- Email: [email protected]
Rectal vascular ectasia associated with watermelon stomach
M Gürsoy, C Baysal, B Demirhan, et al.
Rectal vascular ectasia associated with watermelon stomach Murat Gürsoy, MD, Çaglar ˘ Baysal, MD, Beyhan Demirhan, MD, Gökhan Moray, MD, Sedat Boyacioglu, ˘ MD
Gastric antral vascular ectasia (GAVE) is a rare cause of chronic GI blood loss. The syndrome was first described in 1953 by Rider et al.1 and the term “watermelon stomach” which describes the endoscopic appearance of a subtype of GAVE was coined by Jabbari et al.2 in 1984. The syndrome has both endoscopic and histologic definitions. Endoscopically, the lesions take two forms: diffuse, the most common appearance in patients with cirrhosis, and watermelon stomach, recognized endoscopically as multiple raised, bright red columns of tortuous ectatic blood vessels that radiate outward from the pylorus.3-5 Both forms have identical and characteristic microscopic features including dilation of the capillaries immediately beneath the mucosal epithelium, fibrin thrombi in these capillaries, fibro-muscular hyperplasia of the lamina propria, and perivascular fibrohyalinosis.6 To our knowledge, an association of GAVE and rectal vascular ectasia, where both disorders have an identical histology, has not been reported. CASE REPORT A 46-year-old woman presented in 1994 with end-stage renal failure due to chronic glomerulonephritis. She comFrom Ba¸skent University Faculty of Medicine, Department of Gastroenterology, Pathology, and General Surgery, Ankara, Turkey. Reprint requests: Murat Gürsoy, MD, 1 Cadde, No. 77, Kat. 4, Bahçelievler-06490 Ankara, Turkey; fax: 90-312-223-7333; e-mail: [email protected]. Copyright © 1999 by the American Society for Gastrointestinal Endoscopy 0016-5107/99/$8.00 + 0 37/4/100816 854
GASTROINTESTINAL ENDOSCOPY
Rectal vascular ectasia and watermelon stomach
menced regular hemodialysis three times weekly. In January 1996 the patient became infected with hepatitis C virus. A liver biopsy showed mild inflammatory activity. Doppler US confirmed the absence of splenomegaly and portal hypertension. Administration of 6 million units of interferon-α 2b three times weekly was initiated. The patient experienced fatigue and fever after interferon injections and, in May 1996, she refused to continue this form of treatment. Six months later, she was referred for investigation of iron deficiency anemia and positive fecal occult blood tests. There was no history of hematemesis, melena, or hematochezia. On admission microcytic hypochromic anemia was found with a hemoglobin level of 5.8 gm/dL. Studies confirmed iron deficiency (normal values in parentheses): serum iron 6 µg/dL (50 to 140 µg/dL), unsaturated iron-binding capacity 210 µg/dL (250 to 400 µg/dL), ferritin 62 ng/mL (7 to 280 ng/mL). Serum vitamin B-12 and folate levels were normal. Serum gastrin levels were 625 and 528 pg/mL (normal upper limit 108 pg/mL). All laboratory tests were obtained while the patient was receiving H2 receptor blockers. Upper endoscopy showed a prominent, linear pattern of red stripes in the gastric antrum radiating from the pylorus (Fig. 1A). No bleeding was observed. Biopsies revealed histologic features of GAVE, with dilation of mucosal capillaries and ectasia, and fibromuscular hyperplasia of the lamina propria (Fig. 1B). Neuroendocrine cell hyperplasia was not evident histologically. Colonoscopy demonstrated scattered, raised, erythematous areas in the distal rectum (Fig. 2A). The rest of the colon was normal. There was no evidence of rectal prolapse or significant hemorrhoids. The lesions were present at follow-up sigmoidoscopy 2 and 6 months later. These examinations revealed no bleeding at any of the lesion sites. Biopsies of the erythematous areas showed dilated ectatic mucosal vessels and fibromuscular hyperplasia (Fig. 2B). Because of the extensive nature of the vascular abnormalities in the antrum, we believed that coagulation therapy might be inappropriate. In as much as the patient refused surgery for GAVE, she was treated with H2 receptor blockers and blood transfusion as required. Two months later she was admitted with hematemesis and VOLUME 50, NO. 6, 1999
Rectal vascular ectasia and watermelon stomach
M Gürsoy, C Baysal, B Demirhan, et al.
A
A
B Figure 1. A, Endoscopic view of the gastric antrum showing prominent, red, linear, raised stripes radiating from the pylorus. B, Biopsy specimen from the gastric antral lesions; multiple dilated capillaries (short arrows), fibromuscular hyperplasia (arrowheads), and organizing thrombus (long arrow) (H&E, orig. mag. ×115).
VOLUME 50, NO. 6, 1999
B Figure 2. A, Endoscopic view of the distal rectum revealing scattered raised erythematous areas. B, Photomicrograph of rectal biopsy showing dilated capillaries (short arrows), fibromuscular hyperplasia (arrowheads), and fibrin thrombi (long arrows) (H&E, orig. mag. ×250).
GASTROINTESTINAL ENDOSCOPY
855
M Gürsoy, C Baysal, B Demirhan, et al.
melena. Upper GI endoscopy showed severe hemorrhage in the antrum. The bleeding stopped after two sessions of laser photocoagulation; two further laser photoablation sessions were performed. Due to the extent of the antral lesions and to patient noncompliance, this therapy failed to achieve any significant reduction in the convoluted vascular columns. At 8 months’ follow-up there had been no reduction in blood transfusion requirements. Finally, she was convinced of the need for surgery and underwent a subtotal gastrectomy in February 1998. There has been no further bleeding as of 8 months post-surgery.
DISCUSSION This case illustrates a typical presentation of GAVE with anemia and occult blood loss.2,7-9 On initial endoscopy, the erythematous stripes in the antrum were erroneously diagnosed as erosive gastritis, a fairly common misinterpretation.10 A second endoscopy confirmed the condition was, in fact, watermelon stomach. By definition, GAVE occurs only in the gastric antrum. However, the gastric cardia,11,12 gastric corpus,9 duodenum or jejunum,12-15 and rectum16,17 have all been reported to exhibit ectopic ectasia. In a few cases the lesions found in these other regions have been confirmed histopathologically as having the same features as GAVE, although none in the rectum have been classified this way. To our knowledge, the association of GAVE with rectal ectasia has not been reported. “Watermelon rectum” was noted as an incidental finding in a case of transient eosinophilic syndrome; ectatic blood vessels were not identified in biopsies, and repeat sigmoidoscopy revealed complete resolution of the rectal lesion.16 Abramson17 reported another case of watermelon rectum as a persistent lesion. Associated gastric vascular abnormalities and histologic diagnosis were not mentioned in either of the case reports. GAVE including the typical localization of ectasias to the antrum could be explained by three factors; antral motility disturbance,2,18,19 decreased blood flow to the antrum versus the fundus,4 and the influence of neuro-endocrine factors.20,21 Portal hypertension seems to be a predisposing factor in patients with cirrhosis, but GAVE is not likely the result of increased partial pressure.13,22 Deterioration rather than improvement in the lesions has been reported after portocaval shunt,13 and it appears that portalsystemic shunts should not be performed in an effort to relieve the symptoms of GAVE.13.22 Many investigators have implicated an antral motility disturbance.2,18,19 Jabbari et al.2 suggested that prolapse of the antral mucosa through the pylorus as a possible pathogenesis. Suit et al. and others supported this theory and believe that GAVE 856
GASTROINTESTINAL ENDOSCOPY
Rectal vascular ectasia and watermelon stomach
is likely related to mucosal trauma.7,18 Indeed, histopathologic findings in cases of rectal prolapse and solitary rectal ulcer do resemble those of GAVE. Both regions have similar anatomic and mechanical outlet functions that could lead to a propensity for prolapse. It is probable that humoral factors play roles in the pathogenesis of GAVE.20.21 Some investigators argue that GAVE could be a result of vasoactive factors, such as gastrin, 5-hydroxytryptamine, and vasoactive intestinal polypeptide.21 It has been speculated that hypergastrinemia has a trophic effects on the spindle cells that leads to fibromuscular hyperplasia.8,9 Our patient’s plasma gastrin level was high, a finding that may, in part, be related to her renal disease and long-term H2 receptor blocker therapy. The humoral component theory alone cannot explain the occurrence of this lesion at certain specific sites. However, humoral factors might lead to the propensity for developing this lesion, and perhaps anatomic and mechanical properties determine its specific localizations. Several treatments have been described for GAVE, including antrectomy and endoscopic approaches.23,26 There are no data or guidelines at present as to the best form of therapy in the individual case. The relatively noninvasive and practical aspects of endoscopic techniques such as laser photocoagulation make it the treatment of first choice. Surgical intervention has been suggested for extensive vascular abnormalities and refractory cases that fail to respond favorably to endoscopic treatment. Some studies have reported improvement in gastric mucosal histology and reduction of bleeding with corticosteroid and estrogen-progesterone treatment.23,27,28 Due to the chronic hepatitis C we did not consider treatment with corticosteroids in our patient. In conclusion, ectopic ectasias of the intestinal tract may accompany GAVE. Further studies are needed to determine whether the simultaneous occurrence of GAVE and rectal vascular ectasias is an incidental finding or a different expression of a single pathophysiologic condition. REFERENCES 1. Rider JA, Klotz AP, Kirsner JB. Gastritis with venocapillary ectasia as a source of massive gastric haemorrhage. Gastroenterology 1953;24:118-23. 2. Jabbari M, Cherry R, Lough JO, Daly DS, Kinner DG, Goresky CA. Gastric antral vascular ectasia: the watermelon stomach. Gastroenterology 1984;87:1165-70. 3. Koivisto PVI. Gastric antral vascular ectasia and primary biliary cirrhosis [letter] Endoscopy 1988;20:334. 4. Lee FL, Costello F, Flanagan N, Vasudev KS. Diffuse antral vascular ectasia. Gastrointest Endosc 1984;2:87-90. 5. Cales P, Payen JL, Berg P, Voigt JJ, Desmorat H, Vinel JP, et VOLUME 50, NO. 6, 1999
6.
7. 8. 9.
10. 11.
12. 13.
14.
15. 16. 17.
al. Antral vascular ectasia, new endoscopic and clinical spectrum [abstract ]. Gastroenterology 1991;100:A38. Voigt JJ, Payen JL, Cales P, Selves J, Barbe S, Vinel JP, et al. Les ectasies vasculaires antrales. Aspects anatomo-cliniques a propos de 21 cas (resume) [abstract]. Gastroenterol Clin Biol 1992;16(Suppl):A278. Rawlinson WD, Barr GD. Antral vascular ectasia: The “watermelon” stomach. Med J Aust 1986;144:709-11. Börch G. Diffuse antral vascular ectasia: the watermelon stomach revisited. Am J Gastroenterol 1987;82:1333-4. 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. Gouldesbrough DR, Pell ACH. Gastric antral vascular ectasia: a problem of recognition and diagnosis. Gut 1991;32:954-5. Borsh G, Schafer K, Schimdt G, Menne R, Tiedjen KU. Ectasie vasculaire antrale diffuse: cause rare d’hemorragie gastrointestinale severe. Acta Endosc 1985;15:239-43. Lux G, Fruhmorgen P, Rösch W. Diffuse telangiectasia of the upper GI tract [abstract]. Endoscopy 1979;11:281. Cales P, Voight 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. Wheeler MH, Smith PM, Cotton B, Evans DMD, Lawrie BM. Abnormal blood vessels in the gastric antrum. A cause of gastrointestinal bleeding. Dig Dis Sci 1979;2:155-8. Rose JDR. Endoscopic injection of alcohol for bleeding from gastroduodenal vascular anomalies. BMJ 1987;295:93-4. Steinberg J, Brandt LJ. The watermelon rectum. Gastrointest Endosc 1989;35:340-1. Abramson DA. Hematochezia associated with the watermelon rectum [letter]. Gastrointest Endosc 1992;38:97.
VOLUME 50, NO. 6, 1999
18. 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. 19. Charneau J, Petit R, Cales P, Dauver A, Boyer J. Antral motility in patients with cirrhosis with or without antral vascular ectasia. Gut 1995;37:488-92. 20. Perez-Ayuso RM, Pique JM, Saperas E, Bombi JA, Bordas JM, Elena M, et al. Gastric vascular ectasia in cirrhosis: association with hypoacidity not related to gastric atrophy. Scand J Gastroenterol 1989;24:1073-8. 21. Lowes JR, Rode J. Neuroendocrine cell proliferations in gastric antral vascular ectasia. Gastroenterology 1989;97:207-12. 22. Testard J, Hemet J, Metayer P. Gastrite hemorragique par coagulation intra-vasculaire localisee au cours de l’evolution d’une “cirrhose inflammatoire cryptogenetique.” Sem Hop Paris 1975;51:1235-41. 23. Kruger R, Ryan ME, Dickson KB, Nunez JF. Diffuse vascular ectasia of the gastric antrum. Am J Gastroenterol 1987; 82: 421-6. 24. Frager JD, Brandt LJ, Frank MS, Morecki R. Treatment of a patient with watermelon stomach using transendoscopic laser photocoagulation. Gastrointest Endosc 1988;34: 134-7. 25. Labenz J, Börsch G. Bleeding watermelon stomach treated by Nd-YAG laser photocoagulation. Endoscopy 1993;25:240-2. 26. Gostout CJ Ahlquist DA, Radford CM, Viggiano TR, Bowyer BA, Balm RK. Endoscopic laser therapy for watermelon stomach. Gastroenterology 1989;96:1462-5. 27. Calam J, Walker RJ. Antral vascular lesion, achlorhydria and chronic gastrointestinal blood loss: response to steroids. Dig Dis Sci 1980;25:236-9. 28. Moss SF, Ghosh P, Thomas DM, Jackson JE, Calam J. Gastric antral vascular ectasia: maintenance treatment with oestrogen-progesterone. Gut 1992;33:715-7.
GASTROINTESTINAL ENDOSCOPY
857
Rectal vascular ectasia associated with watermelon stomach Murat Gürsoy, MD, Çaglar ˘ Baysal, MD, Beyhan Demirhan, MD, Gökhan Moray, MD, Sedat Boyacioglu, ˘ MD
Gastric antral vascular ectasia (GAVE) is a rare cause of chronic GI blood loss. The syndrome was first described in 1953 by Rider et al.1 and the term “watermelon stomach” which describes the endoscopic appearance of a subtype of GAVE was coined by Jabbari et al.2 in 1984. The syndrome has both endoscopic and histologic definitions. Endoscopically, the lesions take two forms: diffuse, the most common appearance in patients with cirrhosis, and watermelon stomach, recognized endoscopically as multiple raised, bright red columns of tortuous ectatic blood vessels that radiate outward from the pylorus.3-5 Both forms have identical and characteristic microscopic features including dilation of the capillaries immediately beneath the mucosal epithelium, fibrin thrombi in these capillaries, fibro-muscular hyperplasia of the lamina propria, and perivascular fibrohyalinosis.6 To our knowledge, an association of GAVE and rectal vascular ectasia, where both disorders have an identical histology, has not been reported. CASE REPORT A 46-year-old woman presented in 1994 with end-stage renal failure due to chronic glomerulonephritis. She comFrom Ba¸skent University Faculty of Medicine, Department of Gastroenterology, Pathology, and General Surgery, Ankara, Turkey. Reprint requests: Murat Gürsoy, MD, 1 Cadde, No. 77, Kat. 4, Bahçelievler-06490 Ankara, Turkey; fax: 90-312-223-7333; e-mail: [email protected]. Copyright © 1999 by the American Society for Gastrointestinal Endoscopy 0016-5107/99/$8.00 + 0 37/4/100816 854
GASTROINTESTINAL ENDOSCOPY
Rectal vascular ectasia and watermelon stomach
menced regular hemodialysis three times weekly. In January 1996 the patient became infected with hepatitis C virus. A liver biopsy showed mild inflammatory activity. Doppler US confirmed the absence of splenomegaly and portal hypertension. Administration of 6 million units of interferon-α 2b three times weekly was initiated. The patient experienced fatigue and fever after interferon injections and, in May 1996, she refused to continue this form of treatment. Six months later, she was referred for investigation of iron deficiency anemia and positive fecal occult blood tests. There was no history of hematemesis, melena, or hematochezia. On admission microcytic hypochromic anemia was found with a hemoglobin level of 5.8 gm/dL. Studies confirmed iron deficiency (normal values in parentheses): serum iron 6 µg/dL (50 to 140 µg/dL), unsaturated iron-binding capacity 210 µg/dL (250 to 400 µg/dL), ferritin 62 ng/mL (7 to 280 ng/mL). Serum vitamin B-12 and folate levels were normal. Serum gastrin levels were 625 and 528 pg/mL (normal upper limit 108 pg/mL). All laboratory tests were obtained while the patient was receiving H2 receptor blockers. Upper endoscopy showed a prominent, linear pattern of red stripes in the gastric antrum radiating from the pylorus (Fig. 1A). No bleeding was observed. Biopsies revealed histologic features of GAVE, with dilation of mucosal capillaries and ectasia, and fibromuscular hyperplasia of the lamina propria (Fig. 1B). Neuroendocrine cell hyperplasia was not evident histologically. Colonoscopy demonstrated scattered, raised, erythematous areas in the distal rectum (Fig. 2A). The rest of the colon was normal. There was no evidence of rectal prolapse or significant hemorrhoids. The lesions were present at follow-up sigmoidoscopy 2 and 6 months later. These examinations revealed no bleeding at any of the lesion sites. Biopsies of the erythematous areas showed dilated ectatic mucosal vessels and fibromuscular hyperplasia (Fig. 2B). Because of the extensive nature of the vascular abnormalities in the antrum, we believed that coagulation therapy might be inappropriate. In as much as the patient refused surgery for GAVE, she was treated with H2 receptor blockers and blood transfusion as required. Two months later she was admitted with hematemesis and VOLUME 50, NO. 6, 1999
Rectal vascular ectasia and watermelon stomach
M Gürsoy, C Baysal, B Demirhan, et al.
A
A
B Figure 1. A, Endoscopic view of the gastric antrum showing prominent, red, linear, raised stripes radiating from the pylorus. B, Biopsy specimen from the gastric antral lesions; multiple dilated capillaries (short arrows), fibromuscular hyperplasia (arrowheads), and organizing thrombus (long arrow) (H&E, orig. mag. ×115).
VOLUME 50, NO. 6, 1999
B Figure 2. A, Endoscopic view of the distal rectum revealing scattered raised erythematous areas. B, Photomicrograph of rectal biopsy showing dilated capillaries (short arrows), fibromuscular hyperplasia (arrowheads), and fibrin thrombi (long arrows) (H&E, orig. mag. ×250).
GASTROINTESTINAL ENDOSCOPY
855
M Gürsoy, C Baysal, B Demirhan, et al.
melena. Upper GI endoscopy showed severe hemorrhage in the antrum. The bleeding stopped after two sessions of laser photocoagulation; two further laser photoablation sessions were performed. Due to the extent of the antral lesions and to patient noncompliance, this therapy failed to achieve any significant reduction in the convoluted vascular columns. At 8 months’ follow-up there had been no reduction in blood transfusion requirements. Finally, she was convinced of the need for surgery and underwent a subtotal gastrectomy in February 1998. There has been no further bleeding as of 8 months post-surgery.
DISCUSSION This case illustrates a typical presentation of GAVE with anemia and occult blood loss.2,7-9 On initial endoscopy, the erythematous stripes in the antrum were erroneously diagnosed as erosive gastritis, a fairly common misinterpretation.10 A second endoscopy confirmed the condition was, in fact, watermelon stomach. By definition, GAVE occurs only in the gastric antrum. However, the gastric cardia,11,12 gastric corpus,9 duodenum or jejunum,12-15 and rectum16,17 have all been reported to exhibit ectopic ectasia. In a few cases the lesions found in these other regions have been confirmed histopathologically as having the same features as GAVE, although none in the rectum have been classified this way. To our knowledge, the association of GAVE with rectal ectasia has not been reported. “Watermelon rectum” was noted as an incidental finding in a case of transient eosinophilic syndrome; ectatic blood vessels were not identified in biopsies, and repeat sigmoidoscopy revealed complete resolution of the rectal lesion.16 Abramson17 reported another case of watermelon rectum as a persistent lesion. Associated gastric vascular abnormalities and histologic diagnosis were not mentioned in either of the case reports. GAVE including the typical localization of ectasias to the antrum could be explained by three factors; antral motility disturbance,2,18,19 decreased blood flow to the antrum versus the fundus,4 and the influence of neuro-endocrine factors.20,21 Portal hypertension seems to be a predisposing factor in patients with cirrhosis, but GAVE is not likely the result of increased partial pressure.13,22 Deterioration rather than improvement in the lesions has been reported after portocaval shunt,13 and it appears that portalsystemic shunts should not be performed in an effort to relieve the symptoms of GAVE.13.22 Many investigators have implicated an antral motility disturbance.2,18,19 Jabbari et al.2 suggested that prolapse of the antral mucosa through the pylorus as a possible pathogenesis. Suit et al. and others supported this theory and believe that GAVE 856
GASTROINTESTINAL ENDOSCOPY
Rectal vascular ectasia and watermelon stomach
is likely related to mucosal trauma.7,18 Indeed, histopathologic findings in cases of rectal prolapse and solitary rectal ulcer do resemble those of GAVE. Both regions have similar anatomic and mechanical outlet functions that could lead to a propensity for prolapse. It is probable that humoral factors play roles in the pathogenesis of GAVE.20.21 Some investigators argue that GAVE could be a result of vasoactive factors, such as gastrin, 5-hydroxytryptamine, and vasoactive intestinal polypeptide.21 It has been speculated that hypergastrinemia has a trophic effects on the spindle cells that leads to fibromuscular hyperplasia.8,9 Our patient’s plasma gastrin level was high, a finding that may, in part, be related to her renal disease and long-term H2 receptor blocker therapy. The humoral component theory alone cannot explain the occurrence of this lesion at certain specific sites. However, humoral factors might lead to the propensity for developing this lesion, and perhaps anatomic and mechanical properties determine its specific localizations. Several treatments have been described for GAVE, including antrectomy and endoscopic approaches.23,26 There are no data or guidelines at present as to the best form of therapy in the individual case. The relatively noninvasive and practical aspects of endoscopic techniques such as laser photocoagulation make it the treatment of first choice. Surgical intervention has been suggested for extensive vascular abnormalities and refractory cases that fail to respond favorably to endoscopic treatment. Some studies have reported improvement in gastric mucosal histology and reduction of bleeding with corticosteroid and estrogen-progesterone treatment.23,27,28 Due to the chronic hepatitis C we did not consider treatment with corticosteroids in our patient. In conclusion, ectopic ectasias of the intestinal tract may accompany GAVE. Further studies are needed to determine whether the simultaneous occurrence of GAVE and rectal vascular ectasias is an incidental finding or a different expression of a single pathophysiologic condition. REFERENCES 1. Rider JA, Klotz AP, Kirsner JB. Gastritis with venocapillary ectasia as a source of massive gastric haemorrhage. Gastroenterology 1953;24:118-23. 2. Jabbari M, Cherry R, Lough JO, Daly DS, Kinner DG, Goresky CA. Gastric antral vascular ectasia: the watermelon stomach. Gastroenterology 1984;87:1165-70. 3. Koivisto PVI. Gastric antral vascular ectasia and primary biliary cirrhosis [letter] Endoscopy 1988;20:334. 4. Lee FL, Costello F, Flanagan N, Vasudev KS. Diffuse antral vascular ectasia. Gastrointest Endosc 1984;2:87-90. 5. Cales P, Payen JL, Berg P, Voigt JJ, Desmorat H, Vinel JP, et VOLUME 50, NO. 6, 1999
6.
7. 8. 9.
10. 11.
12. 13.
14.
15. 16. 17.
al. Antral vascular ectasia, new endoscopic and clinical spectrum [abstract ]. Gastroenterology 1991;100:A38. Voigt JJ, Payen JL, Cales P, Selves J, Barbe S, Vinel JP, et al. Les ectasies vasculaires antrales. Aspects anatomo-cliniques a propos de 21 cas (resume) [abstract]. Gastroenterol Clin Biol 1992;16(Suppl):A278. Rawlinson WD, Barr GD. Antral vascular ectasia: The “watermelon” stomach. Med J Aust 1986;144:709-11. Börch G. Diffuse antral vascular ectasia: the watermelon stomach revisited. Am J Gastroenterol 1987;82:1333-4. 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. Gouldesbrough DR, Pell ACH. Gastric antral vascular ectasia: a problem of recognition and diagnosis. Gut 1991;32:954-5. Borsh G, Schafer K, Schimdt G, Menne R, Tiedjen KU. Ectasie vasculaire antrale diffuse: cause rare d’hemorragie gastrointestinale severe. Acta Endosc 1985;15:239-43. Lux G, Fruhmorgen P, Rösch W. Diffuse telangiectasia of the upper GI tract [abstract]. Endoscopy 1979;11:281. Cales P, Voight 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. Wheeler MH, Smith PM, Cotton B, Evans DMD, Lawrie BM. Abnormal blood vessels in the gastric antrum. A cause of gastrointestinal bleeding. Dig Dis Sci 1979;2:155-8. Rose JDR. Endoscopic injection of alcohol for bleeding from gastroduodenal vascular anomalies. BMJ 1987;295:93-4. Steinberg J, Brandt LJ. The watermelon rectum. Gastrointest Endosc 1989;35:340-1. Abramson DA. Hematochezia associated with the watermelon rectum [letter]. Gastrointest Endosc 1992;38:97.
VOLUME 50, NO. 6, 1999
18. 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. 19. Charneau J, Petit R, Cales P, Dauver A, Boyer J. Antral motility in patients with cirrhosis with or without antral vascular ectasia. Gut 1995;37:488-92. 20. Perez-Ayuso RM, Pique JM, Saperas E, Bombi JA, Bordas JM, Elena M, et al. Gastric vascular ectasia in cirrhosis: association with hypoacidity not related to gastric atrophy. Scand J Gastroenterol 1989;24:1073-8. 21. Lowes JR, Rode J. Neuroendocrine cell proliferations in gastric antral vascular ectasia. Gastroenterology 1989;97:207-12. 22. Testard J, Hemet J, Metayer P. Gastrite hemorragique par coagulation intra-vasculaire localisee au cours de l’evolution d’une “cirrhose inflammatoire cryptogenetique.” Sem Hop Paris 1975;51:1235-41. 23. Kruger R, Ryan ME, Dickson KB, Nunez JF. Diffuse vascular ectasia of the gastric antrum. Am J Gastroenterol 1987; 82: 421-6. 24. Frager JD, Brandt LJ, Frank MS, Morecki R. Treatment of a patient with watermelon stomach using transendoscopic laser photocoagulation. Gastrointest Endosc 1988;34: 134-7. 25. Labenz J, Börsch G. Bleeding watermelon stomach treated by Nd-YAG laser photocoagulation. Endoscopy 1993;25:240-2. 26. Gostout CJ Ahlquist DA, Radford CM, Viggiano TR, Bowyer BA, Balm RK. Endoscopic laser therapy for watermelon stomach. Gastroenterology 1989;96:1462-5. 27. Calam J, Walker RJ. Antral vascular lesion, achlorhydria and chronic gastrointestinal blood loss: response to steroids. Dig Dis Sci 1980;25:236-9. 28. Moss SF, Ghosh P, Thomas DM, Jackson JE, Calam J. Gastric antral vascular ectasia: maintenance treatment with oestrogen-progesterone. Gut 1992;33:715-7.
GASTROINTESTINAL ENDOSCOPY
857