CASE REPORT
TREATMENT RESISTANT GASTRIC ANTRAL VASCULAR ECTASIA IN A PATIENT UNDERGOING HAEMODIALYSIS Yeri Ahn, Tom Kai Ming Wang, Joanna Dunlop Department of Renal Medicine, Middlemore Hospital, South Auckland, Papatoetoe, New Zealand
Ahn Y., Wang T.K.M., Dunlop J. (2014). Treatment resistant gastric antral vascular ectasia in a patient undergoing haemodialysis. Journal of Renal Care 40(4), 263–265.
SUMMARY Gastric antral vascular ectasia (GAVE) is an important cause of upper gastrointestinal bleeding and has a high prevalence in patients with renal insufficiency. We report the first documented case of a 52-year-old patient on haemodialysis with GAVE refractory to repeated endoscopic argon plasma coagulation (APC) therapy and highlight the difficulties in its management. We recognise the need for further studies to investigate the optimal management of this condition and suggest alternative treatment strategies to be considered in patients with APC refractory GAVE, such as endoscopic band ligation and changing dialysis modality.
K E Y W O R D S Argon plasma coagulation End-stage kidney disease Gastric antral vascular ectasia Haemodialysis
INTRODUCTION
CLINICAL FINDINGS
Gastric antral vascular ectasia (GAVE) is a rare but important cause of upper gastrointestinal bleeding. We report a case of a patient on haemodialysis with GAVE refractory to standard argon plasma coagulation (APC) therapy and discuss the difficulties and options in managing this condition.
Her other significant co-morbidities include hypertension and non alcoholic liver cirrhosis (Child Pugh score of 7) complicated by portal hypertension, splenomegaly and thrombocytopenia. Two years ago she was investigated for asymptomatic anaemia and found to have a non-bleeding gastric angiodysplastic lesion on gastroscopy, thought not to be the cause of her anaemia. Two months ago, approximately 30 months after her initial investigations, she developed melaena and severe iron-deficiency anaemia. Repeat gastroscopy showed a single gastric antral angiodysplastic lesion with haemorrhage and multiple gastric angioectasias with no bleeding. Histology from biopsies showed dilated, ectatic and congested vessels in the superficial lamina propria of the gastric antral mucosa. Vertically orientated smooth muscle bands were seen without intraluminal thrombi, dysplasia or metaplasia of cells. Our patient was newly diagnosed with GAVE.
PRESENTING CONCERNS A 52-year-old Samoan female with end-stage kidney disease (ESKD) secondary to type 2 diabetes mellitus has been on maintenance haemodialysis for two years. She presented with ongoing melaena, shortness of breath and lethargy, with a serum haemoglobin of 5.5 g/dl.
BIODATA Yeri Ahn finished medical school at the University of Auckland in Auckland, New Zealand in 2011. She is currently a junior doctor working in Middlemore Hospital, South Auckland. Her main interests lie in internal medicine and will continue her RACP training as a medical Registrar. CORRESPONDENCE
Yeri Ahn, Department of Renal Medicine, Middlemore Hospital, Hospital Road, Otahuhu, South Auckland, New Zealand Tel.: þ64 9 276 0000 Fax: þ64 9 276 0156 Email: [email protected]
THERAPEUTIC FOCUS AND ASSESSMENT During her one-month hospitalisation, she was initially treated with intra-lesional adrenaline injections, started on a protonpump inhibitor and underwent haemodialysis sessions without heparin. This was followed by intravenous high-dose protonpump inhibitor, sucralfate, tranexamic acid and desmopressin. She had nine inpatient gastroscopies including four sessions of APC, and required transfusion with 26 units of packed red cells to keep her haemoglobin in the normal range. Given her history of portal hypertension she was also prescribed propranolol. Her case was discussed at a combined gastroenterology and general surgery meeting. She was considered high risk for a
© 2014 European Dialysis and Transplant Nurses Association/European Renal Care Association
Journal of Renal Care 2014
263
Ahn et al.
gastrectomy, and so the decision was made to rest the ulcerated gastric mucosa for three weeks before a repeat gastroscopy. The patient was discharged with an ongoing blood transfusion requirement three times a week on haemodialysis.
FOLLOW-UP AND OUTCOMES Our patient had follow-up endoscopies at four weeks and at nine weeks post discharge. The ectatic appearances on gastroscopy improved but were persistent, and on both occasions, she required further APC treatments to bleeding GAVE lesions. She currently has a reduced but ongoing blood transfusion requirement and it is uncertain whether her GAVE will ever fully resolve.
DISCUSSION GAVE, otherwise known as ‘watermelon stomach’, was initially described in 1953 by Rider et al. (1953). In one series it accounted for 4% of non-variceal upper gastrointestinal haemorrhages seen (Dulai et al. 2004). It is characterised by endoscopic appearances of multiple longitudinal stripes of red ectatic and sacculated mucosal vessels or diffuse spread of vessels mainly around the antrum and pylorus of the stomach (Iguchi et al. 2011). Histological features include hyperplastic gastric antral mucosa, capillary ectasia with thrombosis and fibromuscular hyperplasia in the lamina propria, spindle cell proliferation, fibrohyalinosis, and abnormal submucosal vasculature (Gilliam et al. 1989). Such endoscopic and histological appearances can distinguish GAVE from portal hypertensive gastropathy (PHG). PHG typically involves the fundus or corpus of the stomach with a combination of mosaiclike pattern, cherry red spots and black brown spots. Histological features as mentioned are not specific for PHG (Fuccio et al. 2013). Although most cases are idiopathic, GAVE is associated with autoimmune connective tissues diseases such as Raynaud’s, Sjogren’s syndrome and systemic sclerosis (Fuccio et al. 2013), portal hypertensive gastropathy, cirrhosis (31% in one series Dulai et al. 2004) and other systemic illnesses. Interestingly, a higher prevalence of GAVE has been observed in patients with chronic kidney disease (CKD), with or without being on dialysis (Navab et al. 1989; Tomori et al. 2003; Stefanidis et al. 2006). The exact pathophysiology of GAVE in patients with CKD remains unknown, but potential theories to explain this association include uraemia-induced weakening of gastric emptying, antral dysmotility, platelet dysfunction and impaired
264
Journal of Renal Care 2014
renal excretion of vasoactive mediators such as gastrin (Iguchi et al. 2011). Endoscopic APC is the recommended treatment for GAVE, which reduces bleeding by obliterating the ectatic vasculature (Fuccio et al. 2013). Other therapeutic options include heat, gold or enodymium-yttrium-aluminium garnet (Nd:YAG) laser coagulation. Pharmacological therapies including histamine-2 blockers, proton-pump inhibitors, sucralfate and tranexamic acid have limited efficacy for GAVE because they do not definitively ameliorate ectatic vessels (Burak et al. 2001). Conjugated estrogen-progesterone has also been shown in some studies to reduce bleeding in vascular ectasia of the gastrointestinal tract (Hermans et al. 1996; Tran et al. 1999). Recurrence of GAVE even following endoscopic coagulation therapy is common and reported in 68–77% of cases (Wells et al. 2008; Sato et al. 2012). Repeated endoscopic therapy improves the probability of cure (Potamiano et al. 1994; Liberski et al. 1994) with recommended intervals of 4–6 weeks between sessions to ensure complete healing from previous treatment. Occasionally, as in our case, GAVE is refractory to endoscopic coagulation. An alternative endoscopic treatment for GAVE is band ligation, which is suggested in some observational studies to be superior to endoscopy APC and thermal coagulation (Wells et al. 2008; Sato et al. 2012), but randomised trials are lacking. Surgical antrectomy (Novitsky et al. 2003) is the last-resort therapy for treating endoscopic refractory GAVE, and is mainly utilized in the presence of lifethreatening gastric haemorrhage. There is currently no consensus about what is the best dialysis modality for patients with GAVE and end-stage kidney disease. Three cases of GAVE in pre-dialysis patients entered into remission over a 3–8 months period after initiating haemodialysis (HD) therapy (Iguchi et al. 2011). Another case of switching from haemodialysis to continuous ambulatory peritoneal dialysis leading to resolution of bleeding from GAVE was reported (Yorioka et al. 1996), although other reports of patients changing dialysis modalities showed no substantial therapeutic benefit (Stefanidis et al. 2006).
IMPLICATIONS FOR PRACTICE For patients who suffer from end-stage kidney disease (ESKD) and fail to respond to treatment with APC, changing of their
© 2014 European Dialysis and Transplant Nurses Association/European Renal Care Association
TREATMENT RESISTANT GASTRIC ANTRAL VASCULAR ECTASIA IN A PATIENT UNDERGOING HAEMODIALYSIS
renal replacement modality should be considered. Furthermore, for patients with CKD, GAVE may be considered an indication for starting renal replacement therapy.
CONCLUSION In conclusion, GAVE is an important cause of upper gastrointestinal bleeding and has a higher prevalence in patients with stage 5 CKD. We have reported the first case of GAVE refractory to repeated endoscopic APC therapy, and highlighted the difficulties in its management. Alternative treatment strategies may include endoscopic band ligation. Further investigation is required regarding the optimal dialysis
modality for patients with CKD affected by APC refractory GAVE.
CONFLICT OF INTEREST There were no competing interests in the publication of this case report.
AUTHOR CONTRIBUTIONS YA: Principal author, read and approved the final manuscript. TKMW: Co-author, helped to draft manuscript, read and approved the final manuscript. JD: Supervisor, helped to draft manuscript.
REFERENCES Burak K.W., Lee S.S., & Beck P.L. (2001). Portal hypertensive gastropathy and gastric antral vascular ectasia (GAVE) syndrome. Gut 49, 866– 872. Dulai G.S., Jensen D.M., Kovacs T.O. et al. (2004). Endoscopic treatment outcomes in watermelon stomach patients with and without portal hypertension. Endoscopy 36, 68–72. Fuccio L., Mussetto A, Laterza L. et al. (2013). Diagnosis and management of gastric antral vascular ectasia. World Journal of Gastrointestinal Endoscopy 5(1), 6–13. Gilliam J.H. III, Geisinger K.R., Wu W.C. et al. (1989). Endoscopic biopsy is diagnostic in gastric antral vascular ectasia. The “watermelon stomach.” Digestive Diseases and Sciences 34, 885–888. Hermans C., Goffin E., Horsmans Y. et al. (1996). Watermelon stomach. An unusual cause of recurrent upper GI tract bleeding in the uraemic patient: efficient treatment with oestrogen-progesterone therapy. Nephrology Dialysis Transplantation 11, 871–874. Iguchi A., Kazama J.J., Komatsu M. et al. (2011). Three cases of gastric antral vascular ectasia in chronic renal failure. Case Reports in Nephrology and Urology 1, 15–19. Liberski S.M., McGarrity T.J., Hartle R.J. et al. (1994). The watermelon stomach: long-term outcome in patient streated with Nd;YAG laser therapy. Gastrointestinal Endoscopy 40, 584–587. Navab F., Masters P., Subramani R. et al. (1989). Angiodysplasia in patients with renal insufficiency. The American Journal of Gastroenterology 84, 1297–1301. Novitsky Y.W., Kercher K.W., Czerniach D.R. et al. (2003). Watermelon stomach: pathophysiology, diagnosis, and management. Journal of Gastrointestinal Surgery 7, 652–661.
Potamiano S., Carter C.R., & Anderson J.R. (1994). Endoscopic laser treatment of diffuse gastric antral vascular ectasia. Gut 35, 461– 463. Rider J.A., Klotz A.P., & Kirsner J.B. (1953). Gastritis with veno-capillary ectasia as a source of massive gastric hemorrhage. Gastroenterology 24, 118–123. Sato T., Yamazaki K., & Akaike J. (2012). Endoscopic band ligation versus argon plasma coagulation for gastric antral vascular ectasia associated with liver diseases. Digestive Endoscopy 24, 237– 242. Stefanidis I., Liakopoulos V., Kapsoritakis A.N. et al. (2006). Gastric antral vascular ectasia (watermelon stomach) in patients with ESRD. American Journal of Kidney Diseases 47(6), e77– e82. Tomori K., Nakamoto H., Kotaki S. et al. (2003). Gastric angiodysplasia in patients undergoing maintenance dialysis. Advances in Peritoneal Dialysis 19, 136–142. Tran A., Villeneuve J.P., Bilodeau M. et al. (1999). Treatment of chronic bleeding from gastric antral vascular ectasia (GAVE) with estrogenprogesterone in cirrhotic patients: an open pilot study. American Journal of Gastroenterology 94, 2909–2911. Wells C.D., Harrison M.E., Gurudu S.R. et al. (2008). Treatment of gastric antral vascular ectasia (watermelon stomach) with endoscopic band ligation. Gastrointestinal Endoscopy 68: 231– 236. Yorioka N., Hamaguchi N., Tamiguchi Y. et al. Gastric antral vascular ectasia in a patient on haemodialysis improved with CAPD. Peritoneal Dialysis International 1996; 16: 177–178.
© 2014 European Dialysis and Transplant Nurses Association/European Renal Care Association
Journal of Renal Care 2014
265
TREATMENT RESISTANT GASTRIC ANTRAL VASCULAR ECTASIA IN A PATIENT UNDERGOING HAEMODIALYSIS Yeri Ahn, Tom Kai Ming Wang, Joanna Dunlop Department of Renal Medicine, Middlemore Hospital, South Auckland, Papatoetoe, New Zealand
Ahn Y., Wang T.K.M., Dunlop J. (2014). Treatment resistant gastric antral vascular ectasia in a patient undergoing haemodialysis. Journal of Renal Care 40(4), 263–265.
SUMMARY Gastric antral vascular ectasia (GAVE) is an important cause of upper gastrointestinal bleeding and has a high prevalence in patients with renal insufficiency. We report the first documented case of a 52-year-old patient on haemodialysis with GAVE refractory to repeated endoscopic argon plasma coagulation (APC) therapy and highlight the difficulties in its management. We recognise the need for further studies to investigate the optimal management of this condition and suggest alternative treatment strategies to be considered in patients with APC refractory GAVE, such as endoscopic band ligation and changing dialysis modality.
K E Y W O R D S Argon plasma coagulation End-stage kidney disease Gastric antral vascular ectasia Haemodialysis
INTRODUCTION
CLINICAL FINDINGS
Gastric antral vascular ectasia (GAVE) is a rare but important cause of upper gastrointestinal bleeding. We report a case of a patient on haemodialysis with GAVE refractory to standard argon plasma coagulation (APC) therapy and discuss the difficulties and options in managing this condition.
Her other significant co-morbidities include hypertension and non alcoholic liver cirrhosis (Child Pugh score of 7) complicated by portal hypertension, splenomegaly and thrombocytopenia. Two years ago she was investigated for asymptomatic anaemia and found to have a non-bleeding gastric angiodysplastic lesion on gastroscopy, thought not to be the cause of her anaemia. Two months ago, approximately 30 months after her initial investigations, she developed melaena and severe iron-deficiency anaemia. Repeat gastroscopy showed a single gastric antral angiodysplastic lesion with haemorrhage and multiple gastric angioectasias with no bleeding. Histology from biopsies showed dilated, ectatic and congested vessels in the superficial lamina propria of the gastric antral mucosa. Vertically orientated smooth muscle bands were seen without intraluminal thrombi, dysplasia or metaplasia of cells. Our patient was newly diagnosed with GAVE.
PRESENTING CONCERNS A 52-year-old Samoan female with end-stage kidney disease (ESKD) secondary to type 2 diabetes mellitus has been on maintenance haemodialysis for two years. She presented with ongoing melaena, shortness of breath and lethargy, with a serum haemoglobin of 5.5 g/dl.
BIODATA Yeri Ahn finished medical school at the University of Auckland in Auckland, New Zealand in 2011. She is currently a junior doctor working in Middlemore Hospital, South Auckland. Her main interests lie in internal medicine and will continue her RACP training as a medical Registrar. CORRESPONDENCE
Yeri Ahn, Department of Renal Medicine, Middlemore Hospital, Hospital Road, Otahuhu, South Auckland, New Zealand Tel.: þ64 9 276 0000 Fax: þ64 9 276 0156 Email: [email protected]
THERAPEUTIC FOCUS AND ASSESSMENT During her one-month hospitalisation, she was initially treated with intra-lesional adrenaline injections, started on a protonpump inhibitor and underwent haemodialysis sessions without heparin. This was followed by intravenous high-dose protonpump inhibitor, sucralfate, tranexamic acid and desmopressin. She had nine inpatient gastroscopies including four sessions of APC, and required transfusion with 26 units of packed red cells to keep her haemoglobin in the normal range. Given her history of portal hypertension she was also prescribed propranolol. Her case was discussed at a combined gastroenterology and general surgery meeting. She was considered high risk for a
© 2014 European Dialysis and Transplant Nurses Association/European Renal Care Association
Journal of Renal Care 2014
263
Ahn et al.
gastrectomy, and so the decision was made to rest the ulcerated gastric mucosa for three weeks before a repeat gastroscopy. The patient was discharged with an ongoing blood transfusion requirement three times a week on haemodialysis.
FOLLOW-UP AND OUTCOMES Our patient had follow-up endoscopies at four weeks and at nine weeks post discharge. The ectatic appearances on gastroscopy improved but were persistent, and on both occasions, she required further APC treatments to bleeding GAVE lesions. She currently has a reduced but ongoing blood transfusion requirement and it is uncertain whether her GAVE will ever fully resolve.
DISCUSSION GAVE, otherwise known as ‘watermelon stomach’, was initially described in 1953 by Rider et al. (1953). In one series it accounted for 4% of non-variceal upper gastrointestinal haemorrhages seen (Dulai et al. 2004). It is characterised by endoscopic appearances of multiple longitudinal stripes of red ectatic and sacculated mucosal vessels or diffuse spread of vessels mainly around the antrum and pylorus of the stomach (Iguchi et al. 2011). Histological features include hyperplastic gastric antral mucosa, capillary ectasia with thrombosis and fibromuscular hyperplasia in the lamina propria, spindle cell proliferation, fibrohyalinosis, and abnormal submucosal vasculature (Gilliam et al. 1989). Such endoscopic and histological appearances can distinguish GAVE from portal hypertensive gastropathy (PHG). PHG typically involves the fundus or corpus of the stomach with a combination of mosaiclike pattern, cherry red spots and black brown spots. Histological features as mentioned are not specific for PHG (Fuccio et al. 2013). Although most cases are idiopathic, GAVE is associated with autoimmune connective tissues diseases such as Raynaud’s, Sjogren’s syndrome and systemic sclerosis (Fuccio et al. 2013), portal hypertensive gastropathy, cirrhosis (31% in one series Dulai et al. 2004) and other systemic illnesses. Interestingly, a higher prevalence of GAVE has been observed in patients with chronic kidney disease (CKD), with or without being on dialysis (Navab et al. 1989; Tomori et al. 2003; Stefanidis et al. 2006). The exact pathophysiology of GAVE in patients with CKD remains unknown, but potential theories to explain this association include uraemia-induced weakening of gastric emptying, antral dysmotility, platelet dysfunction and impaired
264
Journal of Renal Care 2014
renal excretion of vasoactive mediators such as gastrin (Iguchi et al. 2011). Endoscopic APC is the recommended treatment for GAVE, which reduces bleeding by obliterating the ectatic vasculature (Fuccio et al. 2013). Other therapeutic options include heat, gold or enodymium-yttrium-aluminium garnet (Nd:YAG) laser coagulation. Pharmacological therapies including histamine-2 blockers, proton-pump inhibitors, sucralfate and tranexamic acid have limited efficacy for GAVE because they do not definitively ameliorate ectatic vessels (Burak et al. 2001). Conjugated estrogen-progesterone has also been shown in some studies to reduce bleeding in vascular ectasia of the gastrointestinal tract (Hermans et al. 1996; Tran et al. 1999). Recurrence of GAVE even following endoscopic coagulation therapy is common and reported in 68–77% of cases (Wells et al. 2008; Sato et al. 2012). Repeated endoscopic therapy improves the probability of cure (Potamiano et al. 1994; Liberski et al. 1994) with recommended intervals of 4–6 weeks between sessions to ensure complete healing from previous treatment. Occasionally, as in our case, GAVE is refractory to endoscopic coagulation. An alternative endoscopic treatment for GAVE is band ligation, which is suggested in some observational studies to be superior to endoscopy APC and thermal coagulation (Wells et al. 2008; Sato et al. 2012), but randomised trials are lacking. Surgical antrectomy (Novitsky et al. 2003) is the last-resort therapy for treating endoscopic refractory GAVE, and is mainly utilized in the presence of lifethreatening gastric haemorrhage. There is currently no consensus about what is the best dialysis modality for patients with GAVE and end-stage kidney disease. Three cases of GAVE in pre-dialysis patients entered into remission over a 3–8 months period after initiating haemodialysis (HD) therapy (Iguchi et al. 2011). Another case of switching from haemodialysis to continuous ambulatory peritoneal dialysis leading to resolution of bleeding from GAVE was reported (Yorioka et al. 1996), although other reports of patients changing dialysis modalities showed no substantial therapeutic benefit (Stefanidis et al. 2006).
IMPLICATIONS FOR PRACTICE For patients who suffer from end-stage kidney disease (ESKD) and fail to respond to treatment with APC, changing of their
© 2014 European Dialysis and Transplant Nurses Association/European Renal Care Association
TREATMENT RESISTANT GASTRIC ANTRAL VASCULAR ECTASIA IN A PATIENT UNDERGOING HAEMODIALYSIS
renal replacement modality should be considered. Furthermore, for patients with CKD, GAVE may be considered an indication for starting renal replacement therapy.
CONCLUSION In conclusion, GAVE is an important cause of upper gastrointestinal bleeding and has a higher prevalence in patients with stage 5 CKD. We have reported the first case of GAVE refractory to repeated endoscopic APC therapy, and highlighted the difficulties in its management. Alternative treatment strategies may include endoscopic band ligation. Further investigation is required regarding the optimal dialysis
modality for patients with CKD affected by APC refractory GAVE.
CONFLICT OF INTEREST There were no competing interests in the publication of this case report.
AUTHOR CONTRIBUTIONS YA: Principal author, read and approved the final manuscript. TKMW: Co-author, helped to draft manuscript, read and approved the final manuscript. JD: Supervisor, helped to draft manuscript.
REFERENCES Burak K.W., Lee S.S., & Beck P.L. (2001). Portal hypertensive gastropathy and gastric antral vascular ectasia (GAVE) syndrome. Gut 49, 866– 872. Dulai G.S., Jensen D.M., Kovacs T.O. et al. (2004). Endoscopic treatment outcomes in watermelon stomach patients with and without portal hypertension. Endoscopy 36, 68–72. Fuccio L., Mussetto A, Laterza L. et al. (2013). Diagnosis and management of gastric antral vascular ectasia. World Journal of Gastrointestinal Endoscopy 5(1), 6–13. Gilliam J.H. III, Geisinger K.R., Wu W.C. et al. (1989). Endoscopic biopsy is diagnostic in gastric antral vascular ectasia. The “watermelon stomach.” Digestive Diseases and Sciences 34, 885–888. Hermans C., Goffin E., Horsmans Y. et al. (1996). Watermelon stomach. An unusual cause of recurrent upper GI tract bleeding in the uraemic patient: efficient treatment with oestrogen-progesterone therapy. Nephrology Dialysis Transplantation 11, 871–874. Iguchi A., Kazama J.J., Komatsu M. et al. (2011). Three cases of gastric antral vascular ectasia in chronic renal failure. Case Reports in Nephrology and Urology 1, 15–19. Liberski S.M., McGarrity T.J., Hartle R.J. et al. (1994). The watermelon stomach: long-term outcome in patient streated with Nd;YAG laser therapy. Gastrointestinal Endoscopy 40, 584–587. Navab F., Masters P., Subramani R. et al. (1989). Angiodysplasia in patients with renal insufficiency. The American Journal of Gastroenterology 84, 1297–1301. Novitsky Y.W., Kercher K.W., Czerniach D.R. et al. (2003). Watermelon stomach: pathophysiology, diagnosis, and management. Journal of Gastrointestinal Surgery 7, 652–661.
Potamiano S., Carter C.R., & Anderson J.R. (1994). Endoscopic laser treatment of diffuse gastric antral vascular ectasia. Gut 35, 461– 463. Rider J.A., Klotz A.P., & Kirsner J.B. (1953). Gastritis with veno-capillary ectasia as a source of massive gastric hemorrhage. Gastroenterology 24, 118–123. Sato T., Yamazaki K., & Akaike J. (2012). Endoscopic band ligation versus argon plasma coagulation for gastric antral vascular ectasia associated with liver diseases. Digestive Endoscopy 24, 237– 242. Stefanidis I., Liakopoulos V., Kapsoritakis A.N. et al. (2006). Gastric antral vascular ectasia (watermelon stomach) in patients with ESRD. American Journal of Kidney Diseases 47(6), e77– e82. Tomori K., Nakamoto H., Kotaki S. et al. (2003). Gastric angiodysplasia in patients undergoing maintenance dialysis. Advances in Peritoneal Dialysis 19, 136–142. Tran A., Villeneuve J.P., Bilodeau M. et al. (1999). Treatment of chronic bleeding from gastric antral vascular ectasia (GAVE) with estrogenprogesterone in cirrhotic patients: an open pilot study. American Journal of Gastroenterology 94, 2909–2911. Wells C.D., Harrison M.E., Gurudu S.R. et al. (2008). Treatment of gastric antral vascular ectasia (watermelon stomach) with endoscopic band ligation. Gastrointestinal Endoscopy 68: 231– 236. Yorioka N., Hamaguchi N., Tamiguchi Y. et al. Gastric antral vascular ectasia in a patient on haemodialysis improved with CAPD. Peritoneal Dialysis International 1996; 16: 177–178.
© 2014 European Dialysis and Transplant Nurses Association/European Renal Care Association
Journal of Renal Care 2014
265
