GERD-Q and Other Diagnostic Tools for GERD Diagnosis
GERD-Q and Other Diagnostic Tools for GERD Diagnosis
Gontar Alamsyah Siregar
Professor, Division of Gastroentero-Hepatology, Department of Internal Medicine, Faculty of
Medicine, University of Sumatera Utara
Introduction
Reflux of gastric contents to the oesophagus is a physiological event: a healthy person typically
has reflux episodes. Gastro-oesophageal reflux disease is defined as reflux
that
causes
troublesome symptoms, mucosal injury in the oesophagus, or both of these. By this
definition, oesophageal lesions (erosions, ulceration, intestinal metaplasia) are not needed for a
diagnosis of the disease. 1 GERD can be further classified as the presence of symptoms without
erosions on endoscopic examination (non-erosive disease or NERD) or GERD symptoms with
erosions present (ERD). 2
In developed countries, the prevalence of gastrooesophageal reflux disease (defined by symptoms
of heartburn, acid regurgitation, or both, at least once a week) is 10–20%, whereas in Asia the
prevalence is roughly less than 5%. In the USA, this disease is the most common gastrointestinal
diagnosis to prompt an outpatient clinic visit (8·9 million visits in 2009). The rising prevalence
of gastro-oesophageal reflux disease seems to be related to the rapidly increasing prevalence of
obesity.
1
Until now, Indonesia has no complete epidemiological data on this condition. The
available data is a report from a study conducted by Lelosutan SAR et al in Faculty of Medicine,
University of Indonesia, Cipto Mangunkusumo Hospital, Jakarta (FKUI/RSCM-Jakarta), which
demonstrates that of 127 study subjects who underwent upper gastrointestinal endoscopy,
22.8% (30 subjects of them) had esophagitis. Another study conducted by Syam AF et al., which
is also from RSCM/FKUI-Jakarta, shows that of 1718 patients who underwent upper
gastrointestinal endoscopy on indication of dyspepsia for 5 years (1997-2002), there is an
increased prevalence of esophagitis, from 5.7% in 1997 to 25.18% in 2002 (mean value of
13.13% per year). 3
Universitas Sumatera Utara
Pathophysiology GERD
Transient lower oesophageal sphincter relaxations (TLESRs)
Many GERD patients have a normal LES resting tone and do not have hiatal hernia, therefore the
abnormal gastro-oesophageal reflux in these subjects is explained by an alternative theory. In
fact, studies in healthy volunteers have identified reflux episodes during sleep and the
postprandial period that are due to an increased number of inappropriate LES relaxations.
TLESRs are brief episodes of LES relaxation unrelated to swallowing or peristalsis.
Neurophysiology studies indicate that TLESRs are visceral reflexes with vagal afferent and
efferent pathways that transmit information to and from the dorsal nucleus of the vagus. Gastric
distension, by stimulation of proximal gastric tension and stretch receptors, has been recognized
as a major factor inducing TLESRs. 4
In normal subjects, gastro-oesophageal reflux occurs only during TLESRs and swallow-induced
LES relaxations, whereas in patients with GERD, TLESRs account for 48-73% of reflux
episodes: thus TLESRs account for the majority of gastro-oesophageal reflux episodes. Patients
with GERD have an equal frequency of TLESRs compared with normal individuals, although
they have a higher percentage of TLESRs associated with reflux. Like LES resting pressure, the
frequency of TLESRs is influenced by foods (fat, chocolate, etc.), alcohol and smoking. 4
Ineffective esophageal motility
Impaired esophageal clearance can be caused by IEM, such as ineffective peristalsis or failed
peristalsis. In 2001, using conventional manometry, IEM was defined as distal esophageal
hypocontractility in ≥ 30% of wet swallows, characterized either as contraction amplitude < 30
mmHg in the distal esophagus, 3 and 8 cm above the LES, or as peristaltic waves that are not
Universitas Sumatera Utara
propagated to the distal esophagus, or absent peristalsis. Hypocontractility is considered the most
prevalent esophageal motor disorder in GERD and this concept has been further supported by
different studies showing that esophageal peristaltic dysfunction was increasingly prevalent with
more severe GERD presentation. Of note, in a group of patients with respiratory symptoms
associated with reflux, IEM was found in 53% of asthmatics, 41% of chronic coughers and 31%
of those with laryngitis. 5
Recently, studies carried out in patients with scleroderma, who are characterized by failed or
absent peristalsis and low basal LES pressure, observed that these patients are frequently affected
by GERD and its complications, thus substantiating the relevant role of esophageal clearance for
the development of GERD. 5
Delayed gastric emptying
It has long been held that delay in gastric emptying results in the extended retention of acidified
gastric contents in the stomach during the postprandial period. This availability of material in the
stomach to reflux may increase the likelihood of GERD. However, the literature has been quite
variable with regard to the potential contribution of gastric emptying in the predisposition to
reflux. Some authors have claimed that as many as 40% of patients with reflux disease ha ve
delayed gastric emptying, but others have cited rates as low as 6%. A recent study demonstrated
that variability in research methodologies accounted for these differences. Using recently
established international control values for scintigraphic gastric emptying assessment, the
investigators were able to standardize the measurement for gastric emptying and revealed that
33% of patients with GERD had intragastric contents greater than the 95 th percentile at 120 min
postprandially and that 26% had abnormal results at 240 min postprandially. It was also shown
Universitas Sumatera Utara
that gastrointestinal symptoms, including dyspepsia and regurgitation, occurred in many patients.
These symptoms were not predictive of delayed gastric emptying. 6
Patients frequently complain of heartburn as well as postprandial dyspepsia or epigastric
discomfort, and it is often difficult for patients to discriminate between these responses. It is
currently believed that delayed gastric emptying contributes to the pathogenesis of GERD in a
small proportion of patients, primarily by increasing available amounts of refluxate and causing
gastric distension. The effects of gastric distension were investigated in a study by inflating an
intragastric balloon in patients with GERD and controls. In both groups of patients, gastric
distension significantly increased the rate of TLESRs, indicating that GERD-associated gastric
distension may be a factor in postprandial GERD. 6
Increased intragastric pressure
Abnormal gastric emptying might contribute to GERD by increasing intra-gastric pressure.
Patients with suspected abnormal gastric emptying should be tested with nuclear markers or
ultrasound. If slow emptying is diagnosed, appropriate therapy should be considered. Medication
such as metoclopramide and Nissen fundoplication improve gastric emptying. 7
There is also strong evidence of a possible link between obesity and GERD. Specifically, it has
been shown that there is a dose-response relationship between increasing body mass index (BMI)
and prevalence of GERD and its complications. Some studies have reported that morbidly obese
patients with GERD have a higher incidence of incompetent LES, transient LES relaxation and
impaired esophageal motility than non-obese patients with GERD. However, a detailed
mathematical analysis has shown that the severity of GERD (based on the DeMeester score) is
associated with BMI, which suggests that obesity plays an independent role in the
pathophysiology GERD, mainly through increased abdominal pressure. 7
Universitas Sumatera Utara
The association of different pulmonary diseases and GERD has recently gained renewed interest.
It has been shown that patients with end-stage lung disease have a high prevalence of GERD; up
to 70%. Although in these patients pan-esophageal motor dysfunction is frequently found, a
more negative thoracic pressure with an increase in the gradient between intra-gastric and intrathoracic pressure might also contribute. 7
Acid pocket
Most meals have a buff ering eff ect that leads to reduced acidity of the stomach in the
postprandial phase. However, acid reflux (as detected by pH monitoring) is generally most
pronounced after meals. In the postprandial period, a layer of unbuff ered acidic gastric juice sits
on top of the meal, close to the cardia, ready to reflux. This occurrence has become known as the
acid pocket and is facilitated by an absence of peristaltic contractions in the proximal stomach. In
patients with gastro-oesophageal reflux disease, the acid pocket is located more proximally with
respect
to
the
manometrically
squamocolumnar
defined lower
junction,
oesophageal
and
it could
even
extend
above
the
sphincter. Treatment with alginate-antacid
preparations abolishes the pocket or increases the distance between the upper border of the acid
pocket and the squamo columnar junction. 1
Oesophageal hypersensitivity
In a subgroup of patients with gastro-oesophageal reflux disease, reflux symptoms are noted
while oesophageal acid exposure is within the normal range; thus, these individuals are
hypersensitive to acid. Hypersensitivity to acid occurs both in people with erosive oesophagitis
and in those with a macroscopically normal mucosa. Experiments in which acid is infused in the
oesophagus indicate that the threshold to development of heartburn and pain is lower in patients
with either erosive oesophagitis or non-erosive reflux disease than in controls. Factors
contributing to the noted increased oesophageal sensitivity are impaired mucosal barrier
function, upregulation of peripheral nociceptors, and central sensitisation. 1
Helicobacter pylori
Universitas Sumatera Utara
Helicobacter pylori does not have an important role in the pathogenesis of gastro-oesophageal
reflux disease. Eradication of the microorganism does not lead to an increased chance of
development of the disorder. 1
Figure 1. Pathophysiology og gastro-oesophageal reflux disease 1
Diagnosis
Careful history taking is the main method to establish GERD diagnosis. Specific symptom of
GERD is heartburn and/or regurgitation that occur after meal. However, it should be emphasized
that most of diagnostic studies of heartburn and regurgitation symptoms are performed in
Caucasian population. In Asia, the symptoms of heartburn and regurgitation are not the typical
features for GERD. However, the experts have agreed that both symptoms are characteristics for
GERD. 3
GERD-Q
GERD Questionnaire (GERD-Q) an instrument of questionnaire developed to assist establishing
the diagnosis of GERD and measuring response to therapy. The questionnaire is developed based
on clinical data and information obtained from high-quality clinical studies as well as from
qualitative interviews with patients in order to evaluate the simplicity of filling up the
questionnaire. GERD questionnaire is a combination of validated questionnaires used in the
DIAMOND study. Improved accuracy of diagnosis by combining several validated questionnaire
Universitas Sumatera Utara
will increase the sensitivity and specificity of diagnosis. An analysis on more than 300 patients at
a primary health care service demonstrates that GERD-Q may provide sensitivity and specificity
of 65% and 71%, which is similar to results obtained by gastroenterologists. Moreover, GERDQ also shows the capacity to evaluate relative impacts of GERD on patients’ life and to provide
assistance in selecting therapy. Table 1 is the GERD-Q that can be filled up by the patients
themselves.
For each question, respondent should fill up according to the frequency of
symptoms that they have experienced in a week. Score 8 or more is the recommended cut-off
point to detect individuals with high tendency to have GERD. GERD-Q has been validated in
Indonesia. A symptom-based approach using GERD-Q reduced health care costs without loss in
efficacy. GERD-Q score or PPI test alone cannot accurately diagnose. A definitive diagnosis of
GERD still depends on endoscopy or 24-h pH monitoring. 3, 8, 9, 10
Table 1. The GERD-Q in Indonesian Language 11
PPI Test
PPI test can be performed to establish the diagnosis in patients with typical symptoms and
without alarm signs or risk for Barret’s esophagus. The test is carried out by administering
double-dose PPI for 1-2 weeks without the preceding endoscopy examination. If the symptoms
subside with PPI administration and recur when the PPI treatment is stopped, then the diagnosis
of GERD can be made. The test is considered as positive result, if there is clinical improvement
of more than 50% in 1 week. A meta-analysis study demonstrates that PPI test has a sensitivity
Universitas Sumatera Utara
of 80% and specificity of 74% for establishing diagnosis of GERD patients with non-cardiac
chest pain. It indicates that PPI test can be considered as a useful strategy and probably has
economic value in management of patients with non-cardiac chest pain without alarm signs of
suspected esophageal abnormalities. 3
Upper Gastrointestinal Endoscopy
Upper gastrointestinal endoscopy (UGIE) is considered the gold standard for establishing the
diagnosis GERD with erosive esophagitis. Using the UGIE, we can find the mucosal break of
esophagus. 3 People who present with alarm symptoms (dysphagia, haematemesis, weight loss)
warrant endoscopy, because they might have clinically significant complications of gastrooesophageal reflux disease or other pathological features. For example, the test serves to rule
out alternative diagnoses, such as eosinophilic oesophagitis, infection, and pill injury;
furthermore, an observation of typical reflux oesophagitis confirms the diagnosis of gastrooesophageal reflux disease. The severity of endoscopically observed reflux oesophagitis is
graded with the Los Angeles classification. 1
Figure 2. Los Angles classification of reflux oesopahgitis 1
In grade A oesophagitis, endoscopic abnormalities are restricted to one or more mucosal lesions with a maximum
length of 5 mm. In grade B, one or more mucosal breaks are present, with a maximum length of more than 5 mm but
non-continuous across mucosal folds. In grade C oesophagitis, mucosal breaks are continuous between at least two
mucosal folds, but less than 75% of oesophageal circumference is involved. In grade D, mucosal breaks encompass
more than 75% of oesophageal circumference. 1
Ambulatory reflux monitoring
Universitas Sumatera Utara
Conventionally, pH monitoring is done with a transnasally inserted catheter with pH sensor,
which is connected to a portable data logger. Every time acid reflux happens a drop in pH is
recorded. These measurements are usually taken for 24 h, a period in which the patient is
ambulatory and in his own environment. Alternatively, a wireless system can be used, 47
whereby a radio transmitter capsule with pH sensor is attached to the oesophageal wall. The
advantage of this technique is that no discomfort is caused by the presence of the nasooesophageal catheter and prolonged measurement can be done. However, the wireless pH
capsules are roughly double the cost of a standard pH catheter. 1
Manometry
Oesophageal manometry is not indicated for diagnosis of gastro-oesophageal reflux disease
because motor dysfunction associated with abnormal reflux is non-specific. The main
indications for manometry are to ascertain the correct position for pH electrode placement and
to exclude severe oesophageal motility disorders such as achalasia and absent peristalsis
before antireflux surgery. Exclusion of other oesophageal disorders is important, because
patients with achalasia can present with heartburn and regurgitation, which could lead to an
erroneous diagnosis of gastro-oesophageal reflux disease. However, whether milder forms of
peristaltic dysfunction predict postoperative dysphagia is uncertain. Manometry
might
be
helpful in patients with predominant regurgitation because it can help to distinguish the
rumination
syndrome
from
gastro-oesophageal
reflux
disease.
This diagnosis is best
accomplished with concurrent pH and impedance monitoring. 1
References
1. Bredenoord AJ, Pandolfino JE, Smout AJPM. Gasto-oesophageal reflux disease. The Lancet. March
2013.
2. Katzs PO, Gerson LB, Vela F. Guidelines for the Diagnosis and Management of Gastroesophageal
Reflux Disease. Am J Gastroenterol. 2013;108:308-328.
3. Gastroenterology TISo. National Consensus on the Management of Gastroesophageal Reflux Disease
in Indonesia. Indones J Intern Med. July 2014;46(3):263-271.
Universitas Sumatera Utara
4. Giorgi F, Palmiero M, Esposito I, al e. Pathophysiology of gastro-oesophageal reflux disease. Acta
Otorhinolaryngol ital. 2006;26(5):241-246.
5. Martinucci I, Bortoli N, Giacchino M, al e. Esophageal motility abnormalities in gastroesophageal
reflux disease. World J Gastrointest Pharmacol Ther. 2014;5(2):86-96.
6. Castell D, Murray J, Tutuian R, al e. Review article: the pathophysiology of gastro-oesophageal reflux
disease − oesophageal manifestations. Alimentary Pharmacology & Therapeutics. 2004;20:14-25.
7. Herbella F, Patti M. Gastroesophageal reflux disease: From pathophysiology to treatment. World J
Gastroenterol. 2010;16(30):3745-49.
8. Bai Y, Du Y, Zou D, et al. Gastroesophageal Reflux Disease Questionnaire (GerdQ) in real-world
practice: A national multicenter surve 8065 patients. Journal of Gastroenterology and Hepatology.
2013:626-631.
9. Jonasson C, Moum B, Bang C, Andersen KR, Hatlebakk JG. Randomised clinical trial: a comparison
between a GerdQ-based algorithm and an endoscopy-based approach for the diagnosis and initial
treatment of GERD. Aliment Pharmacol Ther. 2012;35:1290-1300.
10. ZHOU LY, WANG Y, LU JJ, LIN L. Accuracy of diagnosing gastroesophageal reflux disease by GerdQ,
esophageal impedance monitoring and histology. Journal of Digestive Diseases. 2014(15):230-238.
11. Simadibrata M, Rani A, Adi P, Djumhana A, Abdullah M. The gastro-esophageal reflux disease
questionnaire using Indonesian language: a language validation survey. Med J Indones. May
2011;20:125-130.
Universitas Sumatera Utara
Gontar Alamsyah Siregar
Professor, Division of Gastroentero-Hepatology, Department of Internal Medicine, Faculty of
Medicine, University of Sumatera Utara
Introduction
Reflux of gastric contents to the oesophagus is a physiological event: a healthy person typically
has reflux episodes. Gastro-oesophageal reflux disease is defined as reflux
that
causes
troublesome symptoms, mucosal injury in the oesophagus, or both of these. By this
definition, oesophageal lesions (erosions, ulceration, intestinal metaplasia) are not needed for a
diagnosis of the disease. 1 GERD can be further classified as the presence of symptoms without
erosions on endoscopic examination (non-erosive disease or NERD) or GERD symptoms with
erosions present (ERD). 2
In developed countries, the prevalence of gastrooesophageal reflux disease (defined by symptoms
of heartburn, acid regurgitation, or both, at least once a week) is 10–20%, whereas in Asia the
prevalence is roughly less than 5%. In the USA, this disease is the most common gastrointestinal
diagnosis to prompt an outpatient clinic visit (8·9 million visits in 2009). The rising prevalence
of gastro-oesophageal reflux disease seems to be related to the rapidly increasing prevalence of
obesity.
1
Until now, Indonesia has no complete epidemiological data on this condition. The
available data is a report from a study conducted by Lelosutan SAR et al in Faculty of Medicine,
University of Indonesia, Cipto Mangunkusumo Hospital, Jakarta (FKUI/RSCM-Jakarta), which
demonstrates that of 127 study subjects who underwent upper gastrointestinal endoscopy,
22.8% (30 subjects of them) had esophagitis. Another study conducted by Syam AF et al., which
is also from RSCM/FKUI-Jakarta, shows that of 1718 patients who underwent upper
gastrointestinal endoscopy on indication of dyspepsia for 5 years (1997-2002), there is an
increased prevalence of esophagitis, from 5.7% in 1997 to 25.18% in 2002 (mean value of
13.13% per year). 3
Universitas Sumatera Utara
Pathophysiology GERD
Transient lower oesophageal sphincter relaxations (TLESRs)
Many GERD patients have a normal LES resting tone and do not have hiatal hernia, therefore the
abnormal gastro-oesophageal reflux in these subjects is explained by an alternative theory. In
fact, studies in healthy volunteers have identified reflux episodes during sleep and the
postprandial period that are due to an increased number of inappropriate LES relaxations.
TLESRs are brief episodes of LES relaxation unrelated to swallowing or peristalsis.
Neurophysiology studies indicate that TLESRs are visceral reflexes with vagal afferent and
efferent pathways that transmit information to and from the dorsal nucleus of the vagus. Gastric
distension, by stimulation of proximal gastric tension and stretch receptors, has been recognized
as a major factor inducing TLESRs. 4
In normal subjects, gastro-oesophageal reflux occurs only during TLESRs and swallow-induced
LES relaxations, whereas in patients with GERD, TLESRs account for 48-73% of reflux
episodes: thus TLESRs account for the majority of gastro-oesophageal reflux episodes. Patients
with GERD have an equal frequency of TLESRs compared with normal individuals, although
they have a higher percentage of TLESRs associated with reflux. Like LES resting pressure, the
frequency of TLESRs is influenced by foods (fat, chocolate, etc.), alcohol and smoking. 4
Ineffective esophageal motility
Impaired esophageal clearance can be caused by IEM, such as ineffective peristalsis or failed
peristalsis. In 2001, using conventional manometry, IEM was defined as distal esophageal
hypocontractility in ≥ 30% of wet swallows, characterized either as contraction amplitude < 30
mmHg in the distal esophagus, 3 and 8 cm above the LES, or as peristaltic waves that are not
Universitas Sumatera Utara
propagated to the distal esophagus, or absent peristalsis. Hypocontractility is considered the most
prevalent esophageal motor disorder in GERD and this concept has been further supported by
different studies showing that esophageal peristaltic dysfunction was increasingly prevalent with
more severe GERD presentation. Of note, in a group of patients with respiratory symptoms
associated with reflux, IEM was found in 53% of asthmatics, 41% of chronic coughers and 31%
of those with laryngitis. 5
Recently, studies carried out in patients with scleroderma, who are characterized by failed or
absent peristalsis and low basal LES pressure, observed that these patients are frequently affected
by GERD and its complications, thus substantiating the relevant role of esophageal clearance for
the development of GERD. 5
Delayed gastric emptying
It has long been held that delay in gastric emptying results in the extended retention of acidified
gastric contents in the stomach during the postprandial period. This availability of material in the
stomach to reflux may increase the likelihood of GERD. However, the literature has been quite
variable with regard to the potential contribution of gastric emptying in the predisposition to
reflux. Some authors have claimed that as many as 40% of patients with reflux disease ha ve
delayed gastric emptying, but others have cited rates as low as 6%. A recent study demonstrated
that variability in research methodologies accounted for these differences. Using recently
established international control values for scintigraphic gastric emptying assessment, the
investigators were able to standardize the measurement for gastric emptying and revealed that
33% of patients with GERD had intragastric contents greater than the 95 th percentile at 120 min
postprandially and that 26% had abnormal results at 240 min postprandially. It was also shown
Universitas Sumatera Utara
that gastrointestinal symptoms, including dyspepsia and regurgitation, occurred in many patients.
These symptoms were not predictive of delayed gastric emptying. 6
Patients frequently complain of heartburn as well as postprandial dyspepsia or epigastric
discomfort, and it is often difficult for patients to discriminate between these responses. It is
currently believed that delayed gastric emptying contributes to the pathogenesis of GERD in a
small proportion of patients, primarily by increasing available amounts of refluxate and causing
gastric distension. The effects of gastric distension were investigated in a study by inflating an
intragastric balloon in patients with GERD and controls. In both groups of patients, gastric
distension significantly increased the rate of TLESRs, indicating that GERD-associated gastric
distension may be a factor in postprandial GERD. 6
Increased intragastric pressure
Abnormal gastric emptying might contribute to GERD by increasing intra-gastric pressure.
Patients with suspected abnormal gastric emptying should be tested with nuclear markers or
ultrasound. If slow emptying is diagnosed, appropriate therapy should be considered. Medication
such as metoclopramide and Nissen fundoplication improve gastric emptying. 7
There is also strong evidence of a possible link between obesity and GERD. Specifically, it has
been shown that there is a dose-response relationship between increasing body mass index (BMI)
and prevalence of GERD and its complications. Some studies have reported that morbidly obese
patients with GERD have a higher incidence of incompetent LES, transient LES relaxation and
impaired esophageal motility than non-obese patients with GERD. However, a detailed
mathematical analysis has shown that the severity of GERD (based on the DeMeester score) is
associated with BMI, which suggests that obesity plays an independent role in the
pathophysiology GERD, mainly through increased abdominal pressure. 7
Universitas Sumatera Utara
The association of different pulmonary diseases and GERD has recently gained renewed interest.
It has been shown that patients with end-stage lung disease have a high prevalence of GERD; up
to 70%. Although in these patients pan-esophageal motor dysfunction is frequently found, a
more negative thoracic pressure with an increase in the gradient between intra-gastric and intrathoracic pressure might also contribute. 7
Acid pocket
Most meals have a buff ering eff ect that leads to reduced acidity of the stomach in the
postprandial phase. However, acid reflux (as detected by pH monitoring) is generally most
pronounced after meals. In the postprandial period, a layer of unbuff ered acidic gastric juice sits
on top of the meal, close to the cardia, ready to reflux. This occurrence has become known as the
acid pocket and is facilitated by an absence of peristaltic contractions in the proximal stomach. In
patients with gastro-oesophageal reflux disease, the acid pocket is located more proximally with
respect
to
the
manometrically
squamocolumnar
defined lower
junction,
oesophageal
and
it could
even
extend
above
the
sphincter. Treatment with alginate-antacid
preparations abolishes the pocket or increases the distance between the upper border of the acid
pocket and the squamo columnar junction. 1
Oesophageal hypersensitivity
In a subgroup of patients with gastro-oesophageal reflux disease, reflux symptoms are noted
while oesophageal acid exposure is within the normal range; thus, these individuals are
hypersensitive to acid. Hypersensitivity to acid occurs both in people with erosive oesophagitis
and in those with a macroscopically normal mucosa. Experiments in which acid is infused in the
oesophagus indicate that the threshold to development of heartburn and pain is lower in patients
with either erosive oesophagitis or non-erosive reflux disease than in controls. Factors
contributing to the noted increased oesophageal sensitivity are impaired mucosal barrier
function, upregulation of peripheral nociceptors, and central sensitisation. 1
Helicobacter pylori
Universitas Sumatera Utara
Helicobacter pylori does not have an important role in the pathogenesis of gastro-oesophageal
reflux disease. Eradication of the microorganism does not lead to an increased chance of
development of the disorder. 1
Figure 1. Pathophysiology og gastro-oesophageal reflux disease 1
Diagnosis
Careful history taking is the main method to establish GERD diagnosis. Specific symptom of
GERD is heartburn and/or regurgitation that occur after meal. However, it should be emphasized
that most of diagnostic studies of heartburn and regurgitation symptoms are performed in
Caucasian population. In Asia, the symptoms of heartburn and regurgitation are not the typical
features for GERD. However, the experts have agreed that both symptoms are characteristics for
GERD. 3
GERD-Q
GERD Questionnaire (GERD-Q) an instrument of questionnaire developed to assist establishing
the diagnosis of GERD and measuring response to therapy. The questionnaire is developed based
on clinical data and information obtained from high-quality clinical studies as well as from
qualitative interviews with patients in order to evaluate the simplicity of filling up the
questionnaire. GERD questionnaire is a combination of validated questionnaires used in the
DIAMOND study. Improved accuracy of diagnosis by combining several validated questionnaire
Universitas Sumatera Utara
will increase the sensitivity and specificity of diagnosis. An analysis on more than 300 patients at
a primary health care service demonstrates that GERD-Q may provide sensitivity and specificity
of 65% and 71%, which is similar to results obtained by gastroenterologists. Moreover, GERDQ also shows the capacity to evaluate relative impacts of GERD on patients’ life and to provide
assistance in selecting therapy. Table 1 is the GERD-Q that can be filled up by the patients
themselves.
For each question, respondent should fill up according to the frequency of
symptoms that they have experienced in a week. Score 8 or more is the recommended cut-off
point to detect individuals with high tendency to have GERD. GERD-Q has been validated in
Indonesia. A symptom-based approach using GERD-Q reduced health care costs without loss in
efficacy. GERD-Q score or PPI test alone cannot accurately diagnose. A definitive diagnosis of
GERD still depends on endoscopy or 24-h pH monitoring. 3, 8, 9, 10
Table 1. The GERD-Q in Indonesian Language 11
PPI Test
PPI test can be performed to establish the diagnosis in patients with typical symptoms and
without alarm signs or risk for Barret’s esophagus. The test is carried out by administering
double-dose PPI for 1-2 weeks without the preceding endoscopy examination. If the symptoms
subside with PPI administration and recur when the PPI treatment is stopped, then the diagnosis
of GERD can be made. The test is considered as positive result, if there is clinical improvement
of more than 50% in 1 week. A meta-analysis study demonstrates that PPI test has a sensitivity
Universitas Sumatera Utara
of 80% and specificity of 74% for establishing diagnosis of GERD patients with non-cardiac
chest pain. It indicates that PPI test can be considered as a useful strategy and probably has
economic value in management of patients with non-cardiac chest pain without alarm signs of
suspected esophageal abnormalities. 3
Upper Gastrointestinal Endoscopy
Upper gastrointestinal endoscopy (UGIE) is considered the gold standard for establishing the
diagnosis GERD with erosive esophagitis. Using the UGIE, we can find the mucosal break of
esophagus. 3 People who present with alarm symptoms (dysphagia, haematemesis, weight loss)
warrant endoscopy, because they might have clinically significant complications of gastrooesophageal reflux disease or other pathological features. For example, the test serves to rule
out alternative diagnoses, such as eosinophilic oesophagitis, infection, and pill injury;
furthermore, an observation of typical reflux oesophagitis confirms the diagnosis of gastrooesophageal reflux disease. The severity of endoscopically observed reflux oesophagitis is
graded with the Los Angeles classification. 1
Figure 2. Los Angles classification of reflux oesopahgitis 1
In grade A oesophagitis, endoscopic abnormalities are restricted to one or more mucosal lesions with a maximum
length of 5 mm. In grade B, one or more mucosal breaks are present, with a maximum length of more than 5 mm but
non-continuous across mucosal folds. In grade C oesophagitis, mucosal breaks are continuous between at least two
mucosal folds, but less than 75% of oesophageal circumference is involved. In grade D, mucosal breaks encompass
more than 75% of oesophageal circumference. 1
Ambulatory reflux monitoring
Universitas Sumatera Utara
Conventionally, pH monitoring is done with a transnasally inserted catheter with pH sensor,
which is connected to a portable data logger. Every time acid reflux happens a drop in pH is
recorded. These measurements are usually taken for 24 h, a period in which the patient is
ambulatory and in his own environment. Alternatively, a wireless system can be used, 47
whereby a radio transmitter capsule with pH sensor is attached to the oesophageal wall. The
advantage of this technique is that no discomfort is caused by the presence of the nasooesophageal catheter and prolonged measurement can be done. However, the wireless pH
capsules are roughly double the cost of a standard pH catheter. 1
Manometry
Oesophageal manometry is not indicated for diagnosis of gastro-oesophageal reflux disease
because motor dysfunction associated with abnormal reflux is non-specific. The main
indications for manometry are to ascertain the correct position for pH electrode placement and
to exclude severe oesophageal motility disorders such as achalasia and absent peristalsis
before antireflux surgery. Exclusion of other oesophageal disorders is important, because
patients with achalasia can present with heartburn and regurgitation, which could lead to an
erroneous diagnosis of gastro-oesophageal reflux disease. However, whether milder forms of
peristaltic dysfunction predict postoperative dysphagia is uncertain. Manometry
might
be
helpful in patients with predominant regurgitation because it can help to distinguish the
rumination
syndrome
from
gastro-oesophageal
reflux
disease.
This diagnosis is best
accomplished with concurrent pH and impedance monitoring. 1
References
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Universitas Sumatera Utara
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Universitas Sumatera Utara