Barrett esophagus is metaplastic transformation of esophageal squamous epithelium to columnar cells. A total of 1370 patients who had undergone upper endoscopy because of dyspeptic complaints were enrolled in the study. Age, sex, alcohol and smoking habits, body mass index, type and duration of symptoms (heartburn, epigastric pain, nausea, vomiting), and use of proton pump inhibitors were evaluated in all patients and recorded on standardized forms. Patients were grouped as normal esophagogastric junction, long-segment Barrett esophagus, and short-segment Barrett. Biopsies were taken from at least 6 points and examined histopathologically. Of the 1370 patients involved in the study, 748 (54.6%) were female and 622 (45.4%) were male. Mean age was 47.2 ± 15.30 years. Short-segment Barrett esophagus was detected in 16 patients, and long-segment Barrett was detected in 11 patients. Although Barrett esophagus was detected in 11 cases that were suspected to have Barrett during endoscopy, histopathology was negative in all cases that were not suspected to have Barrett. Barrett esophagus prevalence was significantly higher in people who used alcohol and tobacco and who had hiatal hernia. Although Barrett esophagus was detected in 40% of cases that were suspected to have Barrett during endoscopy, histopathology was negative in all cases that were not suspected to have Barrett. Barrett was detected in 40.7% of cases that were suspected to have Barrett during endoscopy; histopathology was negative in all cases that were not suspected to have Barrett. Senstivity of endoscopy is questionable in detection of short-segment Barrett.

Barrett esophagus (BE) is the metaplastic transformation of esophageal squamous epithelium into columnar cells.1  This histologic alteration is an important complication of gastroesophageal reflux disease (GERD), and it sets the groundwork for adenocarcinoma.2,3  Diagnosis is made by showing goblet cells and intestinal metaplasia in biopsy specimens taken from the lesions directly seen under endoscopy (Fig. 1).4  It has an increasing incidence not only in the United States, New Zealand, and Australia, but also in the rest of the developed world.5,6  Although there are conflicts about the prevalence of BE, reports have demonstrated 1.2% to 25% positivity of BE in endoscopy of asymptomatic patients,7,8  and 8% to 20% positivity in patients who have GER symptoms.9  Factors such as hiatal hernia, obesity, and Helicobacter pylori (HP) are responsible for BE because they provoke acid reflux.10  Recently, BE incidence rates raised after the definition of short-segment BE was introduced.

Fig. 1

Histopathology showing specialized intestinal metaplasia with glandular epithelium and characteristic goblet cells. Hematoxylin-eosin [×50 (left panel), ×100 (right panel)].

Fig. 1

Histopathology showing specialized intestinal metaplasia with glandular epithelium and characteristic goblet cells. Hematoxylin-eosin [×50 (left panel), ×100 (right panel)].

The aim of this study was to compare endoscopic and histopathologic findings in patients who presented with dyspeptic complaints and had upper endoscopy.

A total of 1370 patients who had endoscopy for dyspeptic symptoms between February 2011 and March 2013 were enrolled in the study. Those who had gastric carcinoma, gastrointestinal bleeding during endoscopy, and coagulopathy disorder were excluded from the study. Age, sex, alcohol and smoking habits, heartburn, nausea, vomiting, use of proton pump inhibitors, and duration of symptoms were questioned and recorded on standard forms. Smoking more than 10 cigarettes a day was accepted as habitual smoking.11  Alcohol abuse was identified according to the Diagnostic and Statistical Manual of Mental Disorders 5. Endoscopic examinations were carried out by gastroenterologists or certificated gastrointestinal surgeons using a standard endoscope (Fujinon EPX-4400, System WR, Fujifilm Turkey, Saitama, Japan) under sedation. During the course of endoscopy, esophagogastric junction (EGJ) was examined carefully. Squamocolumnar junction was defined as the line where squamous epithelium turns into salmon-colored columnar mucosa (Fig. 1). Patients were classified as normal EGJ, long-segment BE (intestinal metaplasia ≥3 cm beginning from EGJ), or short-segment BE (SSBE; intestinal metaplasia <3 cm beginning from EGJ; Fig. 2).1214  The presence of more than 2 cm of distance between EGJ and diaphragmatic notch was accepted as hiatal hernia. When normal EGJ was detected, at least 6 biopsies from different sites were taken and examined histopathologically. Of these 6 biopsies, 4 were taken from the squamocolumnar junction and 2 were taken from the gastric antrum. In BE suspected cases, extra biopsies were taken from all possible quadrants and columnar epithelium sites 1 cm distant from each other. All biopsy materials were stored in 10% formalin solution and stained with hematoxylin-eosin and Alcian Blue (Fig. 2). Pathology specimens were reviewed by senior pathologists.

Fig. 2

Salmon-colored columnar mucosa.

Fig. 2

Salmon-colored columnar mucosa.

All patients were notified about the procedures by physicians, and informed consent was taken. Patient data were analyzed using SPSS 15.0 (SPSS Inc, Chicago, Illinois). Student t-test and χ2 tests were used where appropriate. P < 0.05 was accepted as statistically significant.

Of the 1370 patients involved in the study 748 (54.6%) were female and 622 (45.4%) were male. Mean age was 47.2 ± 15.30 years. The demographic and clinical characteristics of patients are shown on Table 1. Alcohol use and smoking were significantly higher in male patients. A total of 19.2% of female and 22.6% of male patients were using proton pump inhibitors, and it was not statistically significant (Table 1). Female patients had more complaints of nausea, vomiting, and heartburn. Durations of symptoms were similar in both sexes. HP was positive in 64.8% of patients who had undergone endoscopy, and no significant difference was found between sexes. Endoscopic findings of patients using the classification described elsewhere15  are listed in Table 2. A total of 27 patients had endoscopically diagnosed BE. Of these, 16 were reported as SSBE and 11 were reported as long-segment BE. Esophagitis was detected in 131 patients, of which 44 (33.5%) were female and 87 (66.5%) were male. The high rate of esophagitis in male patients was statistically significant (P < 0.05). Of the 11 patients (40.7%) with histopathologically diagnosed Barrett, 3 were female and 8 were male. There was not a statistically significant difference between sexes. Hiatal hernia was detected in 7 of 11 patients who were histopathologically identified as Barrett, and this was statistically significant (P < 0.05). Gastrointestinal symptoms, such as nausea, vomiting, and heartburn, were significantly higher in female sex. Alcohol use and smoking were more frequent among males and it was statistically significant (P < 0.05). Durations of symptoms were 46.1 ± 27.0 months in patients with histopathologically proven BE and 41.2 ± 27.8 months in patients who do not have BE, but the difference was not statistically significant. There was no statistically significant difference between sex groups on duration of symptoms (44.7 ± 27.7 months in female patients and 43.2 ± 27.2 months in male patients). When patients were grouped according to body mass index, 15 were underweight (1.1%), 434 (31.6%) were normal weight, 587 (42.9%) were overweight, and 334 (24.4%) were obese. Obesity frequency in our study population was similar to that of the Turkish population.16  There was not a statistically significant association between body mass index and BE (P > 0.05).

Table 1

Demographic and clinical features

Demographic and clinical features
Demographic and clinical features
Table 2

Classification of cases that were diagnosed as Barrett with endoscopy

Classification of cases that were diagnosed as Barrett with endoscopy
Classification of cases that were diagnosed as Barrett with endoscopy
Table 3

Comparison of clinical and endoscopic features of patients with and without histopathologic Barrett diagnosis

Comparison of clinical and endoscopic features of patients with and without histopathologic Barrett diagnosis
Comparison of clinical and endoscopic features of patients with and without histopathologic Barrett diagnosis

Barrett metaplasia is accepted as a precancerous lesion in the development of esophageal adenocarcinoma. In our study BE prevalence in dyspeptic patients who had endoscopy was found as 1.97% endoscopically and 0.8% histologically. Studies carried out in different countries have reached different results. A German study has found BE prevalence as 4.2%, and another study made in Japan reported this prevalence as 0.3% to 0.6%.17  In studies conducted with Turkish patients, histopathologic BE prevalence has been found to be 1.7% and 7.4%.15,18  In our study, most of the 11 patients with pathologically diagnosed BE were male, and the mean age was 46 years. These results are similar to the findings of other series in medical literature.19,20 

SSBE could easily be missed when not carefully looked for during endoscopy, and biopsy could easily be taken from the wrong location. In a study by Padda and Ramirez,21  histopathologic confirmation rates of SSBE and long-segment BE were 38% and 75%, respectively. As with Padda and Ramirez, in our study, only 36% of patients with a diagnosis of having SSBE during endoscopy had histopathologically confirmed BE, whereas most of the patients who were categorized as long-segment BE during endoscopy had histologic BE.

Hiatal hernia is an important factor in the development of GER, which is frequent in patients with BE. In a study by Cameron,22  hiatal hernia was seen in 96% of patients with BE. In addition, hernia sac was longer and wider in patients with BE.22  In our study, hiatal hernia was found in 7 of 11 patients (63.3%) who had histopathologically proven BE.

There are controversies regarding the correlation of esophagitis and BE.23,24  There was no statistically significant difference in esophagitis rates of patients who had BE and who did not have BE in our study. In addition, no relationship was found among dyspeptic symptoms (e.g., nausea, vomiting, heartburn) or duration of symptoms and BE in our study. In studies carried out by Spechler et al24  and Nandurkar et al,25  a relation between SSBE and GER was not found. On the contrary, studies by Johnston et al23  Pereira et al26  showed a significant relation between SSBE and GER. Although we did not find a relation between the presence of esophagitis and BE, nonerosive GER disease that cannot be detected during endoscopic examination may be an important factor in the development of BE.

The relationship between HP infection and BE has not been fully identfied yet. Moreover, some authors argue that HP infection is an inhibitor of BE development by reducing acid secretion.27  On the contrary, no relation between HP infection and BE was found in several studies.28,29  In a such a high-prevalence area as Turkey, it may be difficult to document a relationship between HP infection and BE. In fact, no significant association was found between HP infection and BE in our study.

There are studies reporting that alcohol use provokes GER and thus indirectly reduces BE, but on the other hand there are studies showing no relation between the two.30,31  Although some previous studies have shown inverse correlation with wine use32,33  but positive correlation with liquor use34  and BE development, some authors have argued that alcohol itself, not the type of the different drinks, was directly related to GERD.35  Our study found a significant relationship between BE and alcohol abuse and tobacco use, and demonstrates that BE development increases with alcohol abuse and smoking. Further studies are needed to show the mechanisms and results of risks between foods and drinks and BE.

There are certain reports indicating that there exists a discordance between clinical and pathologic diagnosis of BE among endoscopists in different countries.36  Some authors suggest that the definition of BE should actually be columnar lined esophagus. These further justify the aim of our study.

Patients with dyspeptic or GERD complaints are candidates for BE screening. It is important to raise awareness about SSBE, although it may yield overdiagnosis of SSBE, which may be another problem for beginners in endoscopy. Although BE was detected 40.7% of cases that were suspected to have BE during endoscopy, histopathology was negative in all cases that were not suspected to have BE, thus proving the importance of a careful endoscopic evaluation. Our study points out the fact that senstivity of endoscopy is questionable in detection of SSBE.

1
Spechler
SJ
,
Lee
E
,
Ahnen
D
,
Goyal
RK
,
Hirano
I
,
Ramirez
F
et al
.
Long-term outcome of medical and surgical therapies for gastroesophageal reflux disease: follow-up of a randomized controlled trial
.
JAMA
2001
;
285
(
18
):
2331
2338
2
Banerjee
R
,
Reddy
DN.
Enhanced endoscopic imaging and gastroesophageal reflux disease
.
Indian J Gastroenterol
2011
;
30
(
5
):
193
200
3
Shaheen
NJ
,
Crosby
MA
,
Bozymski
EM
,
Sandler
SM
,
Spechler
SJ.
Is there publication bias in the reporting of cancer risk in Barrett's esophagus
.
Gastroenterology
2000
;
119
(
2
):
333
338
4
Sivri
B.
Low prevalence of Barrett esophagus in Turkey
.
Turk J Gastroenterol
2008
;
19
(
3
):
143
144
5
Blot
WJ
,
Devesa
SS
,
Kneller
RW
,
Fraumeni
JF.
Rising incidence of adenocarcinoma of the esophagus and gastric cardia
.
JAMA
1991
;
265
(
10
):
1287
1289
6
Botterweck
AA
,
Schouten
LJ
,
Volovics
A
,
Dorant
E
,
Brandt
PA.
Trends in incidence of adenocareinoma of the oesophagus and gastric cardia in ten European countries
.
Int J Epidemiol
2000
;
29
(
4
):
645
654
7
Lehmann
FS
,
Renner
EL
,
Meyer-Wyss
B
,
Wilder-Smith
CH
,
Mazzucchelli
L
,
Ruchti
C
et al. Helicobacter pylori and gastric erosions: results of a prevalence study in asymptomatic volunteers
.
Digestion
2000
;
62
(
2–3
):
82
86
8
Ecclissato
C
,
Carvalho
AF
,
Ferraz
JG
,
Nucci
G
,
Souza
CA
,
Pedrazoli
J.
Prevalence of peptic lesions in asymptomatic, healthy volunteers
.
Dig Liver Dis
2001
;
33
(
5
):
403
406
9
Spechler
SJ
,
Goyal
RK.
Barrett's esophagus
.
N Engl J Med
1986
;
315
(
6
):
362
371
10
Kim
JH
,
Rhee
PL
,
Lee
JH
,
Lee
H
,
Choi
YS
,
Son
HJ
et al
.
Prevalence and risk factors of Barrett's esophagus in Korea
.
J Gastroenterol Hepatol
2007
;
22
(
6
):
908
912
11
Alcedo
J
,
Ferrández
A
,
Arenas
J
,
Sopeña
F
,
Ortego
J
,
Sainz
R
et al
.
Trends in Barrett's esophagus diagnosis in Southern Europe: implications for surveillance
.
Dis Esophagus
2009
;
22
(
3
):
239
248
12
Gerson
LB
,
Shetler
K
,
Triadafilopoulos
G.
Prevalence of Barrett's esophagus in asymptomatic individuals
.
Gastroenterology
2002
;
123
(
2
):
461
467
13
Azuma
N
,
Endo
T
,
Arimura
Y
,
Motoya
S
,
Itoh
F
,
Hinoda
Y
et al
.
Prevalence of Barrett's esophagus and expression of mucin antigens detected by a panel of monoclonal antibodies in Barrett's esophagus and esophageal adenocarcinoma in Japan
.
J Gastroenterol
2000
;
35
(
8
):
583
592
14
Hirato
WK
,
Loughney
TM
,
Lazas
DJ
,
Maydonovitch
CL
,
Rohl
V
,
Wong
RK.
Specialized intestinal metaplasia, dysplasia, and cancer of the esophagus and esophagogastric junction: prevalence and clinical data
.
Gastroenterology
1999
;
116
(
2
):
277
285
15
Toruner
M
,
Soykan
I
,
Ensari
A
,
Kuzu
I
,
Yurdaydin
C
,
Ozden
A.
Barrett's esophagus: prevalence and its relationship with dyspeptic symptoms
.
J Gastroenterol Hepatol
2004
;
19
(
5
):
535
540
16
Health Ministry of Republic of Turkey
.
Obesity Report: Perception of Body Mass Index. Ankara 2012; Report no. 894
.
Ankara, Turkey
:
Health Ministry of Republic of Turkey
;
2012
17
Sharma
P
,
McCallum
RW
,
Lundell
L.
The geoprevalence of Barrett's esophagus
.
Presented at: Sixth OESO World Congress; September 2000; Paris, France
18
Dincer
D
,
Besisik
F
,
Sahin
E
,
Demir
K
,
Tuncer
I
,
Cevikbas
U
et al
.
Intestinal metaplasia of the gastric cardia: a study form Turkey
.
Hepatogastroenterology
2002
;
49
(
46
):
1153
1156
19
Gerson
LB
,
Edson
R
,
Lavori
PW
,
Triadafilopoulos
G.
Use of a simple symptom questionnaire to predict Barrett's esophagus in patients with symptoms of gastroesophageal reflux
.
Am J Gastroenterol
2001
;
96
(
7
):
2005
2012
20
Voutilainen
M
,
Farkkila
M
,
Juhola
M
,
Nuorva
K
,
Mauranen
K
,
Mäntynen
T
et al
.
Specialized columnar epithelium of the esophagogastric junction: prevalence and associations
.
Am J Gastroenterol
1999
;
94
(
4
):
913
918
21
Padda
S
,
Ramirez
F.
Accuracy in the diagnosis of SSBE: the role of endoscopic experience
.
Gastrointest Endosc
2001
;
54
(
5
):
605
608
22
Cameron
AJ.
Barrett's esophagus: prevalence and size ofhiatal hernia
.
Am J Gastroenterol
1999
;
94
(
8
):
2054
2059
.
23
Johnston
MH
,
Hammond
AS
,
Laskin
WL
,
Jones
MD.
The prevalence and clinical characteristics of short segments of specialized intestinal metaplasia in the distal esophagus on routine endoscopy
.
Am J Gastroenterol
1996
;
91
(
8
):
1507
1511
24
Spechler
SJ
,
Zeroogian
JM
,
Antonioli
DA
,
Wang
HH
,
Goyal
RK.
Prevalence of metaplasia at the gastroesophageal junction
.
Lancet
1994
;
344
(
8936
):
1533
1536
25
Nandurkar
S
,
Talley
NJ
,
Martin
CJ
,
Adams
TH.
Short segment Barrett's esophagus: prevalence, diagnosis and associations
.
Gut
1997
;
40
(
6
):
710
715
26
Pereira
AD
,
Suspiro
A
,
Chaves
P
,
Saraiva
A
,
Glória
L
,
de Almeida
JC
et al
.
Short segments of Barrett's epithelium and intestinal metaplasia in normal appearing esophagogastric junctions: the same or two different entities?
Gut
1998
;
42
(
5
):
659
662
27
Goldblum
JR
,
Vicari
JJ
,
Falk
GW
,
Rice
TW
,
Peek
RM
,
Easley
K
et al
.
Inflammation and intestinal metaplasia of gastric cardia: the role of gastroesophageal reflux and H. pylori infection
.
Gastroenterology
1998
;
114
(
4
):
633
639
28
Abbas
Z
,
Hussainy
AS
,
Ibrahim
F
,
Jafri
W
,
Shaikh
H
,
Kahn
HA.
Barrett's esophagus and Helicobacter pylori
.
J Gastroenterol Hepatol
1995
;
10
(
3
):
331
333
29
Newton
M
,
Bryan
R
,
Burnham
WR
,
Kamm
MA.
Evaluation of Helicobacter pylori in reflux esophagitis and Barrett's esophagus
.
Gut
1997
;
40
(
1
):
9
13
30
Johansson
J
,
Hakansson
HO
,
Mellblom
L
,
Kempas
A
,
Johansson
KE
,
Granath
F
et al
.
Risk factors for Barrett's oesophagus: a population-based approach
.
Scand J Gastroenterol
2007
;
42
(
2
):
148
156
31
Conio
M
,
Filiberti
R
,
Blanchi
S
,
Ferraris
R
,
Marchi
S
,
Ravelli
P
et al
.
Risk factors for Barrett's esophagus: a case-control study
.
Int J Cancer
2002
;
97
(
2
):
225
229
32
Kubo
A
,
Levin
TR
,
Block
G
,
Rumore
GJ
,
Quesenberry
CP
Jr,
Buffler
P
et al
.
Alcohol types and sociodemographic characteristics as risk factors for Barrett's esophagus
.
Gastroenterology
2009
;
136
(
3
):
806
815
33
Anderson
LA
,
Cantwell
MM
,
Watson
RG
,
Johnston
BT
,
Murphy
SJ
,
Ferguson
HR
et al
.
The association between alcohol and reflux esophagitis, Barrett's esophagus, and esophageal adenocarcinoma
.
Gastroenterology
2009
;
136
(
3
):
799
805
34
Veugelers
PJ
,
Porter
GA
,
Guernsey
,
Casson
AG
.
Obesity and lifestyle risk factors for gastroesophageal reflux disease, Barrett esophagus and esophageal adenocarcinoma
.
Dis Esophagus
2006
(
5
);
19
:
321
328
35
Ronkainen
J
,
Aro
P
,
Storskrubb
T
,
Johansson
SE
,
Lind
T
,
Bolling-Sternevald
E
et al
.
Prevalence of Barrett's esophagus in the general population: an endoscopic study
.
Gastroenterology
2005
;
129
(
6
):
1825
1831
36
Takubo
K
,
Vieth
M
,
Aida
J
,
Sawabe
M
,
Kumagai
Y
,
Hoshihara
Y
et al
.
Differences in the definitions used for esophageal and gastric diseases in different countries: endoscopic definition of the esophagogastric junction, the precursor of Barrett's adenocarcinoma, the definition of Barrett's esophagus, and histologic criteria for mucosal adenocarcinoma or high-grade dysplasia
.
Digestion
2009
;
80
(
4
):
248
257