Digestive and Liver Disease 43 (2011) 345–351

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Digestive and Liver Disease

journal homepage: www.elsevier.com/locate/dld

Review Article

The management of portal hypertensive gastropathy and gastric

antral vascular ectasia
Cristina Ripoll a , Guadalupe Garcia-Tsao b,∗
a
Servicio de Aparato Digestivo, Hospital General Universitario Gregorio Marañón and Centro de Investigación Biomédica en
Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Spain
b
Section of Digestive Diseases, Yale University School of Medicine and VA-CT Healthcare System, New Haven, CT, USA

a r t i c l e i n f o a b s t r a c t

Article history: Portal hypertensive gastropathy and gastric antral vascular ectasia are gastric mucosal lesions that can
Received 31 August 2010 cause chronic gastrointestinal haemorrhage and, consequently, chronic anaemia, in patients with cirrho-
Accepted 11 October 2010 sis. Although chronic anaemia is the most common clinical manifestation, these entities may also lead to
Available online 20 November 2010
acute gastrointestinal bleeding. Despite similar clinical manifestations, their pathophysiology and man-
agement are entirely different. Their diagnosis is endoscopic and although generally each of them has a
Keywords:
characteristic endoscopic appearance and distribution, there are cases in which the differential is difficult
Chronic anaemia
and must rely on histology. This review focuses on the management of both entities. The mainstay of man-
Cirrhosis
Gastrointestinal bleeding
agement of portal hypertensive gastropathy is based on portal-hypotensive pharmacological treatment
Gastropathy whilst gastric antral vascular ectasia benefits from endoscopic therapy. More invasive options should be
Vascular ectasia reserved for refractory cases.
Published by Elsevier Ltd on behalf of Editrice Gastroenterologica Italiana S.r.l.

1. Comparison of clinical picture, prevalence and
epidemiology, pathophysiology and diagnosis of portal
hypertensive gastropathy (PHG) and gastric antral vascular
ectasia (GAVE)
1.1. Clinical picture
PHG and GAVE are two clinical conditions that share many
similarities, although they also have clear differences. The most
relevant similarity is that they both can cause chronic gastroin-
testinal haemorrhage in patients with cirrhosis, manifested by
chronic anaemia. Chronic anaemia is frequently observed in cir-
rhosis (21–87%) depending on the characteristics of the study
population [1,2]. However, a careful differential diagnosis should be
performed in order to identify the cause of anaemia in the cirrhotic
patient (Fig. 1), so that specific treatment can be administered.
in patients with more severe liver disease [3,4] and in patients
with cirrhosis who have had previous endoscopic treatment with
sclerotherapy or endoscopic variceal ligation [5–7]. GAVE is a less
frequent condition, having been reported in only 2% [8] of patients
awaiting liver transplantation or 3% of patients with HCV and
advanced fibrosis [4].
As indicated by its name, PHG is associated with portal hyper-
tension and therefore is frequently found in association to cirrhosis
[9]. It can also be found in non-cirrhotic causes of portal hyper-
tension [10,11]. Conversely, PHG is not observed in patients with
chronic alcoholism without liver disease or in patients with cirrho-
sis who do not have portal hypertension [12].
GAVE is also associated to liver disease but, contrary to PHG, it
can also be observed in patients with other non-hepatic chronic
diseases such as autoimmune connective tissue disorders, bone
marrow transplantation and chronic renal failure [13–17].

1.2. Prevalence and epidemiology 1.3. Pathophysiology

PHG is by far the most frequent of the two entities, with a
prevalence that has been reported to vary between 20% and 80%
depending on patient characteristics. It is more frequently observed
∗ Corresponding author at: Digestive Diseases Section, Yale University School
of Medicine, 333 Cedar Street-1080 LMP, New Haven, CT 06510, USA.
Fax: +1 203 785 7273.
E-mail address: guadalupe.garcia-tsao@yale.edu (G. Garcia-Tsao).
PHG and GAVE appear to have a completely different pathophys-
iology although it has not been clearly determined in either case.
Portal hypertension, estimated by the measurement of the hepatic
venous pressure gradient, correlates with the presence and severity
of PHG [18,19]. Some studies suggest that other factors indepen-
dent of portal hypertension, such as gastric mucosal blood flow or
other local factors may also be involved in its pathogenesis [20,21].
Interestingly, patients with cirrhosis and PHG have more deranged
circulatory abnormalities, with lower systemic vascular resistance

1590-8658/$36.00 Published by Elsevier Ltd on behalf of Editrice Gastroenterologica Italiana S.r.l.

doi:10.1016/j.dld.2010.10.006
346 C. Ripoll, G. Garcia-Tsao / Digestive and Liver Disease 43 (2011) 345–351
Fig. 1. Portal hypertensive gastropathy (PHG) and gastric antral vascular ectasia
(GAVE) are gastric mucosal lesions that may occur in patients with cirrhosis. Both
can lead to chronic or acute gastrointestinal haemorrhage. Diagnosis is endoscopic
but may be difficult in occasions. Treatment is different in both entities. PH = portal
hypertension.
and pulmonary vascular resistance [19] than patients with cirrho-
sis without PHG. Although mucosal changes of PHG do not respond
to antisecretory drugs and histological changes are not compati-
ble with peptic-related disease [22], gastric mucosa from patients
or from animal-models with portal hypertension does have an
increased susceptibility to develop injury by noxious factors and an
impaired healing [23–27]. Furthermore, an increased prevalence of
intestinal metaplasia has been observed in patients with PHG with
and without cirrhosis [28].
On the other hand, portal hypertension does not seem to be
necessary for development of GAVE [29,30] and liver insufficiency
seems to have a more significant role, as this condition is observed
more frequently in patients with more severe liver disease and
has shown to resolve after liver transplantation [8,31]. Vasodilat-
ing mediators such as gastrin [32] and prostaglandin E2 [33] have
been associated to the presence of GAVE. Further accumulation of
these vasodilating and/or other vasodilating or angiogenic media-
tors that are not metabolized by a failing liver could also influence
its development [29]. Lastly, mechanical stress [32] and abnormal
antral motility [34] have also been associated to the development
of GAVE. This is supported by its typical antral distribution and
histological findings of fibromuscular hyperplasia [35].
1.4. Diagnosis
The diagnosis of both entities is established by endoscopy with
mucosal abnormalities observed mainly in the stomach. Although
in occasions the endoscopic differential diagnosis between both
entities is difficult, characteristically PHG is located mainly in the
fundus, whilst GAVE, as its name indicates, is mainly located in the
antrum.
Typically, PHG has a snake-skin mosaic pattern (mild PHG) that
can be accompanied with flat or bulging red or brown spots (severe
PHG). Similar endoscopical lesions as the ones observed in PHG
may be observed in other areas of the gastrointestinal tract [36–42],
findings that have been termed portal hypertensive duodenopathy,
portal hypertensive enteropathy or portal hypertensive colopathy
depending on the location of the characteristic lesions.
GAVE also presents with flat red spots, however without a back-
ground mosaic pattern. In occasions, the red spots can blur together,
so that red and white stripes converge to the pylorus which is
described as a “watermelon stomach”. Contrary to PHG, the typ-
ical lesions of GAVE are only observed in the stomach, and at most
can affect the whole stomach (diffuse form). This last form of GAVE
is the one that is most difficult to distinguish from PHG.
When endoscopic differential diagnosis is difficult, histology is
useful. Both entities are characterized by vascular ectasia in the
mucosa. PHG is characterized by vascular dilatation in mucosa and
submucosa without significant inflammation [22], although usu-
ally biopsies obtained at endoscopy are not deep enough to show
these changes. Gastric mucosal biopsies in GAVE may show regen-
erative mucosal changes, increased lamina propria smooth muscle,
and most typically the presence of fibrin thrombi [35,43]. How-
ever, the latter finding can be frequently overlooked with standard
haematoxylin and eosin staining. A recent study using immuno-
histochemistry with the platelet marker CD61 identified thrombi
more readily by staining platelets within the characteristic thrombi.
These were present in all patients who had a histological diagnosis
of GAVE and in 60% of patients who had an endoscopic diagnosis
of GAVE [44]. This methodology appears to enhance the utility of
histological examination alone and deserves further exploration.
Other non-endoscopic approaches such as computed tomog-
raphy or magnetic resonance have also been tested [45,46]. The
identification of PHG with dynamic computed tomography scan
by observing enhancement of the inner layer of the gastric wall
was evaluated in 32 patients. Enhancement of the inner gastric
layer was observed in 9 of 10 patients with PHG, whilst this was
observed only observed in 5 of the 22 patients without PHG [45].
On the other hand, the evaluation of the calibre of esophagogas-
tric veins by magnetic resonance has not shown to identify PHG
[46]. Finally, in patients with systemic sclerosis antibody patterns
characterized by the absence of antitopoisomerase I antibodies and
presence of antibodies to RNAP III/speckled antinuclear antibody
has been associated to early development of GAVE [17].
Capsule endoscopy has been shown to have only moderate sen-
sitivity and specificity for the detection of PHG [47], although it has
an important role in evaluation of the small bowel involvement
[40,41,48,49].
2. Management of PHG
PHG can be diagnosed in different clinical settings that require
different management (Table 1).
2.1. Asymptomatic PHG
The most frequent setting is finding PHG on a routine endoscopy
performed to evaluate the presence of varices. Endoscopic screen-
ing to establish the need for primary prophylaxis should be
performed every 2–3 years in compensated patients without
varices, or every year in decompensated patients or in patients
with small varices not requiring prophylaxis [50]. In this setting, the
patient may be asymptomatic with no evidence of chronic bleed-
ing. Prophylaxis of bleeding from PHG has not been evaluated in
clinical studies and is therefore not recommended. However, in
patients with varices that require prophylaxis, the use of nonse-
lective betablockers would theoretically lead to further benefit in
a patient with PHG. The presence of concomitant PHG may tip the
balance towards using nonselective beta-blockers in patients with
small varices.
Asymptomatic PHG may also be diagnosed in the setting of sec-
ondary prophylaxis for variceal haemorrhage. Endoscopic therapy
has been associated to an increased incidence of PHG [5–7,51].
There is controversy regarding whether or not PHG that occurs in
the context of endoscopic therapy is as clinically relevant as the
PHG that occurs “spontaneously”. Some studies suggest that PHG
that occurs after endoscopic sclerotherapy or ligation therapy is
 C. Ripoll, G. Garcia-Tsao / Digestive and Liver Disease 43 (2011) 345–351
Table 1
Clinical Management of portal hypertensive gastropathy and gastric vascular ectasia.
Portal hypertensive gastropathy
Asymptomatic No therapy
Chronic bleeding
General measures Iron replacement therapy
Transfusions when necessary
Specific measures Betablockers
Acute bleeding
General measures Adequate resuscitation
Hb between 7 and 8 g/dL in cirrhosis
Antibiotics
Specific measures Vasoactive medication
Rescue therapy TIPS
transient [7,52], whilst another study observed no difference in the
natural history of PHG whether or not previous endoscopic scle-
rotherapy therapy was performed [6]. The natural course of PHG
after ligation therapy seems to be milder than after sclerotherapy
[52]. The association of betablockers to endoscopic variceal liga-
tion, therapy that is recommended for secondary prophylaxis [50],
has been shown to reduce the incidence of PHG [53].
2.2. Chronic bleeding
In some cases, patients may present with chronic iron deficiency
anaemia. Initially, thorough evaluation should be undertaken to
discard any other possible causes of this anaemia. Once the diag-
nosis of PHG has been established as the cause of anaemia, then
specific treatment may be initiated. Iron replacement therapy
should be started in order to avoid depletion of iron deposits. Tak-
ing into account the important role of portal hypertension in the
development of PHG, specific treatment of PHG is mainly based
on portal pressure reducing approaches. The use of non-selective
betablockers, particularly propranolol, has been studied in this set-
ting. Propranolol has been shown to reduce bleeding from both
acute and chronic forms of GI bleeding secondary to PHG.
The first trial that evaluated the use of betablockers in this set-
ting was a randomized controlled trial that included 24 patients
[54]. The presence of varices and PHG was established endoscopi-
cally 6 weeks prior to inclusion. Patients were randomized to the
administration of long acting propranolol (160 mg/day) or placebo
initially for 6 weeks and then crossed-over to the alternative arm
for another 6 weeks. In the period in which patients received pro-
pranolol, there was a lower rate of haemorrhage, an increase in
haemoglobin level and an improvement in the endoscopic appear-
ance of the lesions, compared to the placebo period. However,
given the small number of patients the study was underpowered
to achieve statistical or clinical significance.
Further support for the use of propranolol in the prevention of
recurrent bleeding in patients with cirrhosis and severe PHG was
obtained from a randomized controlled trial that included patients
with previous bleeding, acute or chronic, from PHG. Patients were
randomized to receive propranolol (26 patients) or standard man-
agement of anaemia with iron supplementation if needed (28
patients) [55]. The primary endpoint of the trial was recurrent
haemorrhage from PHG, which was defined by (a) the presence
of acute upper gastrointestinal bleeding with a decrease in hemat-
ocrit and the finding on emergency endoscopy (performed within
the first 12 h) of gastric red spots as the source of bleeding, or (b)
the presence of chronic bleeding defined by occult blood loss with
transfusion requirements of 3 or more units of packed red blood
cells in a 3-month period or continuous iron replacement therapy
for more than 50% of the time of follow-up. Patients randomized to
propranolol remained free of haemorrhage both in the acute (85%
347
Gastric vascular ectasia
No therapy
Iron replacement therapy
Transfusion when necessary
Argon Plasma coagulation
Adequate rescusitation
Hb between 7 and 8 g/dL in cirrhosis
Antibiotics in cirrhosis
Endoscopic therapy
Surgery
vs. 20%) and chronic settings (63% vs. 40% at 30 months), although
the differences were only statistically significant in the former [55].
Multivariate analysis identified the absence of propranolol therapy
as the only factor independently predictive of recurrent haemor-
rhage.
The results of these studies led to the consensus recommenda-
tion that non-selective beta-blockers should be used in the chronic
setting and once the acute episode of bleeding is controlled and the
patient is stable [56].
Most patients are started with propranolol at an initial dose of
20 mg twice a day (BID), although some cases may require a lower
dose. The dose is gradually escalated to a maximum of 160 mg BID
or the maximum tolerated dose, provided heart rate is maintained
around 50–55 bpm. Secondary effects associated to betablockers
such as light-headedness, fatigue, impotence, etc, may limit further
increases in dosage. Besides the beneficial effects of betablock-
ers on the recurrent haemorrhage, one must keep in mind that
betablocker therapy also has other beneficial effects including a
survival benefit in patients who achieve an adequate reduction of
portal pressure estimated by the hepatic venous pressure gradient
[57–59].
Other pharmacologic agents have been tested in individual cases
in PHG such as losartan [60], thalidomide [61] and corticosteroids
[62]. Although there is an interesting rationale behind the use of
these drugs, the clinical evidence that supports their use is weak.
Common sense allows us to define non-response to beta-
blockers when the patient continues to bleed and requires
transfusions despite having attained adequate beta-blockade and
concomitant iron replacement therapy. Although each case should
be evaluated individually, patients who require only occasional
transfusions will most likely not benefit from more invasive
options. In patients that are requiring frequent transfusions, and
given the pathogenic role of portal hypertension, portosystemic
shunt therapies should be considered, either surgical or through
the placement of a transjugular intrahepatic portosystemic shung
(TIPS). Surgical shunt should be mainly considered in patients with
non-cirrhotic portal hypertension or Child-Pugh class A patients
and will depend on local expertise [63–65]. Patients who undergo
shunt surgery have an improvement in the endoscopic appear-
ance of the lesions and a reduction in the number of transfusions
required [63,64]. Patients who receive TIPS have an improvement
of PHG lesions on endoscopy that can be observed as soon as 6
weeks after its placement and up to 3 months in cases with more
severe PHG [30,66–68]. Besides endoscopic improvement of the
lesions, there is also a clinical improvement with a lower number
of transfusion requirements.
Traditionally it is considered that lesions associated to PHG do
not benefit from endoscopic therapy. A recent study has challenged
this, evaluating the use of argon plasma coagulation (APC) in the
treatment of PHG [69]. In this study, 11 patients with bleeding from
348 C. Ripoll, G. Garcia-Tsao / Digestive and Liver Disease 43 (2011) 345–351
PHG were included. APC sessions were aimed to ablate the great-
est amount of mucosal surface as possible, at least 80% in diffuse
lesions. APC was administered at 30–40 W and 1.5–2 l/min of argon
plasma flow. Sessions were repeated every 2–4 weeks. The end-
point, which was defined by the absence of upper GI bleeding or a
reduction in transfusion requirements, was achieved in 81% of the
patients who were bleeding from PHG. Perhaps those patients who
do not respond to betablockers, have severe recurrent bleeding and
are not candidates for TIPS could be considered for an endoscopic
approach.
2.3. Acute bleeding
The development of acute gastrointestinal haemorrhage in a
patient with cirrhosis should immediately raise concern regarding
its most common cause, bleeding varices. In this setting cur-
rent recommendations [50] are (a) adequate resuscitation of the
patient with cautious blood transfusion policy maintaining Hb lev-
els between 7 and 8 g/dL, (b) initiation of vasoconstrictor drug
therapy (terlipressin or somatostatin (or analogues) and antibiotics
(quinolones or 3rd generation cephalosporins) as soon as the pos-
sibility of variceal bleed is suspected (before endoscopy) and (c)
performance of endoscopy as soon as possible.
If it is determined, through endoscopy, that bleeding is from
varices, they should be treated accordingly [50]. Very rarely, no
varices are observed and the only lesion is severe PHG. It must then
be assumed that this is the source of haemorrhage. Endoscopic
treatments of acutely bleeding PHG lesions have not been tested
in randomized controlled trials and therefore clinical judgement
should be used to decide whether or not to treat these lesions endo-
scopically. When varices without stigmata of recent bleeding are
present, and PHG is also observed, determining the cause of haem-
orrhage may be difficult, and should be based on clinical judgement.
If PHG is only mild, it is unlikely that this is the cause of the acute
gastrointestinal bleed. Conversely, if varices are small and PHG is
severe, the more likely source may be the latter.
Once endoscopy establishes PHG as the cause of the acute bleed-
ing episode, specific measures to treat PHG should be undertaken.
No well-designed studies have evaluated the use of endoscopic
therapy of acutely bleeding PHG lesions. However, it seems logical
to consider this therapeutic option in the patient who is bleed-
ing actively, especially if the patient is hemodynamically unstable.
Besides specific local therapy, it would also appear reasonable to
follow the same recommendations that apply to variceal haem-
orrhage, including a cautious transfusion policy and prophylactic
antibiotics. Similarly to variceal bleeding, a portal hypotensive drug
should be administered. The use of betablockers in the acute set-
ting was evaluated in a small open trial in acute severe bleeding
from endoscopically proven PHG with early cessation of bleed-
ing with 3 days of drug initiation [54]. The use of betablockers in
the acute setting has some setbacks, as several days are required
before a hemodynamically effective dose is reached and that this
drug can blunt the physiological compensatory increase in heart
rate. Vasoactive drugs used routinely in the setting of variceal
haemorrhage and that should be preferable in the setting of
acute haemorrhage from PHG are somatostatin and its analogues
(octreotide and vapreotide) and vasopressin and its analogue,
terlipressin [70,71]. Three trials have shown a satisfactory con-
trol of haemorrhage from PHG with somatostatin [72], octreotide
[72,73] and terlipressin [74] although vasopressin [73] did not show
any benefit in comparison to omeprazole. Furthermore, one trial
evaluated different doses of terlipressin and observed a higher pro-
portion of control of haemorrhage and lower recurrence rate in
patients assigned to receive a higher dose (1 mg/4 h) of terlipressin
compared to those who were assigned to receive a lower dose
(0.2 mg/4 h) [74].
In rare occasions, acute haemorrhage is not controlled with
medical therapy. Non-response to medical treatment in the acute
setting may be defined according to the standards of non-response
to variceal bleeding [56], as both are associated to portal hyper-
tension and require a change of therapy. Treatment failure is
considered when there is a new hematemesis after at least 2 h of
treatment initiation, or a 3 g drop in haemoglobin in the absence of
transfusion of packed red blood cells or an inadequate haemoglobin
increase in response to blood transfusions, or death [56]. However,
given the rarity of refractory bleeding from PHG, a careful evalu-
ation for other sources that could have been overlooked on initial
evaluation should be undertaken. Once it has been verified that
refractory bleeding is associated to PHG, rescue therapies are the
same as those recommended in patients who fail standard therapy
for chronic bleeding.
3. Management of gastric vascular ectasia
Similar to PHG, GAVE will most frequently present with chronic
iron deficiency anaemia due to chronic gastrointestinal bleeding.
Although there are many similarities with PHG, the relevance in
establishing an accurate differential diagnosis between these two
entities is based on the completely different therapeutic approach
for both entities (Table 1). Endoscopic treatment of GAVE lesions is
the mainstay of treatment of symptomatic lesions. Similar to PHG,
it is reasonable to not treat lesions that are asymptomatic. If endo-
scopic therapy fails, one may recur to the use of different drugs and
even more invasive options.
Amongst the different endoscopic approaches that have been
evaluated, most studies focus on the use of thermoablative tech-
niques. Independent of the endoscopic technique used, several
sessions will typically be necessary in order to control bleeding
and to correct anaemia.
Argon plasma coagulation is a thermoablative method, which
is based on producing thermal coagulation by applying high
frequency electric current that is passed through with argon
gas without direct contact with the mucosa. This technique
is easily applied and its risk of perforation is lower than
with neodymium:yttrium–aluminium–garnet (Nd:YAG) laser (see
below). Similarly to the Nd:YAG laser, large areas of mucosa can be
treated in a single session, although it does not penetrate as deeply.
It has been associated to the development of hyperplasic polyps
[75–77] and gastric outlet obstruction [78,79]. It does not require
a position perpendicular to the mucosa and can be applied with
focal pulse and “paint brush” approach. The settings are 20–80 W
of electrical power and gas flow between 0.5 and 2 L/min. The ses-
sions should be repeated every 2–6 weeks as needed. This is the
thermoablative method that has been most reported in the treat-
ment of GAVE and has been shown to have a beneficial effect
with a reduction in bleeding and blood transfusion requirement
[69,77,78,80–86].
The Nd:YAG laser coagulation can be applied to a large surface
area of the mucosa in a single session and therefore its hemostatic
response is observed earlier. Its main setback is that it has a greater
risk of perforation than with other thermoablative approaches as it
penetrates deeper within the mucosa. The Nd:YAG laser is placed
1 cm away from mucosa surface and is used with a power setting
between 40 and 90 W with short pulse durations (0.5–1 s). Sessions
should be repeated every 2–4 weeks until the therapeutic goal is
achieved. In the setting of GAVE it has shown to be effective in
reducing rebleeding and transfusion requirements [13,14,87–90].
Other endoscopic approaches have less evidence supporting
its use although they may offer some additional advantages.
Cryotherapy [91,92] consists of rapid expansion in the stomach of
compressed nitrous oxide resulting in a local decrease of the tem-
perature with consequent freezing of the mucosa allowing a faster
 C. Ripoll, G. Garcia-Tsao / Digestive and Liver Disease 43 (2011) 345–351
and more extensive treatment of diffuse lesions. The cryospray
is applied with a specific catheter until ice is formed. Endoscopy
should be repeated until all lesions are fully treated. Recently, the
use of banding in the stomach antrum with the same system that
is used for variceal ligation has been evaluated for the treatment
of GAVE [93,94]. This method offers the advantage that a large
area of mucosa can be treated at once and it is a technique that
is easily accessible in many centres. In a controlled trial comparing
banding to thermoablative treatment, patients who received band-
ing had a significantly greater increase in haemoglobin, decrease
in blood transfusion requirements and hospital admissions [93].
Other endoscopic therapeutic options reported in case reports, such
as the use of coagulation snares swept over the mucosa surface [95]
or endoscopic mucosectomy [96] require further study. Sclerother-
apy and heater probe ablation [97] do not offer any advantages over
the previously described methods.
If endoscopic therapy is not effective or if it is not feasible,
one can recur to other options for which there is very lim-
ited experience. Pilot studies have suggested that the use of
oestrogen–progesterone may be useful [98–100]. Some success has
been described in case reports with the use of octreotide [101], cor-
ticosteroids [102,103], tranexamic acid [104], thalidomide [105],
and a serotonin antagonist [106]. It seems that control of the under-
lying disease such as liver transplantation in patients with cirrhosis
[8,31] or the use of immunosuppressive therapy in connective tis-
sue disorders [107] can lead to improvement in GAVE, although
other reports suggest that despite controlling the underlying dis-
ease (systemic sclerosis and interstitial pneumonitis [108]) there is
no improvement in GAVE.
Surgical treatment with antrectomy and Billroth I anastomo-
sis can be considered in extreme cases in which the combination
of endoscopic and pharmacological treatment is unsuccessful
[109–111], although this obviously should be evaluated on an
individual basis. A thorough endoscopic evaluation of the gas-
trointestinal tract should be performed in order to exclude other
causes of haemorrhage before turning to surgery. This is the most
definitive therapy with low rates of rebleeding and anaemia. How-
ever, morbidity and mortality are high, although it will depend
on the underlying disease. Morbidity and mortality of abdomi-
nal surgery is highest in patients with cirrhosis, especially with
decompensated disease. A recent case report described the perfor-
mance of laparoscopic distal gastrectomy and gastrojejunostomy
in a case of refractory GAVE [112]. Although this may be an option
in non-cirrhotic patients, it seems unlikely that it will be feasible
in cirrhotic patients in whom abdominal surgery will lead to high
morbidity and mortality, partly due to bleeding from abdominal
portosystemic collaterals.
GAVE can also present as acute gastrointestinal bleeding. In
patients with cirrhosis, similar general therapeutic measures rec-
ommended for patients with cirrhosis and acute variceal or PHG
haemorrhage (see above) will apply to patients with cirrhosis who
bleed acutely from GAVE. Endoscopic evaluation will establish
GAVE as the source of bleeding and specific endoscopic treatment
can then be provided. Endoscopic therapy in acute bleeding is sim-
ilar to the approach on chronic bleeding. Once the diagnosis of
bleeding from GAVE is established vasoactive medication should
be discontinued. Antibiotic prophylaxis in order to avoid bacterial
translocation is recommended independent of the cause of the gas-
trointestinal bleed in patients with cirrhosis [113]. Once the patient
has presented with acute bleeding from GAVE, attempts to prevent
further bleeding should be initiated.
4. Conclusion
Although these two different clinical entities have a common
clinical manifestation, PHG and GAVE have a clearly distinct patho-
349
physiology, endoscopic appearance and therapeutic approach. The
treatment of PHG is based on measures that reduce portal pres-
sure, namely the administration of betablockers. On the other hand,
GAVE responds to endoscopic treatment, mainly argon–plasma
coagulation. Refractory cases can respond to more invasive ther-
apeutic options, although this has to be evaluated individually.
Conflicts of interest
The authors have no conflicts of interest.
Acknowledgements
Supported by grants from Yale Liver Center NIH P30 DK34989
and the Instituto de Salud de Carlos III (ISCIII).
References
[1] Mathurin SA, Aguero AP, Dascani NA, et al. Anemia in hospitalized patients
with cirrhosis: prevalence, clinical relevance and predictive factors. Acta Gas-
troenterol Latinoam 2009;39:103–11.
[2] Qamar AA, Grace ND, Groszmann RJ, et al. Incidence, prevalence, and clinical
significance of abnormal hematologic indices in compensated cirrhosis. Clin
Gastroenterol Hepatol 2009;7:689–95.
[3] Merli M, Nicolini G, Angeloni S, et al. The natural history of portal hypertensive
gastropathy in patients with liver cirrhosis and mild portal hypertension. Am
J Gastroenterol 2004;99:1959–65.
[4] Fontana RJ, Sanyal AJ, Mehta S, et al. Portal hypertensive gastropathy in
chronic hepatitis C patients with bridging fibrosis and compensated cirrhosis:
results from the HALT-C trial. Am J Gastroenterol 2006;101:983–92.
[5] D’Amico G, Montalbano L, Traina M, et al. Natural history of congestive
gastropathy in cirrhosis. The Liver Study Group of V. Cervello Hospital. Gas-
troenterology 1990;99:1558–64.
[6] Primignani M, Carpinelli L, Preatoni P, et al. Natural history of portal hyperten-
sive gastropathy in patients with liver cirrhosis. The New Italian Endoscopic
Club for the study and treatment of esophageal varices (NIEC). Gastroenterol-
ogy 2000;119:181–7.
[7] Sarin SK, Shahi HM, Jain M, et al. The natural history of portal hyper-
tensive gastropathy: influence of variceal eradication. Am J Gastroenterol
2000;95:2888–93.
[8] Ward EM, Raimondo M, Rosser BG, et al. Prevalence and natural history of
gastric antral vascular ectasia in patients undergoing orthotopic liver trans-
plantation. J Clin Gastroenterol 2004;38:898–900.
[9] Iwao T, Toyonaga A, Sumino M, et al. Portal hypertensive gastropathy in
patients with cirrhosis. Gastroenterology 1992;102:2060–5.
[10] Sarin SK, Misra SP, Singal A, et al. Evaluation of the incidence and significance
of the “mosaic pattern” in patients with cirrhosis, noncirrhotic portal fibrosis,
and extrahepatic obstruction. Am J Gastroenterol 1988;83:1235–9.
[11] Mori T, Aisa Y, Yajima T, et al. Esophageal varices and portal hypertensive
gastropathy associated with hepatic veno-occlusive disease after allogeneic
hematopoietic stem cell transplantation. Int J Hematol 2008;87:231–2.
[12] Papazian A, Braillon A, Dupas JL, et al. Portal hypertensive gastric mucosa: an
endoscopic study. Gut 1986;27:1199–203.
[13] Gostout CJ, Viggiano TR, Ahlquist DA, et al. The clinical and endoscopic
spectrum of the watermelon stomach. J Clin Gastroenterol 1992;15:256–
63.
[14] Liberski SM, McGarrity TJ, Hartle RJ, et al. The watermelon stomach: long-
term outcome in patients treated with Nd:YAG laser therapy. Gastrointest
Endosc 1994;40:584–7.
[15] Tobin RW, Hackman RC, Kimmey MB, et al. Bleeding from gastric
antral vascular ectasia in marrow transplant patients. Gastrointest Endosc
1996;44:223–9.
[16] Yamamoto M, Takahashi H, Akaike J, et al. Gastric antral vascular
ectasia (GAVE) associated with systemic sclerosis. Scand J Rheumatol
2008;37:315–6.
[17] Ingraham KM, O’Brien MS, Shenin M, et al. Gastric antral vascular ecta-
sia in systemic sclerosis: demographics and disease predictors. J Rheumatol
2010;37:603–7.
[18] Kim MY, Choi H, Baik SK, et al. Portal hypertensive gastropathy: correlation
with portal hypertension and prognosis in cirrhosis. Digest Dis Sci 2010.
[19] Kumar A, Mishra SR, Sharma P, et al. Clinical, laboratory, and hemodynamic
parameters in portal hypertensive gastropathy: a study of 254 cirrhotics. J
Clin Gastroenterol 2010;44:294–300.
[20] Ohta M, Hashizume M, Higashi H, et al. Portal and gastric mucosal
hemodynamics in cirrhotic patients with portal-hypertensive gastropathy.
Hepatology 1994;20:1432–6.
[21] Curvelo LA, Brabosa W, Rhor R, et al. Underlying mechanism of portal
hypertensive gastropathy in cirrhosis: a hemodynamic and morphological
approach. J Gastroenterol Hepatol 2009;24:1541–6.
[22] McCormack TT, Sims J, Eyre-Brook I, et al. Gastric lesions in por-
tal hypertension: inflammatory gastritis or congestive gastropathy? Gut
1985;26:1226–32.
350 C. Ripoll, G. Garcia-Tsao / Digestive and Liver Disease 43 (2011) 345–351
[23] Sarfeh IJ, Tarnawski A. Gastric mucosal vasculopathy in portal hypertension.
Gastroenterology 1987;93:1129–31.
[24] Sarfeh IJ, Soliman H, Waxman K, et al. Impaired oxygenation of gastric mucosa
in portal hypertension. The basis for increased susceptibility to injury. Digest
Dis Sci 1989;34:225–8.
[25] Kawanaka H, Tomikawa M, Jones MK, et al. Defective mitogen-activated pro-
tein kinase (ERK2) signaling in gastric mucosa of portal hypertensive rats:
potential therapeutic implications. Hepatology 2001;34:990–9.
[26] Kinjo N, Kawanaka H, Akahoshi T, et al. Significance of ERK nitration in por-
tal hypertensive gastropathy and its therapeutic implications. Am J Physiol
Gastrointest Liver Physiol 2008;295:G1016–24.
[27] Tominaga M, Ohta M, Kai S, et al. Increased heat-shock protein 90 expres-
sion contributes to impaired adaptive cytoprotection in the gastric mucosa
of portal hypertensive rats. J Gastroenterol Hepatol 2009;24:1136–41.
[28] Ibrisim D, Cevikbas U, Akyuz F, et al. Intestinal metaplasia in portal hyper-
tensive gastropathy: a frequent pathology. Eur J Gastroenterol Hepatol
2008;20:874–80.
[29] Spahr L, Villeneuve JP, Dufresne MP, et al. Gastric antral vascular ecta-
sia in cirrhotic patients: absence of relation with portal hypertension. Gut
1999;44:739–42.
[30] Kamath PS, Lacerda M, Ahlquist DA, et al. Gastric mucosal responses to intra-
hepatic portosystemic shunting in patients with cirrhosis. Gastroenterology
2000;118:905–11.
[31] Vincent C, Pomier-Layrargues G, Dagenais M, et al. Cure of gastric antral vas-
cular ectasia by liver transplantation despite persistent portal hypertension:
a clue for pathogenesis. Liver Transpl 2002;8:717–20.
[32] Quintero E, Pique JM, Bombi JA, et al. Gastric mucosal vascular ectasias causing
bleeding in cirrhosis. A distinct entity associated with hypergastrinemia and
low serum levels of pepsinogen I. Gastroenterology 1987;93:1054–61.
[33] Saperas E, Perez Ayuso RM, Poca E, et al. Increased gastric PGE2 biosyn-
thesis in cirrhotic patients with gastric vascular ectasia. Am J Gastroenterol
1990;85:138–44.
[34] Charneau J, Petit R, Cales P, et al. Antral motility in patients with cirrhosis
with or without gastric antral vascular ectasia. Gut 1995;37:488–92.
[35] Suit PF, Petras RE, Bauer TW, et al. Gastric antral vascular ectasia. A histologic
and morphometric study of “the watermelon stomach”. Am J Surg Pathol
1987;11:750–7.
[36] Misra SP, Dwivedi M, Misra V. Prevalence and factors influencing hemor-
rhoids, anorectal varices, and colopathy in patients with portal hypertension.
Endoscopy 1996;28:340–5.
[37] Ito K, Shiraki K, Sakai T, et al. Portal hypertensive colopathy in patients with
liver cirrhosis. World J Gastroenterol 2005;11:3127–30.
[38] Bresci G, Parisi G, Capria A. Clinical relevance of colonic lesions in cirrhotic
patients with portal hypertension. Endoscopy 2006;38:830–5.
[39] Menchen L, Ripoll C, Marin-Jimenez I, et al. Prevalence of portal hyperten-
sive duodenopathy in cirrhosis: clinical and haemodynamic features. Eur J
Gastroenterol Hepatol 2006;18:649–53.
[40] Figueiredo P, Almeida N, Lerias C, et al. Effect of portal hypertension in the
small bowel: an endoscopic approach. Dig Dis Sci 2008;53:2144–50.
[41] Goulas S, Triantafyllidou K, Karagiannis S, et al. Capsule endoscopy in the
investigation of patients with portal hypertension and anemia. Can J Gas-
troenterol 2008;22:469–74.
[42] Higaki N, Matsui H, Imaoka H, et al. Characteristic endoscopic features of
portal hypertensive enteropathy. J Gastroenterol 2008;43:327–31.
[43] Payen JL, Cales P, Voigt JJ, et al. Severe portal hypertensive gastropathy and
antral vascular ectasia are distinct entities in patients with cirrhosis. Gas-
troenterology 1995;108:138–44.
[44] Westerhoff M, Tretiakova M, Hovan L, et al. CD61, CD31, and CD34 improve
diagnostic accuracy in gastric antral vascular ectasia and portal hypertensive
gastropathy: an immunohistochemical and digital morphometric study. Am
J Surg Pathol 2010;34:494–501.
[45] Ishihara K, Ishida R, Saito T, et al. Computed tomography features of portal
hypertensive gastropathy. J Comput Assist Tomogr 2004;28:832–5.
[46] Erden A, Idilman R, Erden I, et al. Veins around the esophagus and the stom-
ach: do their calibrations provide a diagnostic clue for portal hypertensive
gastropathy? Clin Imaging 2009;33:22–4.
[47] de Franchis R, Eisen GM, Laine L, et al. Esophageal capsule endoscopy for
screening and surveillance of esophageal varices in patients with portal
hypertension. Hepatology 2008;47:1595–603.
[48] Canlas KR, Dobozi BM, Lin S, et al. Using capsule endoscopy to identify GI tract
lesions in cirrhotic patients with portal hypertension and chronic anemia. J
Clin Gastroenterol 2008;42:844–8.
[49] Abdelaal UM, Morita E, Nouda S, et al. Evaluation of portal hypertensive
enteropathy by scoring with capsule endoscopy: is transient elastography
of clinical impact? J Clin Biochem Nutr 2010;47:37–44.
[50] Garcia-Tsao G, Bosch J. Management of varices and variceal hemorrhage in
cirrhosis. N Engl J Med 2010;362:823–32.
[51] El-Khayat HR, El Khattib A, Nosseir M, et al. Portal hypertensive enteropa-
thy before and after variceal obliteration: an endoscopic, histopathologic and
immunohistochemical study. J Gastrointestin Liver Dis 2010;19:175–9.
[52] Hou MC, Lin HC, Chen CH, et al. Changes in portal hypertensive gastropathy
after endoscopic variceal sclerotherapy or ligation: an endoscopic observa-
tion. Gastrointest Endosc 1995;42:139–44.
[53] Lo GH, Lai KH, Cheng JS, et al. The effects of endoscopic variceal ligation and
propranolol on portal hypertensive gastropathy: a prospective, controlled
trial. Gastrointest Endosc 2001;53:579–84.
[54] Hosking SW. Congestive gastropathy in portal hypertension: variations in
prevalence. Hepatology 1989;10:257–8.
[55] Perez-Ayuso RM, Pique JM, Bosch J, et al. Propranolol in prevention of recur-
rent bleeding from severe portal hypertensive gastropathy in cirrhosis. Lancet
1991;337:1431–4.
[56] de Franchis R. Evolving consensus in portal hypertension. Report of the
Baveno IV consensus workshop on methodology of diagnosis and therapy
in portal hypertension. J Hepatol 2005;43:167–76.
[57] D’Amico G, Garcia-Pagan JC, Luca A, et al. Hepatic vein pressure gradient
reduction and prevention of variceal bleeding in cirrhosis: a systematic
review. Gastroenterology 2006;131:1611–24.
[58] Albillos A, Banares R, Gonzalez M, et al. Value of the hepatic venous pressure
gradient to monitor drug therapy for portal hypertension: a meta-analysis.
Am J Gastroenterol 2007;102:1116–26.
[59] Villanueva C, Aracil C, Colomo A, et al. Acute hemodynamic response to beta-
blockers and prediction of long-term outcome in primary prophylaxis of
variceal bleeding. Gastroenterology 2009;137:119–28.
[60] Wagatsuma Y, Naritaka Y, Shimakawa T, et al. Clinical usefulness of the
angiotensin II receptor antagonist losartan in patients with portal hyperten-
sive gastropathy. Hepatogastroenterology 2006;53:171–4.
[61] Karajeh MA, Hurlstone DP, Stephenson TJ, et al. Refractory bleeding from por-
tal hypertensive gastropathy: a further novel role for thalidomide therapy?
Eur J Gastroenterol Hepatol 2006;18:545–8.
[62] Cremers MI, Oliveira AP, Alves AL, et al. Portal hypertensive gastropathy:
treatment with corticosteroids. Endoscopy 2002;34:177.
[63] Orloff MJ, Orloff MS, Orloff SL, et al. Treatment of bleeding from portal hyper-
tensive gastropathy by portacaval shunt. Hepatology 1995;21:1011–7.
[64] Soin AS, Acharya SK, Mathur M, et al. Portal hypertensive gastropathy in
noncirrhotic patients. The effect of lienorenal shunts. J Clin Gastroenterol
1998;26:64–7 [discussion 68].
[65] Henderson JM, Boyer TD, Kutner MH, et al. Distal splenorenal shunt versus
transjugular intrahepatic portal systematic shunt for variceal bleeding: a ran-
domized trial. Gastroenterology 2006;130:1643–51.
[66] Urata J, Yamashita Y, Tsuchigame T, et al. The effects of transjugular intrahep-
atic portosystemic shunt on portal hypertensive gastropathy. J Gastroenterol
Hepatol 1998;13:1061–7.
[67] Mezawa S, Homma H, Ohta H, et al. Effect of transjugular intrahepatic por-
tosystemic shunt formation on portal hypertensive gastropathy and gastric
circulation. Am J Gastroenterol 2001;96:1155–9.
[68] Vignali C, Bargellini I, Grosso M, et al. TIPS with expanded
polytetrafluoroethylene-covered stent: results of an Italian multicenter
study. AJR Am J Roentgenol 2005;185:472–80.
[69] Herrera S, Bordas JM, Llach J, et al. The beneficial effects of argon plasma coag-
ulation in the management of different types of gastric vascular ectasia lesions
in patients admitted for GI hemorrhage. Gastrointest Endosc 2008;68:440–
6.
[70] Cirera I, Feu F, Luca A, et al. Effects of bolus injections and continuous infu-
sions of somatostatin and placebo in patients with cirrhosis: a double-blind
hemodynamic investigation. Hepatology 1995;22:106–11.
[71] Villanueva C, Planella M, Aracil C, et al. Hemodynamic effects of terlipressin
and high somatostatin dose during acute variceal bleeding in nonresponders
to the usual somatostatin dose. Am J Gastroenterol 2005;100:624–30.
[72] Kouroumalis EA, Koutroubakis IE, Manousos ON. Somatostatin for acute
severe bleeding from portal hypertensive gastropathy. Eur J Gastroenterol
Hepatol 1998;10:509–12.
[73] Zhou Y, Qiao L, Wu J, et al. Comparison of the efficacy of octreotide, vaso-
pressin, and omeprazole in the control of acute bleeding in patients with
portal hypertensive gastropathy: a controlled study. J Gastroenterol Hepatol
2002;17:973–9.
[74] Bruha R, Marecek Z, Spicak J, et al. Double-blind randomized, compara-
tive multicenter study of the effect of terlipressin in the treatment of acute
esophageal variceal and/or hypertensive gastropathy bleeding. Hepatogas-
troenterology 2002;49:1161–6.
[75] Izquierdo S, Rey E, Gutierrez Del Olmo A, et al. Polyp as a complication
of argon plasma coagulation in watermelon stomach. Endoscopy 2005;37:
921.
[76] Baudet JS, Salata H, Soler M, et al. Hyperplastic gastric polyps after argon
plasma coagulation treatment of gastric antral vascular ectasia (GAVE).
Endoscopy 2007;39(Suppl. 1):E320.
[77] Fuccio L, Zagari RM, Serrani M, et al. Endoscopic argon plasma coagulation for
the treatment of gastric antral vascular ectasia-related bleeding in patients
with liver cirrhosis. Digestion 2009;79:143–50.
[78] Probst A, Scheubel R, Wienbeck M. Treatment of watermelon stomach (GAVE
syndrome) by means of endoscopic argon plasma coagulation (APC): long-
term outcome. Z Gastroenterol 2001;39:447–52.
[79] Farooq FT, Wong RC, Yang P, et al. Gastric outlet obstruction as a complication
of argon plasma coagulation for watermelon stomach. Gastrointest Endosc
2007;65:1090–2.
[80] Yusoff I, Brennan F, Ormonde D, et al. Argon plasma coagulation for treatment
of watermelon stomach. Endoscopy 2002;34:407–10.
[81] Roman S, Saurin JC, Dumortier J, et al. Tolerance and efficacy of argon plasma
coagulation for controlling bleeding in patients with typical and atypical man-
ifestations of watermelon stomach. Endoscopy 2003;35:1024–8.
[82] Dulai GS, Jensen DM, Kovacs TO, et al. Endoscopic treatment outcomes
in watermelon stomach patients with and without portal hypertension.
Endoscopy 2004;36:68–72.
 C. Ripoll, G. Garcia-Tsao / Digestive and Liver Disease 43 (2011) 345–351
[83] Sebastian S, McLoughlin R, Qasim A, et al. Endoscopic argon plasma coag-
ulation for the treatment of gastric antral vascular ectasia (watermelon
stomach): long-term results. Dig Liver Dis 2004;36:212–7.
[84] Sato T, Yamazaki K, Toyota J, et al. Efficacy of argon plasma coagulation for
gastric antral vascular ectasia associated with chronic liver disease. Hepatol
Res 2005;32:121–6.
[85] Kwan V, Bourke MJ, Williams SJ, et al. Argon plasma coagulation in the
management of symptomatic gastrointestinal vascular lesions: experience
in 100 consecutive patients with long-term follow-up. Am J Gastroenterol
2006;101:58–63.
[86] Lecleire S, Ben-Soussan E, Antonietti M, et al. Bleeding gastric vascular ectasia
treated by argon plasma coagulation: a comparison between patients with
and without cirrhosis. Gastrointest Endosc 2008;67:219–25.
[87] Labenz J, Borsch G. Bleeding watermelon stomach treated by Nd-YAG laser
photocoagulation. Endoscopy 1993;25:240–2.
[88] Ng I, Lai KC, Ng M. Clinical and histological features of gastric antral vascular
ectasia: successful treatment with endoscopic laser therapy. J Gastroenterol
Hepatol 1996;11:270–4.
[89] Mathou NG, Lovat LB, Thorpe SM, et al. Nd:YAG laser induces long-term remis-
sion in transfusion-dependent patients with watermelon stomach. Lasers
Med Sci 2004;18:213–8.
[90] Selinger RR, McDonald GB, Hockenbery DM, et al. Efficacy of neodymium:YAG
laser therapy for gastric antral vascular ectasia (GAVE) following hematopoi-
etic cell transplant. Bone Marrow Transpl 2006;37:191–7.
[91] Kantsevoy SV, Cruz-Correa MR, Vaughn CA, et al. Endoscopic cryotherapy for
the treatment of bleeding mucosal vascular lesions of the GI tract: a pilot
study. Gastrointest Endosc 2003;57:403–6.
[92] Cho S, Zanati S, Yong E, et al. Endoscopic cryotherapy for the manage-
ment of gastric antral vascular ectasia. Gastrointest Endosc 2008;68:895–
902.
[93] Wells CD, Harrison ME, Gurudu SR, et al. Treatment of gastric antral vascular
ectasia (watermelon stomach) with endoscopic band ligation. Gastrointest
Endosc 2008;68:231–6.
[94] Gill KR, Raimondo M, Wallace MB. Endoscopic band ligation for the treatment
of gastric antral vascular ectasia. Gastrointest Endosc 2009;69:1194.
[95] Chong VH. Snare coagulation for gastric antral vascular ectasia ablation. Gas-
trointest Endosc 2009;69:1195.
[96] Katsinelos P, Chatzimavroudis G, Katsinelos T, et al. Endoscopic mucosal
resection for recurrent gastric antral vascular ectasia. Vasa 2008;37:289–92.
[97] Petrini Jr JL, Johnston JH. Heat probe treatment for antral vascular ectasia.
Gastrointest Endosc 1989;35:324–8.
351
[98] Moss SF, Ghosh P, Thomas DM, et al. Gastric antral vascular ectasia: mainte-
nance treatment with oestrogen–progesterone. Gut 1992;33:715–7.
[99] Manning RJ. Estrogen/progesterone treatment of diffuse antral vascular ecta-
sia. Am J Gastroenterol 1995;90:154–6.
[100] Tran A, Villeneuve JP, Bilodeau M, et al. Treatment of chronic bleeding from
gastric antral vascular ectasia (GAVE) with estrogen–progesterone in cirrhotic
patients: an open pilot study. Am J Gastroenterol 1999;94:2909–11.
[101] Nardone G, Rocco A, Balzano T, et al. The efficacy of octreotide therapy in
chronic bleeding due to vascular abnormalities of the gastrointestinal tract.
Aliment Pharmacol Ther 1999;13:1429–36.
[102] Bhowmick BK. Watermelon stomach treated with oral corticosteroid. J R Soc
Med 1993;86:52.
[103] Suzuki T, Hirano M, Oka H. Long-term corticosteroid therapy for gastric antral
vascular ectasia. Am J Gastroenterol 1996;91:1873–4.
[104] McCormick PA, Ooi H, Crosbie O. Tranexamic acid for severe bleeding gastric
antral vascular ectasia in cirrhosis. Gut 1998;42:750–2.
[105] Dunne KA, Hill J, Dillon JF. Treatment of chronic transfusion-dependent gas-
tric antral vascular ectasia (watermelon stomach) with thalidomide. Eur J
Gastroenterol Hepatol 2006;18:455–6.
[106] Cabral JE, Pontes JM, Toste M, et al. Watermelon stomach: treatment with a
serotonin antagonist. Am J Gastroenterol 1991;86:927–8.
[107] Schulz SW, O’Brien M, Maqsood M, et al. Improvement of severe systemic
sclerosis-associated gastric antral vascular ectasia following immuno-
suppressive treatment with intravenous cyclophosphamide. J Rheumatol
2009;36:1653–6.
[108] Shibukawa G, Irisawa A, Sakamoto N, et al. Gastric antral vascular ectasia
(GAVE) associated with systemic sclerosis: relapse after endoscopic treat-
ment by argon plasma coagulation. Intern Med 2007;46:279–83.
[109] Jabbari M, Cherry R, Lough JO, et al. Gastric antral vascular ectasia: the water-
melon stomach. Gastroenterology 1984;87:1165–70.
[110] Mann NS, Rachut E. Gastric antral vascular ectasia causing severe
hypoalbuminemia and anemia cured by antrectomy. J Clin Gastroenterol
2002;34:284–6.
[111] Pljesa S, Golubovic G, Tomasevic R, et al. “Watermelon stomach” in patients
on chronic hemodialysis. Renal Fail 2005;27:643–6.
[112] Belle JM, Feiler MJ, Pappas TN. Laparoscopic surgical treatment for refractory
gastric antral vascular ectasia: a case report and review. Surg Laparosc Endosc
Percutan Tech 2009;19:e189–93.
[113] Hou MC, Lin HC, Liu TT, et al. Antibiotic prophylaxis after endoscopic ther-
apy prevents rebleeding in acute variceal hemorrhage: a randomized trial.
Hepatology 2004;39:746–53.