Barrett Esophagus: Perspectives
on Its Diagnosis and Management
in Asian Populations
Yuji Amano, MD, PhD, and Yoshikazu Kinoshita, MD, PhD
Dr. Amano serves as Director and Abstract: Barrett esophageal cancer has the fastest growing inci-
Associate Professor in the Division of dence of any cancer in Western countries. In Asian countries, most
Gastrointestinal Endoscopy at Shimane cases of esophageal cancer consist of squamous cell carcinomas, not
University Hospital in Izumo, Japan.
adenocarcinomas. Recently, however, the increase in the number of
Dr. Kinoshita is the Dean in the School
of Medicine at Shimane University in Barrett esophagus cases with subsequent Barrett cancer has become
Izumo, Japan, where he also serves as worrisome in Asian countries, as the number of patients with gastro-
Professor and Chairman in the Department esophageal reflux disease has been increasing in these countries. In
of Gastroenterology and Hepatology. this review, recent reports regarding Barrett esophagus in Asian coun-
tries have been collected and this problem is discussed from various
perspectives. In Asia, long-segment Barrett esophagus is much less
Address correspondence to: prevalent than in Western countries, whereas short-segment Barrett
Dr. Yuji Amano, esophagus is frequently found. In epidemiologic studies, evaluation
Division of Gastrointestinal Endoscopy, of the prevalence of Barrett esophagus is limited by poor interob-
Shimane University Hospital, server diagnostic agreement. Standard criteria for the endoscopic
89-1, Enya-cho, Izumo-shi, diagnosis of Barrett esophagus in Asian patients, especially of the
Shimane 693-8501, Japan;
short-segment type, should be established as soon as possible. A high
Fax: +81-853-20-2187; prevalence of hiatal hernia and a decreasing prevalence of Helico-
E-mail: email@example.com bacter pylori infection may increase the number of Barrett esophagus
cases and subsequent Barrett cancer in Asian countries in the near
future. Therefore, a strategy for the clinical management of Barrett
esophagus in Asian countries should be devised.
arrett esophagus is deﬁned as intestinal metaplasia of the
esophageal mucosa, leading to replacement of the esophageal
squamous epithelium with columnar epithelium.1,2 Esopha-
geal adenocarcinoma, namely Barrett cancer, derived from Barrett
esophagus has been rapidly increasing during the last two decades
in North America, Australia, and Europe. Approximately 60% of
Caucasian patients with esophageal cancer living in the United
States have adenocarcinoma in Barrett esophagus.3 Columnar-lined
esophagus with intestinal metaplasia expressing MUC2 core pro-
Keywords tein can develop into esophageal adenocarcinoma.4-7 Therefore, in
Barrett esophagus, Asian population, endoscopic Western countries, it is quite reasonable to deﬁne columnar-lined
diagnosis, Helicobacter pylori infection esophagus with goblet cell metaplasia as Barrett esophagus with
Gastroenterology & Hepatology Volume 4, Issue 1 January 2008 45
A M A N O A N D K I N O S H I TA
Figure 1. The prevalence of patients
with Barrett esophagus (indicated by the
100 bars) and hiatal hernia (indicated by the
black dots) correlates with increasing
* * age. During the study period of 2004–
75 * 2006, 333 patients with histologically
confirmed Barrett esophagus were found
50 * * in 1,997 patients who underwent eso-
phagogastroduodenoscopy. In patients
25 over 70 years of age, the prevalence of
Barrett esophagus and hiatal hernia
was higher than that in the younger
>29 30–39 40–49 50–59 60–69 70–79 80<
*P<.05, compared to the patients younger than
40 years of age.
malignant potential, as goblet cells express MUC2 core study, Barrett esophagus was signiﬁcantly more prevalent
protein. In Asian countries, the majority of esophageal in patients over 70 years of age than in younger patients.
cancer is squamous cell carcinoma. The number of This ﬁnding suggests that the pathophysiology of Barrett
patients with Barrett cancer is small, and only approxi- esophagus (mainly SSBE) may be diﬀerent in Asia than
mately 1% of cases with esophageal cancer are histo- in the West (which has a high LSBE prevalence).
logically adenocarcinomas.8 One reason for the low Reports examining the prevalence of Barrett esopha-
prevalence of Barrett cancer in Asia may be that Barrett gus in Asian countries are shown in Table 1.7,8,12,23-39
esophagus cases are mainly short-segment (<3 cm). How- LSBE prevalence in Asia is extremely low (<1.0% of all
ever, as with long-segment Barrett esophagus (LSBE; >3 Barrett esophagus patients in most reports). In contrast,
cm), some short-segment Barrett esophagus (SSBE) cases SSBE prevalence in Asia is greater than 96% of all Barrett
also show malignant potential.9-11 Reports of a gradually esophagus patients. The prevalence data vary, as demon-
increasing incidence of Barrett cancer in Asia suggest that strated in Table 1, possibly due to racial diﬀerences in
particular attention should be paid to these patients.12,13 Asian countries23 or diﬀerences in how the Barrett esopha-
Accordingly, the strategy for clinical management of gus was diagnosed (endoscopically vs histologically). The
Barrett esophagus in Asia, as well as in Western countries, prevalence of endoscopic versus histologic Barrett esopha-
should be established. This review article evaluates the gus also varied widely. Armstrong was the ﬁrst researcher
present status of Barrett esophagus in Asia and discusses to recommend that “endoscopic Barrett esophagus” be
perspectives on its diagnosis and treatment. considered synonymous with esophageal columnar-
appearing mucosa or columnar-lined esophagus.40 The
Prevalence of Barrett Esophagus in Asia most important reason for the diﬀerentiation is the dif-
ﬁculty in diagnosing Barrett esophagus endoscopically. In
According to recent reports from Western countries, the particular, the endoscopic diagnosis of SSBE is less reliable
prevalence of Barrett esophagus (histologically conﬁrmed than that of LSBE.41,42
by the presence of goblet cell metaplasia/specialized A multicenter, prospective, nationwide, epidemio-
columnar epithelium), LSBE, and SSBE is 1.6–25.0%, logic study conducted in Japan by the Japanese GERD
0.5–7.2%, and 1.1–17.2%, respectively.14-19 In these Society found an overall prevalence of endoscopically
reports, most of the patients were Caucasian. In patients suspected Barrett esophagus of 24.1%, of which 99.1%
with gastroesophageal reﬂux disease (GERD), the preva- was SSBE.33 Some patients were symptomatic dur-
lence of Barrett esophagus is over 10%.20,21 Cameron ing their annual health check-up, whereas others were
and associates reported that LSBE showed a fairly rapid asymptomatic. The prevalence of Barrett esophagus was
evolution to its full length with little subsequent change. higher in this study than in other studies. Moreover, the
They observed no age-related increase in the prevalence of diagnostic criteria for endoscopic Barrett esophagus were
LSBE.22 On the other hand, in our study, we found that those widely used in Japan, but not in Western countries.
change in the prevalence of Barrett esophagus (which was The distal end of the lower esophageal palisade vessels was
99% SSBE) was age-related, as shown in Figure 1. In our used to deﬁne the gastroesophageal junction.
46 Gastroenterology & Hepatology Volume 4, Issue 1 January 2008
B A R R E T T E S O P H A G U S I N A S I A N P O P U L AT I O N S
Table 1. Prevalence of Barrett Esophagus in Asian Countries
Country or Sample Size Prevalence of
Study Study Period Ethnicity (N) Study Method Barrett Esophagus
Rajendra S, et al.23 1997–2000 1,985 Single center LSBE: 1.6%, SSBE: 4.6%
Hongo M, Shoji T8 1999–2000 7,134 Multicenter LSBE: 0.4%,* SSBE: 0.9%*
Wong WM, et al.24 1997–2001 China 16,606 Single center LSBE: 0.02%, SSBE: 0.04%
Zhang J, et al. 25
2001–2002 China 391 Single center LSBE: 6.6%,* SSBE: 24.0%*
1997 India 150 with FD Single center 2.6%
Dhawan PS, et al.27 2000 India 271 Single center 5.9% (by 1 biopsy specimen)
Punia RS, et al. 28
1999–2002 India 55 with GERD Single center 23.6%
1,248 with LSBE: 0.8%, SSBE: 1.6%,
Bafandeh Y, et al.29 2001–2003 Iran Single center
GERD BE: 8.3%*
2005–2006 Iran 501 0.2%
Azuma N, et al.31 1996–1998 Japan 650 Single center LSBE: 0.6%,* SSBE: 15.1%*†
Hongo M, Skoji T 8
1999–2000 Japan 18,400 Multicenter LSBE: 0.2%,* SSBE: 1.0%*
Fujiwara Y, et al. 32
2001–2003 Japan 548 Multicenter LSBE: 0.2%, SSBE: 12.0%
Kawano T, et al. 33
2003 Japan 2,577 Multicenter LSBE: 0.2%,* SSBE: 20.8%*†
LSBE: 0.2%, SSBE: 19.7%
Amano Y, et al.7 2003–2004 Japan 1,699 Single center
LSBE: 0.4%,* SSBE: 37.7%*
Lee JI, et al.34 2000 Korea 1,553 Multicenter LSBE: 0.32%
LSBE: 0.01%, SSBE: 0.14%
Kim JH, et al.35 1997–2004 Korea 70,103 Multicenter
LSBE: 0.01%,* SSBE: 0.53%*
Choi DW, et al.36 Korea 847 Single center LSBE: 0.5%,* SSBE: 16.5%*
2005 LSBE : 0.1%, SSBE : 3.5%
Kim JY, et al.37 Korea 992 Multicenter
(publication) LSBE: 0.3%,* SSBE: 10.9%*
Rosaida MS, 2004
Malaysia 1,000 Single center 2.0%
Goh KL38 (publication)
Gadour MO, 1999
Saudi Arabia 159 Single center 0.3%
Ayoola EA39 (publication)
Yeh C, et al.12 1991–1992 Taiwan 464 Single center 1.98%
BE=Barrett esophagus; FD=functional dyspepsia; GERD=gastroesophageal reflux disease; LSBE=long-segment Barrett esophagus;
SSBE=short-segment Barrett esophagus.
*Prevalence of endoscopic Barrett esophagus. †Endoscopic Barrett esophagus diagnosed by palisade vessel criteria.
Gastroenterology & Hepatology Volume 4, Issue 1 January 2008 47
A M A N O A N D K I N O S H I TA
Endoscopic Diagnosis of Barrett Esophagus landmark of the EGJ to the guidelines for clinical and
pathologic studies on carcinoma of the esophagus.43
Marked variation in the prevalence of Barrett esophagus Therefore, it is acceptable for Japanese endoscopists to
in Asian countries may stem from diﬀerences in endo- determine the EGJ using both landmarks: the distal end
scopic diagnostic criteria among studies. In the study by of the palisade vessels and the proximal end of the gastric
the Japan GERD Society cited above, the endoscopic folds when the palisade vessels are invisible.
criteria proposed by the Japan Esophageal Society were
utilized.43 In Japan, the distal end of the lower esophageal Histologic Diagnosis of Barrett Esophagus
palisade vessels is believed to coincide with, and is used to
deﬁne, the esophagogastric junction (EGJ).44-48 In Japan, Another reason for variation in the prevalence of Barrett
Barrett esophagus is deﬁned by the presence of columnar esophagus may stem from the lack of a worldwide con-
epithelium between the squamocolumnar junction (SCJ) sensus on the histologic deﬁnition of Barrett esophagus.
and the EGJ, irrespective of the type of columnar epithe- According to the guidelines of the American College
lium and its length (ie, LSBE or SSBE), depending upon of Gastroenterology,1 Barrett esophagus is deﬁned by
the distance of the SCJ from the EGJ. the change of the esophageal epithelium of any length
In Western countries, the landmark for the EGJ is recognized at endoscopy and histologically conﬁrmed
the proximal end of the gastric longitudinal folds. Accord- to contain intestinal metaplasia. Furthermore, a deﬁnite
ing to the Prague C & M Criteria for Barrett Esophagus, histologic diagnosis of Barrett esophagus requires proof
which were proposed by a subgroup of the International of intestinal metaplasia with goblet cells. Kerkhof and
Working Group for the Classiﬁcation of Oesophagitis colleagues showed that intestinal metaplasia can be found
(IWGCO) in order to standardize the objective diagno- easily in biopsy specimens if the length of endoscopic
sis of endoscopic Barrett esophagus using conventional Barrett esophagus is longer than 2 cm.49 However, intes-
endoscopy,40 the landmark for the EGJ is the proximal tinal metaplasia cannot be found easily in many SSBE
end of the gastric folds. As interobserver disagreement cases with uneven distribution of intestinal metaplasia.
regarding endoscopic diagnosis of Barrett esophagus, in According to the proposed guidelines of the British
particular SSBE, results from the diﬃculty of determining Society of Gastroenterology,2 the presence of specialized
the location of the EGJ,41,42 the question arises as to which columnar epithelium is less important for the diagnosis of
landmark is appropriate: the proximal end of the gastric Barrett esophagus than the presence of a proper esopha-
folds or the distal end of the esophageal palisade vessels? geal gland, squamous island, and/or double muscularis
Usually, palisade vessels can be found easily when mucosae.50-53 The eﬃcacy and usefulness of their criteria
the lower esophagus is adequately distended by air insuf- have also been suﬃciently discussed at the Paris Work-
ﬂation. In cases with superﬁcial dysplastic lesions and/or shop on Columnar Metaplasia in the Esophagus and the
intense inﬂammation, palisade vessels sometimes cannot Esophagogastric Junction.54 Like the British Society of
be endoscopically detected, suggesting that the palisade Gastroenterology, the Japan Esophageal Society deﬁnes
vessels criterion may not be useful for endoscopic diagno- Barrett esophagus as the presence of at least 1 of the follow-
sis of Barrett esophagus. ing factors: a proper esophageal gland, squamous island,
On the other hand, an investigation of the Prague and double muscularis mucosae.43 Therefore, diﬀerences
C & M Criteria using video clip images of the EGJ found among studies regarding epidemiologic prevalence data
interobserver disagreement in Barrett esophagus cases for Barrett esophagus may be due to diﬀerences among
less than 1 cm in length, but it also found interobserver these studies regarding their histologic criteria.
agreement in Barrett esophagus cases greater than 1 cm.41
Similarly, in our own study, kappa values were higher Barrett Esophagus and Helicobacter pylori
for endoscopic diagnosis of Barrett esophagus longer Infection in Asia
than 1 cm in length,42 suggesting the unsuitability of the
C & M criteria for diagnosing SSBE. Predictors for the presence of Barrett esophagus include
Utilizing only palisade vessels to determine the old age, male gender, hiatal hernia, and long-lasting
endoscopic deﬁnition of the EGJ resulted in a low kappa reﬂux symptoms.16,55-59 Alcohol and smoking have also
coeﬃcient of reliability. When the upper end of the been reported to be predictors for Barrett esophagus and
longitudinal gastric folds was used, the diagnostic con- Barrett cancer in the West,15,18,49,60 but not in Asia.7,35,37
cordance, though initially low, improved to an acceptable However, hiatal hernia and Helicobacter pylori infection
level after the complete application of Prague C & M are important predictors for Barrett esophagus in Asia.
Criteria for Barrett Esophagus.42 In April 2007, the Japan The presence of hiatal hernia plays an important role
Esophageal Society added gastric folds as an additional for the pathogenesis of reﬂux esophagitis and Barrett
48 Gastroenterology & Hepatology Volume 4, Issue 1 January 2008
B A R R E T T E S O P H A G U S I N A S I A N P O P U L AT I O N S
Table 2. Prevalence of Helicobacter pylori Infection in Patients with Barrett Esophagus in Asian Versus
Study Study Period Country Sample Size (N) Study Method Prevalence
Abe Y, et al.76 1996–2001 Japan 112 with RE Single center
Zhang J, et al.77 2001–2002 China 375 with GERD Single center
Amano Y, et al.78 2002–2003 Japan 400 with BE Single center SSBE: 51.2%
Chinuki D, et al. 79
2003–2004 Japan 266 with BE Single center SSBE: 45.5%
Rajendra S, et al.69 2003–2005 Malaysia 188 with GERD Single center
Vieth M, et al.75 1990–1997 Germany 1,054 with BE Single center 43.9%
Loﬀeld RJ, van der
1994–2004 Netherlands 11,691 Single center 30.7%
Wani S, et al.81 2000–2002 US 46 with BE Single center 6.5%
Weston AP, et al.82 US 289 with BE Single center 35.1%
Veldhuyzen van 2006
Canada 1,040 Multicenter 28.0%
Zanten SJ, et al.83 (publication)
BE=Barrett esophagus; GERD=gastroesophageal reflux disease; LSBE=long-segment Barrett esophagus; RE=reflux esophagitis;
SSBE=short-segment Barrett esophagus.
esophagus, as hiatal hernia induces long-lasting reﬂux of Schenk and associates found that the prevalence of
gastric acid contents.23,38,61 The prevalence of hiatal hernia H. pylori infection was 20.4% and 44.3% in patients with
increases with age in Japan; hiatal hernia was found in and without Barrett esophagus, respectively.84 Weston
approximately 70% of patients over 70 years of age, as and colleagues also found that the incidence of H. pylori
shown in Figure 1. infection is related to the incidence of Barrett carcino-
H. pylori infection is well known to be more preva- genesis (ie, 35.1%, 14.3%, and 15.0% in patients with-
lent in Asian than in Western countries and to protect out dysplastic lesion, with high-grade dysplasia, and with
against the development of GERD and Barrett esopha- Barrett cancer, respectively).82 Moreover, SSBE developed
gus.62-69 In Japan, the prevalence of H. pylori infection in 10.3% of patients who underwent H. pylori eradica-
was approximately 70% among patients born before tion therapy,85 and Barrett esophagus developed after
1950.70 The prevalence of H. pylori infection, however, spontaneous healing of atrophic gastritis in patients with
has decreased during the last two decades.71 The gradual H. pylori antibody titers that had fallen to normal levels.86
decrease of H. pylori seroprevalence was also found in These ﬁndings clearly suggest that H. pylori infection is
many Asian countries.72-74 H. pylori infection protects protective for the development of Barrett esophagus.
against the development of Barrett esophagus via the Vicari and colleagues reported that cytotoxin-associ-
decrease of gastric-acid secretion. Therefore, the high rate ated gene A (CagA)-positive strains of H. pylori, which
of H. pylori infection is believed to account for the lower are known to induce intense inﬂammation in the gastric
prevalence of Barrett esophagus in Asian countries. Vieth mucosa and are closely correlated with the incidence
and coworkers determined the prevalence of H. pylori of gastric carcinogenesis, protect against the develop-
infection from a meta-analysis of 23 studies, including ment of Barrett esophagus.87 Although the prevalence of
their own, and concluded that 35.6% of 2,084 patients H. pylori infection was not signiﬁcantly lower in patients
with Barrett esophagus in Western countries were infected with Barrett esophagus (approximately 34%) than in the
with H. pylori.75 As shown in Table 2,69,75-83 the prevalence control group, the prevalence of CagA-positive H. pylori
of H. pylori infection in patients with Barrett esophagus is infection was signiﬁcantly decreased in patients with
higher in Asian than in Western countries. Barrett esophagus (13.3%). This protective eﬀect was
Gastroenterology & Hepatology Volume 4, Issue 1 January 2008 49
A M A N O A N D K I N O S H I TA
conﬁrmed by other investigations in Asian and Western detect dysplastic Barrett lesions with high sensitivity and
countries.88-91 Thus, it is suggested that H. pylori infec- speciﬁcity in both LSBE and SSBE cases. Magnifying
tion aﬀects the prevalence of Barrett esophagus and may endoscopy combined with acetate enhancement or nar-
account for the lower prevalence of this disease in Asia row band imaging is also useful, though it is time-con-
than in the West. suming in LSBE cases. These new endoscopic procedures
On the other hand, several investigators found no may have advantages over the random biopsy diagnostic
relationship between H. pylori infection and the devel- method in Asian patients with SSBE.
opment of Barrett esophagus or Barrett cancer.75,77,92-94 Strategies for the treatment and management of
Henihan and coworkers found that H. pylori infection Barrett esophagus and the prevention of Barrett cancer
induces severe chronic inﬂammation in Barrett esopha- should also be established in Asia. Proton pump inhibitors
gus and, thereby, is not protective against development (PPIs) are used to shorten the length of Barrett esophagus.
of Barrett esophagus.95 Thus, the relationship between Nonsteroidal anti-inﬂammatory drugs (NSAIDs), such as
H. pylori infection and Barrett esophagus is still ambigu- aspirin, or selective cyclooxygenase-2 (COX-2) inhibitors
ous. Koike and associates demonstrated that the prevalence are used to prevent Barrett carcinogenesis. PPIs suppress
of H. pylori infection was signiﬁcantly lower in patients cellular proliferation105,106 and facilitate the regression
with adenocarcinoma at the EGJ than in patients with of Barrett esophagus.107-109 NSAIDs such as aspirin are
gastric cancer, though not as low as in patients with erosive known to decrease the risk of many types of cancer, and
esophagitis and Barrett esophagus.96 This ﬁnding suggests in patients with Barrett esophagus, they decrease the risk
that preservation of gastric acid secretion may be impor- of carcinogenesis from Barrett esophagus.6,110-112 Recent
tant for the development of adenocarcinoma at the EGJ, studies have discussed the prophylactic eﬀects of selective
regardless of the presence of H. pylori infection. Thus, a COX-2 inhibitors for Barrett carcinogenesis.113-115 The
high infection rate of H. pylori does not completely explain eﬃcacy of their drugs must be evaluated in Asian patients
the lower prevalence of Barrett esophagus and shorter with Barrett esophagus, as little data from Asian countries
Barrett segments in Asian than in Western countries. are available.
Issues Related to Incidence Conclusion
of Barrett Esophagus in Asia
Barrett esophagus is not rare, even in Asia, where the
According to the comprehensive registry of the Japan majority of it is in the form of SSBE. Endoscopic diag-
Esophageal Society during 1995–1997, esophageal aden- nosis of SSBE has several problems, and an endoscopic
ocarcinoma accounted for only 1.4% of all esophageal surveillance policy should be established. As patients with
cancers.8 However, as GERD is gradually increasing SSBE have a somewhat higher risk for developing cancer,
in Asia,97 Barrett esophagus may increase. Most Barrett an appropriate treatment strategy for SSBE should also be
esophagus in Asia is SSBE, which also has a malignant established in Asia.
potential. Therefore, the establishment of strategies for
diagnosing and treating Barrett esophagus is an important References
goal in Asia, as well as in the West.
First, new criteria need to be established for the 1. Sampliner RE. Practice guidelines on the diagnosis, surveillance, and therapy
of Barrett esophagus. The Practice Parameters Committee of the American College
endoscopic diagnosis of Barrett esophagus, as the Prague of Gastroenterology. Am J Gastroenterol. 1998;93:1028-1032.
C & M criteria proposed by IWGCO are not helpful 2. Watson A, Heading RC, Shepherd NA, eds. Guidelines for the diagnosis and
for the diagnosis and classiﬁcation of SSBE.41,42 Second, management of Barrett columnar-lined oesophagus. A report of the working party
of the British Society of Gastroenterology. British Society of Gastroenterology [web
a systematic method for the endoscopic surveillance of page]. August 2005. Available at http://www.bsg.org.uk/pdf_word_docs/Bar-
SSBE should also be established. Most Barrett cancer in retts_Oes.pdf. Accessed December 10, 2007.
Asian countries develops from SSBE. Although a stepwise 3. Blot WJ, Devesa SS, Fraumeni JF Jr. Continuing climb in rates of esophageal
adenocarcinoma: an update. JAMA. 1993;270:1320.
4-quadrant biopsy procedure is the gold standard for 4. Guillem P, Billeret V, Buisine MP, Flejou JF, Lecomte-Houcke M, et al. Mucin
the surveillance of dysplastic Barrett esophagus in many expression and cell diﬀerentiation in human normal, premalignant, and malignant
Western countries, it is not an ideal method from the esophagus. Int J Cancer. 2000;88:856-861.
5. Warson C, Van De Bovenkamp JH, Korteland-Van Male AM, Büller HA, Ein-
standpoint of safety, labor, or cost-eﬀectiveness, and it erhand AW, et al. Barrett esophagus is characterized by expression of gastric-type
should be avoided if guidance methods such as crystal mucins (MUC5AC, MUC6) and TFF peptides (TFF1 and TFF2), but the risk of
violet chromoendoscopy,98,99 magnifying endoscopy with carcinoma development may be indicated by the intestinal-type mucin, MUC2.
Hum Pathol. 2002;33:660-668.
acetate enhancement100,101 or narrow band imaging,102,103 6. Amano Y, Ishihara S, Kushiyama Y, Yuki T, Takahashi Y, et al. Barrett oesopha-
or autoﬂuorescence endoscopy104 can be used to obtain gus with predominant intestinal metaplasia correlates with superﬁcial cyclo-
the target biopsy. Crystal violet chromoendoscopy can oxygenase-2 expression, increased proliferation and reduced apoptosis: changes
50 Gastroenterology & Hepatology Volume 4, Issue 1 January 2008
B A R R E T T E S O P H A G U S I N A S I A N P O P U L AT I O N S
that are partially reversed by non-steroidal anti-inﬂammatory drugs usage. Aliment 32. Fujiwara Y, Higuchi K, Shiba M, Watanabe T, Tominaga K, et al. Associa-
Pharmacol Ther. 2004;20:793-802. tion between gastroesophageal ﬂap valve, reﬂux esophagitis, Barrett epithelium,
7. Amano Y, Kushiyama Y, Yuki T, Takahashi Y, Moriyama I, et al. Prevalence of and atrophic gastritis assessed by endoscopy in Japanese patients. J Gastroenterol.
and risk factors for Barrett esophagus with intestinal predominant mucin pheno- 2003;38:533-539.
type. Scand J Gastroenterol. 2006;41:873-879. 33. Kawano T, Kouzu T, Ohara S, Kusano M. The prevalence of Barrett
8. Hongo M, Shoji T. Epidemiology of reﬂux disease and CLE in East Asia. mucosa in the Japanese [in Japanese with English abstract]. Gastroenterol Endosc.
J Gastroenterol. 2003;38(suppl 15):25-30. 2005;47:951-961.
9. Schnell TG, Sontag SJ, Chejfec G. Adenocarcinoma arising in tongues or short 34. Lee JI, Park H, Jung HY, Rhee PL, Song CW, Choi MG. Prevalence of Barrett
segments of Barrett esophagus. Dig Dis Sci. 1992;37:137-143. esophagus in an urban Korean population: a multicenter study. J Gastroenterol.
10. Drewitz DJ, Sampliner RE, Garewal HS. The incidence of adenocarcinoma 2003;38:23-27.
in Barrett esophagus: a prospective study of 170 patients followed 4.8 years. Am J 35. Kim JH, Rhee PL, Lee JH, Lee H, Choi YS, et al. Prevalence and risk factors
Gastroenterol. 1997;92:212-215. of Barrett esophagus in Korea. J Gastroenterol Hepatol. 2007;22:908-912.
11. Sharma P, Morales TG, Bhattacharyya A, Garewal HS, Sampliner RE. 36. Choi DW, Oh SN, Baek SJ, Ahn SH, Chang YJ, et al. Endoscopically observed
Dysplasia in short-segment Barrett esophagus: a prospective 3-year follow-up. Am lower esophageal capillary patterns. Korean J Intern Med. 2002;17:245-248.
J Gastroenterol. 1997;92:2012-2016. 37. Kim JY, Kim YS, Jung MK, Park JJ, Kang DH, et al. Prevalence of Barrett
12. Yeh C, Hsu CT, Ho AS, Sampliner RE, Fass R. Erosive esophagitis and Barrett esophagus in Korea. J Gastroenterol Hepatol. 2005;20:633-636.
esophagus in Taiwan: a higher frequency than expected. Dig Dis Sci. 1997;42: 38. Rosaida MS, Goh KL. Gastro-oesophageal reﬂux disease, reﬂux oesophagitis
702-706. and non-erosive reﬂux disease in a multiracial Asian population: a prospective,
13. Chen PH. Review: Barrett oesophagus in Taiwan. J Gastroenterol Hepatol. endoscopy based study. Eur J Gastroenterol Hepatol. 2004;16:495-501.
1997; 12:S19-22. 39. Gadour MO, Ayoola EA. Barrett oesophagus and oesophageal cancer in Saudi
14. Johnston MH, Hammond AS, Laskin W, Jones DM. The prevalence and Arabia. Trop Gastroenterol. 1999;20:111-115.
clinical characteristics of short segments of specialized intestinal metaplasia in the 40. Armstrong D. Review article: towards consistency in the endoscopic diag-
distal esophagus on routine endoscopy. Am J Gastroenterol. 1996;91:1507-1511. nosis of Barrett oesophagitis and columnar metaplasia. Aliment Pharmacol Ther.
15. Hirota WK, Loughney TM, Lazas DJ, Maydonovitch CL, Rholl V, Wong 2004;20(suppl 5):40-47.
RK. Specialized intestinal metaplasia, dysplasia, and cancer of the esophagus 41. Sharma P, Dent J, Armstrong D, Bergman JJ, Gossner L, et al. The develop-
and esophagogastric junction: prevalence and clinical data. Gastroenterology. ment and validation of an endoscopic grading system for Barrett esophagus: the
1999;116:277-285. Prague C & M criteria. Gastroenterology. 2006;131:1392-1399.
16. Gerson LB, Shetler K, Triadaﬁlopoulos G. Prevalence of Barrett esophagus in 42. Amano Y, Ishimura N, Furuta K, Takahashi Y, Chinuki D, et al. Which land-
asymptomatic individuals. Gastroenterology. 2002;123:461-467. mark results in a more consistent diagnosis of Barrett esophagus, the gastric folds
17. Rex DK, Cummings OW, Shaw M, Cumings MD, Wong RK, et al. Screen- or the palisade vessels? Gastrointest Endosc. 2006;64:206-211.
ing for Barrett esophagus in colonoscopy patients with and without heartburn. 43. The Japan Esophageal Society. Guidelines for the clinical and pathologic stud-
Gastroenterology. 2003;125:1670-1677. ies on carcinoma of the esophagus. 10th ed. Tokyo, Japan: Kanehara Co.
18. Ronkainen J, Aro P, Storskrubb T, Johansson SE, Lind T, et al. Prevalence of 44. Hoshihara Y, Kogure T, Yamamoto T, Hoshimoto M, Hoteya O. Endoscopic
Barrett esophagus in the general population: an endoscopic study. Gastroenterology. diagnosis of Barrett esophagus [in Japanese with English abstract]. Nippon Rinsho.
19. Ward EM, Wolfsen HC, Achem SR, Loeb DS, Krishna M, et al. Barrett 45. Hoshihara Y, Kogure T. What are longitudinal vessels? Endoscopic observation
esophagus is common in older men and women undergoing screening colonoscopy and clinical signiﬁcance of longitudinal vessels in the lower esophagus. Esophagus.
regardless of reﬂux symptoms. Am J Gastroenterol. 2006;101:12-17. 2006;3:145-150.
20. Romero Y, Cameron AJ, Schaid DJ, McDonnell SK, Burgart LJ, et al. Barrett 46. de Carvalho CA. Sur l’angioarchitecture veineuse de la zone de transition
esophagus: prevalence in symptomatic relatives. Am J Gastroenterol. 2002;97: oesophagogastrique et son interpretation functionnelle. Acta Anat. 1966;64:
21. Westhoﬀ B, Brotze S, Weston A, McElhinney C, Cherian R, et al. The 47. Noda T. Angioarchitectural study of esophageal varices. With special reference
frequency of Barrett’s esophagus in high-risk patients with chronic GERD. to variceal rupture. Virchows Arch A Pathol Anat Histopathol. 1984;404:381-392.
Gastrointest Endosc. 2005;61:226-231. 48. Vianna A, Hayes PC, Moscoso G, Driver M, Portmann B, et al. Normal
22. Cameron AJ, Lomboy CT. Barrett esophagus: age, prevalence, and extent of venous circulation of the gastroesophageal junction. A route to understanding
columnar epithelium. Gastroenterology. 1992;103:1241-1245. varices. Gastroenterology. 1987;93:876-889.
23. Rajendra S, Kutty K, Karim N. Ethnic diﬀerences in the prevalence of endo- 49. Kerkhof M, Steyerberg EW, Kusters JG, Kuipers EJ, Siersema PD. Predict-
scopic esophagitis and Barrett esophagus: the long and short of it all. Dig Dis Sci. ing presence of intestinal metaplasia and dysplasia in columnar-lined esophagus: a
2004;49:237-242. multivariate analysis. Endoscopy. 2007;39:772-778.
24. Wong WM, Lam SK, Hui WM, Lai KC, Chan CK, et al. Long-term prospec- 50. Takubo K, Sasajima K, Yamashita K, Tanaka Y, Fujita K. Double muscularis
tive follow-up of endoscopic oesophagitis in southern Chinese: prevalence and mucosae in Barrett esophagus. Hum Pathol. 1991;22:1158-1161.
spectrum of the disease. Aliment Pharmacol Ther. 2002;16:2037-2042. 51. Takubo K, Nixon JM, Jass JR. Ducts of esophageal glands proper and Paneth
25. Zhang J, Chen XL, Wang KM, Guo XD, Zuo AL, Gong J. Barrett esophagus cells in Barrett esophagus: frequency in biopsy specimens. Pathology. 1995;27:
and its correlation with gastroesophageal reﬂux in Chinese. World J Gastroenterol. 315-317.
2004;10:1065-1068. 52. Long JD, Orlando RC. Esophageal submucosal glands: structure and func-
26. Amarapurkar AD, Vora IM, Dhawan PS. Barrett esophagus. Indian J Pathol tion. Am J Gastroenterol. 1999;94:2818-2824.
Microbiol. 1998;41:431-435. 53. Takubo K, Vieth M, Aryal G, Honma N, Sawabe M, et al. Islands of squamous
27. Dhawan PS, Alvares JF, Vora IM, Joseph TK, Bhatia SJ, et al. Prevalence of epithelium and their surrounding mucosa in columnar-lined esophagus: a pathog-
short segments of specialized columnar epithelium in distal esophagus: association nomonic feature of Barrett esophagus? Hum Pathol. 2005;36:269-274.
with gastroesophageal reﬂux. Indian J Gastroenterol. 2001;20:144-147. 54. Paris Workshop on Columnar Metaplasia in the Esophagus and the Esopha-
28. Punia RS, Arya S, Mohan H, Duseja A, Bal A. Spectrum of clinico-pathologi- gogastric Junction, Paris, France, December 11-12 2004. Endoscopy. 2005;37:
cal changes in Barrett oesophagus. J Assoc Physicians India. 2006;54:187-189. 879-920.
29. Bafandeh Y, Esmaili H, Aharizad S. Endoscopic and histologic ﬁndings in 55. Campos GM, DeMeester SR, Peters JH, Oberg S, Crookes PF, et al. Predic-
Iranian patients with heartburn. Indian J Gastroenterol. 2005;24:236-238. tive factors of Barrett esophagus: multivariate analysis of 502 patients with gastro-
30. Rezailashkajani M, Roshandel D, Shafaee S, Zali MR. High prevalence of esophageal reﬂux disease. Arch Surg. 2001;136:1267-1273.
reﬂux oesophagitis among upper endoscopies of Iranian patients. Eur J Gastroenterol 56. Conio M, Filiberti R, Blanchi S, Ferraris R, Marchi S, et al. Risk factors for
Hepatol. 2007;19:499-506. Barrett esophagus: a case-control study. Int J Cancer. 2002;97:225-229.
31. Azuma N, Endo T, Arimura Y, Motoya S, Itoh F, et al. Prevalence of Barrett 57. Avidan B, Sonnenberg A, Schnell TG, Sontag SJ. Hiatal hernia and acid
esophagus and expression of mucin antigens detected by a panel of monoclo- reﬂux frequency predict presence and length of Barrett esophagus. Dig Dis Sci.
nal antibodies in Barrett esophagus and esophageal adenocarcinoma in Japan. 2002;47:256-264.
J Gastroenterol. 2000;35:583-592.
Gastroenterology & Hepatology Volume 4, Issue 1 January 2008 51
A M A N O A N D K I N O S H I TA
58. Wakelin DE, Al-Mutawa T, Wendel C, Green C, Garewal HS, Fass R. A 83. Veldhuyzen van Zanten SJ, Thomson AB, Barkun AN, Armstrong D, Chiba
predictive model for length of Barrett esophagus with hiatal hernia length and N, et al. The prevalence of Barrett oesophagus in a cohort of 1040 Canadian pri-
duration of esophageal acid exposure. Gastrointest Endosc. 2003;58:350-355. mary care patients with uninvestigated dyspepsia undergoing prompt endoscopy.
59. Avidan B, Sonnenberg A, Schnell TG, Chejfec G, Metz A, Sontag SJ. Hiatal Aliment Pharmacol Ther. 2006;23:595-599.
hernia size, Barrett length, and severity of acid reﬂux are all risk factors for esopha- 84. Schenk BE, Kuipers EJ, Klinkenberg-Knol EC, Eskes SA, Meuwissen SG.
geal adenocarcinoma. Am J Gastroenterol. 2002;97:1930-1936. Helicobacter pylori and the eﬃcacy of omeprazole therapy for gastroesophageal
60. de Jonge PJ, Steyerberg EW, Kuipers EJ, Honkoop P, Wolters LM, et al. Risk reﬂux disease. Am J Gastroenterol. 1999;94:884-887.
factors for the development of esophageal adenocarcinoma in Barrett esophagus. 85. Yachida S, Saito D, Kozu T, Gotoda T, Inui T, et al. Endoscopically demon-
Am J Gastroenterol. 2006;101:1421-1429. strable esophageal changes after Helicobacter pylori eradication in patients with
61. Amano K, Adachi K, Katsube T, Watanabe M, Kinoshita Y. Role of hiatus gastric disease. J Gastroenterol Hepatol. 2001;16:1346-1352.
hernia and gastric mucosal atrophy in the development of reﬂux esophagitis in the 86. Kokkola A, Sipponen P, Haapiainen R, Rautelin H, Karjalainen-Lindsberg
elderly. J Gastroenterol Hepatol. 2001;16:132-136. ML, Puolakkainen P. Development of Barrett esophagus after 'spontaneous' heal-
62. Kim JH, Kim HY, Kim NY, Kim SW, Kim JG, et al. Seroepidemiological ing of atrophic corpus gastritis. Helicobacter. 2003;8:590-593.
study of Helicobacter pylori infection in asymptomatic people in South Korea. 87. Vicari JJ, Peek RM, Falk GW, Goldblum JR, Easley KA, et al. The
J Gastroenterol Hepatol. 2001;16:969-975. seroprevalence of cagA positive Helicobacter pylori strains in the spectrum of gastro-
63. Singh V, Trikha B, Nain CK, Singh K, Vaiphei K. Epidemiology of Helico- oesophageal reﬂux disease. Gastroenterology. 1998;115:50-57.
bacter pylori and peptic ulcer in India. J Gastroenterol Hepatol. 2002;17:659-665. 88. Chow WH, Blaser MJ, Blot WJ, Gammon MD, Vaughan TL, et al. An
64. Brown LM, Thomas TL, Ma JL, Chang YS, You WC, et al. Helicobacter pylori inverse relation between cag A+ strains of Helicobacter pylori infection and risk of
infection in rural China: demographic, lifestyle and environmental factors. Int J esophageal and gastric cardia adenocarcinoma. Cancer Res. 1998;58:588-590.
Epidemiol. 2002;31:638-645. 89. Clark GW. Eﬀect of Helicobacter pylori infection in Barrett esophagus and the
65. Tan HJ, Rizal AM, Rosmadi MY, Goh KL. Distribution of Helicobacter genesis of esophageal adenocarcinoma. World J Surg. 2003;27:994-998.
pylori cagA, cagE and vacA in diﬀerent ethnic groups in Kuala Lumpur, Malaysia. 90. Vaezi MF, Falk GW, Peek RM, Vicari JJ, Goldblum JR, et al. CagA-posi-
J Gastroenterol Hepatol. 2005;20:589-594. tive strains of Helicobacter pylori may protect against Barrett esophagus. Am J
66. Jais M, Barua S. Seroprevalence of anti Helicobacter pylori IgG/IgA in asymp- Gastroenterol. 2000;95:2206-2211.
tomatic population from Delhi. J Commun Dis. 2004;36:132-135. 91. Ackermark P, Kuipers EJ, Wolf C, Breumelhof R, Seldenrijk CA, et al. Colo-
67. Lin HY, Chuang CK, Lee HC, Chiu NC, Lin SP, Yeung CY. A seroepidemio- nization with cagA-positive Helicobacter pylori strains in intestinal metaplasia of
logic study of Helicobacter pylori and hepatitis A virus infection in primary school the esophagus and the esophagogastric junction. Am J Gastroenterol. 2003;98:
students in Taipei. J Microbiol Immunol Infect. 2005;8:176-182. 1719-1724.
68. Khan MA, Ghazi HO. Helicobacter pylori infection in asymptomatic subjects 92. Ferrández A, Benito R, Arenas J, García-González MA, Sopeña F, et al.
in Makkah, Saudi Arabia. J Pak Med Assoc. 2007;57:114-117. CagA-positive Helicobacter pylori infection is not associated with decreased risk
69. Rajendra S, Ackroyd R, Robertson IK, Ho JJ, Karim N, Kutty KM. Helico- of Barrett esophagus in a population with high H. pylori infection rate. BMC
bacter pylori, ethnicity, and the gastroesophageal reﬂux disease spectrum: a study Gastroenterol. 2006;6:7.
from the East. Helicobacter. 2007;12:177-183. 93. Quddus MR, Henley JD, Sulaiman RA, et al. Helicobacter pylori infection and
70. Asaka M, Kimura T, Kudo M, Takeda H, Mitani S, et al. Relationship of adenocarcinoma arising in Barrett esophagus. Hum Pathol. 1997;28:1007-1009.
Helicobacter pylori to serum pepsinogens in an asymptomatic Japanese population. 94. Geoﬀrey WB, Clark GWB. Eﬀect of Helicobacter pylori infection in
Gastroenterology. 1992;102:760-766. Barrett esophagus and the genesis of esophageal adenocarcinoma. World J Surg.
71. Fujisawa T, Kumagai T, Akamatsu T, Kiyosawa K, Matsunaga Y. Changes in 2003;27:994-998.
seroepidemiological pattern of Helicobacter pylori and hepatitis A virus over the last 95. Henihan RD, Stuart RC, Nolan N, Gorey TF, Hennessy TP, O'Morain CA.
20 years in Japan. Am J Gastroenterol. 1999;94:2094-2099. Barrett esophagus and the presence of Helicobacter pylori. Am J Gastroenterol.
72. Yim JY, Kim N, Choi SH, Kim YS, Cho KR, et al. Seroprevalence of Helico- 1998;93:542-546.
bacter pylori in South Korea. Helicobacter. 2007;12:333-340. 96. Koike T, Ohara S, Inomata Y, Abe Y, Iijima K, Shimosegawa T. The prevalence
73. Lee SY, Park HS, Yu SK, Sung IK, Jin CJ, et al. Decreasing prevalence of of Helicobacter pylori infection and the status of gastric acid secretion in patients
Helicobacter pylori infection: a 9-year observational study. Hepatogastroenterology. with gastroesophageal junction adenocarcinoma in Japan. Inﬂammopharmacology.
74. Chen J, Bu XL, Wang QY, Hu PJ, Chen MH. Decreasing seroprevalence of 97. Wong BC, Kinoshita Y. Systematic review on epidemiology of gastroesopha-
Helicobacter pylori infection during 1993-2003 in Guangzhou, southern China. geal reﬂux disease in Asia. Clin Gastroenterol Hepatol. 2006;4:398-407.
Helicobacter. 2007;12:164-169. 98. Amano Y, Kushiyama Y, Ishihara S, Yuki T, Miyaoka Y, et al. Crystal violet
75. Vieth M, Masoud B, Meining A, Stolte M. Helicobacter pylori infection: pro- chromoendoscopy with mucosal pit pattern diagnosis is useful for surveillance of
tection against Barrett mucosa and neoplasia? Digestion. 2000;62:225-231. short-segment Barrett esophagus. Am J Gastroenterol. 2005;100:21-26.
76. Abe Y, Ohara S, Koike T, Sekine H, Iijima K, et al. The prevalence of Heli- 99. Yuki T, Amano Y, Kushiyama Y, Takahashi Y, Ose T, et al. Evaluation of
cobacter pylori infection and the status of gastric acid secretion in patients with modiﬁed crystal violet chromoendoscopy procedure using new mucosal pit pattern
Barrett esophagus in Japan. Am J Gastroenterol. 2004;99:1213-1221. classiﬁcation for detection of Barrett dysplastic lesions. Dig Liver Dis. 2006;38:
77. Zhang J, Chen XL, Wang KM, Guo XD, Zuo AL, Gong J. Relationship of 296-300.
gastric Helicobacter pylori infection to Barrett esophagus and gastro-esophageal 100. Guelrud M, Herrera I, Essenfeld H, Castro J. Enhanced magniﬁcation
reﬂux disease in Chinese. World J Gastroenterol. 2004;10:672-675. endoscopy: a new technique to identify specialized intestinal metaplasia in Barrett
78. Amano Y, Kushiyama Y, Yuki T, Takahashi Y, Chinuki D, et al. Predictors esophagus. Gastrointest Endosc. 2001;53:559-565.
for squamous re-epithelialization of Barrett esophagus after endoscopic biopsy. 101. Sharma P, Weston AP, Topalovski M, Cherian R, Bhattacharyya A, Sampliner
J Gastroenterol Hepatol. 2007;22:901-907. RE. Magniﬁcation chromoendoscopy for the detection of intestinal metaplasia and
79. Chinuki D, Amano Y, Ishihara S, et al. REG Ia protein expression in Barrett dysplasia in Barrett oesophagus. Gut. 2003;52:24-27.
esophagus. J Gastroenterol Hepatol. In press. 102. Kara MA, Ennahachi M, Fockens P, ten Kate FJ, Bergman JJ. Detection and
80. Loﬀeld RJ, van der Putten AB. Helicobacter pylori and gastro-oesophageal classiﬁcation of the mucosal and vascular patterns (mucosal morphology) in Barrett
reﬂux disease: a cross-sectional epidemiological study. Neth J Med. 2004;62: esophagus by using narrow band imaging. Gastrointest Endosc. 2006;64:155-166.
188-191. 103. Goda K, Tajiri H, Ikegami M, Urashima M, Nakayoshi T, Kaise M. Use-
81. Wani S, Sampliner RE, Weston AP, Mathur S, Hall M, et al. Lack of predic- fulness of magnifying endoscopy with narrow band imaging for the detection
tors of normalization of oesophageal acid exposure in Barrett oesophagus. Aliment of specialized intestinal metaplasia in columnar-lined esophagus and Barrett
Pharmacol Ther. 2005;22:627-633. adenocarcinoma. Gastrointest Endosc. 2007;65:36-46.
82. Weston AP, Badr AS, Topalovski M, Cherian R, Dixon A, Hassanein RS. 104. Kara MA, Peters FP, Fockens P, ten Kate FJ, Bergman JJ. Endoscopic video-
Prospective evaluation of the prevalence of gastric Helicobacter pylori infec- autoﬂuorescence imaging followed by narrow band imaging for detecting early
tion in patients with GERD, Barrett esophagus, Barrett dysplasia, and Barrett neoplasia in Barrett esophagus. Gastrointest Endosc. 2006;64:176-185.
adenocarcinoma. Am J Gastroenterol. 2000;95:387-394.
52 Gastroenterology & Hepatology Volume 4, Issue 1 January 2008
B A R R E T T E S O P H A G U S I N A S I A N P O P U L AT I O N S
105. Ouatu-Lascar R, Fitzgerald RC, Triadaﬁlopoulos G. Diﬀerentiation and pro- 111. Anderson LA, Johnston BT, Watson RG, Murphy SJ, Ferguson HR, et
liferation in Barrett esophagus and the eﬀects of acid suppression. Gastroenterology. al. Nonsteroidal anti-inﬂammatory drugs and the esophageal inﬂammation-
1999;117:327-335. metaplasia-adenocarcinoma sequence. Cancer Res. 2006;66:4975-4982.
106. Amano Y, Chinuki D, Yuki T, Takahashi Y, Ishimura N, et al. Eﬃcacy of 112. Triadaﬁlopoulos G, Kaur B, Sood S, Traxler B, Levine D, Weston A. The
proton pump inhibitors for cellular proliferation and apoptosis in Barrett oesopha- eﬀects of esomeprazole combined with aspirin or rofecoxib on prostaglandin
gus with diﬀerent mucin phenotypes. Aliment Pharmacol Ther. 2006;24(suppl E2 production in patients with Barrett oesophagus. Aliment Pharmacol Ther.
107. Peters FT, Ganesh S, Kuipers EJ, Sluiter WJ, Klinkenberg-Knol EC, et al. 113. Oyama K, Fujimura T, Ninomiya I, Miyashita T, Kinami S, et al. A COX-
Endoscopic regression of Barrett oesophagus during omeprazole treatment; a ran- 2 inhibitor prevents the esophageal inﬂammation-metaplasia-adenocarcinoma
domised double blind study. Gut. 1999;45:489-494. sequence in rats. Carcinogenesis. 2005;26:565-570.
108. Wilkinson SP, Biddlestone L, Gore S, Shepherd NA. Regression of colum- 114. Lanas A, Ortego J, Sopeña F, Alcedo J, Barrio E, et al. Eﬀects of long-term
nar-lined (Barrett) oesophagus with omeprazole 40 mg daily: results of 5 years of cyclo-oxygenase 2 selective and acid inhibition on Barrett oesophagus. Aliment
continuous therapy. Aliment Pharmacol Ther. 1999;13:1205-1209. Pharmacol Ther. 2007;26:913-923.
109. Srinivasan R, Katz PO, Ramakrishnan A, Katzka DA, Vela MF, Castell DO. 115. Heath EI, Canto MI, Piantadosi S, Montgomery E, Weinstein WM, et al.
Maximal acid reﬂux control for Barrett oesophagus: feasible and eﬀective. Aliment Secondary chemoprevention of Barrett esophagus with celecoxib: results of a ran-
Pharmacol Ther. 2001;15:519-524. domized trial. J Natl Cancer Inst. 2007;99:545-557.
110. Vaughan TL, Dong LM, Blount PL, Ayub K, Odze RD, et al. Non-steroidal
anti-inﬂammatory drugs and risk of neoplastic progression in Barrett oesophagus:
a prospective study. Lancet Oncol. 2005;6:945-952.
We invite our readers to submit case studies for publication.
For cases, please send a description of the case followed
by your treatment question(s). Case studies are published Gastro-Hep Communications, Inc.
alongside an expert commentary. Case studies should include 611 Broadway, Suite 310
a description of the case and a brief literature review. Specific New York, NY 10012
inquiries for the reviewer should also be stated. Inclusion Contact telephone number:
of tables and/or figures is encouraged. All submissions are (212) 995-5569
To submit your case study or manuscript, please send an
electronic file to firstname.lastname@example.org and mail a single
printed copy to the address provided.
Gastroenterology & Hepatology Volume 4, Issue 1 January 2008 53