New frontiers in gastroesophageal reflux disease:
Gespeichert in:
Format: | Buch |
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Sprache: | English |
Veröffentlicht: |
Philadelphia [u.a.]
Saunders
2002
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Schriftenreihe: | Gastroenterology clinics of North America
31,4, Suppl. |
Schlagworte: | |
Online-Zugang: | Inhaltsverzeichnis |
Beschreibung: | XII, 120 S. Ill., graph. Darst. |
Internformat
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245 | 1 | 0 | |a New frontiers in gastroesophageal reflux disease |c Ronnie Fass, guest ed. |
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490 | 1 | |a Gastroenterology clinics of North America |v 31,4, Suppl. | |
650 | 7 | |a Reflux oesophagitis |2 gtt | |
650 | 4 | |a Esophagogastric Junction |x physiopathology | |
650 | 4 | |a Gastroesophageal Reflux | |
650 | 4 | |a Gastroesophageal reflux | |
650 | 4 | |a Heartburn |x etiology | |
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Datensatz im Suchindex
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adam_text | NEW FRONTIERS IN GASTROESOPHAGEAL REFLUX DISEASE
CONTENTS
Preface
Ronnie Fass xi
Gastroesophageal Reflux Disease Revisited SI
Ronnie Fass
For decades, gastroesophageal reflux disease (GERD) has been ap¬
proached as a spectrum of disease. On one end of the spectrum are
the patients with classic symptoms of GERD and normal esopha
geal mucosa. The other end of the spectrum is occupied by patients
with GERD complications such as stricture, Barrett s esophagus,
and adenocarcinoma of the esophagus. Removing the spectrum
concept and approaching the GERD population as three unique
groups of patients (nonerosive reflux disease, erosive esophagitis,
and Barrett s esophagus) will dramatically shift our focus from eso
phageal mucosal injury to mechanisms leading to symptom gen¬
eration in each group and foster specific therapeutic modalities
that benefit each individual group of patients. The new paradigm
suggests that each of the unique groups of GERD should be eval¬
uated individually for the underlying mechanisms, therapeutic ap¬
proaches, and potential complications. This process will enable us
to better characterize each group and thus help to develop better
strategies for diagnosis and treatment.
GERD Mechanisms
Central Mechanisms of Lower Esophageal
Sphincter Control Sll
Pamela J. Hornby, T. Patrick Abrahams, and
Elita R. Partosoedarso
Lower esophageal sphincter (LES) tone is decreased during swal¬
lowing, during transient LES relaxations (TLESRs), and before em
esis, and this decrease is due primarily to increasing inhibitory
vagal output to the LES. Reflex evoked relaxation of the LES is
mediated by long loop vagovagal reflexes that are coordinated
VOLUME 31 • NUMBER 4 • DECEMBER 2002 Supplement V
by the dorsal vagal complex in the hindbrain medulla. A sequence
of events occurs. Central control of TLESRs has not been studied
directly; the information on how drugs may work centrally to re¬
duce TLESRs is extrapolated from knowledge of how the brain
evokes LES relaxation. Reduction of the frequency of TLESRs by
a GABAB agonist, baclofen, is due to inhibition of vagal afferents,
information transfer between the nucleus tractus solitarius and
dorsal motor nucleus of the vagus, and vagal efferent outflow. Pre¬
liminary data show that cannabinoid receptor activation reduces
information transfer between the nucleus tractus solitarius and
dorsal motor nucleus of the vagus. The potential therapeutic use¬
fulness of these types of agents that reduce TLESRs by acting cen¬
trally is promising.
Peripheral Mechanisms Affecting the Lower Esophageal
Sphincter Tone S21
Samer Gawrieh and Reza Shaker
The lower esophageal sphincter (LES) tone is controlled by central
and peripheral mechanisms. This article reviews the various factors
that affect LES motor function, with emphasis on peripheral factors
including the crural diaphragm, pharyngo LES, and laryngo LES
inhibitory reflexes, as well as distention of the esophagus and the
stomach.
Pathogenesis of Gastroesophageal Reflux Disease S35
Roy C. Orlando
The pathophysiology of gastroesophageal reflux disease involves
contact of the esophageal epithelium with acid/pepsin in the
refluxate. For this contact to occur with sufficient duration, there
must be a combination of defects in antireflux and luminal clear¬
ance mechanisms for acid/pepsin to overwhelm an intact epi¬
thelium; otherwise, defects within the epithelium develop that
subsequently enable normal acid contact times to become dama¬
ging to the epithelium. In either case, the final common pathway
is damage to the esophageal epithelium—damage that is reflected
in the development of heartburn, esophageal necrosis and inflam¬
mation, or both.
Assessment of Relationship Between Acid Reflux
and Heartburn Using Receiver Operating
Characteristic Curves S45
Joseph Steinbach, Ronnie Fass, and Ravinder K. Mittal
Reflux of acid from the stomach into the esophagus is thought to be
the cause of heartburn. The relationship between acid reflux and
heartburn, as detected by prolonged ambulatory pH monitoring,
is not clear. The authors tested the strength of association between
acid reflux and heartburn using receiver operative characteristic
vi CONTENTS
(ROC) curves. Esophageal pH at 1 and 6 cm above the lower eso
phageal sphincter was recorded in 236 patients referred for symp¬
tom evaluation. In the 76 patients reporting heartburn during the
monitoring period, the acid reflux frequency and number of reflux
episodes associated with heartburn were higher at 1 cm compared
with 6 cm above the lower esophageal sphincter. The number of re¬
flux episodes associated with heartburn was lower at 1 cm. Fisher
exact test revealed a statistically significant correlation between
acid reflux and heartburn, but the ROC curves revealed a weak as¬
sociation between heartburn and acid reflux, with area under the
curve ranging from 0.59 to 0.72. This weak association indicates
a lack of direct cause and effect relationship between acid reflux
and heartburn. These findings indicate that factors either in addi¬
tion to acid or other than acid in the esophagus determine the
occurrence of heartburn symptoms.
GERD Outcome
Natural History of Nonerosive Reflux Disease:
Is All Reflux Disease the Same? S59
G. Richard Locke III
This article describes the natural history of nonerosive reflux
disease, which is contrasted with that of erosive esophagitis. The
question is whether nonerosive reflux disease and erosive disease
represent two points on a spectrum of gastroesophageal reflux dis¬
ease or whether they represent dichotomous disease states with
different pathogeneses and natural histories. Such information is
important in educating patients regarding prognosis and in design¬
ing treatment approaches for the future.
Decision Making in Gastroesophageal Reflux Disease:
What Are the Critical Issues? S67
Joshua J. Ofman
Gastroesophageal reflux disease (GERD) is a common condition
characterized by heartburn and acid regurgitation. The total health
care costs of GERD are high, and the medications used to treat
symptoms are expensive. There is interest in defining better the
quality of life and economic consequences of GERD. Additionally,
the development of complications of GERD, such as Barrett s eso¬
phagus, esophageal stricture, and esophageal adenocarcinoma,
seems to drive many aspects of decision making. These decisions,
including the use of endoscopy and screening and surveillance
strategies in Barrett s esophagus, have substantial economic ramifi¬
cations from the patient s, payer s, and society s perspectives. This
article reviews the crucial determinants of decision making. The
focus is on the evidence that supports decisions related to screening
and surveillance for Barrett s esophagus and alternative manage¬
ment strategies.
CONTENTS vii
GERD Treatment
Persistent Gastroesophageal Reflux Disease Symptoms on
Standard Proton pump Inhibitor Therapy S77
Stephen J. Sontag
In this study, eight patients with refractory gastroesophageal reflux
disease (GERD) symptoms were controlled over a mean of 15.4
years only by the addition of a benzodiazepine to once daily or
twice daily proton pump inhibitor (PPI) therapy. In selected pa¬
tients with refractory GERD, as defined by continued reflux symp¬
toms despite twice daily PPIs, the addition of a benzodiazepine to
the PPI regimen may provide additional control of GERD symp¬
toms.
Novel Methods of Using Proton pump
Inhibitors S85
Nimish Vakil
Proton pump inhibitors (PPIs) are used widely in the treatment of
gastroesophageal reflux disease. On demand therapy with PPIs has
been shown to be effective in patients with nonerosive reflux dis¬
ease or mild erosive reflux disease. This strategy can reduce the
cost of maintenance therapy and is appealing in patients with no
evidence of mucosal disease. The long term efficacy and safety of
on demand PPI therapy have not been established. Nocturnal re¬
flux may be important in patients with complicated reflux disease
or Barrett s esophagus. Data on combining PPIs with H2 receptor
antagonists (H2RAs) suggest that nocturnal gastric pH can be con¬
trolled by the administration of H2RAs at bedtime. There are few
data on nocturnal symptoms, and some studies suggest that tachy
phylaxis may develop with H2RA therapy. More data are required
on the clinical effectiveness of combination therapy administered
long term.
Surgical and Endoscopic Treatment of
Gastroesophageal Reflux Disease S89
J. Patrick Waring
This article crystallizes the current thinking regarding the long
term management of patients with GERD, emphasizing the current
role of laparoscopic antireflux surgery. The advantages and disad¬
vantages of antireflux surgery are discussed separately, followed
by a discussion of the changing ideas regarding proper patient
selection and preoperative evaluation. The management of post¬
operative problems is discussed. Finally a brief discussion of the
emerging endoscopic therapies is included.
viii CONTENTS
Novel Medical Therapies for Gastroesophageal Reflux
Disease Beyond Proton pump Inhibitors Sill
Joel E. Richter
The control of transient lower esophageal sphincter relaxations is a
novel pharmacologic approach to the treatment of gastroesopha¬
geal reflux disease. It is applicable in most reflux patients character¬
ized as having nonerosive disease or patients with mild erosive
disease. Currently, only the GABAB agonist baclofen is available
for oral therapy, although side effects may be a limiting factor.
Future drug development requires a better understanding of the
central and peripheral mechanisms controlling transient lower
esophageal sphincter relaxations.
Index S117
CONTENTS •*
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spelling | New frontiers in gastroesophageal reflux disease Ronnie Fass, guest ed. Philadelphia [u.a.] Saunders 2002 XII, 120 S. Ill., graph. Darst. txt rdacontent n rdamedia nc rdacarrier Gastroenterology clinics of North America 31,4, Suppl. Reflux oesophagitis gtt Esophagogastric Junction physiopathology Gastroesophageal Reflux Gastroesophageal reflux Heartburn etiology Refluxösophagitis (DE-588)4137773-4 gnd rswk-swf (DE-588)4143413-4 Aufsatzsammlung gnd-content Refluxösophagitis (DE-588)4137773-4 s DE-604 Fass, Ronnie Sonstige (DE-588)132037955 oth Gastroenterology clinics of North America 31,4, Suppl. (DE-604)BV000613725 31,4,S HBZ Datenaustausch application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=010147756&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis |
spellingShingle | New frontiers in gastroesophageal reflux disease Gastroenterology clinics of North America Reflux oesophagitis gtt Esophagogastric Junction physiopathology Gastroesophageal Reflux Gastroesophageal reflux Heartburn etiology Refluxösophagitis (DE-588)4137773-4 gnd |
subject_GND | (DE-588)4137773-4 (DE-588)4143413-4 |
title | New frontiers in gastroesophageal reflux disease |
title_auth | New frontiers in gastroesophageal reflux disease |
title_exact_search | New frontiers in gastroesophageal reflux disease |
title_full | New frontiers in gastroesophageal reflux disease Ronnie Fass, guest ed. |
title_fullStr | New frontiers in gastroesophageal reflux disease Ronnie Fass, guest ed. |
title_full_unstemmed | New frontiers in gastroesophageal reflux disease Ronnie Fass, guest ed. |
title_short | New frontiers in gastroesophageal reflux disease |
title_sort | new frontiers in gastroesophageal reflux disease |
topic | Reflux oesophagitis gtt Esophagogastric Junction physiopathology Gastroesophageal Reflux Gastroesophageal reflux Heartburn etiology Refluxösophagitis (DE-588)4137773-4 gnd |
topic_facet | Reflux oesophagitis Esophagogastric Junction physiopathology Gastroesophageal Reflux Gastroesophageal reflux Heartburn etiology Refluxösophagitis Aufsatzsammlung |
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