Eur Arch Otorhinolaryngol (2012) 269:1189–1194
DOI 10.1007/s00405-011-1905-3
LARYNGOLOGY
Risk factors for laryngopharyngeal reXux
Murat Saruç · Elif Ayanoglu Aksoy · Eser Vardereli ·
Mehmet Karaaslan · Bahattin Çiçek · Ümit Ãnce ·
Ferhan Öz · Nurdan Tözün
Received: 2 September 2011 / Accepted: 20 December 2011 / Published online: 30 December 2011
© Springer-Verlag 2011
Abstract The aim of this study was to evaluate the demo-
graphic and clinicopathologic characteristics of gastro-
esophageal reXux disease (GERD) with and without
laryngopharyngeal reXux (LPR) to determine the risk fac-
tors for the occurrence of LPR in patients with GERD. This
is a retrospective study of GERD patients with and without
LPR. From the outpatient computer program of our hospital
we randomly enrolled 45 GERD patients with LPR into the
Wrst group and another 45 GERD patients without LPR to
the second group. Medical records of the patients in both
groups were examined. All patients underwent upper
This research results have been presented on European laryngological
Society (ELS) and American Bronchoesophagological Association
Workshop on Laryngopharyngeal ReXux and Swallowing Disorders in
Antalya, Turkey 24–26 May, 2007.
M. Saruç · E. Vardereli · B. Çiçek · N. Tözün
Gastroenterology Division, Acibadem University School
of Medicine, Istanbul, Turkey
E. A. Aksoy (&)
Otorhinolaryngology Head and Neck Surgery Department,
Acibadem University School of Medicine, Maslak Hospital,
ATASEHIR 38 ADA SEDEF CAD ATA ¾ D 229 KADIKOY,
3758 Istanbul, Turkey
e-mail: elifayanoglu@yahoo.com
M. Karaaslan
Internal Medicine Department, Acibadem University School
of Medicine, Istanbul, Turkey
F. Öz
Otorhinolaryngology Head and Neck Surgery Department,
Acibadem Health Care Group, Bakirkoy Hospital,
Istanbul, Turkey
Ü. Ãnce
Pathology Department, Acibadem University School
of Medicine, Istanbul, Turkey
gastrointestinal system endoscopy. LPR was conWrmed by
laryngoscopy, and LPR-related laryngoscopy scoring. Non-
erosive GERD (NERD), erosive GERD (ERD) and Bar-
rett’s esophagus (BE) were diagnosed by endoscopy and
histopathology. Various clinical parameters including sta-
tus of Helicobacter pylori (H. pylori) infection, topography
of gastritis were analyzed. For therapy, lansoprazole in a
dosage of 30 mg BID for at least 8 weeks were given to all
patients in both groups. GERD patients with and without
LPR were compared according to demographic, clinic,
endoscopic and histopathological parameters. The results
revealed that patients with LPR were younger than
the patients without LPR (38.7 § 10.2 years and
43.8 § 11.5 years; p = 0.08); however, there was no statis-
tical signiWcance. Patients without LPR showed no gender
predilection (55% male) while LPR patients showed male
preponderance (71% male). In LPR group, 11 patients
(24%) had NERD, while 28 (62%) and 6 (13%) patients
had ERD and BE, respectively. Twenty-seven (60%)
patients without LPR were diagnosed as NERD, 15 patients
(33%) without LPR had ERD and only 3 patients (6.6%)
showed the histological Wndings of BE. The patients in
LPR group had higher body mass index. Hiatal hernia was
more frequent in the patients with LPR (53%) than in the
patients without LPR (24%) (p = 0.005). LPR patients had
longer duration of reXux symptoms than the patients with-
out LPR (p = 0.04). H. pylori status was not diVerent in
both groups but the patients without LPR had more corpus
gastritis than the patients with LPR. Eight weeks of lansop-
razole treatment was successful in 71% of patients with
LPR, and 86% of patients without LPR. We concluded that
male gender, hiatal hernia, longer duration of symptoms,
high BMI, having ERD and BE seems as risk factors for the
occurrence of LPR in patients with GERD. H. pylori status
did not have any eVect on the development of LPR. Corpus
123
1190
dominant gastritis may have a protective role against the
development of LPR. Proton pump inhibitor therapy is less
eVective in patients with LPR.
Keywords Laryngopharyngeal reXux · LFR ·
Risk factors · Gastroesophageal reXux disease ·
GERD · H. pylori · Corpus dominant gastritis
Introduction
Gastroesophageal reXux is the Xow of gastric contents back
into the esophagus and the upper airways [1]. This term can
cause confusion since small quantities of gastric content
may be found in esophagus physiologically. Therefore, it is
named as gastroesophageal reXux disease (GERD) when
this event develops symptoms or causes tissue damage [2].
An epidemiological review reported a prevalence of GERD
of 10–20% and 5% in Western and Asian countries, respec-
tively [3]. Laryngopharyngeal reXux (LPR) is a common
condition in patients with chronic refractory ear, nose and
throat (ENT) symptoms. It is one of the most important eti-
ological factors for many inXammatory disorders of the
ENT [4, 5]. Typical symptoms of GERD are pyrosis, regur-
gitation, and back breastbone pain. LPR is considered when
the relevance of the symptomatological procession con-
cerns the symptoms and/or the signs that bring the patient
to the ENT specialist. These symptoms are called as atypi-
cal symptoms such as cough, globe, hoarseness, vocal
fatigue, frequent throat clearing, and dry throat etc. [1].
Estimates for acid reXux causing laryngitis have ranged
from 18 to 80% [5–7]. There are two major proposed mech-
anisms for GERD-associated LPR. One is acid stimulation
of vagal aVerents in the distal and/or proximal esophagus.
The other is the direct laryngeal contact with acid, pepsin
and other substances present in the gastroesophageal reXux-
ate [4]. The relation between GERD and LPR is well
known but risk factors are not clear. The aim of this study
was to evaluate the demographic and clinicopathologic
characteristics of the GERD with and without LPR to deter-
mine the risk factors for the occurrence of LPR in patients
with GERD.
Patients and methods
This is a retrospective study of GERD patients with and
without LPR. From the outpatient computer program of our
medical center, we randomly enrolled 45 GERD patients
with LPR to the Wrst group and another 45 GERD patients
without LPR to the second group. Medical records of the
patients in both groups were examined. This study was
approved by the institutional review board of the institution
123
Eur Arch Otorhinolaryngol (2012) 269:1189–1194
where the work was carried out. All patients underwent
upper gastrointestinal system endoscopy. Non-erosive
GERD (NERD), erosive GERD (ERD) and Barrett’s esopha-
gus (BE) were diagnosed by endoscopy and histopathology.
Patients were excluded if they had received non-steroidal
anti-inXammatory drugs, bismuth compounds, proton pump
inhibitors, oral anticoagulants, or antibiotics known to be
active against Helicobacter pylori (H. Pylori) within the pre-
vious 3 months, as were those who had received the recent
blood transfusions, had undergone gastric surgery, or had
bleeding diathesis. The symptoms of the patients were
recorded according to type, duration, frequency and severity
of reXux symptoms. Subjects underwent an upper gastroin-
testinal endoscopy and biopsy specimens were taken from
the gastric antrum, body, and fundus. They were then pre-
scribed lansoprazole (30 mg bid), clarithromycin (500 mg
bid), and amoxycillin (1 g bid) for a week. At the eighth
week, a second endoscopy was performed and further biopsy
specimens were obtained from same sites with initial endos-
copy to determine the eradication of H. pylori. Compliance
with medication was assessed by tablet counting and by
direct questioning at the second endoscopy. Possible side
eVects of treatment were also assessed at these times by open
and direct questioning, by the same gastroenterologist,
according to a preset questionnaire. Endoscopy was per-
formed under sedation with from 0 to 5 mg of intravenous
midazolam. Olympus video gastroscope was used and it was
thoroughly cleaned and disinfected between endoscopies.
This involved internal and external brushing using a neutral
detergent, and then being put into an endoscope washer and
given a further 7-min wash with neutral detergent, and 4-min
disinfection with 2.2% glutaraldehyde. To determine the sta-
tus of H. pylori, pre-entry and at eighth week, biopsy speci-
mens were taken from the antrum (within 2 cm of the
pylorus, two for histology and one for rapid urease test), cor-
pus (half-way along greater curvature, two for histology),
and fundus (high in the fundal vault, two for histology). Var-
ious measures were taken to minimize cross contamination of
H. pylori between biopsy specimens from diVerent sites.
First, suction was not used during the procedure until the
Wnal biopsy specimen had been taken. Second, biopsy for-
ceps were changed between sites. Third, samples were
always taken in the order fundus, corpus, and antrum. An
antral specimen was put immediately into a tube for a rapid
urease test. Biopsy specimens were submitted in formalde-
hyde solution for the histological examination at the pathol-
ogy laboratory. Tissues were processed routinely, embedded
in paraYn and cut in 5- sections. Along with the usual
hematoxylin–eosine stain all sections were also stained with
toluidine blue in order to better reveal the bacteria. Slides
were examined independently by two pathologists according
to Sydney system [8]. Various clinical parameters including
status of H. pylori infection, topography of gastritis were
Eur Arch Otorhinolaryngol (2012) 269:1189–1194 1191

Table 1 ReXux symptom index

Within the past month, how did the following problems aVect you? 0 = No problem

5 = Severe problem

1. Hoarseness or a problem with your voice? 0 1 2 3 4 5

2. Clearing your throat 0 1 2 3 4 5
3. Excess throat mucous or postnasal drip 0 1 2 3 4 5
4. DiYculty swallowing food, liquids or pills 0 1 2 3 4 5
5. Cough after you eating and after lying down 0 1 2 3 4 5
6. Breathing diYculties and choking episodes 0 1 2 3 4 5
7. Troublesome and annoying cough 0 1 2 3 4 5
8. Sensations of something sticking in your 0 1 2 3 4 5
throat or a lump in your throat
9. Heartburn, chest pain, indigestion, 0 1 2 3 4 5
or stomach acid coming up
Total
Adapted from Belafsky et al. [9]

analyzed. For therapy, lansoprazole in a dosage of 30 mg
BID for at least 8 weeks were given to all patients in both
groups. GERD patients with and without LPR were com-
pared according to demographic, clinic, endoscopic and his-
topathological parameters. LPR was conWrmed by indirect
laryngoscopy, and graded by LPR-related laryngoscopy scor-
ing system. Indirect laryngoscopy was done using a Karl
Storz videoendoscopy system with a rigid endoscope. LPR
was deWned by the ReXux Symptom Index (RSI) [9] and
ReXux Finding Score (RFS) [10] (Tables 1, 2). RSI is a pre-
viously validated self-administered questionnaires used to
assess the clinical severity of symptoms at diagnosis and
after treatment. The maximal score for RSI is 45. Patients
rate nine symptoms (throat clearing, hoarseness, diYculty
swallowing…etc.) on a scale from 0 to 5. Any score greater
than 13 is considered abnormal [9]. The RFS is an 8-item
scale attempts to document the physical Wndings noted on
laryngoscopy that are associated with LPR and document the
clinical severity of LPR. RFS, grades eight diVerent laryn-
geal Wndings: subglottic edema (or pseudosulcus), ventricular
obliteration (indicative of vocal-fold edema), vocal-fold or
arytenoid erythema/hyperemia, posterior commissure hyper-
trophy, diVuse laryngeal edema, granuloma, excessive
mucus, and vocal-fold edema. Although each item on the
RFS is entirely subjective, the overall score documents evi-
dence of LPR. The worst possible score on RFS is 26, and a
score above 7 is felt to be abnormal [11, 12].
Mann–Whitney U and Chi-square tests were used for the
statistical analyses and p < 0.05 was accepted statistically
signiWcant.
Results
The patients with LPR were younger than the patients with-
out LPR (38.7 § 10.2 years and 43.8 § 11.5 years;
p = 0.08); however, there was no statistical signiWcance.
Table 3 shows the demographic and clinicopathologic char-
acteristics of the GERD with and without LPR. Patients
without LPR showed no gender predilection (55% male)
while LPR patients showed male preponderance (71%
male). In LPR group, 11 patients (24%) had NERD, while
28 (62%) and 6 (13%) patients had ERD and BE, respec-
tively. Twenty-seven (60%) patients without LPR were
diagnosed as NERD, 15 patients (33%) without LPR had
ERD and only 3 patients (6.6%) showed the histological
Wndings of BE. The patients in LPR group had higher body
mass index (BMI) (p = 0.04). Hiatal hernia was more fre-
quent in the patients with LPR (53%) than in the patients
without LPR (24%) (p = 0.005). LPR patients had longer
duration of reXux symptoms than the patients without LPR
(p = 0.04). H. pylori status was not diVerent in both groups
but the patients without LPR had more corpus gastritis than
the patients with LPR. Eight weeks lansoprazole treatment
was successful in 71% of patients with LPR, and 86% of
patients without LPR.
Discussion
The present study demonstrated that age is not a risk factor
for the development of LPR. In the literature, there is only
one study which searched the relationship between BMI of
patients and the occurrence of LPR [13]. In that study,
Halum et al. [13] reviewed 285 patients with LPR and com-
pared their BMI with those of patients with GERD but
without LPR. LPR did not correlate with increasing BMI;
however, abnormal esophageal reXux events correlated
with increasing BMI. The mean number of pharyngeal
reXux events was not elevated in obese patients, whereas
the mean number of esophageal reXux events was signiW-
cantly elevated in obese when compared with non-obese

123
1192 Eur Arch Otorhinolaryngol (2012) 269:1189–1194

Table 2 ReXux Wndings score Table 3 Demographic and clinicopathologic characteristics of the
Pseudosulcus (infraglottic GERD with and without LPR
edema)
0 = Absent GERD GERD p value
with LPR without LPR
2 = Present
Ventricular obliteration Age (years) 38.7 § 10.2 43.8 § 11.5 0.08
0 = Absent Gender (male) 71% 55% 0.04
2 = Partial ERD 62% 33% 0.001
4 = Complete BE 13% 6.6% 0.01
Erythema/hyperemia BMI (kg/m2) 34.2 § 8.1 29.1 § 6.3 0.04
0 = Absent Hiatal hernia 53% 24% 0.005
2 = Arytenoids only Disease duration (years) 18.1 § 6.2 12.4 § 4.2 0.04
4 = DiVuse H. pylori frequency 60% 62% >0.05
Vocal-fold edema Corpus gastritis 24% 33% 0.04
0 = None
GERD gastroesophageal reXux disease, LPR laryngopharyngeal reXux,
1 = Mild ERD erosive reXux disease, BE Barrett esophagus, BMI body mass
2 = Moderate index
3 = Severe
4 = Polypoid 58 patients with pH-documented LPR, 40% (23 of 58) had
DiVuse laryngeal edema heartburn and 48% (28 of 58) had abnormal esophageal
0 = None reXux (by pH monitoring criteria); by transnasal esopha-
1 = Mild goscopy with biopsy, 12% (7 of 58) had esophagitis and
2 = Moderate another 7% (4 of 58) had BE. But in another study, authors
3 = Severe found that the prevalence of BE was 20.4% overall and
4 = Obstructing 15.6% in pure laryngopharyngeal reXux patients [16]. This
Posterior commissure indicates that, although these patients may sense reXux
hypertrophy diVerently, they have similar risks as patients with typical
0 = None symptoms. Further, the identiWcation of BE in the absence
1 = Mild of typical reXux symptoms suggests the potential for occult
2 = Moderate disease progression and late discovery of cancer. Symp-
3 = Severe toms of LPR are more prevalent in patients with esophageal
4 = Obstructing adenocarcinoma than typical GERD symptoms and may
Granuloma/granulation represent the only sign of disease. LPR symptoms better
0 = Absent predict the presence of esophageal adenocarcinoma than
2 = Present typical GERD symptoms [17]. Hiatal hernia is a well-
Thick endolaryngeal mucus known risk factor for GERD, but the results are conXicting
0 = Absent for LPR. Studies revealed a predisposition for LPR in
Adapted from Belafsky et al. patients with hiatal hernias, but the cause–eVect relation-
2 = Present
[10]
ship is unclear [18, 19]. Some authors claimed that the
dynamic anatomy of the esophagogastric junction high-
patients. Our study had the same result with the only study lights the diYculty of deWning hiatal hernia and of elucidat-
in the literature demonstrating that pharyngeal reXux was ing the relation between hiatal hernia, the diaphragmatic
not associated with increasing BMI or obesity in LPR hiatus, the lower esophageal sphincter, and GERD, includ-
patients. But Halum et al. [13] also reported that GERD ing LPR [17]. Rate of response to proton pump inhibitor
was associated with increasing BMI and obesity. In a trial treatment was lower in LPR group in our study just like
patients with LPR had the mean age of 49 years, and 53% most of the other studies in the literature [20, 21]. Authors
(31 of 58) were women showing no risk diVerence accord- agree that proton pump inhibitor therapy remains the cor-
ing to gender [14]. But in the present group, male gender nerstone of treatment [1, 20, 21]. The current management
appeared as a risk factor. ERD and BE were risk factors for recommendation for patients with LPR is empiric therapy
the development of LPR in our study. In the literature, it with twice-daily proton pump inhibitors for 3 months [22].
was also shown that patients with reXux esophagitis had a Meta-analysis of eight controlled studies about PPI treat-
higher risk to develop extra esophageal disorders of the ment of LPR showed that PPI therapy may oVer a modest
pharynx, larynx and lungs [15]. Koufman et al. [14] studied but nonsigniWcant clinical beneWt over placebo in patients

123
Eur Arch Otorhinolaryngol (2012) 269:1189–1194
with suspected LPR [23]. In the majority of those who are
unresponsive to such therapy, other causes of laryngeal irri-
tation are considered. Although some patients respond to
conservative behavioral and medical management, as is the
case with GERD, most require more aggressive and pro-
longed treatment to achieve regression of symptoms and
laryngeal tissue changes [21]. Surgical fundoplication is the
most eVective in those who are responsive to acid-suppres-
sive therapy [20].
Disease duration was not well studied in patients with
LPR. In our study having GERD symptoms for longer time
was associated with higher risk for having LPR by low sta-
tistical signiWcance. The relationship between H. pylori and
GERD was well studied but conXicting data are continuing
to be gathered. Most of these researches showed that there
is no cause–eVect relation and eradication of H. pylori does
not improve GERD symptoms or provide tissue healing
[24, 25]. It has revealed that H. pylori infection is associ-
ated with the pattern of gastritis, but shows no relationship
to the incidence of ERD. High density of H. pylori coloni-
zation in gastric corpus may reduce the esophageal acid
exposure. DiVuse atrophic gastritis may protect the patients
from ERD [24]. But in another study, the increased preva-
lence of H. pylori colonization in the cardia was associated
with ERD which was just opposite of our Wndings [24]. In
our study, there was no diVerence between the rates of H.
pylori infection but corpus gastritis was less frequent in
patients with LPR. We are now aware that inXammation of
corpus decreases the acid secretion of the stomach. Further
controlled clinical study is still required to show the impact
of H. pylori infection and topography of gastritis in patients
with LPR.
The most frequent lesions related to LPR in our study
were edema or erythema in diVerent districts of the larynx,
granulomas, and polyps. The most frequently involved
laryngeal region was the interarytenoid region. But these
laryngological Wndings are not meant to independently
identify reXux as their cause but instead should be taken as
a composite score to indicate the presence or absence of
LPR [10]. The pseudosulcus alone was not accepted a reli-
able sign of LPR, but if it was associated with signs and
symptoms of LPR then it was included. The diagnosis of
LPR was made by a combination of the history and physi-
cal examination. Lack of 24 h pH-monitoring or pH-imped-
ance measurement in the diagnosis of LPR patients is a
limitation of our study. But as we have patients whom we
think have LPR have normal pH studies, clinical diagnosis
of LPR is reliable most of the times.
In a study it was stated that if pseudosulcus was with
reXux symptoms, the probability of reXux rose to 70% [11].
Since symptoms of LPR may be sign of higher incidence of
BE and esophageal adenocarcinoma, some experts suggests
that patients with LPR should have an upper gastrointesti-
1193
nal endoscopy, even if no classical symptoms of GERD are
present [26]. But still there is a debate going on about the
indication of upper gastrointestinal endoscopy among LPR
patients. Reichel et al. [27] reported that esophagogas-
troduodenoscopy is indicated in at least those LPR patients
reporting heartburn as their main complaint. Because in
their group of patients they found that BE or grade B esoph-
agitis was diagnosed only in patients with heartburn as their
main presenting symptom.
Conclusion
Male gender, hiatal hernia, longer duration of symptoms,
high BMI, having ERD and BE seems as risk factors for the
occurrence of LPR in patients with GERD. H. pylori status
did not have any eVect on the development of LPR. Corpus
dominant gastritis may have a protective role against the
development of LPR. Proton pump inhibitor therapy is less
eVective in patients with LPR. Further research is needed to
identify the patients who may need higher doses or pro-
longed duration of proton pump inhibitors or the patients
who may beneWt from surgical treatment of GERD. As
symptoms of LPR may be a sign of higher incidence of BE
and esophageal adenocarcinoma, patients with LPR should
have an upper gastrointestinal endoscopy, even if no classi-
cal symptoms of GERD are present.
ConXict of interest The authors do not have any conXict of interest.
References
1. Mosca F, Rossillo V, Leone CA (2006) Manifestations of gastro-
pharyngo-laryngeal reXux disease. Acta Otorhinolaryngol Ital
26(5):247–251
2. Vakil N et al (2006) The Montreal deWnition and classiWcation of
gastroesophageal reXux disease: a global evidence-based consen-
sus. Am J Gastroenterol 101(8):1900–1920 (quiz 1943)
3. Dent J et al (2005) Epidemiology of gastro-oesophageal reXux dis-
ease: a systematic review. Gut 54(5):710–717
4. Wong RK et al (2000) ENT manifestations of gastroesophageal
reXux. Am J Gastroenterol 95(8):S15–S22
5. Gatta L et al (2007) Meta-analysis: the eYcacy of proton pump
inhibitors for laryngeal symptoms attributed to gastro-oesophageal
reXux disease. Aliment Pharmacol Ther 25(4):385–392
6. Wilson JA et al (1989) Gastroesophageal reXux and posterior lar-
yngitis. Ann Otol Rhinol Laryngol 98(6):405–410
7. Koufman JA (1991) The otolaryngologic manifestations of gas-
troesophageal reXux disease (GERD): a clinical investigation of
225 patients using ambulatory 24-hour pH monitoring and an
experimental investigation of the role of acid and pepsin in the
development of laryngeal injury. Laryngoscope 101(4 Pt 2 Suppl
53):1–78
8. Dixon MF et al (1996) ClassiWcation, grading of gastritis. The
updated Sydney System. International Workshop on the Histopa-
thology of Gastritis, Houston 1994. Am J Surg Pathol 20(10):
1161–1181
123
1194
9. Belafsky PC, Postma GN, Koufman JA (2002) Validity and reli-
ability of the reXux symptom index (RSI). J Voice 16:274–277
10. Belafsky PC, Postma GN, Koufman JA (2001) The validity and re-
liabilty of reXux Wnding score (RFS). Laryngoscope 111:1313–1317
11. Ylitalo R, Lindestad PA, Hertegard S (2004) Is pseudosulcus alone
a reliable sign of gastroesophago-pharyngeal reXux? Clin Otolar-
yngol Allied Sci 29(1):47–50
12. Hill RK et al (2004) Pachydermia is not diagnostic of active laryn-
gopharyngeal reXux disease. Laryngoscope 114(9):1557–1561
13. Halum SL et al (2005) Patients with isolated laryngopharyngeal
reXux are not obese. Laryngoscope 115(6):1042–1045
14. Koufman JA et al (2002) Prevalence of esophagitis in patients
with pH-documented laryngopharyngeal reXux. Laryngoscope
112(9):1606–1609
15. Suazo J, Facha MT, Valdovinos MA (1998) Case and control
study of atypical manifestations in gastroesophageal reXux dis-
ease. Rev Invest Clin 50(4):317–322
16. Perry KA et al (2008) The integrity of esophagogastric junction
anatomy in patients with isolated laryngopharyngeal reXux symp-
toms. J Gastrointest Surg 12(11):1880–1887
17. Reavis KM, Morris CD, Gopal DV, Hunter JG, Jobe BA (2004)
Laryngopharyngeal reXux symptoms better predict the presence of
esophageal adenocarcinoma than typical gastroesophageal reXux
symptoms. Ann Surg 239(6):849–856
18. Kahrilas PJ (2001) Supraesophageal complications of reXux dis-
ease and hiatal hernia. Am J Med 111(Suppl 8A):51S–55S
19. Mjones AB et al (2007) Hoarseness and misdirected swallowing in
patients with hiatal hernia. Eur Arch Otorhinolaryngol 264(12):
1437–1439
123
Eur Arch Otorhinolaryngol (2012) 269:1189–1194
20. Abou-Ismail A, Vaezi MF (2011) Evaluation of patients with sus-
pected laryngopharyngeal reXux: a practical approach. Curr Gas-
troenterol Rep 13(3):213–218
21. Ford CN (2005) Evaluation and management of laryngopharyn-
geal reXux. JAMA 294(12):1534–1540
22. Koufman JA, Aviv JE, Casiano RR, Shaw GY (2002) Laryngo-
pharyngeal reXux: position statement of the committee on speech,
voice and swallowing disorders of the American Academy of Oto-
laryngology—Head and Neck Surgery. Otolaryngol Head Neck
Surg 127:32–35
23. Qadeer MA, Phillips CO, Lopez AR et al (2006) Proton pump
inhibitor therapy for suspected GERD-related chronic laryngitis: a
meta-analysis of randomized controlled trials. Am J Gastroenterol
101:2646–2654
24. Gao BX et al (2006) The roles of Helicobacter pylori and pattern
of gastritis in the pathogenesis of reXux esophagitis. Zhonghua Yi
Xue Za Zhi 86(38):2674–2678
25. Abdul-Razzak KK, Bani-Hani KE (2007) Increased prevalence of
Helicobacter pylori infection in gastric cardia of patients with reX-
ux esophagitis: a study from Jordan. J Dig Dis 8(4):203–206
26. Hammer HF (2009) ReXux-associated laryngitis and laryngopha-
ryngeal reXux: a gastroenterologist’s point of view. Dig Dis
27(1):14–17
27. Reichel O, Issing WJ (2007) Should patients with pH-documented
laryngopharyngeal reXux routinely undergo oesophagogas-
troduodenoscopy? A retrospective analysis. J Laryngol Otol
121(12):1165–1169