Management of Gastroesophageal Reflux Disease

Management of Gastroesophageal RefluxDisease

RADU TUTUIAN, MD; DONALD O. CASTELL, MD

ABSTRACT: Gastroesophageal reflux disease (GERD) isa chronic condition requiring long-term treatment. Sim-ple lifestyle modifications are the first methods em-ployed by patients and, because of their low cost andsimplicity, should be continued even when more potenttherapies are initiated. Potent acid-suppressive therapyis currently the most important and successful medicaltherapy. Whereas healing of the esophageal mucosa isachieved with a single dose of any proton pump inhib-itor (PPI) in more than 80% of cases, symptoms are moredifficult to control. Patients with persistent symptoms ontherapy should be tested (preferably with combinedmultichannel intraluminal impedance and pH) for asso-ciation of symptoms with acid, nonacid, or no GER.Long-term follow-up studies indicate that PPIs are effi-cacious, tolerable, and safe medication. So far, promo-tility agents have shown limited efficacy, and their side-

effect profile outweighs their benefits. Antireflux surgeryin carefully selected patients (ie, young, typical GERDsymptoms, abnormal pH study, and good response toPPI) is as effective as PPI therapy and should be offeredto these patients as an alternative to medication. Still,patients should be informed about the risks of antirefluxsurgery (ie, risk of postoperative dysphagia; decreasedability to belch, possibly leading to bloating; increasedflatulence). Endoscopic antireflux procedures are rec-ommended only in selected patients and given the rel-ative short experience with these techniques, patientstreated with endoscopic procedures should be enrolledin a rigorous follow-up program. KEY INDEXINGTERMS: Gastroesophageal reflux disease (GERD); Protonpump inhibitors; Antireflux surgery. [Am J Med Sci2003;326(5):309–318.]

Approximately 40% of the US population hassymptoms of gastroesophageal reflux disease

(GERD),1 making it the fourth most prevalent gas-trointestinal disease in the United States.2 GERD isa chronic disease requiring long-term therapy. As ageneral rule, the management of GERD should fol-low a step-wise approach, starting with simple ther-apeutic modalities and gradually advancing to morepotent and more aggressive modalities based on 2goals: healing of lesions and alleviation ofsymptoms.

The pattern of presentation and therapy is well-expressed by the “heartburn iceberg” shown in Fig-ure 1. The vast majority of patients have only occa-sional symptoms and will empirically treatheartburn with over-the-counter (OTC) medicationsand not seek medical attention.3 Patients with fre-quent symptoms will seek medical attention and areoften evaluated by primary care physicians andgiven prescriptions for acid-suppressive therapy.Because acid-suppressive therapy is very effective

and has few side effects, specialists (gastroenterolo-gists and gastrointestinal surgeons) are likely to seeonly the “tip of the iceberg” represented by patientswith severe or persistent symptoms not responsiveto standard treatment.4 When evaluated by gastro-enterologists, treatment targets reduction of esoph-ageal acid exposure. Supported by a good correlationbetween control of intragastric pH and healing oferosive esophagitis,5 medical strategies employpharmacological suppression of gastric acid produc-tion, whereas surgical and endoscopic strategies em-ploy augmentation of the gastroesophageal junction.

The above concepts have primarily been studied inpatients with so-called “typical” symptoms of GERD(heartburn, regurgitation) but apply equally to thosewith atypical (chest pain, asthma/cough, hoarse-ness, sore throat) symptoms or complications (ulcer-ation, strictures, metaplasia) of the disease.

Simple Therapeutic Modalities (LifestyleModifications)

In the current days of very potent acid-suppres-sive therapy, simple, alternative, patient-driven,and less expensive GERD treatments tend to beforgotten. Most of these methods were the maintherapeutic modalities before the late 1970s andinclude elevation of head of the bed, wearing loose-

From the Division of Gastroenterology/Hepatology, MedicalUniversity of South Carolina, Charleston, South Carolina.

Correspondence: Radu Tutuian, M.D., Division of Gastroenter-ology/Hepatology, Medical University of South Carolina, 96Jonathan Lucas Street, 210 CSB, Charleston, SC 29425 (E-mail:[email protected]).

309THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES

fitting clothing, avoidance of meals before bedtime,weight loss, and restriction of smoking, alcohol, cof-fee, and fat.6 Today, these lifestyle modificationsoften also include use of antacids, alginate, andover-the-counter (OTC) doses of histamine-2 recep-tor antagonists (H2RA).

Elevation of the head of the bed helps improve-ment of esophageal acid clearance and decreases thetotal recumbent acid exposure.7 These hypothesesare supported by studies indicating significant re-duction in nocturnal acid clearance time and totalnocturnal acid exposure using 6-inch blocks to ele-vate the head of the bed.8 A more patient-friendlyalternative is to sleep predominantly on the leftside.9 Avoidance of meals for 3 hours before bedtimeis based on studies indicating that postprandial re-cumbency leads to a significant increase in the num-ber and duration of reflux events10

Wearing loose-fitting clothing as a measure toreduce gastroesophageal reflux is based on the hy-pothesis that tight clothing increases intragastricpressure and therefore the gastroesophageal pres-sure gradient across the lower esophageal sphincter(LES),11 the so-called “tight pants syndrome.” Eventhough there are no good studies supporting thishypothesis, this relatively simple and intuitive mea-sure should not be ignored.

Based on studies showing a correlation of morbidobesity with reflux and lower LES pressures,12

weight reduction in the attempt to improve GERD isa rational approach. Even though not formally stud-ied, it is commonly believed that typical GERDsymptoms improve in patients during weightreduction.

Recommendations to avoid certain foods and limit

smoking and alcohol are based on studies indicatingdecreases in LES pressures and/or increased num-ber of gastroesophageal reflux episodes. Ingestion ofhigh-fat meals decreases LES pressure,13 increasesfrequency of transient lower esophageal relax-ations,14 and increases esophageal acid exposure forup to 3 hours after meals.15 Increased esophagealacid exposure has been documented after ingestionof chocolate16 and alcohol17 and after smoking.18,19

The use of antacids in treatment of GERD relieson the neutralizing capabilities of these compoundson acid gastric secretions. The superiority of antac-ids over placebo was proven in double-blind studiesin patients with reflux esophagitis.20,21 Other place-bo-controlled studies have shown the superiority ofan alginic acid-antacid combination in controllingreflux symptoms.22 The observation of the floatingnature of alginic acid within the stomach suggestedthat it might work well in patients with symptomsduring the upright position,23 a hypothesis sup-ported in subsequent studies.24

After several years of proven efficacy and safety ofstandard-dose H2RAs, the class of medication be-came available as low-dose over-the-counter (OTC)preparations for “conservative” treatment of GERD.There is only limited information available showingsymptomatic improvement with OTC doses ofH2Ras,25 although several studies have documentedthe ability of these preparations to decrease intra-gastric acidity.26,27 In 2002, the American Gastroen-terology Association (AGA) issued a consensus state-ment declaring OTC H2RA and antacid the first lineof treatment for patients with mild GERD symp-toms. The combination H2RA/antacid was consid-ered better at symptom relief than its constituentcomponents alone.

Table 1 summarizes the life-style modification ap-proach to GERD. Even though recently developedacid-suppressive agents are highly effective in treat-ment of GERD, these simple measures should bediscussed with patients. Their simplicity and lowcost justify them as phase 1 therapy to be continuedin all patients suffering from this disorder. OTCantacids or even H2RAs should be recommended foroccasional “breakthrough” symptoms while patientsare receiving more potent therapies.

Figure 1. Pattern of presentation and therapy of GERD patientsexpressed by the “heartburn iceberg.” Endo, endoscopic antirefluxprocedure.

Table 1. Lifestyle Modifications That Can Help Improve GERDSymptoms

Sleep with the head of the bed elevatedSleep on the left sideAvoid late meals/avoid recumbent position 3 hours after mealsAvoid high-fat mealsUse smaller mealsUse saliva-stimulating agents (ie, hard candies, chewing gum)Wear loose-fitting clothingRestrict smoking, alcohol, coffee, chocolateLose weight

Management of Gastroesophageal Reflux Disease

310 November 2003 Volume 326 Number 5

Pharmacologic Management of GERD

The objectives of pharmacological treatment ofGERD are relief of symptoms, avoidance of compli-cations, and healing of esophageal mucosa. Theprincipal classes of pharmacological agents are: acidsuppressive drugs [H2RAs, proton pump inhibitors(PPIs)], promotility agents (bethanechol, metoclo-pramide, cisapride, domperidone, erythromycin, te-gaserod), mucosal protective agents (sucralfate), andagents to reduce transient lower esophageal sphinc-ter relaxation (TLESR) (baclofen).

Acid-Suppressive DrugsHistamine-2 Receptor Antagonists. H2RAs

were the antisecretory therapy of choice from themid-1970s until the introduction of PPIs into clinicalpractice in the late 1980s.28 Currently in the UnitedStates, 4 H2RAs are available for clinical use: rani-tidine (Zantac), famotidine (Pepcid), cimetidine(Tagamet), and nizatidine (Axid). Even though themore recently developed PPIs have been shown tobe superior, the H2RAs still remain useful intreatment of milder forms of the disease and foron-demand therapy, particularly for nocturnalGERD symptoms.

Prescription dosages of H2RAs can be groupedinto standard dose (150 mg of ranitidine, 20 mg offamotidine, 400 mg of cimetidine, and 150 mg ofnizatidine, each twice daily) and high dose (obtainedby doubling the standard doses). The healing rateswith H2RAs range between 50 and 70% at 8 weeksand 60 to 80% at 12 weeks.29 Most studies haveshown superiority of H2RAs to placebo but no sig-nificant differences among high and standard doses(possible type II error, because most studies werepowered to show differences from placebo). It wassoon recognized that esophageal healing rates cor-related with decrease of esophageal acid exposure,duration of acid suppressive therapy, and degree ofesophagitis.30 Studies have shown that esophagealhealing rates at 12 weeks were higher than healingrates at 8 weeks,31 but 24 weeks of H2RA could not

heal erosive esophagitis not healed at 12 weeks.32

H2RAs relieve GERD symptoms in about half ofpatients after 6 to 12 weeks.33

Even in this era of potent acid-suppressive PPIs,H2RAs provide the advantage of prompt relief ofheartburn,34 and when administered at bedtime,they improve nocturnal gastric acid control in GERDpatients taking PPIs.35

Proton Pump Inhibitors. PPIs are superior toH2RAs in treating erosive esophagitis36 and its com-plications,37 relieving symptoms from erosive andnonerosive GERD,38,39 and preventing recurrence ofGERD-associated symptoms.40 Studies by Zeitoun,41

Lundell et al,42 Vantrappen et al,43 and Klinken-berg-Knol et al36 indicate superiority of the PPIversus H2RA. Thus, they have surpassed H2RAs asthe antisecretory agents of choice (Figure 2). PPIsare substituted benzimidazoles that irreversiblybind the H�,K�-ATPase, the final common step inacid secretion.44

Currently, 5 PPIs are commercially available inthe United States: omeprazole, lansoprazole, rabe-prazole, pantoprazole, and esomeprazole. FDA-ap-proved doses (20- and 40-mg omeprazole, 15- and30-mg lansoprazole, 20-mg rabeprazole, 40-mg pan-toprazole, and 40-mg esomeprazole) are for use oncedaily, which provides sufficient acid suppression toeffectively treat most patients. Symptom relief canbe expected in about 78% of cases (range, 62–94%)and esophagitis healing in 83% (range, 71–96%).45

Whether one PPI is superior to the others is con-troversial. For every study showing that one PPI issuperior to another, there is another study showingthe opposite. Overall, based on similar esophagealhealing rates of over 80% at 8 weeks46 and similarintragastric pH profiles after 7 days of dosing,47 allfirst-generation PPIs (omeprazole, lansoprazole, ra-beprazole, pantoprazole) can be considered to haveequivalent effectiveness (Figure 3). Minor differ-ences in pharmacodynamics and price exist.48 How-ever, individual variability in patient response toPPI can vary widely. Therefore, we recommend

Figure 2. Comparison of omeprazole versus raniti-dine in healing reflux esophagitis after 8 weeks oftreatment. Studies by Zeitoun,41 Lundell et al,42

Vantrappen et al,43 and Klinkenberg-Knol et al36

indicate superiority of the PPI versus H2RA. Num-bers indicate dose of omeprazole used in the study.

Tutuian and Castell


switching to another PPI as the first step in patientsnot responding to one PPI.

The most recent “second-generation” PPI, esome-prazole, the active S-isomer in the racemic mixtureof omeprazole,49 has been reported to have slightlybetter effect on GERD.50 Results from a large, dou-ble-blind study suggest that the advantages of es-omeprazole become more important in patients withmore severe disease (Figure 4).51

The timing of administering the PPI in relationwith meals is important. The ideal window to takethe PPI is 15 to 30 minutes before meals. This allowsthe medication to be absorbed to be available to theproton pumps when they are activated by the meal.PPIs taken before meals provide better intragastricpH control compared with being taken after themeal.52 Inadequate timing is frequently seen clini-cally, especially when patients are prescribed PPItwice daily without further instructions; patientsfrequently take the medication in the morning andbefore bedtime (without a meal).

Despite the efficacy of single-dose proton pumpinhibitor in controlling intragastric acidity, improv-ing symptoms, and healing of erosive esophagitis,some patients do not heal as well and may requireincreased dosing. In addition, patients with extrae-sophageal presentations (asthma, cough, or laryngi-tis) may require higher doses for effective symptomcontrol.53–55 Rather than doubling the single doseamount, it is preferable to give the PPI twice daily.This recommendation is based on studies in healthysubjects indicating that 20 mg of omeprazole beforebreakfast and before dinner was superior in control-ling intragastric pH compared with 40 mg of ome-prazole before breakfast or before dinner.56

A more recent discovery has been that PPIs maynot achieve adequate control of intragastric pH57;even with twice-daily dosing, they are not alwaysable to control nocturnal acid breakthrough.58 Asingle dose of H2RAs added at bedtime to the PPIcan reduce nocturnal acid breakthrough (Figure5).59 Concerns that combination of PPI and H2RAs

Figure 3. Comparison of first-generation PPIs for short-termtreatment healing rates. Bars indicate percentage healing after 8weeks of treatment. Numbers indicate patients in respectivestudies.

Figure 4. Comparison of esomeprazole versus lan-soprazole in 8-week healing rates of erosive esoph-agitis by baseline grade of esophagitis. The benefitsof esomeprazole are higher in more severe cases ofesophagitis.

Figure 5 . Proportion of patients with nocturnal acid break-through (defined as intragastric pH � 4 for at least 60 continuousminutes) on PPI bid � H2RA at bedtime versus PPI twice per dayalone.35



might decrease the efficacy of PPIs were cleared bystudies indicating similar intragastric acid controlon daily PPI after placebo or H2RAs the night be-fore.60 Therefore H2RAs are still potentially effec-tive drugs for on-demand therapy of both daytimeand nocturnal GERD symptoms.

Based on existing data we propose the step-uptherapeutic approach to acid suppression guided asillustrated in Table 2. Symptom response to a trial ofPPI therapy is currently a popular recommendeddiagnostic approach to GERD (“PPI-trial”).61 Pa-tients failing PPI trials or not responding to PPItherapy should undergo reflux testing to evaluatethe amount of reflux and its relation to symptoms.For more than 20 years, esophageal pH testing hasbeen the accepted standard for diagnosingGERD.62,63 For optimal study interpretation pa-tients should be off PPI therapy for at least 7 daysbefore undergoing esophageal pH testing. Patientswith GERD who failed to respond to standard PPItreatment because of insufficient dosing might ex-perience symptom exacerbation during this periodthat may help clarify the diagnosis.

An important alternative diagnosis in patientswith persistent symptoms on therapy is the possi-bility of symptomatic nonacid reflux, which will bemissed by conventional pH testing because of thelimitations of this technique in identifying nonacidreflux.64,65 Currently, combined multichannel in-traluminal impedance and pH (MII-pH) is evolvingas dual modality reflux testing. Because MII-pHdetects reflux by changes in intraluminal electricconductivity, both acid and nonacid reflux eventscan be identified.66,67 Preliminary data from a mul-ticenter collaborative study suggest that only 20% ofpatients with persistent symptoms on acid-suppres-sive therapy have their symptoms related to acidreflux. The other 80% usually present a diagnosticdilemma as to whether their symptoms are associ-ated with nonacid reflux or not associated with anytype of GER. Combined MII-pH will further clarify-ing this possible association, including recognitionthat 40% of patients with persistent symptoms ontherapy have no temporal correlation betweensymptoms and any type of reflux. Therefore, webelieve that combined MII-pH should be consideredthe next step in diagnostic management of patientsnot responding to PPI therapy (Figure 6).

As mentioned before, GERD is a chronic diseaserequiring long-standing therapy. Although dailymaintenance therapy on standard-dose PPI sustainsrelapse rates well under 20% for 12 months,68,69

change to H2RAs or placebo will increase the relapseto more than 50 to 70% and 70 to 90%, respective-ly.70,71 Long-term safety and efficacy of standardPPI doses are supported by European studies withpatient follow-up over a decade.72

Promotility Agents (PMAs)The rationale for using PMAs in treatment of

GERD is based on the hypothesis that normalizingunderlying dysmotility or augmenting existing mo-tility would decrease esophageal acid contact time.An overall comment regarding PMAs in GERD isthat as a group, they have limited effectiveness orundesirable side effects.

Bethanechol is a cholinergic agonist that will in-crease esophageal peristalsis and LES pressure butalso stimulate gastric secretion. Compared with pla-cebo, it will improve GERD symptoms but has noadvantages in healing esophagitis.73,74 At the recom-mended dose for treatment of GERD (25 mg 4 timesper day), it may have cholinergic side effects, includ-ing diarrhea, abdominal cramping, fatigue, andblurred vision.

Metoclopramide is a smooth-muscle stimulantthat inhibits dopamine receptors. It enhances gas-tric emptying and LES pressure but has no effect onesophageal peristalsis. Even though it may improveGERD symptoms, it does not show healing rates tojustify its side-effect profile: galactorrhea, men-strual dysfunction, lethargy, and extrapyramidalmotor defects. The most concerning side effect istardive dyskinesia, which can occur in up to 20% ofpatients and can be permanent.75

Cisapride stimulates acetylcholine release, in-creasing LES pressure, aiding esophageal peristal-sis, and accelerating gastric emptying. Placebo-con-trolled trials have shown significant improvements

Table 2. Suggested Approach to Acid Suppressive Therapy

Step Medical regimen

1 Single-dose PPI (AM before meals)2 Switch to another PPI3 PPI AM plus evening (or bedtime) H2RA4 PPI twice daily before meals5 PPI twice daily before meals plus H2RA at bedtime

Figure 6. Suggested diagnostic GERD algorithm.

Tutuian and Castell


in GERD symptoms76; because of its cardiovascularside effects, however, it is no longer available.

Tegaserod, a selective 5-HT4 receptor partial ago-nist, is a potent promotility agent throughout thegastrointestinal tract that is also considered to de-crease visceral sensitivity77 and promote gastricemptying.78 In 1 study in GERD patients, it wasshown to decrease postprandial esophageal acid ex-posure79 suggesting a potential role in treatment ofGERD.

Domperidone and erythromycin are the other pro-motility agents currently being investigated fortreatment of GERD. Both agents enhance gastricemptying but do not have significant effects onesophageal peristalsis. Their side effect profiles mayalso limit their clinical utility.

Mucosal Protective AgentsThe role of sucralfate in treatment of GERD has

not been studied as extensively as H2RAs and PPIs.Sucralfate is believed to physically adhere to injuredmucosa and thereby create a protective barrieragainst acid gastric secretions. Randomized compar-isons showed superiority to placebo and healingcomparable with standard dose H2RAs.80

Agents to Reduce TLESRsRecently, transient lower esophageal sphincter re-

laxations (TLESRs) have been recognized to be themajor mechanism of gastroesophageal reflux.81–83

Baclofen, an agonist of �-aminobutyric acid type B,was shown to reduce the rate of postprandialTLESRs and acid reflux episodes in healthy volun-teers84 and patients with reflux esophagitis.85 In amechanistic study using combined MII-pH inhealthy volunteers and patients with GERD, a sin-gle dose of 40 mg of baclofen significantly reduced alltypes (acid and nonacid) of postprandial reflux.86

The side-effect profile of dizziness or nausea mayrestrict its clinical utility.

Surgical Management of GERD

Surgical antireflux procedures are highly effectivetreatment modalities in appropriately selected pa-tients. Before potent acid suppressive therapy be-came available, surgery was considered superior tomedical therapies.87 The rationales for antirefluxsurgery have evolved parallel to clarifications inpathophysiologic mechanisms of reflux disease. Al-though hiatal hernia was considered to be of majorimportance in production of GERD, antireflux sur-gery was performed to reduce the hiatal hernia andkeep the LES within the abdominal cavity.88 Re-ports showing that only 9% of patients with hiatalhernia had typical reflux symptoms89 suggested thatother factors might play a more important role.When low LES pressures were considered the majorfactor in gastroesophageal junction incompetence,

antireflux procedures were done to increase LESpressure.90 At present, given that TLESR is consid-ered the main mechanism by which GERD occurs,surgery is done to lengthen the intraabdominal por-tion of the LES, to reduce the volume of the gastricfundus and prevent effacing of the LES during gas-tric distention in the postprandial period.91

Preoperative evaluation of patients undergoingantireflux surgery includes: esophageal manometry,upper gastrointestinal endoscopy, 24-hour esopha-geal pH monitoring, barium esophagogram, and gas-tric emptying studies.92 This is necessary to selectthe ideal candidates for the procedure, who shouldbe young (because they will require long-term GERDtherapy), should have typical GERD symptoms(heartburn, regurgitation), should have an abnor-mal ambulatory pH test, and should have respondedto PPI therapy. Antireflux procedures should beused with caution in patients with atypical manifes-tations (ie, chest pain, acid taste), in patients notresponding to PPI therapy, and patients with inef-fective esophageal motility. Contraindications toperform surgical interventions are major esophagealmotility abnormalities (ie, achalasia, scleroderma).

Recently, a randomized clinical trial in 310 pa-tients comparing surgery and omeprazole showedsimilar success/failure rates over a 5-year period.93

Results from community hospitals report rates ofcomplications/defective fundoplication (ie, dyspha-gia, 31%; bloating, 46%; flatulence, 67%; and recur-rent esophagitis, 26%) during a 78-month follow-up,94 which underlined the importance of having anexperienced surgeon in a hospital that has a highprocedure volume.

Endoscopic Management of GERD

Recent development in endoscopic techniques pro-posed a series of procedures to treat GERD. Radio-frequency ablation of the lower esophageal sphincter(Stretta procedure) uses a balloon-tipped 4-needlecatheter that delivers radiofrequency (RF) energy tothe smooth muscle of the gastroesophageal junction.The initial proposed mechanism of action was con-sidered to be generation of a scarring tissue thatwould decrease the amount of reflux.95 Subse-quently, it was proposed that RF ablation of the LESmight in fact decrease the number of transient loweresophageal sphincter relaxations.96 This procedureis recommended in patients suffering from chronicheartburn requiring maintenance antisecretorytherapy but without a hiatal hernia �2 cm, severeesophagitis, or complications of gastroesophageal re-flux disease. After the initial success, more recentstudies indicate that the procedure improves symp-toms (ie, severity of GERD, scores on GERD-relatedquestionnaires), but results regarding improvementof esophageal acid exposure are conflicting.97,98

Around the same time, the FDA approved a sec-



ond endoscopic antireflux technique (EndoCinch)that is based on endoscopic placement of suturesbelow the gastroesophageal junction. This procedureis not indicated in the presence of dysphagia, grade3 or 4 esophagitis, obesity, or hiatal hernia �2 cm inlength. Initial results and recently published fol-low-up studies indicate symptomatic improvementas well as improvement in esophageal acid exposureparameters.99,100 Other endoscopic antireflux proce-dures are currently in advanced stages of evaluationusing injected materials, endoscopic fundoplication,etc.

Summary

Gastroesophageal reflux disease (GERD) is achronic condition requiring long-term treatment.Simple, life-style modifications are the first methodsemployed by patients; because of their low cost andsimplicity, they should be continued even whenmore potent therapies are initiated.

Potent acid-suppressive therapy is currently themost important and successful medical therapy. Al-though healing of esophageal mucosa is achievedwith a single dose of any PPI in more than 80% ofcases, symptoms are more difficult to control. Forsymptom control, additional dosing or combinationtherapy with H2RA might be required. Patientswith persistent symptoms on therapy should betested (preferable with combined MII-pH) for asso-ciation of symptoms with acid, nonacid, or no GER.Long-term follow-up studies indicate that PPIs areeffective, tolerable, and safe medications. So far,PMAs have shown limited efficacy and their side-effect profiles outweigh benefits.

Antireflux surgery, in carefully selected patients(ie, young, typical GERD symptoms, abnormal pHstudy, and good response to PPI) is as effective asPPI therapy and should be offered to these patientsas an alternative to medication. Still, patientsshould be informed about the risks of antirefluxsurgery (ie, risk of postoperative dysphagia; de-creased ability to belch, possibly leading to bloatingand increased flatulence).

Endoscopic antireflux procedures are recom-mended only in selected patients; given the rela-tively short experience with these techniques, pa-tients treated with endoscopic procedures should beenrolled in a rigorous follow-up program.

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Management of Gastroesophageal Reflux Disease

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