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Prevalence of Barrett's esophagus in systemic sclerosis.

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ARTHRITIS & RHEUMATISM
Vol. 52, No. 9, September 2005, pp 2882–2888
DOI 10.1002/art.21261
© 2005, American College of Rheumatology
Prevalence of Barrett’s Esophagus in Systemic Sclerosis
J. Wipff,1 Y. Allanore,1 F. Soussi,1 B. Terris,1 V. Abitbol,1 J. Raymond,2
S. Chaussade,1 and A. Kahan1
dysplasic BE. Long-term prospective studies are warranted to determine the phenotype of SSc patients at
high risk of developing dysplasia or esophageal adenocarcinoma.
Objective. The esophagus is the most commonly
affected gastrointestinal area in systemic sclerosis
(SSc). Patients with SSc frequently develop gastroesophageal reflux, esophageal injury, and sometimes,
intestinal metaplasia, or Barrett’s esophagus (BE),
which may increase the risk of esophageal adenocarcinoma. This study sought to determine the prevalence of
BE and esophageal adenocarcinoma in a cohort of SSc
patients.
Methods. One hundred ten SSc patients who were
receiving long-term treatment with proton-pump inhibitors (PPIs) were assessed systematically by esophageal
manometry and endoscopy. Esophageal biopsies were
performed when macroscopic abnormalities were detected, and BE was diagnosed histologically.
Results. Among the 110 patients, 14 had BE
(12.7%). None of the patients with BE had adenocarcinoma, but 3 of the 14 patients (21%) had dysplasia on
esophageal biopsy. Similar proportions of patients with
and without BE had abnormal peristalsis and decreased
lower esophageal sphincter pressure. No association
between BE and other disease characteristics was demonstrated.
Conclusion. In this study, 12.7% of SSc patients
who had been treated with PPIs for long periods had
BE, similar to the prevalence in patients with gastroesophageal reflux disease. Although none of the patients
had esophageal adenocarcinoma, patients with BE
should be followed up closely, particularly patients with
Systemic sclerosis (SSc) is a connective tissue
disease characterized by early vascular involvement,
which culminates in excessive deposition of collagen in
the skin and internal organs. The gastrointestinal tract is
the second most commonly involved site (1). The most
frequently involved area of this tract is the esophagus,
affecting 75–90% of patients with SSc (1–4). Damage is
prominent in the distal two-thirds of the esophagus,
resulting in abnormal esophageal motility. Manometry
reveals a dysfunctioning lower esophageal sphincter and
diminution or abolition of esophageal peristalsis, with
poor clearance of acidic material following reflux (3).
This increases the time of contact between acid and the
esophageal mucosa, thus creating a predisposition to
esophageal injury.
The pathophysiologic mechanism of esophageal
involvement is thought to depend on early vascular
impairment, as indicated by the relationship between
aperistalsis and Raynaud’s phenomenon (5), followed by
neurologic abnormalities that lead to muscular disturbance (3,6). Regardless of its etiology, chronic gastroesophageal reflux can be complicated by a columnarlined epithelium with goblet cells, known as Barrett’s
esophagus (BE). This complication affects between 5%
and 15% of patients with chronic gastroesophageal
reflux disease (GERD) (7,8). Furthermore, BE increases the risk of esophageal adenocarcinoma (9).
Only a few studies have determined the prevalence of BE and esophageal adenocarcinoma in SSc, and
the results are contradictory (10,11). The aims of our
present cross-sectional study were to use systematic
endoscopy to investigate the prevalence of BE and
esophageal adenocarcinoma, and to try to identify a
disease phenotype associated with these lesions.
1
J. Wipff, MD, Y. Allanore, MD, PhD, F. Soussi, MD, B.
Terris, MD, PhD, V. Abitbol, MD, S. Chaussade, MD, PhD, A. Kahan,
MD, PhD: Cochin Hospital, AP-HP Paris 5 University, Paris, France;
2
J. Raymond, MD: Saint-Vincent de Paul Hospital, Paris 5 University,
Paris, France.
Drs. Wipff and Allanore contributed equally to this work.
Address correspondence and reprint requests to Y. Allanore,
MD, PhD, Service de Rhumatologie A, Hôpital Cochin, 27 rue du
faubourg St Jacques, 75014 Paris, France. E-mail: yannick.allanore@
cch.ap-hop-paris.fr.
Submitted for publication December 29, 2004; accepted in
revised form June 3, 2005.
2882
BARRETT’S ESOPHAGUS IN SYSTEMIC SCLEROSIS
2883
Table 1. Characteristics of systemic sclerosis (SSc) patients with and without Barrett’s esophagus (BE)*
Age, mean ⫾ SD years
Sex, female/male
Tobacco use
Alcohol use
PPI dose
Mean mg/day
20 mg/day
⬎20 mg/day
Nonsteroidal antiinflammatory drugs
Platelet antiaggregating
Prednisone ⬍10 mg per day
Calcium channel blockers
Angiotensin-converting enzyme inhibitors
Diffuse/limited cutaneous form of SSc
SSc duration, mean ⫾ SD years
Raynaud’s phenomenon duration, mean ⫾ SD years
Pulmonary arterial hypertension
Pulmonary fibrosis on CT scan
Positive antinuclear antibodies
Positive anti–topoisomerase I antibodies
Positive anticentromere antibodies
Decreased FVC†
Decreased DLCO/VA‡
All SSc
patients
(n ⫽ 110)
SSc patients
with BE
(n ⫽ 14)
SSc patients
without BE
(n ⫽ 96)
58 ⫾ 12
93/17
4
0
110 (100)
31
65 (59)
45 (41)
14 (13)
33 (30)
44 (40)
95 (86)
35 (32)
45 (41)/65 (59)
9⫾8
13 ⫾ 11
18 (16)
55 (50)
79 (72)
32 (29)
19 (17)
27 (25)
44 (40)
53 ⫾ 13
12/2
0
0
14 (100)
33
5 (36)
9 (64)
3 (21)
3 (21)
6 (43)
12 (86)
6 (43)
6 (43)/8 (57)
10 ⫾ 9
13 ⫾ 11
3 (21)
8 (57)
12 (86)
4 (29)
3 (21)
4 (29)
7 (50)
59 ⫾ 12
81/15
4
0
96 (100)
27
60 (62)
36 (37)
11 (11)
30 (31)
38 (40)
83 (86)
29 (30)
39 (41)/57 (59)
9⫾8
13 ⫾ 11
15 (16)
47 (49)
67 (70)
28 (29)
16 (17)
23 (24)
37 (39)
* Except where indicated otherwise, values are the no. (%) of patients. PPI ⫽ proton-pump inhibitor; CT ⫽ computed
tomography.
† Abnormal forced vital capacity (FVC) defined as ⬍75% of normal value.
‡ Abnormal diffusing capacity for carbon monoxide divided by alveolar volume (DLCO/VA) defined as ⬍75% of normal
value.
PATIENTS AND METHODS
All patients who were hospitalized consecutively with a
diagnosis of SSc in accordance with the classification criteria
established by the American College of Rheumatology (formerly, the American Rheumatism Association) (12) and who
were followed up systematically during a 2-year period were
included. All patients gave their informed consent for all
procedures. The following clinical data were collected: age,
sex, cutaneous SSc subtype according to the definition by
LeRoy et al (13), duration of disease (date of first nonRaynaud’s symptom), duration of Raynaud’s phenomenon,
digital ulceration, and prostacyclin use. Pulmonary fibrosis was
diagnosed on the basis of a computed tomography scan and
abnormal results on respiratory function tests (forced vital
capacity, and diffusing capacity for carbon monoxide divided
by alveolar volume, with abnormal defined as ⬍75% of
predicted values) (14). Pulmonary arterial hypertension was
defined as a pulmonary arterial pressure higher than 40 mm
Hg at rest on Doppler echocardiography. The following biologic tests were carried out: standard blood tests, immunofluorescence on HEp-2 cells for antinuclear and anticentromere
antibodies, and counterimmunoelectrophoresis for anti–
topoisomerase I and anti-RNP.
Gastroesophageal involvement was screened by manometry to analyze lower esophageal sphincter pressure, with
a normal cutoff level of 10 mm Hg (14 cm H2O). Patients were
divided into 3 groups according to peristaltic wave propagation: aperistalsis (⬍10% of waves propagated), abnormal
propagation (⬍50% of waves propagated), and normal propagation. Manometry was performed after a 3-day washout
period to eliminate drugs that may interfere with esophageal
motility (cisapride, metoclopramide, calcium channel blockers). All included patients underwent an endoscopy with a
Fujinon EG 200FP or 450FP endoscope (Fujinon, Saitama,
Japan). In more than 80% of patients, the endoscopy was
performed after administration of general anesthesia (propofol), which is standard procedure for all patients in the
gastroenterology department.
When macroscopic lesions suggestive of BE, esophagitis, or strictures were detected, several biopsy samples (an
average of 4) were collected from each patient. BE was defined
by the finding of intestinal architecture in the lower esophagus
displaying a villiform columnar-lined mucosa with goblet cells;
these features of BE were identified by classic coloration on
hematoxylin and eosin staining. Long-segment BE, which is
suspected to confer a higher risk of adenocarcinoma, was
defined by the presence of lesions ⬎3 cm. We did not take the
fundic metaplasia into account. All patients with a normal
macroscopic aspect on endoscopy were considered to be free
of metaplasia.
2884
WIPFF ET AL
Figure 1. Histologic pattern of Barrett’s esophagus (BE) occurring in 2 patients. A, Biopsy sample of the distal esophagus
showing BE without dysplasia. B, Distal esophageal mucosa showing BE with high-grade dysplasia; the intestinal epithelium
contains cells with markedly enlarged nuclei. These atypia involve not only the glands, but also the mucosal surface.
(Hematoxylin and eosin stained; original magnification ⫻ 800.)
In the final 12 months of followup, all patients who
underwent endoscopy were tested for Helicobacter pylori. The
method for detection of H pylori was an enzyme-linked immunosorbent assay (Helico Premier; Meridian Diagnostic, Cincinnati, OH).
The chi-square test and the Mann-Whitney U test were
used to compare data. P values less than 0.05 were considered
significant.
RESULTS
One hundred ten patients were included in the
study. All patients had been treated with proton-pump
inhibitors (PPIs) since receiving the diagnosis of SSc or
since the initial commercial marketing of omeprazole in
1989, and had also been treated, when necessary, with
prokinetic agents. The characteristics of the SSc patients
are summarized in Table 1. Fourteen patients (12.7%)
were diagnosed with BE on the basis of histologic
findings (Figure 1A). Macroscopic findings were
suggestive of BE in 24 patients, but the diagnosis was
confirmed in only 14 of the patients. Intestinal metaplasia was found in several biopsy sites in 8 of the 14
patients with BE. None of these patients developed
adenocarcinoma. However, 3 of the 14 patients with BE
(21%) had dysplasia on intestinal metaplasia; among
Table 2. Results of gastroesophageal assessments in systemic sclerosis (SSc) patients with and without Barrett’s
esophagus (BE)*
BE
Short-segment (⬍3 cm)
Long-segment (⬎3 cm)
Dysplasia
Esophageal adenocarcinoma
Manometric aperistalsis
Manometric abnormal peristalsis
Manometric decreased lower esophageal
sphincter pressure (⬍14 cm H2O)
Helicobacter pylori–positive on serology
* Values are the no. (%) of patients.
All SSc patients
(n ⫽ 110)
SSc patients with BE
(n ⫽ 14)
SSc patients without BE
(n ⫽ 96)
14 (12.7)
13 (12)
1 (1)
3 (3)
0
41 (37)
80 (73)
62 (56)
14 (100)
13 (93)
1 (7)
3 (21)
0
8 (57)
13 (93)
9 (64)
–
–
–
0
0
33 (34)
67 (70)
53 (55)
18/50 (36)
1/10 (10)
17/40 (42.5)
BARRETT’S ESOPHAGUS IN SYSTEMIC SCLEROSIS
Table 3. Studies of Barrett’s esophagus (BE) in systemic sclerosis
(SSc) patients
Study design, author, year (ref.)
Retrospective
Recht et al, 1988 (30)
Weston et al, 1998 (31)
Marie et al, 2001 (29)
Cross-sectional
Present study
Case report
Cameron and Payne, 1978 (15)
Agha and Dabich, 1985 (16)
Anderson and Seymour, 1987 (17)
Chang et al, 1991 (18)
Dill, 1983 (19)
Halpert et al, 1983 (20)
Ilan et al, 1996 (21)
Lambert et al, 1987 (22)
McKinley and Sherlock, 1984 (23)
Maekawa and Nogami, 1993 (24)
Navon et al, 1991 (25)
Niv et al, 1988 (26)
Sprung and Gibb, 1985 (27)
Szigeti et al, 2001 (28)
Total
No. (%) of SSc
No. (%) of
patients with
SSc patients
BE and
with BE
adenocarcinoma
10 (37)
9 (16)
1 (2)
2
–
–
14 (13)
–
2
2
3
1
1
2
1
1
1
1
1
1
3
5
59
–
–
–
–
–
2
1
–
1
1
–
1
–
–
8 (14)
these patients, 2 had low-grade dysplasia (one-fifth of
biopsy sites) and 1 had high-grade dysplasia (high
grade in one-fourth [Figure 1B] and low grade in
two-fourths).
Of the patients with dysplasia, all 3 were women
who had a limited cutaneous form of SSc and a long
duration of Raynaud’s phenomenon (duration of 37
years, 21 years, and 15 years). These 3 women had
recurrent digital ulcerations, and in 2 of the 3, the
ulcerations were treated with prostacyclin. Esophageal
manometry showed abnormal propagation in all 3
women and aperistalsis in 2 of them. Sphincter pressure
in the lower esophagus was markedly decreased, with
levels below 12 cm H2O in all 3 patients.
The manometry results for the whole population
are shown in Table 2. In patients with BE compared with
those without BE, there was a trend toward a higher
frequency of aperistalsis (57% versus 34%, respectively;
P not significant [NS]), a lower wave propagation (93%
versus 70%, respectively; P NS), and a higher frequency
of abnormal (⬍14 cm H2O) lower esophageal sphincter
pressure (64% versus 55%, respectively; P NS) (Table
2). We found a trend toward a higher frequency of
abnormal manometry results (abnormal peristalsis or
2885
abnormal sphincter pressure in the lower esophagus) in
the BE group (100%) than in the non-BE group (76%)
(P ⫽ 0.09). Patients with BE were significantly less likely
to be H pylori–positive than were patients without BE
(10% versus 42.5%, respectively; P ⬍ 0.05).
We found no significant difference in the clinical
and biologic characteristics between patients with BE
and those without BE (Table 1). Notably, patients with
and without BE had a similar mean duration of disease
(mean ⫾ SD 10 ⫾ 9 years versus 9 ⫾ 8 years, respectively) and mean duration of Raynaud’s phenomenon
(both 13 ⫾ 11 years), and were equally likely to have the
limited cutaneous (57% versus 59%, respectively) or
diffuse (43% versus 41%, respectively) forms of SSc.
DISCUSSION
In this series of 110 SSc patients who underwent
long-term treatment with PPIs and were analyzed by
systematic endoscopy, the prevalence of BE was 12.7%.
Since the initial description of an association between
BE and SSc by Cameron and Payne in 1978 (15),
numerous case reports (16–28) and 3 retrospective
series (29–31) (Table 3) have been published. In the
earliest retrospective series, the prevalence of BE was
estimated to be 37% among patients who were assessed
by endoscopy following reports of clinical gastrointestinal symptoms (30), and 16% among patients referred to
a gastroenterology department (31). SSc patients who
undergo endoscopy because of digestive symptoms may
represent the subgroup with the most severe esophageal
involvement, thus increasing the prevalence of BE. In
the other retrospective series, systematic esophageal
manometry and endoscopy were performed in 43 patients, with BE detected in only 1 patient (prevalence of
2%) (29). The discrepancy in the prevalence between
the latter study and our results could be related mainly
to the fact that the study by Marie et al was not designed
to determine the prevalence of BE, but rather to investigate the link between esophageal involvement and
pulmonary involvement in SSc.
Abnormalities of esophagus motility leading to
BE can occur in asymptomatic patients (2,4,32); 30–40%
of patients with esophageal lesions are asymptomatic
(1). Indeed, we did not take the digestive symptoms of
our patients into account because they were receiving
PPIs, which would thus mask gastrointestinal symptoms.
Long-term systematic treatment with PPIs that may also
influence the prevalence of BE has been proven to be
effective in ameliorating symptoms and macroscopic
2886
lesions when erosive esophagitis occurs in GERD (33),
and to be effective in reducing symptoms of esophagitis
in SSc patients by decreasing the time with pH under 4,
as demonstrated by pH-metry (34). However, PPIs have
less influence on biliary reflux, and therefore this may
account for the generation of BE in our patients.
GERD is a recognized risk factor for BE (30). In
our cross-sectional series, the frequency of BE in patients with SSc seemed to be similar to that in patients
with GERD, 5–15% of whom are thought to develop BE
(7,8). The typical BE risk factors associated with intestinal metaplasia include male sex, white race, obesity,
and alcohol or tobacco use (35). In contrast, 85% of our
SSc patients were female, all had a body mass index ⬍30
kg/m2, and the majority did not consume tobacco or
alcohol. Although nonsteroidal antiinflammatory drugs
are known to decrease the evolution of BE until dysplasia,
only 21% of our patients with BE were currently receiving
these drugs; therefore, this will need further investigation.
It is possible that BE associated with SSc could be a
particular entity with a different pathophysiologic mechanism.
The only common risk factor between SSc and
GERD patients with BE is the H pylori status. The
presence of H pylori is believed to protect against GERD
and associated long-segment BE (36–38). In our series,
BE patients were less likely to be H pylori–positive than
were non-BE patients (10% versus 42.5%, respectively;
P ⬍ 0.05), confirming the potential protective role of H
pylori. The prevalence of H pylori was lower in our SSc
population than that demonstrated in previous studies
(39); however, the H pylori test was not similar and H
pylori prevalence differs according to age and sociocultural conditions (mostly in childhood).
The incidence of esophageal adenocarcinoma has
not been clearly established in GERD patients, whereas
the risk of carcinoma is elevated in patients with Barrett’s metaplasia (9,40,41). In fact, the incidence of
esophageal adenocarcinoma is estimated to be 0.5% per
BE patient-year (35). Strategies for the management of
patients with GERD have thus been proposed, suggesting that patients with chronic GERD symptoms should
be assessed for detection of BE, and those patients with
established BE should be screened by endoscopy every 2
or 3 years, every year if low-grade dysplasia occurs, and
every 3 months in the case of high-grade dysplasia (7).
The findings of one study suggested that 8 (14%)
of 59 SSc patients with BE had developed esophageal
adenocarcinoma (35). However, that study took into
WIPFF ET AL
account only the patients with the most severe symptoms; therefore, because of publication bias, those findings cannot be extrapolated to the whole SSc population.
Among 680 SSc patients with a mean followup of 12
years, Segel et al (11) found only 1 case of adenocarcinoma; the prevalence of BE was not provided in that
study. Our results are in accordance with the findings of
Segel et al, since none of our patients with SSc (mean
followup of 9 years) had esophageal adenocarcinoma.
However, given the low incidence of esophageal adenocarcinoma and the number of patients screened, we
cannot draw any conclusion about this risk.
Although SSc patients with BE exhibit strikingly
different characteristics from those observed in the
typical patient with BE, 3 of the 14 patients in our study
developed dysplasia, suggesting that BE associated with
SSc can evolve in the same way as classic BE. Our
patient with high-grade dysplasia had been treated with
plasma argon, showing that followup of BE can lead to
a specific treatment. Other endoscopic techniques have
also been validated for premalignant lesion treatment
(42).
Our results did not highlight a specific manometric pattern associated with BE. Manometry is a highly
sensitive method for the detection of esophageal injury
in SSc (43); this is emphasized by our finding that 80%
of the SSc patients screened and 100% of the SSc
patients with BE had at least 1 abnormality. However,
manometry is less accurate in patients with severe
esophageal involvement, such as can occur in patients
with BE.
The fact that patients with BE were more frequently receiving a high dose of PPIs (9 of 14, or 64%)
than were patients without BE (36 of 96, or 37%) (P NS,
because of low effectiveness) may suggest that BE
patients could have more severe or more symptomatic
esophageal involvement. However, the cross-sectional
and observational methods of our study limit our ability
to investigate this aspect.
It has previously been suggested that esophageal
abnormalities could be more frequently associated with
the limited cutaneous subtype of SSc than with the
diffuse cutaneous subtype (10). However, other data
suggest that it can occur regardless of the cutaneous
subtype and regardless of disease duration (44,45).
In this cross-sectional study of 110 patients with a
mean SSc disease duration of 9 years who were systematically treated with PPIs, we found a prevalence of BE
of 12.7% and no adenocarcinoma. This prevalence of
BE in SSc patients is similar to that found in patients
BARRETT’S ESOPHAGUS IN SYSTEMIC SCLEROSIS
with GERD (7,8). An increased risk of adenocarcinoma
has been demonstrated in GERD patients with BE, and
recommendations for detection and followup of these
patients are available (7). Whether the same recommendations (i.e., use of periodic endoscopic assessments)
should be applied to SSc patients remains to be further
validated in long-term prospective studies.
REFERENCES
1. Clements PJ, Becvar R, Drosos AA, Ghattas L, Gabrielli A.
Assessment of gastrointestinal involvement. Clin Exp Rheumatol
2003;21:S15–8.
2. Poirier T, Rankin M. Gastrointestinal manifestations of progressive systemic scleroderma based on a review of 364 cases. Am J
Gastroenterol 1972;58:30–44.
3. Sjogren RW. Gastrointestinal motility disorders in scleroderma.
Arthritis Rheum 1994;37:1265–82.
4. Turner R, Lipshutz W, Miller W, Rittenberg G, Schumacher HR,
Cohen S. Esophageal dysfunction in collagen disease. Am J Med
Sci 1973;265:191–9.
5. Stevens MB, Hookman P, Siegel C, Esterly JR, Shulman L,
Hendrix T. Aperistalsis of the esophagus in patients with connective-tissue disorders and Raynaud’s phenomenon. N Engl J Med
1964;270:1218–22.
6. Kahan A, Menkes CJ. Gastrointestinal involvement in systemic
sclerosis [review]. Clin Dermatol 1994;12:259–65.
7. Chang JT, Katzka DA. Gastroesophageal reflux disease, barrett
esophagus, and esophageal adenocarcinoma. Arch Intern Med
2004;164:1482–8.
8. Shaheen N, Ransohoff DF. Gastroesophageal reflux, barrett
esophagus and esophageal cancer. JAMA 2002;287:1972–86.
9. Heath E, Limburg P, Hawk E, Forastiere AA. Adenocarcinoma of
the esophagus: risk factors and prevention. Oncology 2000;14:
507–23.
10. Katzka D, Reynolds JC, Saul S, Plotkin A, Lang C, Ouyang A, et
al. Barrett’s metaplasia and adenocarcinoma of the esophagus in
scleroderma. Am J Med 1987;82:46–52.
11. Segel M, Campbell W, Medsger T, Roumm A. Systemic sclerosis
(scleroderma) and esophageal adenocarcinoma: is increased patient screening necessary? Gastroenterology 1985;89:485–8.
12. Subcomittee for Scleroderma Criteria of the American Rheumatism Association Diagnostic and Therapeutic Criteria Committee.
Preliminary criteria for the classification of systemic sclerosis
(scleroderma). Arthritis Rheum 1980;23:581–90.
13. LeRoy EC, Black C, Fleischmajer R, Jablonska S, Krieg T,
Medsger TA Jr, et al. Scleroderma (systemic sclerosis): classification, subsets and pathogenesis [editorial]. J Rheumatol 1988;15:
202–5.
14. Matucci-Cerinic M, D’Angelo S, Denton CP, Vlachoyiannopoulos
P, Silver R. Assessment of lung involvement. Clin Exp Rheumatol
2003;21 Suppl 29:S19–23.
15. Cameron A, Payne W. Barrett’s esophagus occurring as a complication of scleroderma. Mayo Clin Proc 1978;53:612–5.
16. Agha F, Dabich L. Barrett’s esophagus complicating scleroderma.
Gastrointest Radiol 1985;20:325–9.
17. Anderson M, Seymour E. Association of Barrett’s esophagus and
scleroderma. South Med J 1987;80:764–5.
18. Chang CP, Huang Y, Tsay S, Lai K, Lee S. Primary biliary
cirrhosis and scleroderma complicated by Barrett’s oesophagus. S
Afr Med J 1991;79:397–8.
19. Dill J. Barrett’s epithelium in scleroderma. Gastrointest Endosc
1983;29:296–7.
2887
20. Halpert R, Laufer I, Thompson J, Feczko P. Adenocarcinoma of
the esophagus in patients with scleroderma. Am J Roentgenol
1983;140:920–7.
21. Ilan Y, Shouval D, Galun E, Goldin E, Ligumsky M, Friedman G, et
al. Esophageal malignancy after liver transplantation in a patient with
Barrett’s esophagus. Scand J Gastroenterol 1996;31:415–6.
22. Lambert DR, Llanrza P, Gaglani R, Lach R, Beaver W. Esophageal-atrial fistula. J Clin Gastroenterol 1987;9:345–9.
23. McKinley M, Sherlock P. Barrett’s esophagus with adenocarcinoma in scleroderma. Am J Gastroenterol 1984;79:438–9.
24. Maekawa Y, Nogami R. A case of progressive systemic sclerosis
associated with sarcoidosis and esophageal adenocarcinoma. J
Dermatol 1993;20:45–8.
25. Navon P, Klar A, Hurvitz H, Adler S, Branski D. Barrett’s
esophagus in a young patient with Raynaud’s phenomenon.
J Rheumatol 1991;18:1735–6.
26. Niv Y, Abu-Avid S, Yelin A, Liberman Y. Barrett’s epithelium and
esophageal adenocarcinoma in scleroderma. Am J Gastroenterol
1988;83:792–3.
27. Sprung J, Gibb P. Dysplasic Barrett’s esophagus in scleroderma.
Am J Gastroenterol 1985;80:518–22.
28. Szigeti N, Fabian G, Gomori E, Czirjak L. Barrett esophagus in
systemic sclerosis. Orv Hetil 2001;142:671–4.
29. Marie I, Dominique S, Levesque H, Ducrotte P, Denis P, Hellot
MF, et al. Esophageal involvement and pulmonary manifestations
in systemic sclerosis. Arthritis Rheum 2001;45:346–54.
30. Recht M, Levine M, Katzka D, Reynolds J, Saul S. Barrett’s
esophagus in scleroderma: increased prevalence and radiographic
findings. Gastrointest Radiol 1988;13:1–5.
31. Weston S, Thumshirn M, Wiste J, Camilleri M. Clinical and upper
gastrointestinal motility features in systemic sclerosis and related
disorders. Am J Gastroenterol 1998;93:1085–9.
32. Atkinson M, Summerling M. Oesophageal changes in systemic
sclerosis. Gut 1966;7:402–8.
33. Modlin I, Kidd M. GERD 2003: issues from the past and consensus for the future. Drugs Today (Barc) 2004;40 Suppl A:3–8.
34. Hendel L, Hage E, Hendel J, Stentoft P. Omeprazole in the
long-term treatment of severe gastro-oesophageal reflux disease in
patients with systemic sclerosis. Aliment Pharmacol Ther 1992;6:
565–77.
35. Sharma P, McQuaid K, Dent J, Fennerty MB, Sampliner R,
Spechler S, et al. Review of the diagnosis and management of
Barrett’s esophagus: the AGA Chicago workshop. Gastroenterol
2004;127:310–30.
36. Wu JC, Chan FK, Ching JY, Leung WK, Hui Y, Leong R, et al.
Effect of Helicobacter pylori on treatment of gastroesophageal
reflux disease: a double blind, placebo controlled, randomised
trial. Gut 2004;2:174–9.
37. Zhang J, Chen XL, Wang KM, Guo XD, Zuo AL, Gong J.
Relationship of gastric Helicobacter pylori infection to Barrett’s
esophagus and gastroesophageal reflux disease in Chinese. World
J Gastroenterol 2004;5:672–5.
38. Abe Y, Ohara S, Koike T, Sekine H, Iijima K, Kawamura M, et al.
The prevalence of Helicobacter pylori infection and the status of
gastric acid secretion in patients with Barrett’s esophagus in Japan.
Am J Gastroenterol 2004;77:1213–21.
39. Yazawa N, Fujimoto M, Kikuchi K, Kubo M, Ihn H, Sato S, et al.
High seroprevalence of Helicobacter pylori infection in patients
with systemic sclerosis: association with esophageal involvement.
J Rheumatol 1998;25:650–3.
40. Haggit RC, Tryzelaar J, Ellis FM, Ellis FH, Colcher H. Adenocarcinoma complicating columnar epithelium-lined (Barrett’s)
esophagus. Am J Clin Pathol 1978;70:1–5.
41. Sarr M, Hamilton S, Marrone G, Cameron J. Barrett’s esophagus: its
prevalence and association with adenocarcinoma in patients with
symptoms of gastroesophageal reflux. Am J Surg 1985;149:187–93.
2888
42. Pech O, May A, Gossner L, Rabenstein T, Ell C. Management of
pre-malignant and malignant lesions by endoscopic resection. Best
Pract Res Clin Gastroenterol 2004;18:61–76.
43. Bassotti G, Battaglia E, Debernardi V, Germani U, Quiriconi F,
Dughera L, et al. Esophageal dysfunction in scleroderma: relationship with disease subsets. Arthritis Rheum 1997;40:2252–9.
WIPFF ET AL
44. Fulp S, Castell D. Scleroderma esophagus. Dysphagia 1990;5:
204–10.
45. Furst DE, Clements PJ, Saab M, Sterz MG, Paulus HE. Clinical
and serological comparison of 17 chronic progressive systemic
sclerosis and 17 CREST syndrome patients for sex, age, and
disease duration. Ann Rheum Dis 1984;43:794–801.
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