1. health and fitness
2. disease
3. gerd and acid reflux

Management of Gastroesophageal Reflux
Disease
RADU TUTUIAN, MD; DONALD O. CASTELL, MD
ABSTRACT: Gastroesophageal reflux disease (GERD) is
a chronic condition requiring long-term treatment. Simple lifestyle modifications are the first methods employed by patients and, because of their low cost and
simplicity, should be continued even when more potent
therapies are initiated. Potent acid-suppressive therapy
is currently the most important and successful medical
therapy. Whereas healing of the esophageal mucosa is
achieved with a single dose of any proton pump inhibitor (PPI) in more than 80% of cases, symptoms are more
difficult to control. Patients with persistent symptoms on
therapy should be tested (preferably with combined
multichannel intraluminal impedance and pH) for association of symptoms with acid, nonacid, or no GER.
Long-term follow-up studies indicate that PPIs are efficacious, tolerable, and safe medication. So far, promotility agents have shown limited efficacy, and their side-
effect profile outweighs their benefits. Antireflux surgery
in carefully selected patients (ie, young, typical GERD
symptoms, abnormal pH study, and good response to
PPI) is as effective as PPI therapy and should be offered
to these patients as an alternative to medication. Still,
patients should be informed about the risks of antireflux
surgery (ie, risk of postoperative dysphagia; decreased
ability to belch, possibly leading to bloating; increased
flatulence). Endoscopic antireflux procedures are recommended only in selected patients and given the relative short experience with these techniques, patients
treated with endoscopic procedures should be enrolled
in a rigorous follow-up program. KEY INDEXING
TERMS: Gastroesophageal reflux disease (GERD); Proton
pump inhibitors; Antireflux surgery. [Am J Med Sci
2003;326(5):309–318.]
A
and has few side effects, specialists (gastroenterologists and gastrointestinal surgeons) are likely to see
only the “tip of the iceberg” represented by patients
with severe or persistent symptoms not responsive
to standard treatment.4 When evaluated by gastroenterologists, treatment targets reduction of esophageal acid exposure. Supported by a good correlation
between control of intragastric pH and healing of
erosive esophagitis,5 medical strategies employ
pharmacological suppression of gastric acid production, whereas surgical and endoscopic strategies employ augmentation of the gastroesophageal junction.
The above concepts have primarily been studied in
patients with so-called “typical” symptoms of GERD
(heartburn, regurgitation) but apply equally to those
with atypical (chest pain, asthma/cough, hoarseness, sore throat) symptoms or complications (ulceration, strictures, metaplasia) of the disease.
pproximately 40% of the US population has
symptoms of gastroesophageal reflux disease
(GERD),1 making it the fourth most prevalent gastrointestinal disease in the United States.2 GERD is
a chronic disease requiring long-term therapy. As a
general rule, the management of GERD should follow a step-wise approach, starting with simple therapeutic modalities and gradually advancing to more
potent and more aggressive modalities based on 2
goals: healing of lesions and alleviation of
symptoms.
The pattern of presentation and therapy is wellexpressed by the “heartburn iceberg” shown in Figure 1. The vast majority of patients have only occasional symptoms and will empirically treat
heartburn with over-the-counter (OTC) medications
and not seek medical attention.3 Patients with frequent symptoms will seek medical attention and are
often evaluated by primary care physicians and
given prescriptions for acid-suppressive therapy.
Because acid-suppressive therapy is very effective
From the Division of Gastroenterology/Hepatology, Medical
University of South Carolina, Charleston, South Carolina.
Correspondence: Radu Tutuian, M.D., Division of Gastroenterology/Hepatology, Medical University of South Carolina, 96
Jonathan Lucas Street, 210 CSB, Charleston, SC 29425 (E-mail:
[email protected]).
THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES
Simple Therapeutic Modalities (Lifestyle
Modifications)
In the current days of very potent acid-suppressive therapy, simple, alternative, patient-driven,
and less expensive GERD treatments tend to be
forgotten. Most of these methods were the main
therapeutic modalities before the late 1970s and
include elevation of head of the bed, wearing loose309
Management of Gastroesophageal Reflux Disease
Table 1. Lifestyle Modifications That Can Help Improve GERD
Symptoms
Sleep with the head of the bed elevated
Sleep on the left side
Avoid late meals/avoid recumbent position 3 hours after meals
Avoid high-fat meals
Use smaller meals
Use saliva-stimulating agents (ie, hard candies, chewing gum)
Wear loose-fitting clothing
Restrict smoking, alcohol, coffee, chocolate
Lose weight
Figure 1. Pattern of presentation and therapy of GERD patients
expressed by the “heartburn iceberg.” Endo, endoscopic antireflux
procedure.
fitting clothing, avoidance of meals before bedtime,
weight loss, and restriction of smoking, alcohol, coffee, and fat.6 Today, these lifestyle modifications
often also include use of antacids, alginate, and
over-the-counter (OTC) doses of histamine-2 receptor antagonists (H2RA).
Elevation of the head of the bed helps improvement of esophageal acid clearance and decreases the
total recumbent acid exposure.7 These hypotheses
are supported by studies indicating significant reduction in nocturnal acid clearance time and total
nocturnal acid exposure using 6-inch blocks to elevate the head of the bed.8 A more patient-friendly
alternative is to sleep predominantly on the left
side.9 Avoidance of meals for 3 hours before bedtime
is based on studies indicating that postprandial recumbency leads to a significant increase in the number and duration of reflux events10
Wearing loose-fitting clothing as a measure to
reduce gastroesophageal reflux is based on the hypothesis that tight clothing increases intragastric
pressure and therefore the gastroesophageal pressure gradient across the lower esophageal sphincter
(LES),11 the so-called “tight pants syndrome.” Even
though there are no good studies supporting this
hypothesis, this relatively simple and intuitive measure should not be ignored.
Based on studies showing a correlation of morbid
obesity with reflux and lower LES pressures,12
weight reduction in the attempt to improve GERD is
a rational approach. Even though not formally studied, it is commonly believed that typical GERD
symptoms improve in patients during weight
reduction.
Recommendations to avoid certain foods and limit
310
smoking and alcohol are based on studies indicating
decreases in LES pressures and/or increased number of gastroesophageal reflux episodes. Ingestion of
high-fat meals decreases LES pressure,13 increases
frequency of transient lower esophageal relaxations,14 and increases esophageal acid exposure for
up to 3 hours after meals.15 Increased esophageal
acid exposure has been documented after ingestion
of chocolate16 and alcohol17 and after smoking.18,19
The use of antacids in treatment of GERD relies
on the neutralizing capabilities of these compounds
on acid gastric secretions. The superiority of antacids over placebo was proven in double-blind studies
in patients with reflux esophagitis.20,21 Other placebo-controlled studies have shown the superiority of
an alginic acid-antacid combination in controlling
reflux symptoms.22 The observation of the floating
nature of alginic acid within the stomach suggested
that it might work well in patients with symptoms
during the upright position,23 a hypothesis supported in subsequent studies.24
After several years of proven efficacy and safety of
standard-dose H2RAs, the class of medication became available as low-dose over-the-counter (OTC)
preparations for “conservative” treatment of GERD.
There is only limited information available showing
symptomatic improvement with OTC doses of
H2Ras,25 although several studies have documented
the ability of these preparations to decrease intragastric acidity.26,27 In 2002, the American Gastroenterology Association (AGA) issued a consensus statement declaring OTC H2RA and antacid the first line
of treatment for patients with mild GERD symptoms. The combination H2RA/antacid was considered better at symptom relief than its constituent
components alone.
Table 1 summarizes the life-style modification approach to GERD. Even though recently developed
acid-suppressive agents are highly effective in treatment of GERD, these simple measures should be
discussed with patients. Their simplicity and low
cost justify them as phase 1 therapy to be continued
in all patients suffering from this disorder. OTC
antacids or even H2RAs should be recommended for
occasional “breakthrough” symptoms while patients
are receiving more potent therapies.
November 2003 Volume 326 Number 5
Tutuian and Castell
Pharmacologic Management of GERD
The objectives of pharmacological treatment of
GERD are relief of symptoms, avoidance of complications, and healing of esophageal mucosa. The
principal classes of pharmacological agents are: acid
suppressive drugs [H2RAs, proton pump inhibitors
(PPIs)], promotility agents (bethanechol, metoclopramide, cisapride, domperidone, erythromycin, tegaserod), mucosal protective agents (sucralfate), and
agents to reduce transient lower esophageal sphincter relaxation (TLESR) (baclofen).
Acid-Suppressive Drugs
Histamine-2 Receptor Antagonists. H2RAs
were the antisecretory therapy of choice from the
mid-1970s until the introduction of PPIs into clinical
practice in the late 1980s.28 Currently in the United
States, 4 H2RAs are available for clinical use: ranitidine (Zantac), famotidine (Pepcid), cimetidine
(Tagamet), and nizatidine (Axid). Even though the
more recently developed PPIs have been shown to
be superior, the H2RAs still remain useful in
treatment of milder forms of the disease and for
on-demand therapy, particularly for nocturnal
GERD symptoms.
Prescription dosages of H2RAs can be grouped
into standard dose (150 mg of ranitidine, 20 mg of
famotidine, 400 mg of cimetidine, and 150 mg of
nizatidine, each twice daily) and high dose (obtained
by doubling the standard doses). The healing rates
with H2RAs range between 50 and 70% at 8 weeks
and 60 to 80% at 12 weeks.29 Most studies have
shown superiority of H2RAs to placebo but no significant differences among high and standard doses
(possible type II error, because most studies were
powered to show differences from placebo). It was
soon recognized that esophageal healing rates correlated with decrease of esophageal acid exposure,
duration of acid suppressive therapy, and degree of
esophagitis.30 Studies have shown that esophageal
healing rates at 12 weeks were higher than healing
rates 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 of
patients after 6 to 12 weeks.33
Even in this era of potent acid-suppressive PPIs,
H2RAs provide the advantage of prompt relief of
heartburn,34 and when administered at bedtime,
they improve nocturnal gastric acid control in GERD
patients taking PPIs.35
Proton Pump Inhibitors. PPIs are superior to
H2RAs in treating erosive esophagitis36 and its complications,37 relieving symptoms from erosive and
nonerosive GERD,38,39 and preventing recurrence of
GERD-associated symptoms.40 Studies by Zeitoun,41
Lundell et al,42 Vantrappen et al,43 and Klinkenberg-Knol et al36 indicate superiority of the PPI
versus H2RA. Thus, they have surpassed H2RAs as
the antisecretory agents of choice (Figure 2). PPIs
are substituted benzimidazoles that irreversibly
bind the H⫹,K⫹-ATPase, the final common step in
acid secretion.44
Currently, 5 PPIs are commercially available in
the United States: omeprazole, lansoprazole, rabeprazole, pantoprazole, and esomeprazole. FDA-approved doses (20- and 40-mg omeprazole, 15- and
30-mg lansoprazole, 20-mg rabeprazole, 40-mg pantoprazole, and 40-mg esomeprazole) are for use once
daily, which provides sufficient acid suppression to
effectively treat most patients. Symptom relief can
be 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 controversial. For every study showing that one PPI is
superior to another, there is another study showing
the opposite. Overall, based on similar esophageal
healing rates of over 80% at 8 weeks46 and similar
intragastric pH profiles after 7 days of dosing,47 all
first-generation PPIs (omeprazole, lansoprazole, rabeprazole, pantoprazole) can be considered to have
equivalent effectiveness (Figure 3). Minor differences in pharmacodynamics and price exist.48 However, individual variability in patient response to
PPI can vary widely. Therefore, we recommend
Figure 2. Comparison of omeprazole versus ranitidine in healing reflux esophagitis after 8 weeks of
treatment. Studies by Zeitoun,41 Lundell et al,42
Vantrappen et al,43 and Klinkenberg-Knol et al36
indicate superiority of the PPI versus H2RA. Numbers indicate dose of omeprazole used in the study.
THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES
311
Management of Gastroesophageal Reflux Disease
Figure 3. Comparison of first-generation PPIs for short-term
treatment healing rates. Bars indicate percentage healing after 8
weeks of treatment. Numbers indicate patients in respective
studies.
Figure 5 . Proportion of patients with nocturnal acid breakthrough (defined as intragastric pH ⬍ 4 for at least 60 continuous
minutes) on PPI bid ⫹ H2RA at bedtime versus PPI twice per day
alone.35
switching to another PPI as the first step in patients
not responding to one PPI.
The most recent “second-generation” PPI, esomeprazole, the active S-isomer in the racemic mixture
of omeprazole,49 has been reported to have slightly
better effect on GERD.50 Results from a large, double-blind study suggest that the advantages of esomeprazole become more important in patients with
more severe disease (Figure 4).51
The timing of administering the PPI in relation
with meals is important. The ideal window to take
the PPI is 15 to 30 minutes before meals. This allows
the medication to be absorbed to be available to the
proton pumps when they are activated by the meal.
PPIs taken before meals provide better intragastric
pH control compared with being taken after the
meal.52 Inadequate timing is frequently seen clinically, especially when patients are prescribed PPI
twice daily without further instructions; patients
frequently take the medication in the morning and
before bedtime (without a meal).
Despite the efficacy of single-dose proton pump
inhibitor in controlling intragastric acidity, improving symptoms, and healing of erosive esophagitis,
some patients do not heal as well and may require
increased dosing. In addition, patients with extraesophageal presentations (asthma, cough, or laryngitis) may require higher doses for effective symptom
control.53–55 Rather than doubling the single dose
amount, it is preferable to give the PPI twice daily.
This recommendation is based on studies in healthy
subjects indicating that 20 mg of omeprazole before
breakfast and before dinner was superior in controlling intragastric pH compared with 40 mg of omeprazole before breakfast or before dinner.56
A more recent discovery has been that PPIs may
not achieve adequate control of intragastric pH57;
even with twice-daily dosing, they are not always
able to control nocturnal acid breakthrough.58 A
single dose of H2RAs added at bedtime to the PPI
can reduce nocturnal acid breakthrough (Figure
5).59 Concerns that combination of PPI and H2RAs
Figure 4. Comparison of esomeprazole versus lansoprazole in 8-week healing rates of erosive esophagitis by baseline grade of esophagitis. The benefits
of esomeprazole are higher in more severe cases of
esophagitis.
312
November 2003 Volume 326 Number 5
Tutuian and Castell
Table 2. Suggested Approach to Acid Suppressive Therapy
Step
Medical regimen
1
2
3
4
5
Single-dose PPI (AM before meals)
Switch to another PPI
PPI AM plus evening (or bedtime) H2RA
PPI twice daily before meals
PPI twice daily before meals plus H2RA at bedtime
might decrease the efficacy of PPIs were cleared by
studies indicating similar intragastric acid control
on daily PPI after placebo or H2RAs the night before.60 Therefore H2RAs are still potentially effective drugs for on-demand therapy of both daytime
and nocturnal GERD symptoms.
Based on existing data we propose the step-up
therapeutic approach to acid suppression guided as
illustrated in Table 2. Symptom response to a trial of
PPI therapy is currently a popular recommended
diagnostic approach to GERD (“PPI-trial”).61 Patients failing PPI trials or not responding to PPI
therapy should undergo reflux testing to evaluate
the amount of reflux and its relation to symptoms.
For more than 20 years, esophageal pH testing has
been the accepted standard for diagnosing
GERD.62,63 For optimal study interpretation patients should be off PPI therapy for at least 7 days
before undergoing esophageal pH testing. Patients
with GERD who failed to respond to standard PPI
treatment because of insufficient dosing might experience symptom exacerbation during this period
that may help clarify the diagnosis.
An important alternative diagnosis in patients
with persistent symptoms on therapy is the possibility of symptomatic nonacid reflux, which will be
missed by conventional pH testing because of the
limitations of this technique in identifying nonacid
reflux.64,65 Currently, combined multichannel intraluminal impedance and pH (MII-pH) is evolving
as dual modality reflux testing. Because MII-pH
detects reflux by changes in intraluminal electric
conductivity, both acid and nonacid reflux events
can be identified.66,67 Preliminary data from a multicenter collaborative study suggest that only 20% of
patients with persistent symptoms on acid-suppressive therapy have their symptoms related to acid
reflux. The other 80% usually present a diagnostic
dilemma as to whether their symptoms are associated with nonacid reflux or not associated with any
type of GER. Combined MII-pH will further clarifying this possible association, including recognition
that 40% of patients with persistent symptoms on
therapy have no temporal correlation between
symptoms and any type of reflux. Therefore, we
believe that combined MII-pH should be considered
the next step in diagnostic management of patients
not responding to PPI therapy (Figure 6).
THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES
Figure 6. Suggested diagnostic GERD algorithm.
As mentioned before, GERD is a chronic disease
requiring long-standing therapy. Although daily
maintenance therapy on standard-dose PPI sustains
relapse rates well under 20% for 12 months,68,69
change to H2RAs or placebo will increase the relapse
to more than 50 to 70% and 70 to 90%, respectively.70,71 Long-term safety and efficacy of standard
PPI doses are supported by European studies with
patient follow-up over a decade.72
Promotility Agents (PMAs)
The rationale for using PMAs in treatment of
GERD is based on the hypothesis that normalizing
underlying dysmotility or augmenting existing motility would decrease esophageal acid contact time.
An overall comment regarding PMAs in GERD is
that as a group, they have limited effectiveness or
undesirable side effects.
Bethanechol is a cholinergic agonist that will increase esophageal peristalsis and LES pressure but
also stimulate gastric secretion. Compared with placebo, it will improve GERD symptoms but has no
advantages in healing esophagitis.73,74 At the recommended dose for treatment of GERD (25 mg 4 times
per day), it may have cholinergic side effects, including diarrhea, abdominal cramping, fatigue, and
blurred vision.
Metoclopramide is a smooth-muscle stimulant
that inhibits dopamine receptors. It enhances gastric emptying and LES pressure but has no effect on
esophageal peristalsis. Even though it may improve
GERD symptoms, it does not show healing rates to
justify its side-effect profile: galactorrhea, menstrual dysfunction, lethargy, and extrapyramidal
motor defects. The most concerning side effect is
tardive dyskinesia, which can occur in up to 20% of
patients and can be permanent.75
Cisapride stimulates acetylcholine release, increasing LES pressure, aiding esophageal peristalsis, and accelerating gastric emptying. Placebo-controlled trials have shown significant improvements
313
Management of Gastroesophageal Reflux Disease
in GERD symptoms76; because of its cardiovascular
side effects, however, it is no longer available.
Tegaserod, a selective 5-HT4 receptor partial agonist, is a potent promotility agent throughout the
gastrointestinal tract that is also considered to decrease visceral sensitivity77 and promote gastric
emptying.78 In 1 study in GERD patients, it was
shown to decrease postprandial esophageal acid exposure79 suggesting a potential role in treatment of
GERD.
Domperidone and erythromycin are the other promotility agents currently being investigated for
treatment of GERD. Both agents enhance gastric
emptying but do not have significant effects on
esophageal peristalsis. Their side effect profiles may
also limit their clinical utility.
Mucosal Protective Agents
The role of sucralfate in treatment of GERD has
not been studied as extensively as H2RAs and PPIs.
Sucralfate is believed to physically adhere to injured
mucosa and thereby create a protective barrier
against acid gastric secretions. Randomized comparisons showed superiority to placebo and healing
comparable with standard dose H2RAs.80
Agents to Reduce TLESRs
Recently, transient lower esophageal sphincter relaxations (TLESRs) have been recognized to be the
major mechanism of gastroesophageal reflux.81– 83
Baclofen, an agonist of ␥-aminobutyric acid type B,
was shown to reduce the rate of postprandial
TLESRs and acid reflux episodes in healthy volunteers84 and patients with reflux esophagitis.85 In a
mechanistic study using combined MII-pH in
healthy volunteers and patients with GERD, a single dose of 40 mg of baclofen significantly reduced all
types (acid and nonacid) of postprandial reflux.86
The side-effect profile of dizziness or nausea may
restrict its clinical utility.
Surgical Management of GERD
Surgical antireflux procedures are highly effective
treatment modalities in appropriately selected patients. Before potent acid suppressive therapy became available, surgery was considered superior to
medical therapies.87 The rationales for antireflux
surgery have evolved parallel to clarifications in
pathophysiologic mechanisms of reflux disease. Although hiatal hernia was considered to be of major
importance in production of GERD, antireflux surgery was performed to reduce the hiatal hernia and
keep the LES within the abdominal cavity.88 Reports showing that only 9% of patients with hiatal
hernia had typical reflux symptoms89 suggested that
other factors might play a more important role.
When low LES pressures were considered the major
factor in gastroesophageal junction incompetence,
314
antireflux procedures were done to increase LES
pressure.90 At present, given that TLESR is considered the main mechanism by which GERD occurs,
surgery is done to lengthen the intraabdominal portion of the LES, to reduce the volume of the gastric
fundus and prevent effacing of the LES during gastric distention in the postprandial period.91
Preoperative evaluation of patients undergoing
antireflux surgery includes: esophageal manometry,
upper gastrointestinal endoscopy, 24-hour esophageal pH monitoring, barium esophagogram, and gastric emptying studies.92 This is necessary to select
the ideal candidates for the procedure, who should
be young (because they will require long-term GERD
therapy), should have typical GERD symptoms
(heartburn, regurgitation), should have an abnormal ambulatory pH test, and should have responded
to PPI therapy. Antireflux procedures should be
used with caution in patients with atypical manifestations (ie, chest pain, acid taste), in patients not
responding to PPI therapy, and patients with ineffective esophageal motility. Contraindications to
perform surgical interventions are major esophageal
motility abnormalities (ie, achalasia, scleroderma).
Recently, a randomized clinical trial in 310 patients comparing surgery and omeprazole showed
similar success/failure rates over a 5-year period.93
Results from community hospitals report rates of
complications/defective fundoplication (ie, dysphagia, 31%; bloating, 46%; flatulence, 67%; and recurrent esophagitis, 26%) during a 78-month followup,94 which underlined the importance of having an
experienced surgeon in a hospital that has a high
procedure volume.
Endoscopic Management of GERD
Recent development in endoscopic techniques proposed a series of procedures to treat GERD. Radiofrequency ablation of the lower esophageal sphincter
(Stretta procedure) uses a balloon-tipped 4-needle
catheter that delivers radiofrequency (RF) energy to
the smooth muscle of the gastroesophageal junction.
The initial proposed mechanism of action was considered to be generation of a scarring tissue that
would decrease the amount of reflux.95 Subsequently, it was proposed that RF ablation of the LES
might in fact decrease the number of transient lower
esophageal sphincter relaxations.96 This procedure
is recommended in patients suffering from chronic
heartburn requiring maintenance antisecretory
therapy but without a hiatal hernia ⬎2 cm, severe
esophagitis, or complications of gastroesophageal reflux disease. After the initial success, more recent
studies indicate that the procedure improves symptoms (ie, severity of GERD, scores on GERD-related
questionnaires), but results regarding improvement
of esophageal acid exposure are conflicting.97,98
Around the same time, the FDA approved a secNovember 2003 Volume 326 Number 5
Tutuian and Castell
ond endoscopic antireflux technique (EndoCinch)
that is based on endoscopic placement of sutures
below the gastroesophageal junction. This procedure
is not indicated in the presence of dysphagia, grade
3 or 4 esophagitis, obesity, or hiatal hernia ⬎2 cm in
length. Initial results and recently published follow-up studies indicate symptomatic improvement
as well as improvement in esophageal acid exposure
parameters.99,100 Other endoscopic antireflux procedures are currently in advanced stages of evaluation
using injected materials, endoscopic fundoplication,
etc.
Summary
Gastroesophageal reflux disease (GERD) is a
chronic condition requiring long-term treatment.
Simple, life-style modifications are the first methods
employed by patients; because of their low cost and
simplicity, they should be continued even when
more potent therapies are initiated.
Potent acid-suppressive therapy is currently the
most important and successful medical therapy. Although healing of esophageal mucosa is achieved
with a single dose of any PPI in more than 80% of
cases, symptoms are more difficult to control. For
symptom control, additional dosing or combination
therapy with H2RA might be required. Patients
with persistent symptoms on therapy should be
tested (preferable with combined MII-pH) for association of symptoms with acid, nonacid, or no GER.
Long-term follow-up studies indicate that PPIs are
effective, tolerable, and safe medications. So far,
PMAs have shown limited efficacy and their sideeffect profiles outweigh benefits.
Antireflux surgery, in carefully selected patients
(ie, young, typical GERD symptoms, abnormal pH
study, and good response to PPI) is as effective as
PPI therapy and should be offered to these patients
as an alternative to medication. Still, patients
should be informed about the risks of antireflux
surgery (ie, risk of postoperative dysphagia; decreased ability to belch, possibly leading to bloating
and increased flatulence).
Endoscopic antireflux procedures are recommended only in selected patients; given the relatively short experience with these techniques, patients treated with endoscopic procedures should be
enrolled in a rigorous follow-up program.
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