Gastric antral vascular ectasia: A case report and literature review

Open access

Abstract

Gastric antral vascular ectasia (GAVE) is a rare but an important cause of upper gastrointestinal bleeding (UGIB) and commonly presents as occult bleeding that manifests as iron deficiency anemia (IDA). GAVE is commonly associated with chronic illnesses, most frequently liver cirrhosis and connective tissue diseases. The pathogenesis of GAVE is still obscure, and many hypotheses such as mechanical stress, hormonal factors, and autoimmune factors, have been proposed. Upper gastrointestinal endoscopy has a major role in the diagnosis and treatment of GAVE.

Abstract

Gastric antral vascular ectasia (GAVE) is a rare but an important cause of upper gastrointestinal bleeding (UGIB) and commonly presents as occult bleeding that manifests as iron deficiency anemia (IDA). GAVE is commonly associated with chronic illnesses, most frequently liver cirrhosis and connective tissue diseases. The pathogenesis of GAVE is still obscure, and many hypotheses such as mechanical stress, hormonal factors, and autoimmune factors, have been proposed. Upper gastrointestinal endoscopy has a major role in the diagnosis and treatment of GAVE.

Introduction

Gastric antral vascular ectasia (GAVE) is a rare cause of upper gastrointestinal bleeding (UGIB), accounting for about 4% of non-variceal UGIB and commonly presents as occult bleeding that manifests in iron deficiency anemia (IDA). GAVE is commonly associated with chronic illnesses, most frequently liver cirrhosis and connective tissue diseases.[1] In this report, we present one case of GAVE, discussing the etiology, endoscopic features, histology, pathogenesis, and optimal management for this rare entity.

Case Report

A 76-years-old male patient, known to have multiple medical problems, was admitted electively in late July 2013 for further work up for symptomatic anemia. Patient was complaining of fatigability, dizziness, and occasional black stool for about 6 months before admission. No history of hematemesis or rectal bleeding was noted. Patient’s past medical history includes hypertension, diabetes mellitus, dyslipidemia, ischemic heart disease, atrial fibrillation, congestive heart failure, pulmonary hypertension, severe tricuspid valve regurgitation, chronic kidney disease, benign prostatic hypertrophy, and vitiligo. His past surgical history was significant for bilateral total knee replacement for osteoarthritis and cataract surgery. His medications are tamsulosin, acetaminophen, darbepoetin alpha, folic acid, esomeprazole, metoprolol, warfarin, and torsemide. Family history was unremarkable. He is a nonsmoker and nonalcohol drinker.

Upon examination, he looked pale and lethargic but with stable vital signs and without postural hypotension. Unremarkable abdominal examination was noted, and digital rectal examination revealed no melena at this time. The cardiovascular examination revealed slow atrial fibrillation, a pansystolic murmur, a prominent jugular venous pressure, and bilateral lower limb edema. The chest examination was remarkable, with signs of right pleural effusion. Skin examination showed vitiligo.

At the time of present admission, laboratory data revealed low hemoglobin (7.6 g/dL) and hematocrit (0.242) with normal mean corpuscular volume. Platelets and white blood cells count were normal. Serum iron study showed low serum iron and ferritin levels. Vitamin B12 and red blood cell (RBC) folate levels were normal. Serology for celiac disease was negative. Urea and creatinine levels were elevated, 21 mmol/L and 192 µmol/L, respectively. Liver profile was normal, and his international normalized ratio (INR) was therapeutic at 2.5. Before admission, he has undergone upper and lower endoscopy. Upper endoscopy was reported as mild to moderate gastritis involving the antrum and the distal body (Figure 1) and the gastric biopsy from the antrum was reported as mild Helicobacter pylori-negative gastritis. Colonoscopy revealed only diminutive polyp in the sigmoid colon. RBC nuclear scan was negative.

Figure 1

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Figure 1

Upper endoscopic image labeled as gastritis.

Citation: Journal of Translational Internal Medicine 6, 1; 10.2478/jtim-2018-0010

During admission, the patient received blood transfusion, and his heart failure treatment optimized then capsule endoscopy (CE) was done. CE showed multiple red punctuate lesions around the pylorus (Figure 2) suggestive of angioectasias or GAVE. Small bowel was looking normal on CE. A repeat gastroscopy was performed and confirmed endoscopic diagnosis of GAVE. Active bleeding was noted from the lesions during endoscopy. Argon plasma coagulation (APC) was applied and good homeostasis was achieved. Warfarin was held temporarily during active bleeding episodes and during endoscopic therapy but was resumed thereafter. His hemoglobin was stable over a period of 2 months and follow up at 10 g/dL; then he developed melena and drop in hemoglobin level to 8.4 g/dL and required three sessions of APC before stabilization of the hemoglobin level at 11.7 g/dL. No further gastrointestinal (GI) bleeding event was noted until writing this article.

Figure 2

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Figure 2

Picture obtained with capsule endoscopy (CE): multiple red punctuate lesions around the pylorus.

Citation: Journal of Translational Internal Medicine 6, 1; 10.2478/jtim-2018-0010

Discussion

GAVE was reported for the first time by Rider et al. in 1953,[2] and since then, multiple cases were reported with more understanding of its clinical and endoscopic features. Although GAVE is a rare cause of UGIB, it can cause significant and serious GI bleeding specially in the elderly patients with multiple medical problems. GAVE affects most commonly females (71%), with an average age of 73 years at presentation. GAVE usually presents with IDA (89% of patients) due to chronic blood loss but occasionally causes severe acute GI bleeding.[3]

GAVE is usually associated with chronic illnesses, most commonly liver and connective tissue diseases. Liver cirrhosis has been found in 30% of the cases.[4] It has also been reported to be common in scleroderma and calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia syndrome.[4-5] Case reports of GAVE in patients with essential hypertension,[6] chronic renal failure,[7] acute myeloid leukemia[8] and GAVE in patients who have undergone bone marrow transplant[9] have been published.

In the literature, two characteristic endoscopic appearances of GAVE have been reported. First is the diffuse punctuate lesions in the antrum, similar to that observed in our patient (Figure 2). This type of GAVE is typically seen in male, patients with cirrhosis and commonly accompanied by acute bleeding. Our patient is a male, does not have liver disease, and is presented with chronic blood loss rather than acute bleeding. Second one is the red lesions organized in stripes radially departing from the pylorus, known as watermelon stomach (Figure 3). This type is mostly common in females with connective tissue diseases and usually present with occult bleeding.[10-11]

Figure 3

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Figure 3

Striped watermelon appearance of gastric antral vascular ectasia.

Citation: Journal of Translational Internal Medicine 6, 1; 10.2478/jtim-2018-0010

GAVE is typically located in the gastric antrum; however, it may be also found rarely in other areas of the GI tract, including cardia,[12-13] duodenum, jejunum,[14] and rectum [15-16] The involvement of the proximal part of the stomach is very rare and commonly located within a diaphragmatic hernia.[17,18]

The main differential diagnosis of GAVE on endoscopy is portal hypertensive gastropathy (PHG) and antral gastritis. PHG is typically more predominant in the fundus and the body of the stomach, whereas GAVE mainly involves the antrum. Furthermore, severe PHG can extend up to the antrum and can resemble GAVE. GAVE can be easily confused with gastritis on upper GI endoscopy; however, the histological pattern of GAVE, although not pathognomonic, can differentiate between the two entities. On histology, GAVE is characterized by vascular ectasia of the mucosal capillaries, focal thrombosis, spindle cell proliferation (smooth muscle cell and myofibroblast hyperplasia), and fibrohyalinosis, which consist of homogeneous substance around the ectatic capillaries of the lamina propria (Figure 4).[19,20,21]

Figure 4

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Figure 4

Gastric antral vascular ectasia (GAVE). Histology shows dilated capillaries (c) in the superficial gastric mucosa with occasional thrombi (arrow). Fibromuscular spindle cells are prominent.

Citation: Journal of Translational Internal Medicine 6, 1; 10.2478/jtim-2018-0010

The peculiar thing in our patient is that GAVE was misinterpreted as gastritis on upper GI endoscopy and the diagnosis was detected through CE. Sidhu et al. reported similar scenario in six patients.[18] It is not clear why the diagnosis in our patient was missed on an initial upper GI endoscopy that was performed by an expert endoscopy consultant. One possible explanation of this is the variation in endoscopic appearances of GAVE over time, possibly related to blood flow, hemoglobin concentration, or synchronous other gastric pathology such as gastritis. CE can be regarded as “physiologic” endoscopy, without the need for air insufflation and subsequent compression of the gastric vasculature, and this may make lesions such as GAVE more prominent on CE.

The pathogenesis of GAVE is still obscure, and many hypotheses such as mechanical stress, hemodynamic alterations, and hormonal and autoimmune factors have been proposed. Mechanical stress represented by strong gastric peristalsis is thought to induce prolapse and trauma of antral mucosa and intermittent obstruction of blood vessels, which can lead to fibromuscular hyperplasia and vascular ectasia.[22] Increased levels of hormones with vasodilating properties, such as gastrin and prostaglandin E2, have been observed in patients with GAVE, and it has been suggested that failure of liver processing functions may lead to a build-up of these hormones, contributing to the pathogenesis of GAVE.[23] Up to 60% of patients with GAVE have associated autoimmune diseases, specially connective tissue diseases, and test positive for autoantibodies such as antinuclear antibodies and anti-centromere antibodies; therefore, an autoimmune pathogenesis is suggested.[9]

The mainstay of therapy for GAVE remains endoscopic. Neodymium:yttrium-aluminum-garnet (Nd:YAG) laser has been widely used in the treatment of GAVE. All series have confirmed the efficacy of this endoscopic thermal therapy by reducing or abolishing the need of blood transfusions in 50–80% of cases.[24,25,26,27] However, APC has been found to be equally effective in the treatment of GAVE and is superior to ND:YAG laser in cost, convenience, and complication rates.[28] Multiple sessions of APC may be required to reduce bleeding episodes and/or decrease transfusion dependence. Several other endoscopic therapies, such as cryotherapy,[29] band ligation,[30,31,32] and radiofrequency ablation,[33] have been proposed in the past years. Although initial reports of these endoscopic modalities are encouraging, well-performed, larger, prospective studies are needed before providing any definitive conclusion.

Multiple drugs, such as hormonal (estrogen-progesterone) therapy,[34-35] octreotide,[36-37] steroids,[38-39] and transexamic acid,[40] have been tried to control GAVE-related bleeding. After all, no one has clearly shown satisfactory results in order to consider medical therapy as a valid alternative to an invasive approach.

Before the advent of endoscopic therapy, GAVE was commonly treated by antrectomy. However, surgical resection is often associated with significant morbidity and mortality and should be reserved only for patients who are refractory to medical and endoscopic therapy.

Conclusion

GAVE is a rare but an important cause of UGIB. Diagnosis of GAVE can be overlooked during upper GI endoscopy and must always be considered specially in obscure GI bleeding. Endoscopic therapy using APC is the main treatment option.

Conflict of interest: None for all authors.

References

  • 1

    Dulai GS, Jensen DM, Kovacs TO, Grainek IM, Jutabha R. Endoscopic treatment outcomes in watermelon stomach patients with and without portal hypertension. Endoscopy 2004; 36: 68-72.

  • 2

    Rider JA, Klotz AP, Kirsner JB. Gastritis with veno-capillary ectasia as a source of massive gastric hemorrhage. Gastroenterology 1953; 24:118-23.

  • 3

    Gostout CJ, Viggiano TR, Ahlquist DA, Wang KK. Larson MV, Balm R. The clinical and endoscopic spectrum of the watermelon stomach. J Clin Gastroenterol 1992; 15: 256-63.

  • 4

    Ward EM, Raimondo M, Rosser BG, Wallace MB, Dickson RD. Prevalence and natural history of gastric antral vascular ectasia in patients undergoing orthotopic liver transplantation. J Clin Gastroenterol 2004; 38: 898-900.

  • 5

    Beales IL. Watermelon stomach in the CREST syndrome. Postgrad Med J 1994; 70: 766-7

  • 6

    Watson M, Hally RJ, McCue PA, Varga J, Jiménez SA. Gastric antral vascular ectasia (watermelon stomach) in patients with systemic sclerosis. Arthritis Rheum 1996; 39: 341-6.

  • 7

    Liberski SM, McGarrity TJ, Hartle RJ, Varano V, Reynolds D. The watermelon stomach: long-term outcome in patients treated with Nd:YAG laser therapy. Gastrointest Endosc 1994; 40: 584-7.

  • 8

    Takahashi T, Miya T, Oki M, Sugawara N, Yoshimoto M, Tsujisaki M. Severe hemorrhage from gastric vascular ectasia developed in a patient with AML. Int J Hematol 2006; 83: 467-8.

  • 9

    Tobin RW, Hackman RC, Kimmey MB, Durtschi MB, Hayashi A, Malik R, et al. Bleeding from gastric antral vascular ectasia in marrow transplant patients. Gastrointest Endosc 1996; 44: 223-9.

  • 10

    Gostout CJ, Viggiano TR, Ahlquist DA, Wang KK. Larson MV, Balm R. The clinical and endoscopic spectrum of the watermelon stomach. J Clin Gastroenterol 1992; 15: 256-63.

  • 11

    Ito M, Uchida Y, Kamano S, Kawabata H, Nishioka M. Clinical comparisons between two subsets of gastric antral vascular ectasia. Gastrointest Endosc 2001; 53: 764-70.

  • 12

    Chaves DM, Sakai P, Oliveira CV, Cheng S, Ishioka S. Watermelon stomach: clinical aspects and treatment with argon plasma coagulation. Arq Gastroenterol 2006; 43: 191-5.

  • 13

    Stotzer PO, Willén R, Kilander AF. Watermelon stomach: not only an antral disease. Gastrointest Endosc 2002; 55: 897-90.

  • 14

    Shaffer RA, Scobey MW. Ring around the cardia: a watermelon stomach variant. Gastrointest Endosc 2003; 57: 280-2.

  • 15

    Calès P, Voigt JJ, Payen JL, Bloom E, Berg P, Vinel JP, et al. Diffuse vascular ectasia of the antrum, duodenum, and jejunum in a patient with nodular regenerative hyperplasia. Lack of response to portosystemic shunt or gastrectomy. Gut 1993; 34: 558-61.

  • 16

    Gürsoy M, Baysal C, Demirhan B, Moray G, Boyacioğlu S. Rectal vascular ectasia associated with watermelon stomach. Gastrointest Endosc 1999; 50: 854-7.

  • 17

    Singh D, Shill M, Kaur H. The watermelon rectum. J Clin Gastroenterol 2001; 33: 164-6.

  • 18

    Sidhu R, Sanders DS, McAlindon ME. Does capsule endoscopy recognise gastric antral vascular ectasia more frequently than conventional endoscopy? J Gastrointestin Liver Dis 2006; 15: 375-7.

  • 19

    Gostout CJ, Viggiano TR, Ahlquist DA, Wang KK, Larson MV, Balm R. The clinical and endoscopic spectrum of the watermelon stomach. J Clin Gastroenterol 1992; 15: 256-63.

  • 20

    Suit PF, Petras RE, Bauer TW, Petrini JL. Gastric antral vascular ectasia. A histologic and morphometric study of “the watermelon stomach”. Am J Surg Pathol 1987; 11: 750-7.

  • 21

    Gilliam JH, Geisinger KR, Wu WC, Weidner N, Richter JE. Endoscopic biopsy is diagnostic in gastric antral vascular ectasia. The “watermelon stomach”. Dig Dis Sci 1989; 34: 885-8.

  • 22

    Payen JL, Calès P, Voigt JJ, Barbe S, Pilette C, DubuissonL, et al. Severe portal hypertensive gastropathy and antral vascular ectasia are distinct entities in patients with cirrhosis. Gastroenterology 1995; 108: 138-44.

  • 23

    Quintero E, Pique JM, Bombi JA, Bordas JM, Sentis J, Elena M, 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.

  • 24

    Ripoll C, Garcia-Tsao G. The management of portal hypertensive gastropathy and gastric antral vascular ectasia. Digest Liv Dis 2011; 43: 345-51.

  • 25

    Gostout CJ, Ahlquist DA, Radford CM, Viggiano TR, Bowyer BA, et al. Endoscopic laser therapy for watermelon stomach. Gastroenterology 1989; 96: 1462-5.

  • 26

    Sargeant IR, Loizou LA, Rampton D, Tulloch M, Bown SG. Laser ablation of upper gastrointestinal vascular ectasias: long term results. Gut 1993; 34: 470-5.

  • 27

    Potamiano S, Carter CR, Anderson JR. Endoscopic laser treatment of diffuse gastric antral vascular ectasia. Gut 1994; 35: 461-3.

  • 28

    Rosenfeld G, Enns R. Argon photocoagulation in the treatment of gastric antral vascular ectasia and radiation proctitis. Curr Endoscop Prac 2009; 23: 801-4.

  • 29

    Cho S, Zanati S, Yong E, Cirocco M, Kandel G, Kortan P, et al. Endoscopic cryotherapy for the management of gastric antral vascular ectasia. Gastrointest Endosc 2008; 68: 895-902.

  • 30

    Sinha SK, Udawat HP, Varma S, Lal A, Rana SS, Bhasin DK. Watermelon stomach treated with endoscopic band ligation. Gastrointest Endosc 2006; 64: 1028-31.

  • 31

    Kumar R, Mohindra S, Pruthi HS. Endoscopic band ligation: a novel therapy for bleeding gastric antral vascular ectasia. Endoscopy 2007; 39(S1): E56-7.

  • 32

    Wells CD, Harrison ME, Gurudu SR, Crowell MD, Byrne TJ, Depetris G, et al. Treatment of gastric antral vascular ectasia (watermelon stomach) with endoscopic band ligation. Gastrointest Endosc 2008; 68: 231-6.

  • 33

    Gross SA, Al-Haddad M, Gill KR, Schore AN, Wallace MB. Endoscopic mucosal ablation for the treatment of gastric antral vascular ectasia with the HALO90 system: a pilot study. Gastrointest Endosc 2008; 67: 324-7.

  • 34

    Moss SF, Ghosh P, Thomas DM, Jackson JE, Calam J. Gastric antral vascular ectasia: maintenance treatment with oestrogen-progesterone. Gut 1992; 33: 715-7.

  • 35

    Tran A, Villeneuve JP, Bilodeau M, Willems B, Marleau D, Fenyves D, 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.

  • 36

    Nardone G, Rocco A, Balzano T, Budillon G. The efficacy of octreotide therapy in chronic bleeding due to vascular abnormalities of the gastrointestinal tract. Aliment Pharmacol Ther 1999; 13: 1429-36.

  • 37

    Barbara G, De Giorgio R, Salvioli B, Stanghellini V, Corinaldesi R. Unsuccessful octreotide treatment of the watermelon stomach. J Clin Gastroenterol. 1998; 26: 345-6.

  • 38

    Bhowmick BK. Watermelon stomach treated with oral corticosteroid. J R Soc Med 1993; 86: 52.

  • 39

    Calam J, Walker RJ. Antral vascular lesion, achlorhydria, and chronic gastrointestinal blood loss: response to steroids. Dig Dis Sci 1980; 25: 236-9.

  • 40

    McCormick PA, Ooi H, Crosbie O. Tranexamic acid for severe bleeding gastric antral vascular ectasia in cirrhosis. Gut 1998; 42: 750-2.

1

Dulai GS, Jensen DM, Kovacs TO, Grainek IM, Jutabha R. Endoscopic treatment outcomes in watermelon stomach patients with and without portal hypertension. Endoscopy 2004; 36: 68-72.

2

Rider JA, Klotz AP, Kirsner JB. Gastritis with veno-capillary ectasia as a source of massive gastric hemorrhage. Gastroenterology 1953; 24:118-23.

3

Gostout CJ, Viggiano TR, Ahlquist DA, Wang KK. Larson MV, Balm R. The clinical and endoscopic spectrum of the watermelon stomach. J Clin Gastroenterol 1992; 15: 256-63.

4

Ward EM, Raimondo M, Rosser BG, Wallace MB, Dickson RD. Prevalence and natural history of gastric antral vascular ectasia in patients undergoing orthotopic liver transplantation. J Clin Gastroenterol 2004; 38: 898-900.

5

Beales IL. Watermelon stomach in the CREST syndrome. Postgrad Med J 1994; 70: 766-7

6

Watson M, Hally RJ, McCue PA, Varga J, Jiménez SA. Gastric antral vascular ectasia (watermelon stomach) in patients with systemic sclerosis. Arthritis Rheum 1996; 39: 341-6.

7

Liberski SM, McGarrity TJ, Hartle RJ, Varano V, Reynolds D. The watermelon stomach: long-term outcome in patients treated with Nd:YAG laser therapy. Gastrointest Endosc 1994; 40: 584-7.

8

Takahashi T, Miya T, Oki M, Sugawara N, Yoshimoto M, Tsujisaki M. Severe hemorrhage from gastric vascular ectasia developed in a patient with AML. Int J Hematol 2006; 83: 467-8.

9

Tobin RW, Hackman RC, Kimmey MB, Durtschi MB, Hayashi A, Malik R, et al. Bleeding from gastric antral vascular ectasia in marrow transplant patients. Gastrointest Endosc 1996; 44: 223-9.

10

Gostout CJ, Viggiano TR, Ahlquist DA, Wang KK. Larson MV, Balm R. The clinical and endoscopic spectrum of the watermelon stomach. J Clin Gastroenterol 1992; 15: 256-63.

11

Ito M, Uchida Y, Kamano S, Kawabata H, Nishioka M. Clinical comparisons between two subsets of gastric antral vascular ectasia. Gastrointest Endosc 2001; 53: 764-70.

12

Chaves DM, Sakai P, Oliveira CV, Cheng S, Ishioka S. Watermelon stomach: clinical aspects and treatment with argon plasma coagulation. Arq Gastroenterol 2006; 43: 191-5.

13

Stotzer PO, Willén R, Kilander AF. Watermelon stomach: not only an antral disease. Gastrointest Endosc 2002; 55: 897-90.

14

Shaffer RA, Scobey MW. Ring around the cardia: a watermelon stomach variant. Gastrointest Endosc 2003; 57: 280-2.

15

Calès P, Voigt JJ, Payen JL, Bloom E, Berg P, Vinel JP, et al. Diffuse vascular ectasia of the antrum, duodenum, and jejunum in a patient with nodular regenerative hyperplasia. Lack of response to portosystemic shunt or gastrectomy. Gut 1993; 34: 558-61.

16

Gürsoy M, Baysal C, Demirhan B, Moray G, Boyacioğlu S. Rectal vascular ectasia associated with watermelon stomach. Gastrointest Endosc 1999; 50: 854-7.

17

Singh D, Shill M, Kaur H. The watermelon rectum. J Clin Gastroenterol 2001; 33: 164-6.

18

Sidhu R, Sanders DS, McAlindon ME. Does capsule endoscopy recognise gastric antral vascular ectasia more frequently than conventional endoscopy? J Gastrointestin Liver Dis 2006; 15: 375-7.

19

Gostout CJ, Viggiano TR, Ahlquist DA, Wang KK, Larson MV, Balm R. The clinical and endoscopic spectrum of the watermelon stomach. J Clin Gastroenterol 1992; 15: 256-63.

20

Suit PF, Petras RE, Bauer TW, Petrini JL. Gastric antral vascular ectasia. A histologic and morphometric study of “the watermelon stomach”. Am J Surg Pathol 1987; 11: 750-7.

21

Gilliam JH, Geisinger KR, Wu WC, Weidner N, Richter JE. Endoscopic biopsy is diagnostic in gastric antral vascular ectasia. The “watermelon stomach”. Dig Dis Sci 1989; 34: 885-8.

22

Payen JL, Calès P, Voigt JJ, Barbe S, Pilette C, DubuissonL, et al. Severe portal hypertensive gastropathy and antral vascular ectasia are distinct entities in patients with cirrhosis. Gastroenterology 1995; 108: 138-44.

23

Quintero E, Pique JM, Bombi JA, Bordas JM, Sentis J, Elena M, 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.

24

Ripoll C, Garcia-Tsao G. The management of portal hypertensive gastropathy and gastric antral vascular ectasia. Digest Liv Dis 2011; 43: 345-51.

25

Gostout CJ, Ahlquist DA, Radford CM, Viggiano TR, Bowyer BA, et al. Endoscopic laser therapy for watermelon stomach. Gastroenterology 1989; 96: 1462-5.

26

Sargeant IR, Loizou LA, Rampton D, Tulloch M, Bown SG. Laser ablation of upper gastrointestinal vascular ectasias: long term results. Gut 1993; 34: 470-5.

27

Potamiano S, Carter CR, Anderson JR. Endoscopic laser treatment of diffuse gastric antral vascular ectasia. Gut 1994; 35: 461-3.

28

Rosenfeld G, Enns R. Argon photocoagulation in the treatment of gastric antral vascular ectasia and radiation proctitis. Curr Endoscop Prac 2009; 23: 801-4.

29

Cho S, Zanati S, Yong E, Cirocco M, Kandel G, Kortan P, et al. Endoscopic cryotherapy for the management of gastric antral vascular ectasia. Gastrointest Endosc 2008; 68: 895-902.

30

Sinha SK, Udawat HP, Varma S, Lal A, Rana SS, Bhasin DK. Watermelon stomach treated with endoscopic band ligation. Gastrointest Endosc 2006; 64: 1028-31.

31

Kumar R, Mohindra S, Pruthi HS. Endoscopic band ligation: a novel therapy for bleeding gastric antral vascular ectasia. Endoscopy 2007; 39(S1): E56-7.

32

Wells CD, Harrison ME, Gurudu SR, Crowell MD, Byrne TJ, Depetris G, et al. Treatment of gastric antral vascular ectasia (watermelon stomach) with endoscopic band ligation. Gastrointest Endosc 2008; 68: 231-6.

33

Gross SA, Al-Haddad M, Gill KR, Schore AN, Wallace MB. Endoscopic mucosal ablation for the treatment of gastric antral vascular ectasia with the HALO90 system: a pilot study. Gastrointest Endosc 2008; 67: 324-7.

34

Moss SF, Ghosh P, Thomas DM, Jackson JE, Calam J. Gastric antral vascular ectasia: maintenance treatment with oestrogen-progesterone. Gut 1992; 33: 715-7.

35

Tran A, Villeneuve JP, Bilodeau M, Willems B, Marleau D, Fenyves D, 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.

36

Nardone G, Rocco A, Balzano T, Budillon G. The efficacy of octreotide therapy in chronic bleeding due to vascular abnormalities of the gastrointestinal tract. Aliment Pharmacol Ther 1999; 13: 1429-36.

37

Barbara G, De Giorgio R, Salvioli B, Stanghellini V, Corinaldesi R. Unsuccessful octreotide treatment of the watermelon stomach. J Clin Gastroenterol. 1998; 26: 345-6.

38

Bhowmick BK. Watermelon stomach treated with oral corticosteroid. J R Soc Med 1993; 86: 52.

39

Calam J, Walker RJ. Antral vascular lesion, achlorhydria, and chronic gastrointestinal blood loss: response to steroids. Dig Dis Sci 1980; 25: 236-9.

40

McCormick PA, Ooi H, Crosbie O. Tranexamic acid for severe bleeding gastric antral vascular ectasia in cirrhosis. Gut 1998; 42: 750-2.

Journal Information

Figures

  • View in gallery

    Upper endoscopic image labeled as gastritis.

  • View in gallery

    Picture obtained with capsule endoscopy (CE): multiple red punctuate lesions around the pylorus.

  • View in gallery

    Striped watermelon appearance of gastric antral vascular ectasia.

  • View in gallery

    Gastric antral vascular ectasia (GAVE). Histology shows dilated capillaries (c) in the superficial gastric mucosa with occasional thrombi (arrow). Fibromuscular spindle cells are prominent.

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