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REVIEW
Gastroesophageal Reflux Disease (GERD) and Irritable Bowel
Syndrome (IBS)—Is It One Disease or an Overlap of Two
Disorders?
Anita Gasiorowska ÆChoo Hean Poh Æ
Ronnie Fass
Received: 27 August 2008 / Accepted: 17 October 2008
ÓSpringer Science+Business Media, LLC 2008
Abstract Up to 79% of IBS patients report gastroesoph-
ageal reflux disease (GERD) symptoms, and up to 71% of
GERD patients report irritable bowel syndrome (IBS)
symptoms. There are two principal hypotheses for the
common presence of IBS symptoms in GERD patients. The
first theory suggests that GERD and IBS overlap in a sig-
nificant number of patients. The second theory suggests that
IBS-like symptoms are part of the spectrum of GERD
manifestation. The first theory is supported by genetic
studies and similarities in gastrointestinal sensory-motor
abnormalities potentially due to general gastrointestinal
disorder of smooth muscle or sensory afferents. The other
theory is primarily supported by studies demonstrating
improvement of IBS-like symptoms in GERD patients
receiving anti-reflux treatment. The close relationship
between GERD and IBS could be explained by either
GERD affecting different levels of the GI tract or a high
overlap rate between GERD and IBS due to similar
underlying GI dysfunction.
Keywords Gastroesophageal reflux disease (GERD)
Irritable bowel syndrome (IBS) Pathophysiologic
mechanism Symptom assessment Visceral hyperalgesia
Introduction
Gastroesophageal reflux disease (GERD) and irritable
bowel syndrome (IBS) are very common in the general
population. The prevalence of IBS in North America
ranges from 3–20%, with most prevalence estimates
ranging from 10–15% [1]. Thus far, there is limited
information about the epidemiology of IBS in specific
patient populations such as the elderly and ethnic groups
other than Caucasians. IBS has a female predominance,
and it peaks from the ages 20 to 45 years [1–3]. IBS
accounts for 25–50% of referrals to gastroenterologists
[4].
GERD is also very common. Population-based studies
demonstrated that 32–57% of the general adult population
in Western countries demonstrated typical GERD-related
symptoms within the last year. The community prevalence
of weekly heartburn ranges from 10–21% [5]. Both GERD
and IBS are less common in Asia than in Western popu-
lations. The reported population prevalence of GERD in
East Asia ranges from 3 to 7% for weekly symptoms of
heartburn and/or acid regurgitation [6,7].
Most epidemiologic studies show a significant overlap
between the different functional disorders of the digestive
tract in the general population [8–11]. Consequently, the
presence of IBS-related symptoms in patients with GERD
may suggest an overlap between two distinct disorders that
share a similar pathophysiologic mechanism, such as vis-
ceral hypersensitivity or gastrointestinal (GI) dysmotility
[2,12]. Alternatively, lower abdominal symptoms may be
part of the overall clinical presentation of GERD, sug-
gesting that the underlying mechanism for GERD may lead
to upper as well as lower gut symptoms.
The classic symptoms of GERD are heartburn, acid
regurgitation, dysphagia, and belching. Extra-esophageal
and atypical symptoms of GERD may include wheezing,
chronic cough, hoarseness, chest pain, and sleep deprivation.
However, a variety of other symptoms have been seen in
GERD patients. Some appear to originate from other levels
A. Gasiorowska C. H. Poh R. Fass (&)
Neuroenteric Clinical Research Group, Southern Arizona VA
Health Care System, University of Arizona, GI Section
(1-111G-1), 601 S. 6th Avenue, Tucson, AZ 85723-0001, USA
e-mail: Ronnie.Fass@va.gov
123
Dig Dis Sci
DOI 10.1007/s10620-008-0594-2
of the gastrointestinal tract. These include flatulence,
abdominal discomfort, and alteration in bowel movement
[13].
Irritable bowel syndrome is a chronic, relapsing, gas-
trointestinal disorder commonly presenting with abdominal
pain, bloating, and alteration in bowel movement. Although
IBS is not known to lead to serious disease or excess
mortality, it has a significant impact on patients’ quality of
life and social functioning. The clinical presentation of IBS
is quite diverse. Many of the patients report a wide range of
colonic and extra-colonic symptoms [2,14,15].
This article reviews two principal hypotheses about the
potential relationship between GERD- and IBS-related
symptoms. The first theory suggests that GERD and IBS
overlap in a significant number of patients, and the second
theory proposes that IBS-like symptoms are part of the
spectrum of GERD presentation.
The Prevalence of IBS in GERD
Many epidemiologic studies have demonstrated that
patients with GERD frequently report IBS-related symp-
toms (see Table 1).
Kennedy et al. [16] in a population-based study,
explored the relationship between IBS, GERD, and bron-
chial hyper-responsiveness (BHR) using a symptom
questionnaire. The 12-month prevalence of IBS-related
symptoms for men and women was 10.5% and 22.9%,
respectively. The 12-month prevalence of GERD-related
symptoms was 29.4% and 28.2%, respectively. Of the 910
subjects who were found to have GERD, 19% reported IBS-
like symptoms and of the 546 IBS patients, 32% were found
to have GERD. The authors revealed that IBS and GERD
symptoms occur more frequently together than expected
and that the conditions are associated with each other.
De Vries et al. [17] studied GERD patients seeking care
and demonstrated that IBS is more prevalent in GERD
patients than in the general population (35% vs. 0.6–6%).
In another study, Pimentel et al. [12] determined the
prevalence of IBS, as defined by Rome I criteria, in sub-
jects with GERD as compared with non-GERD controls.
Of the 35 GERD subjects, 71% were positive for IBS,
whereas only 35% of the 49 non-GERD control subjects
had IBS. The study demonstrated that the prevalence of
IBS was significantly more common in the GERD group
than in the non-GERD group. Additionally, in this study, a
subset of GERD patients underwent 24-h esophageal pH
monitoring, and 64% of those with IBS had abnormal pH
test results.
Zimmerman [18] evaluated the prevalence of IBS in non-
erosive reflux disease (NERD) patients. In this study, half of
the NERD patients met the diagnostic criteria for IBS as
defined by the Rome I criteria. The authors also reported
that the extent of esophageal acid exposure, as measured by
24-h esophageal pH monitoring, was unrelated to symptoms
of irritable bowel syndrome. Interestingly, Fass et al. [19],
who summarized the results of 14 clinical therapeutic trials,
demonstrated that lower abdominal complaints were pres-
ent in 60% of both erosive esophagitis and NERD patients.
In a large epidemiologic study that evaluated 3,318 adult
patients from general practice clinics, 72% of the GERD
patients were found to have functional bowel disorders
[20]. Among these patients, 27% had symptoms suggestive
of IBS according to the Rome II criteria, 16% functional
dyspepsia, and 57% had varied functional bowel symp-
toms. The most commonly reported symptoms were gas
and flatulence (81%), transit disorders (62%), and
abdominal distension (58%).
Recently, Nastaskin et al. [21] conducted a systematic
review of the literature evaluating the prevalence of IBS and
GERD in the general population and the rate of overlapping
symptoms between the 2 disorders. The average prevalence
of GERD was 19.4% and IBS 12.1%. Several of the included
studies determined that the GERD maximum mean preva-
lence in patients already diagnosed with IBS was 39.3%.
There was a significant variability in the GERD prevalence,
ranging from 17 to 80%. The likely reason for the wide
range of GERD prevalence in IBS patients appeared to
depend on the method for diagnosing GERD. The maximum
mean prevalence of IBS in subjects with already-known
GERD was 48.8%. The prevalence of IBS in GERD patients
also had a wide range (31–71%) and was clearly dependent
on the criteria used to diagnose IBS (Manning, Rome I, or
Table 1 The prevalence of IBS
in GERD
a
The maximum mean
prevalence
Sample size Prevalence of IBS (%) IBS definition
Kennedy et al. [16] 910 19 Modified Manning
De Vries et al. [17] 263 35 Rome II
Pimentel et al. [12] 35 71 Rome I
Zimmerman [18] 256 50 Rome I
Fass et al. [19] 6,810 60 ReQuest
Gillemot et al. [20] 3,318 27 Rome II
Nataskin et al. [21] Systematic review 48.8
a
–
Dig Dis Sci
123
Rome II). This systematic review demonstrated that IBS and
GERD appear to overlap to a degree that is greater than their
individual prevalence in the community. The authors con-
cluded that the prevalence of IBS in the non-GERD
community was only 5.1%. These data suggested strong
overlap between GERD and IBS and postulated that IBS
appears to be relatively uncommon in the absence of GERD.
The Prevalence of GERD in IBS
Several studies examining extra-colonic features of IBS
clearly demonstrated that these patients frequently report
typical GERD-related symptoms (see Table 2). The rela-
tionship between GERD and functional GIdisorders has been
primarily studied in IBS patients. The prevalence of GERD is
higher in IBS patients than what has been observed in the
general population and varies from 40 to 79% [2,16,22].
Smart et al. [22] assessed the nature and frequency of
gastroesophageal reflux symptoms in 25 patients with IBS.
Symptoms like heartburn, acid regurgitation, and dyspha-
gia were significantly more common in the IBS patients
than in an age- and sex-matched control group. Esophageal
symptoms were present daily in 28% and once a week in
52% of the IBS patients. Ambulatory 24-h esophageal pH
monitoring showed abnormal esophageal acid exposure in
50% of the IBS patients. This study also demonstrated that
significant reduction in lower esophageal sphincter pres-
sure accompanies irritable bowel syndrome, but no
disturbances of esophageal body motor activity could be
found. The results of this study provided clear confirmation
that esophageal symptoms are significantly more common
in IBS patients than in the general population [22].
In contrast, some authors showed that heartburn, which
is a common complaint in IBS, was reported by nearly a
third of the patients but is observed as frequently as in the
control group [23].
Talley et al. [8] enrolled consecutive patients with IBS,
who were classified according to their leading complaint
(constipation or diarrhea predominant). Overlap with
GERD-related symptoms was observed in 32.9% of the
IBS-constipation predominant and 40.9% of the IBS-diar-
rhea predominant patients. In another study, reflux
symptoms were found to be significantly higher in IBS
patients as compared with patients with inflammatory
bowel disease [15].
Recently, Cheung et al. [6] examined the association
between GERD and IBS in a Chinese population in Hong
Kong. The prevalence of IBS, according to Rome I criteria,
and GERD were 4% and 5%, respectively. These findings
were consistent with other studies in this region. Thirteen
percent of the subjects with GERD and 11% with IBS
suffered from both GERD and IBS. Gender did not have a
significant effect on the chances of having IBS or GERD,
but overlap of the two disorders occurred predominantly in
male subjects. In this study, younger subjects were also
more prone to having both IBS and GERD. The prevalence
of IBS has been shown to be higher in younger subjects in
the Chinese population as it was documented in Caucasians
and gradually decreases with age. In contrast, the preva-
lence of GERD increases with age. However, Agreus et al.
[10] found a different pattern in a sample of a Swedish
population. Over 7 years, they described the prevalence of
gastroesophageal reflux symptoms as stable, whereas IBS
increased over time independent of aging of the study
sample.
Hypothesis 1. IBS and GERD: Two Different Disorders
with a Common Pathophysiology
The first hypothesis proposes that IBS and GERD are two
distinct disorders that share a common pathophysiologic
process [24,25]. Consequently, each disorder requires
specific treatment, and one therapeutic intervention direc-
ted towards GERD or IBS will have limited effect on the
symptoms of the other disorder.
Recent studies in twins have suggested that there is
probably a distinct genetic contribution to the development
of IBS and GERD. Genetic modeling confirmed the inde-
pendent additive genetic effects in GERD and IBS [26].
Estimates for genetic variance were 22% for IBS and 13%
for GERD.
Some authors have postulated that IBS patients may
have motility disturbances similar to those seen in GERD
in the upper GI tract. Ineffective esophageal motility and
Table 2 The prevalence of
GERD in IBS
a
The maximum mean
prevalence
Sample size Prevalence of GERD (%) IBS definition
Smart et al. [22] 25 52 Manning
Whorwell et al. [23] 100 33 Authors determined
Talley et al. [8] 76 (constipation predominant) 32.9 Rome II
45 (diarrhea predominant) 40.9 Rome II
Cheung et al. [6] 79 11 Rome I
Nataskin et al. [21] Systematic review 39.3
a
–
Dig Dis Sci
123
impaired primary peristalsis have been suggested to be
contributing factors to the pathophysiology of GERD [27].
In IBS, alteration in colonic transit and small-bowel
motility are demonstrable. Thus, some authors speculated
that a general smooth-muscle dysfunction of the GI tract
may explain the close relationship between IBS and GERD
[28]. Smart et al. [22] performed esophageal manometry in
IBS subjects and demonstrated a significant reduction in
lower esophageal sphincter basal pressure, which could
explain GERD-related symptoms in these patients.
Several other studies suggested that GERD and IBS
overlap because of general visceral hyperalgesia [6,9,29,
30]. Visceral hyperalgesia, particularly rectal hyperalgesia,
has long been associated with IBS. Trimble et al. [31]
showed that IBS subjects had lower rectal sensory thresholds
for pain as compared with healthy controls and concomi-
tantly exhibited significantly lower sensory thresholds for
both perception and discomfort in the esophagus.
Another study by Costantini et al. [29] demonstrated
that IBS subjects have a significantly lower threshold for
esophageal symptoms during esophageal provocative test-
ing (bethanechol subcutaneously and balloon distension
test), but there was no difference in esophageal motility or
lower esophageal sphincter basal pressure when compared
with controls. The authors hypothesized that IBS subjects
do not have pathologic reflux but are rather more sensitive
to physiologic reflux.
Proton pump inhibitors (PPIs) provide the most effective
form of medical therapy for patients with GERD. Despite
this fact, it has been estimated that between 10 and 40% of
patients with GERD fail to respond or respond only partially
to standard-dose proton pump inhibitors [32]. Patients with
typical GERD symptoms including heartburn and regurgi-
tation are more likely to respond to PPI therapy than those
with extra-esophageal symptoms such asthma, hoarseness,
or cough. Additionally, patients with NERD are less likely
to respond to PPI therapy than those with erosive esopha-
gitis. The predictors of response to PPI therapy have only
been partially characterized. There are several putative
mechanisms for refractory GERD including weakly acidic
reflux, duodeno-gastroesophageal reflux, delayed gastric
emptying, psychologic comorbidity and concomitant func-
tional bowel disorders [33]. GERD patients who also had
IBS perceived their symptoms as more severe and tended
not to achieve the same degree of improvement in GERD
symptoms while treated with PPI as those without IBS.
Rubenstein et al. [30] found that esophageal hypersen-
sitivity is associated with features of psychiatric disorders
and IBS, which might partly explain the etiology of
heartburn symptoms that are refractory to PPI therapy. This
study suggested that visceral afferent hypersensitivity is a
general gastrointestinal phenomenon that is not limited to a
particular segment of the gastrointestinal tract.
Recently, Zimmerman and Hershcovici [9] estimated
the presence of IBS features in NERD patients. The authors
demonstrated that bowel symptoms were associated with
reflux symptom scores but not with esophageal acid
exposure. In this study, the presence of IBS features in a
large proportion of the NERD patients may further suggest
that visceral hypersensitivity could aggravate symptoms
resulting from the exposure of the esophageal mucosa to
acid. The findings of this study are in accordance with
previous observations about the association between vis-
ceral hypersensitivity and GERD.
Jung et al. [34] conducted a population-based cross-
sectional survey to determine the prevalence and risk fac-
tors for the overlap of GERD and IBS (as defined by Rome
III criteria). This study confirmed previous observations
that IBS and GERD occurred more commonly together
than expected by chance. The authors also revealed that
higher body mass index (BMI) is a predictor for increasing
IBS and GERD overlap. The authors identified specific
subgroups of people with both IBS and GERD. Self-
reported insomnia and frequent abdominal pain were risk
factors for IBS-GERD overlap as compared with IBS alone
and GERD alone.
Nojkov et al. [35] evaluated the influence of comorbid
IBS and psychologic distress on the response to PPI ther-
apy of patients with GERD. Patients with IBS reported
more severe GERD symptoms at baseline but experienced
a similar magnitude of improvement in GERD symptoms
as compared to patients without IBS while on PPI therapy.
The authors found that comorbid IBS and psychologic
distress, but not the presence or absence of erosive
esophagitis, influenced symptom perception and disease-
specific quality of life before and after PPI therapy.
Hypothesis 2. IBS-Like Symptoms Are Part of GERD
Manifestations
Some studies suggest that IBS-like symptoms are part of
the symptom spectrum of GERD and can represent an
extra-esophageal, but GI-related, manifestation of GERD
[20,36]. Evidence to support this hypothesis originates
from therapeutic trials in GERD patients. In these studies,
lower abdominal symptoms, suggestive of IBS, signifi-
cantly improved after medical or surgical anti-reflux
treatment. In one study, up to 24% of patients with GERD
reported a significant or complete improvement of their
bowel symptoms following acid suppressive therapy,
mainly proton pump inhibitors [20]. In another study, 30%
of GERD patients who underwent laparoscopic fundopli-
cation were found to have IBS using Rome II criteria and,
of those, 81% reported significant improvement of their
IBS symptoms postoperatively [36].
Dig Dis Sci
123
Kountouras et al. [37] demonstrated that 41% of
patients with GERD and IBS reported complete resolution
of their IBS symptoms after receiving esomeprazole
20 mg daily for 3 months. However, the results of this
study should be interpreted cautiously because of lack of
a placebo arm.
The underlying pathophysiologic mechanism that
explains how gastroesophageal reflux can cause IBS-like
symptoms has yet to be elucidated. It is likely that the
recently growing interest in the full spectrum of GERD
symptoms, which includes atypical and extra-esophageal
manifestations as well as sleep abnormalities, has led to the
recognition that lower abdominal complaints may also be
encountered in patients with GERD.
Additional support for the concept that GERD is a more
systemic disorder than is currently accepted was provided
by the recently introduced GERD questionnaire, the
ReQuest (Nycomed; Constance, Germany). The developers
of the ReQuest incorporated lower GI complaints sugges-
tive of IBS into the questionnaire after demonstrating that
patients and physicians perceive that these symptoms are
part of the symptom spectrum of GERD [38]. Therapeutic
studies that used the ReQuest as an evaluative tool clearly
demonstrated a significant reduction in lower abdomen and
dyspepsia-like symptoms in response to proton pump
inhibitor (PPI) therapy. [39–41].
Summary
Studies clearly demonstrate that GERD is prevalent in IBS
patients and vice versa. The reason for this close rela-
tionship between the two disorders remains unknown.
Presently, there are two leading hypotheses that attempt to
explain this relationship. The first suggests that IBS-like
symptoms are part of the spectrum of GERD manifesta-
tions. The other suggests that IBS and GERD are two
different disorders with a similar underlying pathophysi-
ology. Both hypotheses need to be further evaluated.
Acknowledgments The authors wish to acknowledge the grant
support from AstraZeneca, Eisai, TAP, and Vecta.
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