How We Are Treating GERD
Lifestyle changes
Lifestyle changes are aimed at decreasing distal esophageal acid exposure.
Alterations that are recommended include losing weight, stopping smoking, and
wearing loose-fitting clothing. Decreasing the size of each meal may be
helpful.8 Certain foods, including chocolate, peppermint, high fat
foods including fried foods, alcohol-based drinks, caffeinated beverages,
citrus drinks, and tomato-based foods should all be avoided.4,8 Patients
may get relief from symptoms by not lying down immediately (3 hours) after
meals.4
Overview of medical therapy
Three classes of medications are available to treat GERD: promotility agents,
histamine2-receptor antagonists (H2RAs), and PPIs.
Promotility Agents
Defective esophageal and gastric motility are key elements of GERD pathogenesis.8
Promotility agents increase lower esophageal sphincter pressure, augment
gastric emptying, stimulate peristalsis, and increase the amplitude of
esophageal contractions.10,17 Metoclopramide is the only promotility
agent approved by the Food and Drug Administration (FDA) for use in the U.S.
Side effects occur in 20% to 30% of patients; the most serious are depression
and tardive dyskinesia.10
H2RAs
H2RAs suppress gastric acid by occupying H2 receptors.18
Four H2RAs are available; they are equivalent in efficacy.10
Symptom relief is seen in approximately 60% of patients.8,10,19 Healing
of erosions is seen in about half of patients treated with twice-daily H2RAs.8,10,18
As a class they are well tolerated .10,18 Studies have shown that
patients develop tolerance to H2RA therapy.8,20 In
addition, H2RA absorption is decreased by food.21
PPIs
PPIs provide the highest levels of symptom relief, esophageal healing, and
prevention of relapse and complications.8,22 They are the first
choice for therapy in most GERD patients with or without esophageal mucosal
injury and in those with extraesophageal manifestations.8,17,23-26 The
most common side effects are headache, nausea, and diarrhea. Some of the PPIs
may interact with other drugs metabolized via the cytochrome P450 system and
cause an increase in their plasma levels.
Nonerosive GERD (Symptomatic GERD with normal upper endoscopy)
Therapeutic goals in uncomplicated GERD include symptom resolution and
prevention of relapse. The practice of a step-up approach to the treatment of
GERD is now reserved for initial treatment of those with mild, sporadic,
uncomplicated GERD who experience heartburn less than two to three times a
week. However, even patients with infrequent heartburn can present with severe
GERD complications, including Barrett's esophagus; thus, the appropriateness of
this strategy in any patients with GERD is unclear.27
Howden et al compared the effectiveness of management of heartburn symptoms in
patients with GERD by sustained treatment with an H2RA, a PPI, a
step-up regimen of the PPI and the H2RA, or a step-down regimen of
the PPI and the H2RA.19 At the end of 20 weeks, the group
treated continuously with the PPI experienced less severe heartburn and more
twenty-four (24) hour heartburn-free periods than the other three groups.
Evidence suggests that the therapeutic requirements of patients with non-erosive
GERD are similar to those with erosive esophagitis (EE). However, PPIs may be
less effective in patients with nonerosive GERD than in patients with EE. This
suggests that some patients with nonerosive GERD may have symptoms mediated by
factors other than acid or they may require more acid control to relieve
symptoms.
Erosive GERD or Erosive Esophagitis (EE)
PPIs are the mainstay of therapy for severe and complicated GERD. A once-daily
dose of a PPI is effective for acute and long-term management of GERD. Healing
rates for EE range from 78% to 94% at eight weeks.29-31 Maintenance
studies report continued healing of EE in 80% to 87% of patients over 12 months
of study.32,33 When patients are prescribed higher doses of a PPI,
one would expect higher rates of response, but few data are available to
support this.
Barrett's Esophagus
The goals of therapy in patients with Barrett's esophagus include elimination of
GERD symptoms, maintenance of healed mucosa, and prevention of disease
progression. However, these patients have greater esophageal acid exposure than
other patients with GERD and control of symptoms may require higher doses of
PPIs.34 No studies have proven that aggressive antireflux therapy
alters the natural history of Barrett's esophagus. The importance of
duodenogastro esophageal reflux is being increasingly recognized in the
pathogenesis of severe GERD especially in patients with Barrett's esophagus.27,35
Aggressive acid suppression with a PPI decreases both acid and duodenogastric
esophageal reflux in these patients.36
Maintenance Therapy
Many patients with GERD require some form of maintenance therapy. Recurrence
rates of esophageal erosions among individuals with documented EE range from
75% to 92% following discontinuation of the PPI.37 Vigneri et al
compared five maintenance regimens for patients with healed EE and showed
significantly higher remission rates with PPI therapy than with H2RAs
or prokinetics.
The data supporting step-down therapy are weak. In one study, patients who
initially had nonerosive, symptomatic GERD and became asymptomatic after
treatment with a PPI stopped their PPIs in a stepwise fashion.41 After
one year of follow-up, only 15% remained asymptomatic without any medication of
any class. Younger age and heartburn as the predominant symptoms predicted
unsuccessful PPI step-down management.
Management of the Patient with Refractory GERD
PPIs do not afford symptom relief or heal mucosal injury in all patients for
several reasons: the diagnosis of GERD may be incorrect, the patient may have
nonacid gastroesophageal reflux, or PPI therapy in this patient may not control
gastric acidity.
Esophageal acid exposure appears to be infrequent in normal subjects and
patients with uncomplicated GERD but may be seen in up to 50% of patients with
Barrett's esophagus.42 To ascertain the degree of association
between acid reflux and symptoms in patients who have breakthrough symptoms
combined intragastric and intraesophageal pH monitoring should be performed. If
there is nocturnal acid breakthrough, the approach may be to add a bedtime H2RA
to twice-a-day PPI therapy. In patients with ineffective gastric pH control
despite maximal dose of one PPI, changing from that PPI to another may be
worthwhile.43 These patients are poor candidates for surgery,
because the best predictor of surgical success is complete response to medical
therapy and the ideal candidate is the patient who has complete elimination of
symptoms with medications but does not want to take them long term.4