2009 SSAT PLENARY PRESENTATION
Preoperative Gastric Acid Secretion and the Risk to Develop
Barrett’s Esophagus After Esophagectomy
for Chagasic Achalasia
Julio Rafael Mariano da Rocha & Ivan Cecconello &
Ulysses Ribeiro Jr & Elisa R. Baba &
Adriana Vaz Safatle-Ribeiro & Kiyoshi Iriya &
Rubens A. A. Sallum & Paulo Sakai & Sérgio Szachnowicz
Received: 3 June 2009 /Accepted: 14 August 2009 /Published online: 9 September 2009
# 2009 The Society for Surgery of the Alimentary Tract
Introduction The aim of this study was to determine the contribution of preoperative gastric secretory and hormonal
response, to the appearance of Barrett’s esophagus in the esophageal stump following subtotal esophagectomy.
Methods Thirty-eight end-stage chagasic achalasia patients submitted to esophagectomy and cervical gastric pull-up were
followed prospectively for a mean of 13.6±9.2 years. Gastric acid secretion, pepsinogen, and gastrin were measured
preoperatively in 14 patients who have developed Barrett’s esophagus (Group I), and the results were compared to 24
patients who did not develop Barrett’s esophagus (Group II).
Results In the group (I), the mean basal and stimulated preoperative gastric acid secretion was significantly higher than in
the group II (basal: 1.52 vs. 1.01, p=0.04; stimulated: 20.83 vs. 12.60, p=0.01). Basal and stimulated preoperative
pepsinogen were also increased at the Group I compared to Group II (Basal=139.3 vs. 101.7, p=0.02; stimulated=186.0 vs.
156.5, p=0.07. There was no difference in preoperative gastrin between the two groups. Gastritis was present during
endoscopy in 57.1% of the Group I, while it was detected in 16.6% of the Group II, p=0.014.
Conclusions Barrett’s esophagus in the esophageal stump was associated to high preoperative levels of gastric acid
secretion, serum pepsinogen, and also gastritis in the transposed stomach.
In the era of globalization, Chagas’ disease has also
expanded its borders to the northern hemisphere. Economic
adversity and political tribulations have increased migration
from Chagas’ endemic areas, and many of these patients
will develop gastrointestinal symptoms. In the USA, more
than seven million people from Trypanosoma cruzi endem-
ic countries become legal residents between 1981 and
2005.1–4Nonetheless, Europe has also witnessed an
increased risk, mainly due to the migration to Spain and
Portugal. Consequently, US and European clinicians are
Manuscript was presented at the 50th Annual Meeting of the Society
for Surgery of the Alimentary Tract, in Chicago, IL, USA, in
May 30–June 3, 2009.
J. R. M. da Rocha:I. Cecconello:U. Ribeiro Jr:E. R. Baba:
A. V. Safatle-Ribeiro:R. A. A. Sallum:P. Sakai:
Digestive Surgery Division, Department of Gastroenterology,
University of São Paulo School of Medicine,
São Paulo, Brazil
E. R. Baba:K. Iriya
Department of Pathology,
University of São Paulo School of Medicine,
São Paulo, Brazil
J. R. M. da Rocha (*)
Rua Oscar Freire, 1546 Apto:171,
05409-010 São Paulo, SP, Brazil
J Gastrointest Surg (2009) 13:1893–1899
likely to see an increasing number of patients with
suspected or confirmed chronic Chagas’ disease.5
T. cruzi, the cause of Chagas’ disease, leads to diverse
stages of destruction of the intramural plexuses of the
gastrointestinal tract. The clinical symptoms are usually
limited to the esophagus and colon; however, the entire
gastrointestinal tract plexuses are also partially affected.6
Chagasic achalasia is a well-defined manifestation of this
disease and may be treated by surgical techniques targeting
the esophagogastric junction (i.e., Heller myotomy and
partial fundoplication) in patients with non-advanced form
of chagasic achalasia.7
Esophagectomy and gastric pull-up with cervical anas-
tomosis represents the main treatment for the advanced end-
stage of this disease, with acceptable morbidity, mortality,
and reasonable postoperative outcome for a benign dis-
ease.7,8However, previous study on postoperative outcome
of chagasic patients who have undergone esophagectomy
with gastric pull up showed some complications including
bleeding severe gastritis, gastric ulcers in the transposed
stomach, and also esophagitis, esophageal ulcers, and
Barrett’s epithelium in the esophageal cervical remnant.9–14
The contributing factors to Barrett’s esophagus develop-
ment, in this situation, are not completely known.
Thus, the aim of this study was to determine the
contribution of preoperative conditions, regarding gastric
secretory and hormonal response, to the appearance of
Barrett’s esophagus in the esophageal stump, in patients
who underwent subtotal esophagectomy with gastric pull-
up for end-stage chagasic achalasia.
Patients and Methods
Thirty-eight consecutive patients were studied preopera-
tively and postoperatively, regarding gastric acid secretion
(GAS), serum pepsinogen (SP), and serum gastrin (SG).
These patients with end-stage chagasic achalasia (severe
dysphagia, dilation greater than 7 cm, sigmoid esophagus,
and esophageal atony, and complications of previous
surgical therapies) were submitted to subtotal esophagec-
tomy and gastric pull-up with pyloroplasty at the Digestive
Surgery Division of the Gastroenterology Department of
the University of Sao Paulo, School of Medicine. This
patient population is part of a published series of 101
esophagectomy patients followed by our group.13
Twenty (52.6%) patients were male and 18 (47.4%) were
female, with a mean age of 43.6±12.1 ranging from 19 to
65 years old. All were epidemiologically and serologically
positive for Chagas’ disease. Symptoms of dysphagia,
regurgitation, weight loss, and heartburn were present in all
patients. Diagnosis of advanced achalasia was confirmed by
Barium X-ray, upper endoscopic examination and manomet-
ric studies. The patients were followed prospectively for a
mean of 13.6±9.2 years (ranging from 2 to 25 years).
This study was approved by the Research and Ethics
Committee of the University of São Paulo, School of
Medicine, and patient writing consent was obtained from all
A transhiatal subtotal esophagectomy with gastric pull-up
to the cervical region was performed. The mean length of
the cervical esophageal stump was 5 cm. Anterior extra-
mucosal pyloromyotomy was performed in all patients.
Clinical and Radiological Assessment
Before and after surgical treatment all patients were
assessed by clinical, radiological, and endoscopic examina-
tions. Postoperatively, clinical and endoscopic evaluation
was performed every 1 to 2 years. The following clinical
parameters were studied: dysphagia, regurgitation, heart-
burn, diarrhea, Dumping Syndrome, fasting gastric resi-
dues, and body mass index (BMI). Imaging control, X-Ray
study of upper gastro-intestinal tract, and gastric emptying
time was studied before and after surgical treatment.
and gastric biopsies were performed in all patients every
2 years. The presence of esophagitis (Savary–Miller grades
mucosa in the esophageal stump (Fig. 1). The presence of
gastritis, or bile in the transposed stomach was also described.
Figure 1 Endoscopic view of metaplastic columnar mucosa in the
esophageal stump. Red salmon color mucosa may be seen.
1894J Gastrointest Surg (2009) 13:1893–1899
Gastric Acid Secretion in Basal Condition
and After Pentagastrin Stimulation
The functional studies were performed between 1 to
4 weeks before the operation to assure data reliability, and
at fourth postoperative year.
Due to the achalasia, patients were kept on a liquid diet
for 3 days, and the esophagus was cleaned with water using
a 30-Fr oral tube on the previous evening, followed by a
12-h fasting period. GAS was evaluated as described
elsewhere.15The GAS results were expressed in mEq of
hydrochloric acid per hour (mEq/h), as basal secretion and
peak acid output after pentagastrin stimulation.15
Basal and Betazole® Stimulated Serum Pepsinogen Levels
The first blood sample was collected for estimating basal
serum pepsinogen. Then, 1.7 mg/kg of body weight of
Betazole® was given intramuscularly. Antihistamine prod-
ucts (promethazine and hydrocortisone sodium succinate)
were always available in the event of hypersensitivity to the
injected drug. Basal blood samples of 8 ml were obtained
from a peripheral vein at 60, 90, and 120 min after
Betazole® stimulation. Serum pepsinogen was determined
according to the method described by Uete et al.16and
standardized by Saez-Alquezar et al.17, in the Biochemistry
Laboratory of the University Hospital of the University of
São Paulo Medical School.
Basal Serum Gastrin
Eight milliliters of venous blood sample was collected to
analyze basal serum gastrin in duplicate. Serum gastrin was
estimated by radioimmunoassay using Gama Dab/125
Gastrin, Radioimmunoassay Kit, Clinical assays, Division
of Travenal Laboratories Inc., Cambridge, Massachusetts,
Collected biopsies were stained by H&E and the patholog-
ical results were reviewed by experienced pathologists.
Barrett’s epithelium in the esophageal remnant was defined
by the presence of esophageal columnar epithelium with
specialized intestinal metaplasia (Fig. 2).
Nonparametric data were analyzed using Chi-Square and
Fisher’s exact test for contingency tables. For parametric
data, an unpaired t test was used for comparison of
differences between means in the groups. Statistical
significance was endorsed by a p value of less than 0.05.
Barrett’s esophagus was always preceded by esophagitis
and was first observed at 18 months postoperatively, with a
mean of Barrett’s appearance = 7.73 years (1.6–17 years).
Table1 shows the relationship between clinical–pathologic
parameters and the occurrence of Barrett’s esophagus in the
esophageal stump. There was a significant association
between the development of Barrett’s epithelium and the
time interval post-esophagectomy. The presence of bile in the
gastric conduit, and subjective symptoms of pyrosis and
gastritis were also associated with the development of
Barrett’s. On the other hand, there was no statistically
significant association between Barrett’s and age, gender,
and body mass index (Table 1).
Gastric Acid Secretion
Results of basal and pentagastrin stimulated GAS are pre-
sented in Table 1. In the Barrett’s group (I), the mean basal
and pentagastrin-stimulated gastric acid secretion was signif-
icantly higher than in the non-Barrett’s group (basal: 1.52 vs.
1.01, p=0.04; stimulated: 20.83 vs. 12.60 mEq/h,
At 4 years postoperative, basal and stimulated GAS were
also increased in Group I compared to Group II (basal = 1.38
vs. 1.1, p=0.28; stimulated = 15.8 vs. 11.6, p=0.08)
however, the differences were not statistically significant.
Barrett’s development in the esophageal stump after
esophagectomy and gastric pull occurred at the mean time
of 7 years. Thus, when patients were stratified according to
the time of development of Barrett’s esophagus, early
Barrett’s appearance, i.e. less than 7 years postoperatively
(eight cases, mean = 4.62±2.25 years), was associated with
higher preoperative acidity when compared to those with
Figure 2 Histological appearance of Barrett’s epithelium with the
presence of specialized cells (intestinal metaplasia; ×200).
J Gastrointest Surg (2009) 13:1893–18991895
late occurrence (six cases, mean = 11.76±3.26 years;
Table 2). Therefore, higher preoperative GAS levels were
also associated with early Barrett’s development. (Table 2).
Basal and Betazole® stimulated SP are shown in Table 1.
Preoperative basal and stimulated pepsinogen were
increased in Group I compared to Group II (basal =
139.35 vs. 101.7, p=0.02; stimulated = 186.05 vs. 156.5,
At 1 year postoperative, basal and stimulated pepsino-
gen were also increased in Group I compared to Group II
(basal = 96.6 vs. 71.7, p=0.008; stimulated = 146.2 vs.
Basal Serum Gastrin
There was no difference in basal SG values in the Barrett’s
patients compared to the non-Barrett’ subjects, p=0.89
Esophagectomy and gastric pull-up with cervical anasto-
mosis is currently the procedure of choice in the manage-
ment of end-stage chagasic achalasia.7,8However, this type
of reconstruction after esophageal resection causes mod-
ifications in anatomy and physiology in the upper gastro-
Barrett’s (14 patients)Non-Barrett’s (24 patients)p value
Preoperative gastric acid secretiond
Postoperative gastric acid secretion (4 years)d
Basal1.38±0.94 mEq/l (0.1–3.3)
M.A.O.15.8±9.20 mEq/l (4.4–32.2)
Preoperative pepsinogen levels
Basal139.3±60.9 (65–263 ug/ml)
Stimulated 186.0±63.6 (99–308 ug/ml)
Postoperative pepsinogen levels (1 year)
Basal 96.6±37.4 (57 to 156 ug/ml)
Stimulated146.2 + 43.0(92–210 ug/ml)
Preoperative basal gastrin
Gastrin80.44 (40 to 157 pg/ml)
44 (24–60) SE=2.98
Male = 50%
22.97 (19.9–27.78) SE = 0.76
43.12 (19–65) SE=2.57
Male = 45.83%
20.92 (19.9–25.3) SE = 0.96
Present = 11/14 (78.6%)
Present = 11/14 (78.6%)
Present = 9/24 (37.5%)
Present = 12/24 (50%)
Present = 8/14 (57.1%)
Present = 11/14 (78.6%)
Present = 4/24 (16.7%)
Present = 11/24 (45.83%)
1.52±1.01 mEq/l (0.15–3.9)
20.83±9.45 mEq/l (7.7–37.4)
1.01±0.53 mEq/l (0.17–1.83)
12.60±4.57 mEq/l (1.48–18.8)
1.1±0.45 mEq/l (0.4–2.1)
11.6±5.2 mEq/l (1.76–21.4)
101.7±37.0 (60–190 ug/ml)
156.5±45.2 (105–248 ug/ml)
71.7±21.5 (53–120 ug/ml)
110.5±32.0 (62 to 192 ug/ml)
82.75 (10.1 to 184.74 pg/ml)0.89a
Table 1 Comparisons of
Patients with and without
Barrett’s Esophagus in the
Esophageal Stump Regarding
Clinical and Laboratorial
cFisher’s exact test
Table 2 Barrett’s Esophagus in the Esophageal Remnant and its Relationship to Preoperative Gastric Acid Secretion and Timing of Occurrence
Preoperative gastric acid secretionEarly (8 cases; <7years) Late (6 cases; >7years)p value
1.56±1.13 mEq/h (0.2–3.9)
23.16±8.92 mEq/h (12.3–37.4)
1.26±0.24 mEq/h (0.9–1.4)
11.91±6.57 mEq/h (4.36–13.3)
aUnpaired t test
1896J Gastrointest Surg (2009) 13:1893–1899
Long-term follow-up of these patients has shown
complications that, if adequately treated, did not influence
the clinical outcome, but were associated with downstream
clinical findings that raised some concerns: (1) esophagitis
in the esophageal cervical stump rose over time and (2)
diffuse gastritis and peptic ulcer of the transposed stomach,
starting at 5 or more years of follow-up.9Based on these
findings, our group initiated a prospective study that
included quantifying preoperative gastric acid secretion,
pepsinogen, and basal gastrin as well as clinical and
endoscopic evaluation, biannually.
We have demonstrated that after esophagectomy with
vagotomy, the GAS and SP levels decrease from 6 months
to 1 year postoperative, and that there is a recovery of the
GAS and SP levels to near preoperative values after 4 years
of surgical treatment.9,13
In 1991 and 1992 we reported for the first time the
presence of Barrett’s epithelium developing in the esoph-
ageal stump of chagasic achalasia patients.10,11The
occurrence of ectopic columnar metaplasia and Barrett’s
esophagus in the esophageal stump was not detected in the
first 18 months of follow-up but did rise over time; 10.9%
between 1 and 5 years; 29.5 between 5 to 10 years and
57.5% at 10 or more years of follow-up.13
Resection or disruption of natural antireflux mecha-
nisms, esophagogastric direct anastomosis, pyloroplasty,
impairment of gastric motility, recovery of acid secretion
from gastric conduit, and impaired motility of esophageal
remnant all have the potential to contribute to esophageal
stump mucosal damage.12–14,18
We sought in this study to evaluate the contribution of
preoperative conditions, regarding gastric secretory and
hormonal response, to the appearance of Barrett’s esopha-
gus in the esophageal stump, in patients who underwent
subtotal esophagectomy for end-stage chagasic achalasia.
In patients that underwent esophagectomy mainly for
cancer, O’ Riordan et al.19reported a 50% incidence of
columnar metaplasia above the anastomosis in 48 post-
esophagectomy patients, with a median follow-up of
26 months (range = 12–67 months). Specialized intestinal
metaplasia was detected in 54% of those patients. Accord-
ing to the authors, the prevalence of columnar metaplasia
did not relate to the magnitude of acid or bile reflux, to
preoperative neo-adjuvant therapies, or to the original
tumor histology. However, the duration of the reflux was
the most significant parameter, with increasing prevalence
over time. The authors concluded that the duration of acid
and bile reflux, rather than the volume of reflux, underlies
the development of metaplasia.19
In the present study, clinical alterations including the
presence of gastritis and bile in the gastric conduit noted
during endoscopic surveillance, and intense pyrosis were all
associated with Barrett’s appearance. Unfortunately, we did
not have the equipment to measure the presence of bile in
gastric and the esophageal mucosa and their harmful effects
are strengthened by the action of gastric secretion.9,22,23
In the present investigation, chagasic gastric acid secretion,
serum pepsinogen, and basal serum gastrin were analyzed in
patients who had developed Barrett’s esophagus in the
esophagealstump andcomparedtothose whodidnot develop
Barrett’s epithelium. In the Barrett’s group, the preoperative
mean basal and pentagastrin-stimulated GAS was significant-
ly higher than in the non-Barrett’s group. Postoperative GAS
measured at 4 years was also increased in the Barrett’s group,
however, statistically marginally significant. These results
may be confounded by the presence of duodenogastric reflux
due to pyloromyotomy.
Our data demonstrated that GAS and pepsinogen produc-
tion can be stimulated despite chagasic involvement of the
intramural stomach plexuses. This evidence implies that the
majority of parietal and chief cells, in chagasic patients,
maintain the functional capacity in basal condition and after
stimulation.5Barrett’s group serum pepsinogen values were
higher compared to the non-Barrett’s group. Other authors
have found an association between GAS and serum
pepsinogen; however, the scattering of individual values
was such that serum pepsinogen could not be used as an
index of gastric acid secretion in clinical practice.24
In the present research, basal serum gastrin showed a
significantly higher basal value in both groups, nonetheless
serum gastrin did not influence the appearance of Barrett’s
metaplasia. A possible explanation for this finding might be
the gastric hypoacidity observed in Chagas’ disease
patients,5,25,26acting as a continuous stimuli to the parietal
cells. Other mechanisms are postulated to explain the basal
hypergastrinemia in Chagas’ disease patients: (1) hypersen-
sitivity of the “G” cells due to the autonomic denervation
and/or (2) increased production of extra-gastric gastrin
under these circumstances.25–28
Therefore, the present study enabled us to evaluate
clinical, exocrine, and endocrine aspects of the behavior of
gastric secretion and their relationship to the Barrett’s
esophagus in the esophageal remnant. We were able to
demonstrate the association between high gastric acid
secretion and high serum pepsinogen levels with earlier
development of Barrett’s esophagus in the esophageal
stump. Additionally, the presence of gastritis in the
transposed stomach, probably due to exposure to duodeno-
gastric reflux, may also indicate higher risk for developing
Barrett in the esophageal stump.
Posner, University of Chicago, for revising the manuscript and for his
The authors are grateful to Professor Mitchell C.
J Gastrointest Surg (2009) 13:1893–18991897
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Dr. Ulysses Ribeiro, Jr, Presenter (University of Sao
Paulo, Sao Paulo, Brazil)
Dr. Marco Patti (University of Chicago): Congratulations
on a very nice presentation and a very interesting study.
Clearly your group has a unique experience in the treatment
of esophageal achalasia.
I have three questions for you.
As you mention in the manuscript, most of these patients
had failed every other modality of treatment, including
dilatation or Heller myotomy, before undergoing esophagec-
tomy. How many of these patients had esophagitis or Barrett's
esophagus before undergoing esophagectomy?
You showed that there is an increase in the acid gastric
secretion and an increased level of pepsinogen. However,
based on the endoscopy that is not very reliable, you
assume that bile reflux plays a predominant role. Have you
decided to assess bile reflux in a more objective way such
as by the Bilitec or by pH/impedance monitoring?
Finally, assuming that duodeno gastric esophageal reflux
plays a major role in the development of the cervical
metaplasia, have consider some form of bile diversion in
Dr. Ulysses Ribeiro, Jr: Thank you, Dr. Patti, for your
We have not seen any Barrett's before the surgery in
1898 J Gastrointest Surg (2009) 13:1893–1899
The patients did not have important gastroesophageal Download full-text
reflux before surgery because the esophageal junction was
functionally closed due to achalasia, with a very high
degree of dysphagia. So, dilatation and or myotomy have
failled in these patients.
I know that the endoscopic view of the bile is not so
reliable, but we didn't have bilitec R to do the measure-
ments. Thus, we have included the bile endoscopic view to
evaluate the duodenogastric reflux.
Considering bile diversion, we are thinking about it.
But, postoperatively Roux en Y bile diversion would be a
difficult and risky operation, with high complication rates.
So, that's a way to go, but I'm not sure if we are going to
do it because of the referred complications.
Dr. Steve Demeester (USC, Los Angeles): Just a quick
question. We know that the severity of reflux after gastric
pullup is related to the height of the anastomosis, if it is low
in the chest reflux is worse.
In the videos it looked like there was quite a bit of
residual cervical esophagus. Do you have an idea of where
your anastomosis were placed in most of these individuals?
Dr. Ulysses Ribeiro Jr:
esophageal stump is around 5 to 6 centimeters.
The mean length of the
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