Clin J Gastroenterol (2013) 6:231–236 DOI 10.1007/s12328-013-0385-y
CASE REPORT
Successful treatment of refractory gastric antral vascular ectasia using transcatheter arterial embolization Haruka Yoshida • Hiroki Takahashi • Hiromichi Akoshima Nobuyuki Chida • Kenji Noguchi • Nobukazu Tanabe • Yutaka Mano • Katsuaki Ukai • Keiichi Tadokoro
•
Received: 22 January 2013 / Accepted: 30 April 2013 / Published online: 23 May 2013 Ó Springer Japan 2013
Abstract In January 2008, a 67-year-old woman was admitted to our hospital because of hepatitis C virus-related cirrhosis and hepatocellular carcinoma (HCC). In February 2010, she had tarry stools and anemia resulting from gastric antral vascular ectasia (GAVE). Argon plasma coagulation (APC) treatment for GAVE was performed at that time. She revisited our hospital in July 2010 because of tarry stools and anemia caused by GAVE recurrence, which required 5 APC sessions and blood transfusion to control the bleeding. In October 2010, she arrived at our hospital by ambulance because of hemorrhagic shock resulting from GAVE recurrence. Despite performing 5 APC sessions and multiple blood transfusions, the tarry stools and anemia persisted during the hospitalization period. In December 2010 and January 2011, second-stage selective transcatheter arterial embolization (TAE) of the right gastric and right gastroepiploic arteries using microcoils was performed for the treatment of the refractory GAVE. Upper gastrointestinal endoscopy performed after TAE revealed the disappearance of mucosal diffuse spotty redness. In addition, no complications such as gastric ulcer and necrosis were observed. Selective TAE, effectively resolved the GAVE and anemia, and no recurrence has been observed during the last 24 months. Therefore, TAE may be a safe and radical treatment for refractory GAVE.
H. Yoshida (&) H. Takahashi H. Akoshima K. Noguchi N. Tanabe Y. Mano K. Ukai K. Tadokoro Department of Gastroenterology, Sendai Medical Center, 2-8-8 Miyagino, Sendai, Miyagi 983-8520, Japan e-mail: [email protected] N. Chida Chida Medical Clinic, Sendai, Japan
Keywords Argon plasma coagulation Gastric antral vascular ectasia Transcatheter arterial embolization
Introduction Gastric antral vascular ectasia (GAVE), characterized by the presence of red spots or streaks in the antral mucosa on endoscopic examination [1], is responsible for *4 % of all non-variceal upper gastrointestinal bleeding events[2]. Typical initial presentations range from occult bleedings causing blood transfusion-dependent chronic iron-deficiency anemia, to severe acute upper gastrointestinal bleeding. Various treatments have been reported, including medical, surgical, and endoscopic therapy. Argon plasma coagulation (APC) therapy is the most common treatment for GAVE-related bleeding. However, we sometimes experience recurrent GAVE even though there is repeated APC therapy. Hence, we report a case of recurrent GAVE refractory to the repeated APC treatments and successfully controlled by selective transcatheter arterial embolization (TAE).
Case report In January 2008, a 67-year-old woman was admitted to our hospital because of hepatitis C virus-related cirrhosis (Child-Pugh grade A) and hepatocellular carcinoma (HCC). Transcatheter arterial chemoembolization (TACE) for HCC was performed during the same month. Systemic treatment with sorafenib was initiated in April 2008 but was terminated after 3 months because of thrombocytopenia. TACE was performed 4 times between January 2010 and December 2010 for recurrent HCC. In February 2010,
123
232
the patient was found to have tarry stools and anemia (hemoglobin [Hb] level, 4.4 g/dL) resulting from GAVE associated with cirrhosis. APC treatment for GAVE was performed and a proton-pump inhibitor was prescribed. Each APC session has been performed using a 2.3-mm diameter probe with a heat-resistant ceramic tip (APC probe; ERBEÒ Electromedizin, Tu¨bingen, Germany). An argon plasma coagulation unit, including a high-frequency
Fig. 1 Endoscopic examination prior to argon plasma coagulation (APC) treatment revealed the presence of gastric antral vascular ectasia (GAVE), as indicated by mucosal diffuse spotty redness spreading over the antrum of the stomach and oozing from the GAVE lesion
Clin J Gastroenterol (2013) 6:231–236
electrosurgical generator (ERBEÒ ICC 200) and an argon delivery unit (ERBEÒ APC 300), was used. The argon gas flow was set at 2.0 l/min and 60 W power was used. The patient was then discharged from the hospital. In May 2010, sorafenib therapy was resumed for treatment of recurrent HCC. The patient revisited our hospital in July 2010 because of recurrent tarry stools and anemia. A laboratory examination upon hospitalization revealed an Hb level of 8.2 g/dL. Upper gastrointestinal endoscopy revealed no varices; however, a coalescence of numerous angiectatic lesions that resembled a ‘‘honeycomb stomach’’ was noted from the pylorus to the antrum, and the patient was diagnosed with recurrent GAVE (Fig. 1). Total colonoscopy and capsule endoscopy did not detect any other causes of anemia. In addition to oral iron and intravenous tranexamic acid therapies, multiple blood transfusions (a total of 10 units of packed red blood cells) were needed and 5 APC sessions were performed upon hospitalization. Each session was performed once or twice a week when the patient had tarry stools or her Hb level decreased. The vascular lesions were treated until most of the telangiectasias were coagulated. In October 2010, the patient arrived at our hospital by ambulance because of hemorrhagic shock, and her Hb level was 5.4 g/dL. Despite discontinuing sorafenib therapy on admission and performing 7 APC sessions, the tarry stools and anemia persisted, requiring frequent blood transfusions (a total of 26 units of packed red blood cells). We concluded that the GAVE could not be controlled by APC treatment. Hence, we sought a more effective therapy to treat GAVE and found a domestic case report in which TAE was performed
RGA
CHA
SDA
PSPDA ASPDA
RGEA
Fig. 2 Right gastric angiography revealed arteriovenous shunting in the right gastric arterial territory and the antral branch of the right gastroepiploic artery spread over the antrum. Microcoils were used in the left hepatic artery for treatment of vascular injury during the prior angiography for hepatocellular carcinoma. CHA Common hepatic
123
artery, RGA right gastric artery, SDA supraduodenal artery, PSPDA posterior superior pancreaticoduodenal artery, ASPDA anterior superior pancreaticoduodenal artery, RGEA right gastroepiploic artery. Gray shading indicates arteriovenous malformation
Clin J Gastroenterol (2013) 6:231–236
233
Fig. 3 First-stage transcatheter arterial embolization (TAE) was performed using microcoils. The right gastric artery was embolized using microcoils and the arteriovenous shunting area was reduced. PHA Proper hepatic artery, SA splenic artery, Filled triangle indicates microcoils
PHA RGA
SA
SDA PSPDA
RGEA
Fig. 4 Second-stage TAE was performed at the antral branch of the right gastroepiploic artery, after which arteriovenous shunting was rarely detected. RGEA branch: antral branch of right gastroepiploic artery
RGA RGEA brach
CHA
SDA
PSPDA
RGEA
for GAVE [3]. Angiography was performed in December 2010, and arteriovenous shunting was detected in the right gastric arterial territory and the antral branch of the right gastroepiploic artery (Fig. 2). For first-stage TAE, the right gastric artery was embolized using microcoils in December 2010 (Fig. 3). Two weeks after the first-stage TAE was performed, upper gastrointestinal endoscopy revealed no complications such as gastric ulcer and ischemia; however, a few red spots were detected. In January 2011, 3 weeks after the first-stage TAE was performed, second-stage TAE was performed using microcoils at the antral branch of the right gastroepiploic artery (Fig. 4). Four days after the second-stage TAE was performed, upper gastrointestinal endoscopy detected no complications. Five days after the second-stage TAE was performed, the patient was discharged from the hospital. In December 2011, endoscopy
revealed remarkable reduction of red spots and no ischemic change (Fig. 5). Selective TAE of the right gastric and right gastroepiploic arteries effectively resolved the GAVE and anemia (Fig. 6). As of January 2013, the patient has had no recurrence of GAVE or anemia during the last 24 months.
Discussion GAVE was first described in 1953 as erosive gastritis with venocapillary ectasia in a patient with severe chronic irondeficiency anemia [4]. In 1984, Jabbari et al. [5] more accurately defined GAVE as ‘‘longitudinal red folds traversing the antrum and converging on the pylorus, each containing a visible convoluted column of vessels’’ and
123
234
Clin J Gastroenterol (2013) 6:231–236
coined the term ‘‘watermelon stomach’’ on endoscopic examination. Lee et al. [6] described a stomach with diffuse red spots representing dilated blood vessels in the antrum as a ‘‘honeycomb stomach.’’ Most GAVE patients are elderly, with a preponderance of women [7, 8]. GAVE has been associated with cirrhosis, renal failure, bone marrow transplantation, and scleroderma [9]. Although various treatments have been reported, no optimal therapy for GAVE has been established. Recently, pharmacological agents and endoscopic therapy have become the first-line treatments for GAVE [9].
Fig. 5 Endoscopy performed in December 2011 revealed a remarkable reduction of red spots and oozing was not detected
Fig. 6 Serial hemoglobin concentrations, blood transfusion requirements, and the number of APC sessions, showing the effects of TAE therapy
Medical treatment of GAVE includes corticosteroids [5], a combination of estrogen and progesterone [10], octreotide [7], tranexamic acid [11], and cyclophosphamide [12]. In the present case, tranexamic acid was used but was considered ineffective. Furthermore, whether the other treatments are effective or have strong adverse effects remains to be elucidated. Endoscopic therapy includes Nd:YAG laser coagulation [13], APC [14], endoscopic mucosal ablation [15], and endoscopic band ligation (EBL) [9]. Of these therapies, APC is the most frequently used endoscopic treatment for GAVE-related bleeding. Lecleire et al. [16] reported that APC treatment of bleeding GAVE was efficient in more than 80 % of cases, and the mean number of APC sessions in 17 GAVE patients with cirrhosis required to attain a stable hemoglobin level was 2.18 (±1.74; median, 2). In our case, melena persisted despite performing 7 APC sessions. Moreover, the patient showed recurrence within 6 months of treatment [17]. Thus, we concluded that the patient had refractory GAVE. APC treatment failure was reported to be infrequent and was primarily described in patients with hemorrhagic diathesis resulting from thrombocytopenia, or long-term anticoagulation or antiplatelet therapy [14]. In our case, the platelet count in October 2010 was only 4.2 9 104/lL, which might have affected the treatment-resistant hemorrhage. Sorafenib is a multikinase inhibitor that targets vascular endothelial growth factor (VEGF)-mediated angiogenesis. A recent meta-analysis of randomized controlled VEGF trials showed a significant 2-fold increase in the risk of allgrade bleeding events [18]. In our case, sorafenib might
Clinical course
1 unit blood transfusion
APC Hb(g/dl) 16
TAE for GAVE
14 12 10 8 6 4 2 0 -60 -30
0
30
60
hospitalization
123
90
120
150
hospitalization
180
210
240
270
300
330 360
390
420
450
480 510
day
Clin J Gastroenterol (2013) 6:231–236
have affected the patient’s tolerance to the APC therapy. However, despite discontinuing the sorafenib therapy and performing 7 APC sessions, the refractory GAVE and anemia persisted during the hospitalization period. Nakamura et al. [17] reported that the effectiveness of APC therapy is temporary and that APC is not always effective as a medium-term and long-term treatment. The authors revealed that early recurrence seemed to be induced by the development of new GAVE, fragility of local blood vessels, stagnation of mucosal blood flow, and mechanical irritation. Perente et al. [19] reported the endosonographic findings of regional wall thickening and a spongy appearance in the second and third layer of the vascular structural areas. Because of the limited depth of thermal injury, APC treatment might not be effective in some cases. TAE for GAVE treatment is rarely reported, and its effectiveness has not yet been established. Jabbari et al. [5] reported negative results from angiography studies performed in 3 cases. Robertson et al. [20] considered the reason why angiogram for GAVE patients would be negative. The angiographic findings may be subtle because clearance of contrast material from the vessels within the gastric antrum occurred early and the late venous-phase films appeared normal. Furthermore, superimposition of the gastric antrum on the right renal pelvicaliceal system may obscure hypervascularity and arteriovenous shunting. They also described recent improvements in digital subtraction angiographic equipment and techniques have produced superior contrast resolution, allowing optimum detection of subtle venous phase abnormalities. So negative results of angiography for GAVE patients might have been caused by the technical problems. Terawaki et al. [3] performed successful TAE for GAVE treatment despite the lack of abnormal vessels on angiography. They reported that TAE was effective because blood flow reduction in the antrum might improve the venous dilatation. Potential complications of TAE include gastric ulcer and necrosis resulting from gastric ischemia. Ashiya et al. [21] presented to the academy of the Japanese Society of Gastroenterology that TAE of the right and left gastric arteries resulted in gastric ulcers. In our case, however, no complications were encountered and the angiography performed in December 2011 revealed no recurrence of arteriovenous shunting in the antral area. This result may have occurred because we performed selective TAE. For cases in which GAVE cannot be controlled by endoscopic treatments such as APC and EBL, we recommend TAE. If the culprit vessels are detected, a more selective and safer TAE procedure could be performed. We report that selective TAE may be a safe and radical treatment for the management of recurrent GAVE refractory to other treatments.
235 Conflict of interest of interest.
The authors declare that they have no conflict
References 1. Payen J, Cales P, Voigt J, et al. Severe portal hypertensive gastropathy and antral vascular ectasia are distinct entities in patients with cirrhosis. Gastroenterology. 1995;108:138–44. 2. 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. 3. Terawaki H, Kobayashi S, Kato J, et al. A case report of hemodialysis patient who presented recurrent bleeding from gastric antral vascular ectasia (GAVE) associated with liver cirrhosis: the effectiveness of trans-arterial embolization to bilateral gastric arteries. J Jpn Soc Dial Ther. 2008;41:803–8. 4. Rider JA, Klotz AP, Kirsner JB. Gastritis with veno-capillary ectasia as a source of massive gastric hemorrhage. Gastroenterology. 1953;24:118–23. 5. Jabbari M, Cherry R, Lough JO, et al. Gastric antral vascular ectasia: the watermelon stomach. Gastroenterology. 1984;87: 1165–70. 6. Lee FL, Costello F, Flanagan N, et al. Diffuse antral vascular ectasia. Gastrointest Endosc. 1984;30:87–90. 7. Sebastian S, O’Morain CA, Buckley MJ. Review article: current therapeutic options for gastric antral vascular ectasia. Aliment Pharmacol Ther. 2003;18:157–65. 8. Gostout CJ, Viggiano TR, Ahlquist DA, et al. The clinical and endoscopic spectrum of the watermelon stomach. J Clin Gastroenterol. 1992;15:256–63. 9. Sato T, Yamazaki K, Akaike J, et al. Endoscopic band ligation for refractory gastric antral vascular ectasia associated with liver cirrhosis. Clin J Gastroenterol. 2011;4:108–11. 10. Moss SF, Ghosh P, Thomas DM, et al. Gastric antral vascular ectasia: maintenance treatment with estrogen-progesterone. Gut. 1992;33:715–7. 11. McCormick PA, Ooi H, Crosbie O. Tranexamic acid for severe bleeding gastric antral vascular ectasia in cirrhosis. Gut. 1998;42:750–2. 12. Peterson A, Varga J. Cyclophosphamide: a novel treatment of gastric antral vascular ectasia associated with systemic sclerosis? Curr Rheumatol Rep. 2010;12:4–7. 13. Sargeant IR, Loizou LA, Rampton D, et al. Laser ablation of upper gastrointestinal vascular ectasias: long term results. Gut. 1993;34:470–5. 14. Fuccio L, Zagari RM, Serrani M, et al. Endoscopic argon plasma coagulation for the treatment of gastric antral vascular ectasiarelated bleeding in patients with liver cirrhosis. Digestion. 2009;79:143–50. 15. Gross SA, Al-Haddad M, Gill KRS, et al. Endoscopic mucosal ablation for the treatment of gastric antral vascular ectasia with the HALO90 system: a pilot study. Gastrointest Endosc. 2008;67: 324–7. 16. 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. 17. Nakamura S, Mitsunaga A, Konishi H, et al. Long-term follow up of gastric vascular ectasia treated by argon plasma coagulation. Dig Endosc. 2006;18:128–33. 18. Je Y, Schutz FA, Choueiri TK. Risk of bleeding with vascular endothelial growth factor receptor tyrosine-kinase inhibitors sunitinib and sorafenib: a systematic review and meta-analysis of clinical trials. Lancet Oncology. 2009;10:967–74.
123
236 19. Parente F, Petrillo M, Vago F, et al. The watermelon stomach: clinical, endoscopic, endosonographic, and therapeutic aspects in three cases. Endoscopy. 1995;27:203–6. 20. Robertson I, Tait N, Jackson J. Vascular ectasia of the gastric antrum: angiographic findings. Am J Roentgenol. 1996;166:87–9.
123
Clin J Gastroenterol (2013) 6:231–236 21. Ashiya E, Yagi N, Shiomi H, et al. A case report of gastric vascular ectasia patient successfully treated by trans-arterial embolization despite the inefficiency of argon plasma coagulation. Jpn J Gastroenterol. 2003;100:A304.
CASE REPORT
Successful treatment of refractory gastric antral vascular ectasia using transcatheter arterial embolization Haruka Yoshida • Hiroki Takahashi • Hiromichi Akoshima Nobuyuki Chida • Kenji Noguchi • Nobukazu Tanabe • Yutaka Mano • Katsuaki Ukai • Keiichi Tadokoro
•
Received: 22 January 2013 / Accepted: 30 April 2013 / Published online: 23 May 2013 Ó Springer Japan 2013
Abstract In January 2008, a 67-year-old woman was admitted to our hospital because of hepatitis C virus-related cirrhosis and hepatocellular carcinoma (HCC). In February 2010, she had tarry stools and anemia resulting from gastric antral vascular ectasia (GAVE). Argon plasma coagulation (APC) treatment for GAVE was performed at that time. She revisited our hospital in July 2010 because of tarry stools and anemia caused by GAVE recurrence, which required 5 APC sessions and blood transfusion to control the bleeding. In October 2010, she arrived at our hospital by ambulance because of hemorrhagic shock resulting from GAVE recurrence. Despite performing 5 APC sessions and multiple blood transfusions, the tarry stools and anemia persisted during the hospitalization period. In December 2010 and January 2011, second-stage selective transcatheter arterial embolization (TAE) of the right gastric and right gastroepiploic arteries using microcoils was performed for the treatment of the refractory GAVE. Upper gastrointestinal endoscopy performed after TAE revealed the disappearance of mucosal diffuse spotty redness. In addition, no complications such as gastric ulcer and necrosis were observed. Selective TAE, effectively resolved the GAVE and anemia, and no recurrence has been observed during the last 24 months. Therefore, TAE may be a safe and radical treatment for refractory GAVE.
H. Yoshida (&) H. Takahashi H. Akoshima K. Noguchi N. Tanabe Y. Mano K. Ukai K. Tadokoro Department of Gastroenterology, Sendai Medical Center, 2-8-8 Miyagino, Sendai, Miyagi 983-8520, Japan e-mail: [email protected] N. Chida Chida Medical Clinic, Sendai, Japan
Keywords Argon plasma coagulation Gastric antral vascular ectasia Transcatheter arterial embolization
Introduction Gastric antral vascular ectasia (GAVE), characterized by the presence of red spots or streaks in the antral mucosa on endoscopic examination [1], is responsible for *4 % of all non-variceal upper gastrointestinal bleeding events[2]. Typical initial presentations range from occult bleedings causing blood transfusion-dependent chronic iron-deficiency anemia, to severe acute upper gastrointestinal bleeding. Various treatments have been reported, including medical, surgical, and endoscopic therapy. Argon plasma coagulation (APC) therapy is the most common treatment for GAVE-related bleeding. However, we sometimes experience recurrent GAVE even though there is repeated APC therapy. Hence, we report a case of recurrent GAVE refractory to the repeated APC treatments and successfully controlled by selective transcatheter arterial embolization (TAE).
Case report In January 2008, a 67-year-old woman was admitted to our hospital because of hepatitis C virus-related cirrhosis (Child-Pugh grade A) and hepatocellular carcinoma (HCC). Transcatheter arterial chemoembolization (TACE) for HCC was performed during the same month. Systemic treatment with sorafenib was initiated in April 2008 but was terminated after 3 months because of thrombocytopenia. TACE was performed 4 times between January 2010 and December 2010 for recurrent HCC. In February 2010,
123
232
the patient was found to have tarry stools and anemia (hemoglobin [Hb] level, 4.4 g/dL) resulting from GAVE associated with cirrhosis. APC treatment for GAVE was performed and a proton-pump inhibitor was prescribed. Each APC session has been performed using a 2.3-mm diameter probe with a heat-resistant ceramic tip (APC probe; ERBEÒ Electromedizin, Tu¨bingen, Germany). An argon plasma coagulation unit, including a high-frequency
Fig. 1 Endoscopic examination prior to argon plasma coagulation (APC) treatment revealed the presence of gastric antral vascular ectasia (GAVE), as indicated by mucosal diffuse spotty redness spreading over the antrum of the stomach and oozing from the GAVE lesion
Clin J Gastroenterol (2013) 6:231–236
electrosurgical generator (ERBEÒ ICC 200) and an argon delivery unit (ERBEÒ APC 300), was used. The argon gas flow was set at 2.0 l/min and 60 W power was used. The patient was then discharged from the hospital. In May 2010, sorafenib therapy was resumed for treatment of recurrent HCC. The patient revisited our hospital in July 2010 because of recurrent tarry stools and anemia. A laboratory examination upon hospitalization revealed an Hb level of 8.2 g/dL. Upper gastrointestinal endoscopy revealed no varices; however, a coalescence of numerous angiectatic lesions that resembled a ‘‘honeycomb stomach’’ was noted from the pylorus to the antrum, and the patient was diagnosed with recurrent GAVE (Fig. 1). Total colonoscopy and capsule endoscopy did not detect any other causes of anemia. In addition to oral iron and intravenous tranexamic acid therapies, multiple blood transfusions (a total of 10 units of packed red blood cells) were needed and 5 APC sessions were performed upon hospitalization. Each session was performed once or twice a week when the patient had tarry stools or her Hb level decreased. The vascular lesions were treated until most of the telangiectasias were coagulated. In October 2010, the patient arrived at our hospital by ambulance because of hemorrhagic shock, and her Hb level was 5.4 g/dL. Despite discontinuing sorafenib therapy on admission and performing 7 APC sessions, the tarry stools and anemia persisted, requiring frequent blood transfusions (a total of 26 units of packed red blood cells). We concluded that the GAVE could not be controlled by APC treatment. Hence, we sought a more effective therapy to treat GAVE and found a domestic case report in which TAE was performed
RGA
CHA
SDA
PSPDA ASPDA
RGEA
Fig. 2 Right gastric angiography revealed arteriovenous shunting in the right gastric arterial territory and the antral branch of the right gastroepiploic artery spread over the antrum. Microcoils were used in the left hepatic artery for treatment of vascular injury during the prior angiography for hepatocellular carcinoma. CHA Common hepatic
123
artery, RGA right gastric artery, SDA supraduodenal artery, PSPDA posterior superior pancreaticoduodenal artery, ASPDA anterior superior pancreaticoduodenal artery, RGEA right gastroepiploic artery. Gray shading indicates arteriovenous malformation
Clin J Gastroenterol (2013) 6:231–236
233
Fig. 3 First-stage transcatheter arterial embolization (TAE) was performed using microcoils. The right gastric artery was embolized using microcoils and the arteriovenous shunting area was reduced. PHA Proper hepatic artery, SA splenic artery, Filled triangle indicates microcoils
PHA RGA
SA
SDA PSPDA
RGEA
Fig. 4 Second-stage TAE was performed at the antral branch of the right gastroepiploic artery, after which arteriovenous shunting was rarely detected. RGEA branch: antral branch of right gastroepiploic artery
RGA RGEA brach
CHA
SDA
PSPDA
RGEA
for GAVE [3]. Angiography was performed in December 2010, and arteriovenous shunting was detected in the right gastric arterial territory and the antral branch of the right gastroepiploic artery (Fig. 2). For first-stage TAE, the right gastric artery was embolized using microcoils in December 2010 (Fig. 3). Two weeks after the first-stage TAE was performed, upper gastrointestinal endoscopy revealed no complications such as gastric ulcer and ischemia; however, a few red spots were detected. In January 2011, 3 weeks after the first-stage TAE was performed, second-stage TAE was performed using microcoils at the antral branch of the right gastroepiploic artery (Fig. 4). Four days after the second-stage TAE was performed, upper gastrointestinal endoscopy detected no complications. Five days after the second-stage TAE was performed, the patient was discharged from the hospital. In December 2011, endoscopy
revealed remarkable reduction of red spots and no ischemic change (Fig. 5). Selective TAE of the right gastric and right gastroepiploic arteries effectively resolved the GAVE and anemia (Fig. 6). As of January 2013, the patient has had no recurrence of GAVE or anemia during the last 24 months.
Discussion GAVE was first described in 1953 as erosive gastritis with venocapillary ectasia in a patient with severe chronic irondeficiency anemia [4]. In 1984, Jabbari et al. [5] more accurately defined GAVE as ‘‘longitudinal red folds traversing the antrum and converging on the pylorus, each containing a visible convoluted column of vessels’’ and
123
234
Clin J Gastroenterol (2013) 6:231–236
coined the term ‘‘watermelon stomach’’ on endoscopic examination. Lee et al. [6] described a stomach with diffuse red spots representing dilated blood vessels in the antrum as a ‘‘honeycomb stomach.’’ Most GAVE patients are elderly, with a preponderance of women [7, 8]. GAVE has been associated with cirrhosis, renal failure, bone marrow transplantation, and scleroderma [9]. Although various treatments have been reported, no optimal therapy for GAVE has been established. Recently, pharmacological agents and endoscopic therapy have become the first-line treatments for GAVE [9].
Fig. 5 Endoscopy performed in December 2011 revealed a remarkable reduction of red spots and oozing was not detected
Fig. 6 Serial hemoglobin concentrations, blood transfusion requirements, and the number of APC sessions, showing the effects of TAE therapy
Medical treatment of GAVE includes corticosteroids [5], a combination of estrogen and progesterone [10], octreotide [7], tranexamic acid [11], and cyclophosphamide [12]. In the present case, tranexamic acid was used but was considered ineffective. Furthermore, whether the other treatments are effective or have strong adverse effects remains to be elucidated. Endoscopic therapy includes Nd:YAG laser coagulation [13], APC [14], endoscopic mucosal ablation [15], and endoscopic band ligation (EBL) [9]. Of these therapies, APC is the most frequently used endoscopic treatment for GAVE-related bleeding. Lecleire et al. [16] reported that APC treatment of bleeding GAVE was efficient in more than 80 % of cases, and the mean number of APC sessions in 17 GAVE patients with cirrhosis required to attain a stable hemoglobin level was 2.18 (±1.74; median, 2). In our case, melena persisted despite performing 7 APC sessions. Moreover, the patient showed recurrence within 6 months of treatment [17]. Thus, we concluded that the patient had refractory GAVE. APC treatment failure was reported to be infrequent and was primarily described in patients with hemorrhagic diathesis resulting from thrombocytopenia, or long-term anticoagulation or antiplatelet therapy [14]. In our case, the platelet count in October 2010 was only 4.2 9 104/lL, which might have affected the treatment-resistant hemorrhage. Sorafenib is a multikinase inhibitor that targets vascular endothelial growth factor (VEGF)-mediated angiogenesis. A recent meta-analysis of randomized controlled VEGF trials showed a significant 2-fold increase in the risk of allgrade bleeding events [18]. In our case, sorafenib might
Clinical course
1 unit blood transfusion
APC Hb(g/dl) 16
TAE for GAVE
14 12 10 8 6 4 2 0 -60 -30
0
30
60
hospitalization
123
90
120
150
hospitalization
180
210
240
270
300
330 360
390
420
450
480 510
day
Clin J Gastroenterol (2013) 6:231–236
have affected the patient’s tolerance to the APC therapy. However, despite discontinuing the sorafenib therapy and performing 7 APC sessions, the refractory GAVE and anemia persisted during the hospitalization period. Nakamura et al. [17] reported that the effectiveness of APC therapy is temporary and that APC is not always effective as a medium-term and long-term treatment. The authors revealed that early recurrence seemed to be induced by the development of new GAVE, fragility of local blood vessels, stagnation of mucosal blood flow, and mechanical irritation. Perente et al. [19] reported the endosonographic findings of regional wall thickening and a spongy appearance in the second and third layer of the vascular structural areas. Because of the limited depth of thermal injury, APC treatment might not be effective in some cases. TAE for GAVE treatment is rarely reported, and its effectiveness has not yet been established. Jabbari et al. [5] reported negative results from angiography studies performed in 3 cases. Robertson et al. [20] considered the reason why angiogram for GAVE patients would be negative. The angiographic findings may be subtle because clearance of contrast material from the vessels within the gastric antrum occurred early and the late venous-phase films appeared normal. Furthermore, superimposition of the gastric antrum on the right renal pelvicaliceal system may obscure hypervascularity and arteriovenous shunting. They also described recent improvements in digital subtraction angiographic equipment and techniques have produced superior contrast resolution, allowing optimum detection of subtle venous phase abnormalities. So negative results of angiography for GAVE patients might have been caused by the technical problems. Terawaki et al. [3] performed successful TAE for GAVE treatment despite the lack of abnormal vessels on angiography. They reported that TAE was effective because blood flow reduction in the antrum might improve the venous dilatation. Potential complications of TAE include gastric ulcer and necrosis resulting from gastric ischemia. Ashiya et al. [21] presented to the academy of the Japanese Society of Gastroenterology that TAE of the right and left gastric arteries resulted in gastric ulcers. In our case, however, no complications were encountered and the angiography performed in December 2011 revealed no recurrence of arteriovenous shunting in the antral area. This result may have occurred because we performed selective TAE. For cases in which GAVE cannot be controlled by endoscopic treatments such as APC and EBL, we recommend TAE. If the culprit vessels are detected, a more selective and safer TAE procedure could be performed. We report that selective TAE may be a safe and radical treatment for the management of recurrent GAVE refractory to other treatments.
235 Conflict of interest of interest.
The authors declare that they have no conflict
References 1. Payen J, Cales P, Voigt J, et al. Severe portal hypertensive gastropathy and antral vascular ectasia are distinct entities in patients with cirrhosis. Gastroenterology. 1995;108:138–44. 2. 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. 3. Terawaki H, Kobayashi S, Kato J, et al. A case report of hemodialysis patient who presented recurrent bleeding from gastric antral vascular ectasia (GAVE) associated with liver cirrhosis: the effectiveness of trans-arterial embolization to bilateral gastric arteries. J Jpn Soc Dial Ther. 2008;41:803–8. 4. Rider JA, Klotz AP, Kirsner JB. Gastritis with veno-capillary ectasia as a source of massive gastric hemorrhage. Gastroenterology. 1953;24:118–23. 5. Jabbari M, Cherry R, Lough JO, et al. Gastric antral vascular ectasia: the watermelon stomach. Gastroenterology. 1984;87: 1165–70. 6. Lee FL, Costello F, Flanagan N, et al. Diffuse antral vascular ectasia. Gastrointest Endosc. 1984;30:87–90. 7. Sebastian S, O’Morain CA, Buckley MJ. Review article: current therapeutic options for gastric antral vascular ectasia. Aliment Pharmacol Ther. 2003;18:157–65. 8. Gostout CJ, Viggiano TR, Ahlquist DA, et al. The clinical and endoscopic spectrum of the watermelon stomach. J Clin Gastroenterol. 1992;15:256–63. 9. Sato T, Yamazaki K, Akaike J, et al. Endoscopic band ligation for refractory gastric antral vascular ectasia associated with liver cirrhosis. Clin J Gastroenterol. 2011;4:108–11. 10. Moss SF, Ghosh P, Thomas DM, et al. Gastric antral vascular ectasia: maintenance treatment with estrogen-progesterone. Gut. 1992;33:715–7. 11. McCormick PA, Ooi H, Crosbie O. Tranexamic acid for severe bleeding gastric antral vascular ectasia in cirrhosis. Gut. 1998;42:750–2. 12. Peterson A, Varga J. Cyclophosphamide: a novel treatment of gastric antral vascular ectasia associated with systemic sclerosis? Curr Rheumatol Rep. 2010;12:4–7. 13. Sargeant IR, Loizou LA, Rampton D, et al. Laser ablation of upper gastrointestinal vascular ectasias: long term results. Gut. 1993;34:470–5. 14. Fuccio L, Zagari RM, Serrani M, et al. Endoscopic argon plasma coagulation for the treatment of gastric antral vascular ectasiarelated bleeding in patients with liver cirrhosis. Digestion. 2009;79:143–50. 15. Gross SA, Al-Haddad M, Gill KRS, et al. Endoscopic mucosal ablation for the treatment of gastric antral vascular ectasia with the HALO90 system: a pilot study. Gastrointest Endosc. 2008;67: 324–7. 16. 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. 17. Nakamura S, Mitsunaga A, Konishi H, et al. Long-term follow up of gastric vascular ectasia treated by argon plasma coagulation. Dig Endosc. 2006;18:128–33. 18. Je Y, Schutz FA, Choueiri TK. Risk of bleeding with vascular endothelial growth factor receptor tyrosine-kinase inhibitors sunitinib and sorafenib: a systematic review and meta-analysis of clinical trials. Lancet Oncology. 2009;10:967–74.
123
236 19. Parente F, Petrillo M, Vago F, et al. The watermelon stomach: clinical, endoscopic, endosonographic, and therapeutic aspects in three cases. Endoscopy. 1995;27:203–6. 20. Robertson I, Tait N, Jackson J. Vascular ectasia of the gastric antrum: angiographic findings. Am J Roentgenol. 1996;166:87–9.
123
Clin J Gastroenterol (2013) 6:231–236 21. Ashiya E, Yagi N, Shiomi H, et al. A case report of gastric vascular ectasia patient successfully treated by trans-arterial embolization despite the inefficiency of argon plasma coagulation. Jpn J Gastroenterol. 2003;100:A304.
