associated with phenothiazines (including akathisia, acute dystonia and potentially irreversible tardive dyskinesia).(13) Such adverse effects, which occur in as many as 20 percent of patients,(8) have tempered physicians’ enthusiasm for long-term use of metoclopramide.
Cisapride
Cisapride stimulates the release of acetylcholine by specific enteric nerves or may directly trigger neuromuscular activity in gastrointestinal smooth muscle. This benzamide compound increases lower esophageal sphincter pressure in patients with hypotensive sphincter tone, strengthens the amplitude of esophageal peristaltic contractions, enhances gastric emptying and improves antroduodenal coordination.(14)(15)(16)
Multicenter randomized studies in the United States and Canada have evaluated cisapride, in a dosage of 10 mg or 20 mg four times daily before meals and at bedtime, in patients with moderate to severe heartburn and endoscopically confirmed esophagitis.(17)(18)(19) In one trial,(17) cisapride consistently relieved symptoms of reflux, with the 10-mg regimen significantly decreasing nighttime heartburn by the fourth week. The 20-mg regimen produced significant symptomatic improvement throughout the 12 weeks of the study. Antacid consumption was significantly reduced in patients receiving the higher dose. At 12 weeks, the 20-mg dose significantly improved esophagitis, but the 10-mg dose did not. In a similar trial,(18) 10 mg of cisapride taken four times daily was highly effective in the treatment of heartburn. However, none of the cisapride trials performed in the United States specifically selected patients likely to benefit from prokinetic therapy, such as those with documented motility defects. The reliance on studies of erosive esophagitis may have been inappropriate with cisapride monotherapy, which appears to perform best in nonerosive disease.
The effectiveness of cisapride was recently confirmed in a study involving 48 symptomatic patients with multigrade esophagitis.(14) Compared with placebo, 10 mg of cisapride taken four times a day for 12 weeks significantly decreased dyspeptic symptoms (heartburn, belching and regurgitation). In patients receiving cisapride, antacid consumption decreased and esophagitis scores improved, but not significantly. These results are less dramatic than results described in earlier European reports that supported the effectiveness of cisapride in the healing of esophagitis.(8)(20)(21)
Comparison with other prokinetic agents has been limited to a report of 30 patients receiving subcutaneous administration of cisapride, 10 mg three times a day, or metoclopramide, 10 mg three times a day.(22) At four weeks, both treatment with metoclopramide and treatment with cisapride significantly improved symptoms. No adverse effects were reported with cisapride, while central nervous system reactions in three patients resulted in discontinuation of metoclopramide.
In a European trial including patients with mild to moderate erosive esophagitis, combination therapy with cimetidine, 1 g per day, and cisapride, 10 mg four times per day, produced greater symptomatic and endoscopic improvements than the histamine [H.sub.2] antagonist administered alone.(23) Another trial showed high symptomatic responses to both ranitidine (Zantac), 150 mg twice a day, and a combined regimen of ranitidine, 150 mg twice a day, and cisapride, 10 mg twice a day. Compared with ranitidine alone, the combination therapy resulted in greater endoscopic improvement at 12 weeks in patients with more severe esophagitis.(24) A European study reported significantly better healing of esophagitis (but not significantly better symptom relief) with the combination of ranitidine, 150 mg twice a day, and cisapride, 10 mg three times a day, than with either agent as monotherapy.(25)
Multicenter European studies of patients with esophagitis that healed acutely with an antisecretory regimen suggest that cisapride can maintain symptomatic and mucosal remission with once- or twice-daily regimens using half the acute therapeutic dose.(26)(27) Twelve-month relapse rates were significantly reduced in patients with mild erosive esophagitis who received cisapride.(26)
Cisapride appears to be safe and well tolerated. The overall incidence of adverse events associated with cisapride therapy does not differ significantly from the incidence with placebo (13.7 percent versus 11.2 percent, respectively).(28) Notably absent are the central nervous system side effects and high prolactin levels associated with metoclopramide therapy.
Investigational Prokinetic Agents
DOMPERIDONE
Like metoclopramide, domperidone (Motilium) blocks dopamine receptors. However, this benzimidazole derivative is primarily a peripheral dopamine antagonist and does not easily or completely cross the blood-brain barrier. It is not yet available in the United States, but approval is believed to be pending. Oral domperidone at clinical doses produces variable effects on lower esophageal sphincter pressure and esophageal peristalsis, but does enhance gastric emptying in a dose-dependent manner.(8) Many clinicians believe that domperidone is particularly useful in the control of nausea.
Results of treatment with domperidone in regimens of 20 mg three or four times a day have been equivocal, with a few reports of symptomatic improvement and healing of esophagitis. Some comparative trials have shown similar efficacy between domperidone and [H.sub.2] antagonists (famotidine [Pepcid] or ranitidine). The combination of domperidone plus an antisecretory drug, however, was not more effective than treatment with either agent alone.(29)(30) Domperidone may work synergistically with cisapride.
Domperidone is associated with few significant side effects and is relatively free of extrapyramidal and other central nervous system side effects. Hyperprolactinemia occurs in about 10 to 15 percent of patients, resulting in breast enlargement, galactorrhea and amenorrhea.
ERYTHROMYCIN
The macrolide antimicrobial erythromycin can stimulate gastrointestinal muscle activity. Its mechanism of activity is not known, but it appears either to be a motilin agonist or to act directly on cholinergic nerve cells. Erythromycin, 250 mg three times a day administered orally, increases postprandial esophageal sphincter pressure and strikingly improves gastric emptying, but shows no effect on esophageal peristalsis.(8)
In patients with gastroesophageal reflux, use of oral erythromycin has led to variable results.(31) Limiting factors include a significant incidence of side effects (including nausea, vomiting and abdominal cramping), the potential for drug interactions, concerns regarding undesired effects on bacterial flora and development of drug tolerance.
Reassessing the Role of Prokinetic Agents
Bethanechol and metoclopramide may relieve mild symptoms of gastroesophageal reflux, but these compounds have inconsistently healed esophagitis. The absence of clear-cut efficacy, plus the potential for central nervous system side effects and other serious adverse reactions, has presented obstacles to greater use of these prokinetic agents. The efficacy of cisapride in healing esophagitis also has not been uniformly demonstrated. Nevertheless, this agent may play a role in initial reflux therapy, in adjunctive treatment with an antisecretory agent and potentially in maintenance treatment.
Given their extensive clinical use and record of efficacy and long-term safety,(32) [H.sub.2]-receptor antagonists are often considered the mainstay of antireflux therapy and as initial agents of choice in patients with moderate to severe, persistent reflux symptoms and/or complications (Table 1). Patients should be counseled to adopt conservative treatment measures, such as elevation of the head of the bed and avoidance of foods and medications that adversely affect lower esophageal sphincter pressure (Table 2).
TABLE 1 Pharmacologic Treatment of Gastroesophageal Reflux Disease(*)
Initial empiric prescription drug therapy
[H.sub.2]-receptor antagonist at standard doses
Cimetidine (Tagamet), up to 800 mg 2 times a day or 400 mg 4 times a day
Famotidine (Pepcid), 20 mg 2 times a day
Nizatidine (Axid), 150 mg 2 times a day
Ranitidine (Zantac), 150 mg 2 times a day
Possible use of prokinetic agent (e.g., cisapride [Propulsid], 10 to 20 mg 4 times a day)
Aggressive medical therapy for severe or refractory disease
Famotidine, nizatidine or ranitidine at double the dosing frequency using the standard dose or more
Combination therapy of [H.sub.2] antagonist and prokinetic agent
Cisapride, 10 to 20 mg 4 times a day before meals and at bedtime
Metoclopramide (Reglan), up to 10 mg or 15 mg 4 times a day
Bethanechol (Urecholine), up to 25 mg 4 times a day
Domperidone (Motilium), [dagger] up to 20 mg 4 times a day
Proton pump inhibitor
Omeprazole (Prilosec), 20 mg every morning or 2 times a day
Lansoprazole (Prevacid), 30 mg every day
Potential next step in aggressive medical therapy
Combination therapy of proton pump inhibitor and prokinetic agent
(*)Excluding use of antacids.
([dagger])Not yet available in the United States.
TABLE 2 Foods and Drugs That Can Decrease Lower Esophageal Sphincter
Pressure
Foods
Carminatives, such as peppermint and spearmint
Chocolate
Foods with high fat content
Onions
Drugs
Alpha-adrenergic antagonists
[Beta.sub.2]-adrenergic agonists
Calcium channel blockers
Diazepam (Valium)
Meperidine (Demerol)
Progesterone-containing oral contraceptives
Theophylline
Most patients will obtain symptom relief and endoscopic healing with standard-dose [H.sub.2]-antagonist regimens. In those who remain symptomatic, endoscopy is advisable since the presence of extensive erosive esophagitis or Barrett’s esophagus along with refractory symptoms may be an indication for acceleration of therapy. If endoscopic results are normal, possibly including endoscopic biopsies, the diagnosis of gastroesophageal reflux disease should be reconsidered and additional tests (such as pH monitoring and motility studies) should be ordered to assess the basis of existing symptoms. If endoscopic results reveal erosive esophagitis, the clinician might proceed to more frequent dosing of [H.sub.2] antagonists or may consider the addition of a prokinetic drug or possibly the use of a proton pump blocker (Table 1).
For patients who are unresponsive to standard-dose [H.sub.2]-antagonist therapy and who do not improve sufficiently with omeprazole, 20 mg per day, a 20-mg twice-daily regimen might be considered. Unfortunately, once proton-pump blockers are started, it may never be possible to return to less potent therapy.(33) Subsequently, physiologic studies may be undertaken in patients truly refractory even to high-dose omeprazole; results might support the addition of a prokinetic agent to subtherapeutic proton pump inhibitor therapy.
Combination antisecretory and prokinetic therapy may prove synergistic in patients previously determined by esophageal manometry or nuclear imaging of gastric emptying to have motility abnormalities. Studies are needed to test the hypothesis that tailoring therapy to abnormal physiology would improve results, although this approach certainly seems logical.
A sampling of weekly costs of different antireflux regimens is provided in Table 3. Although not a comprehensive comparison, it does suggest that at conventional doses, proton pump inhibitors tend to be more expensive than either [H.sub.2] antagonists or prokinetic agents. It should be emphasized, however, that considerations other than relative cost, in particular proven safety, should be weighed in the selection of appropriate therapy. Additionally, standard [H.sub.2]-antagonist doses are based on ulcerhealing regimens and may not reflect the effective regimen for an individual patient.
TABLE 3 Costs of Standard Dosage Prescription Antireflux Regimens
Daily standard dosage regimen Weekly cost of therapy(*)
Selected [H.sub.2]-receptor antagonists
Cimetidine (Tagamet)[dagger], 400 mg 2 $21 (18-19 for generic)
times a day
Famotidine (Pepcid)[dagger], 20 mg 2 21
times a day
Ranitidine (Zantac), 150 mg 2 times a 23
day
Selected prokinetic agents
Metoclopramide (Reglan), 10 mg 4 times 17 (3-5 for generic)
a day
Cisapride (Propulsid), 10 mg 4 times a 17
day
Proton pump inhibitor
Omeprazole (Prilosec), 20 mg every 25
morning
Lansoprazole (Prevacid), 30 mg every 23
morning
(*)Estimated cost to the pharmacist based on average wholesale prices of 30 tables, rounded to the nearest dollar, in Red book. Montvale, N.J.: Medical Economics Data, 1995. Cost to the patient will be higher, depending on prescription filling fee.
([dagger])Cimetidine and famotidine recently have been approved for over-the-counter use in smaller dosage strengths. These over-the-counter preparations will be less expensive than the prescription forms.
A patient information handout on gastroesophageal reflux disease is provided on page 965.
REFERENCES
(1.)Castell DO. Rationale for high-dose [H.sub.2]-receptor blockade in the treatment of gastro-oesophageal reflux disease. Aliment Pharmacol Ther 1991; 5(Suppl 1):59-67.
(2.)Quigley EM. Gastroesophageal reflux disease: the roles of motility in pathophysiology and therapy [Editorial]. Am J Gastroenterol 1993; 88:1649-51.
(3.)Reynolds JC. Prokinetic agents: a key in the future of gastroenterology. Gastroenterol Clin North Am 1989; 18:437-57.
(4.)Saco LS, Orlando RC, Levinson SL, Bozymski EM, Jones JD, Frakes JT. Double-blind controlled trial of bethanechol and antacid versus placebo and antacid in the treatment of erosive esophagitis. Gastroenterology 1982; 82:1369-73.
(5.)Farrell RL, Roling GT, Castell DO. Cholinergic therapy of chronic heartburn. Ann Intern Med 1974; 8:573-6.
(6.)Thanik K, Chey WY, Shak A, Hamilton D, Nadelson N. Bethanechol or cimetidine in the treatment of symptomatic reflux esophagitis: a double-blind control study. Arch Intern Med 1982; 142:1479-81.
(7.)Thanik K, Chey WY, Shak A, Gutierrez JG. Reflux esophagitis. Ann Intern Med 1980; 93:805-8.
(8.)Ramirez B, Richter JE. Promotility drugs in the treatment of gastro-oesophageal reflux disease. Aliment Pharmacol Ther 1993; 7:5-20.
(9.)Bright-Asare P, El-Bassoussi M. Cimetidine, metoclopramide, or placebo in the treatment of symptomatic gastroesophageal reflux. J Clin Gastroenterol 1980; 2:149-56.
(10.)McCallum RW, Ippoliti AF, Cooney C, Sturdevant RA. A controlled trial of metoclopramide in symptomatic gastroesophageal reflux. N Engl J Med 1977; 296:354-7.
(11.)Lieberman DA, Keeffe EB. Treatment of severe reflux esophagitis with cimetidine and metoclopramide. Ann Intern Med 1986; 104:21-6.
(12.)Temple JG, Bradby GV, O’Connor FO, Panesar KS, Mulligan TO, Robinson TJ, et al. Cimetidine and metoclopramide in oesophageal reflux disease. Br Med J [Clin Res] 1983; 286:1863-4.
(13.)Ganzini L, Casey DE, Hoffman WF, McCall AL. The prevalence of metoclopramide-induced tardive dyskinesia and acute extrapyramidal movement disorders. Arch Intern Med 1993; 153:1469-75.
(14.)Robertson CS, Evans DF, Ledingham SJ, Atkinson M. Cisapride in the treatment of gastro-oesophageal reflux disease. Aliment Pharmacol Ther 1993; 7:181-90.
(15.)Gilbert RJ, Dodds WJ, Kahrilas PJ, Hogan WJ, Lipman S. Effect of cisapride, a new prokinetic agent, on esophageal motor function. Dig Dis Sci 1987; 32:1331-6.
(16.)Maddern GJ, Jamieson GG, Myers JC, Collins PJ. Effect of cisapride on delayed gastric emptying in gastro-oesophageal reflux disease. Gut 1991; 32:470-4.
(17.)Faruqui S, Sigmund C, Smith R, Fitch D, Mellow M, Orr W. Cisapride in the treatment of GERD: a double-blind, placebo-controlled multicenter dose-response trial [Abstract]. Gastroenterology 1992; 102(2 Pt 2):A66.
(18.)DeMicco M, Berenson M, Wu W, Castell D, Lanza F, Robinson M, et al. Cisapride in the treatment of GERD: a double-blind, placebo-controlled multicenter dose-response trial [Abstract]. Gastroenterology 1992; 102(2 Pt 2):A59.
(19.)Dodds W, Champion M, Orr W, Robinson M, Spechler S, Gilmore P, et al. Oral cisapride in GERD. Gastroenterology 1989; 96(5 Pt 2):A126.
(20.)McCallum RW. Cisapride: a new class of prokinetic agent. Am J Gastroenterol 1991; 86:135-49.
(21.)Galmiche JP, Fraitag B, Filoche B, Evreux M, Vitaux J, Zeitoun P, et al. Double-blind comparison of cisapride and cimetidine in treatment of reflux esophagitis. Dig Dis Sci 1990; 35:649-55.
(22.)Manousos ON, Mandidis A. Treatment of reflux symptoms in oesophagitis patients. Curr Ther Res Clin Exp 1987; 42:807-13.
(23.)Galmiche JP, Brandstatter G, Evreux M, Hentschel E, Kerstan E, Kratochvil P, et al. Combined therapy with cisapride and cimetidine in severe reflux oesophagitis. Gut 1988; 29:675-81.
(24.)Wienbeck M. The Ranpride Study Group. Does a motor stimulating agent improve the therapeutic effect of [H.sub.2]-blockers in reflux esophagitis? Gastroenterology 1986; 90(5 Pt 2):A1691.
(25.)Duvas A, Papalagara G, Ioarinou A, et al. Comparison of cisapride with ranitidine in the treatment of reflux esophagitis. II. United European Gastroenterology Week, Barcelona. July 19-24, 1993; Abstract no. 170.
(26.)Blum AL, Adami B, Bouzo MH, Brandstatter G, Fumagalli I, Galmiche JP, et al. Effect of cisapride on relapse of esophagitis. A multinational, placebo-controlled trial in patients healed with an antisecretory drug. Dig Dis Sci 1993; 38:551-60.
(27.)Tytgat GN, Anker Hansen OJ, Carling L, de Groot GH, Geldof H, Glise H, et al. Effect of cisapride on relapse of reflux oesophagitis, healed with an antisecretory drug. Scand J Gastroenterol 1992; 27:175-83.
(28.)Verlinden M, Reyntijens A, Schuermans V. Safety profile of cisapride. In: Johnson AG, Lux G, eds. Progress in the treatment of gastrointestinal motility disorders. The role of cisapride. New York: Excerpta Medica, 1988:30-6.
(29.)Guslandi M, Dell’Oca M, Molteni V, Romano R, Passaretti S, Ballarin E. Famotidine versus domperidone, versus a combination of both in the treatment of reflux esophagitis: interim report [Abstract]. Gastroenterology 1989; 96(5 Pt 2):A191.
(30.)Masci E, Testoni PA, Passretti S, Guslandi M, Tittobello A. Comparison of ranitidine, domperidone maleate and ranitidine + domperidone maleate in the short-term treatment of reflux oesophagitis. Drugs Exp Clin Res 1985; 11:687-92.
(31.)Harrison ME, Ruzkowski CJ, Young MF, Sanowski RA. Erythromycin improves gastric emptying and esophageal motility without affecting gastroesophageal reflux [Abstract]. Gastroenterology 1991; 100(2 Pt 2):A80.
(32.)Feldman M, Burton ME. [Histamine.sub.2]-receptor antagonists. Standard therapy for acid-peptic diseases. N Engl J Med 1990; 323:1672-80,1749-55.
(33.)Antonson CW, Robinson MG, Hawkins TM, McIntosh DL, Campbell DR. High doses of histamine antagonists do not prevent relapses of peptic esophagitis following therapy with a proton pump inhibitor [Abstract]. Gastroenterology 1990; 98(5 Pt 2):A16.
RELATED ARTICLE: What You Can Do About Heartburn
What is heartburn?
Heartburn is a burning, painful feeling that occurs behind your breastbone. Despite its name, heartburn involves your esophagus (swallowing tube), not your heart. You may have heartburn if you generally notice the pain one or two hours after you eat, if the pain is worse when you lie down or bend over, or if the burning goes away after you take antacids or drink some liquids.
What causes heartburn?
Heartburn is caused by acid and other irritating substances rising up, or refluxing, from your stomach into your esophagus. This can damage the esophagus.
In healthy people, stomach acid is usually prevented from getting into the esophagus by a tightening of the muscle around the place where the esophagus joins the stomach. This muscle is called the lower esophageal sphincter (LES). Usually, any acid that rises up into the esophagus goes back down into the stomach quickly. With heartburn, the LES muscle is not working at full strength. Sometimes, this can lead to inflammation or swelling of the membranes that line the lower esophagus. This is called reflux esophagitis.
If your doctor suspects that you have reflux esophagitis, he or she may want to do a test called an endoscopy. During an endoscopy, your doctor looks at your esophagus through a tube with a light at the end. Reflux esophagitis can cause permanent narrowing of the esophagus, known as stricture. It can also lead to bleeding.
What can I do to stop having heartburn?
The goal of treatment is to keep stomach acid out of the esophagus, which allows the damaged esophagus to heal and prevents further damage.
The list on the next page gives tips on preventing stomach acid from rising up into your esophagus. You may not get relief of your symptoms right away, but don’t give up. For severe heartburn, changes in lifestyle may need to be permanent. You may need to continue these changes even after your symptoms improve so that your symptoms don’t return.
Tips for Getting Relief from Heartburn
*Use bed blocks
Raise the head of your bed 4 to 6 inches with wood blocks or bricks. Using extra pillows is not as effective. Placing a foam wedge beneath the upper half of your body may also work.
*Take antacids
Antacids can be taken as often as needed for heartburn. Tablet antacids may be more effective than liquid forms.
*Eat smaller meals
Don’t overfill your stomach.
*Avoid foods that can cause your symptoms
Foods to avoid include spicy and fatty foods, tomato and citrus juices (such as grapefruit and orange juices), chocolate, mint, coffee and alcoholic beverages.
*Do not lie down for 4 hours after eating
Eliminate bedtime or evening snacks. Allow gravity to help move food down past the LES to keep acid out of the esophagus.
*Stop smoking
Talk to your doctor about quitting. If you cannot stop, decrease the number of cigarettes you smoke.
*Maintain your ideal weight
Excess weight increases the amount of pressure constantly placed on your stomach, making reflux worse. Even a small amount of weight loss may help.
*Avoid tight clothing
Avoid wearing tight belts and pants or girdles.
What else can I do?
Your doctor may prescribe a medicine for you to take. Some medicines decrease the amount of stomach acid your body makes, while others make it easier for food to go down the esophagus and empty from the stomach. Every medicine does not work for every person. The medicine should be taken just as prescribed by your doctor. You and your doctor can work together to find the treatment that will help you the most.
This information provides a general overview on heartburn and may not apply to everyone. Talk to your family doctor to find out if this information applies to you and to get more information on this subject.
