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Portal hypertensive vasculopathy and mucosal vascular ectasias
July 1995
Effects of purified Clostridium difficile toxin A in the animal intestine of the rat in vivo. Natural Toxins 1 9 9 3 ; 1 : 3 6 9 - 3 7 5 . 3. Cassuto J, Jodal M, Tuttle R, R, Lungren O. On the role of intramural nerves in the pathogenesis of cholera toxin-induced intestinal secretion. Scand J Gastroenterol 1 9 8 1 ; 1 6 : 3 7 7 - 3 8 4 . 4. Cassuto J, Jodal M, Lungren O. The effects of nicotinic and muscarinic receptor blockade on cholera toxin induced intestinal secretion in rats and cats. Acta Physiol Scand 1 9 8 2 ; 1 1 4 : 5 7 3 - 5 7 7 . 5. Pothoulakis C, Castagliuolo I, LaMont JT, Jaffer A, O'Keane JC, Snider RM, Leeman SE. CP-96,345, a substance P antagonist, inhibits rat intestinal responses to Clostridium difficile toxin A but not cholera toxin, Proc Natl Acad Sci USA 1 9 9 4 ; 9 1 : 9 4 7 - 9 5 1 .
Portal Hypertensive Vasculopathy and Mucosal Vascular Ectasias Dear Sir: The recent article by Payen et al. entitled "Severe Portal Hypertensive Gastropathy and Antral Vascular Ectasia Are Distinct Entities in Patients With Cirrhosis" is of interest) The authors examined the clinical and histological differences between cirrhotic patients with portal hypertension who have two different endoscopic patterns of vasculopathy: portal hypertensive gastropathy and gastric antral vascular ectasia. They found that refractory gastrointestinal bleeding develops more often in patients with endoscopic antral vascular ectasia (watermelon stripe or diffuse red spots) than in patients with endoscopic portal hypertensive gastropathy (mosaic pattern and red spots usually present in the gastric body and fundus). Our experience is similar. Significantly, it is often difficult to control bleeding in patients who have only mild to moderate portal hypertension and the endoscopic pattern of antral vascular ectasia. In this circumstance, neither shunting nor endoscopic ablation controls bleeding and therapy relies largely on pharmacological reduction of splanchnic blood flow; results are frequently less than satisfactory. Although we agree that the two endoscopic patterns of vasculoparhy in patients with portal hypertension have prognostic significance, we find that it is more important from the therapeutic point of view to determine whether patients bleeding from antral vascular ectasia have portal hypertension. 2'3 The patients without portal hypertension are usually elderly women who also have atrophic gastritis affecting the proximal stomach and in whom bleeding may be successfully controlled by endoscopic ablation of the mucosal vascular lesions. In addition to noting clinical differences between patients with portal hypertension and different endoscopic patterns ofvasculopathy, the authors describe histological differences in biopsy specimens from areas of endoscopic antral vascular ectasia compared with areas of endoscopic portal hypertensive gastropathy. On the basis of both the clinical and histological differences, the authors conclude that, in the setting of portal hypertension, endoscopic antral vascular ectasia and endoscopic portal hypertensive gastropathy represent distinct entities. We disagree with this conclusion. We have found that the histological alterations in the antral mucosa are the same in patients with endoscopic antral vascular ectasia irrespective of whether they have portal hypertension. Because the histological changes are the same in antral vascular ectasia irrespective of portal pressure and different in patients with portal hypertension depending on the endoscopic pattern, we believe it is likely that the observed differences are the result of other factors, probably factors specific to the antrttrn, such as motility or mucosal prolapse. Indeed, the authors report that 14 patients (64%) with the endoscopic pattern of severe portal hypertensive gastropathy also had the antral vascular ectasia, as shown endoscopically and on biopsy. This also suggests that the endoscopic and histological manifestations of portal hypertension in the gastric mucosa are hetero-
CORRESPONDENCE 333
geneous in appearance, the differences probably relate to coexisting factors and do not necessarily indicate the presence of distinct and separate entities. CHRISTOPHER J. GOSTOUT HERSCHEL A. CARPENTER Mayo Clinic and Mayo Foundation 200 First Street S. W. Rochester, Minnesota 55905 1. Payen J-L, Cal~s P, Voigt JJ, Barbe S, Pilette C, Dubuisson L, Desmorat H, Vinel J-P, Kervran A, Chayvialle J-A, Pascal J-P. Severe portal hypertensive gastropathy and antral vascular ectasia are distinct entities in patients with cirrhosis. Gastroenterology 1995; 1 0 8 : 1 3 8 - 1 4 4 . 2. Viggiano TR, Gostout CJ. Portal hypertensive intestinal vasculopathy: a review of the clinical, endoscopic, and histopathologic features. Am J Gastroenterol 1 9 9 2 ; 8 7 : 9 4 4 - 9 5 3 . 3. Gostout CJ, viggiano TR, Ahlquist DA, et al. The clinical and endoscopic spectrum of the watermelon stomach. J Clin Gastroenterol 1992;15:256-263. Reply. The interesting letter from Drs. Gostout and Carpenter deserves several comments. In our experience, as in theirs, treatment aimed at decreasing the level of portal pressure is ineffective in patients with gastric antral vascular ectasia (GAVE). 1 Likewise, we recently compared a personal series of 85 patients with GAVE, 89% of whom had cirrhosis, to 77 detailed observations of the literature. 2 The following characteristics were more often found in noncirrhotic patients: female sex, anemia, and watermelon stomach. However, we must emphasize that the recruitment of patients with or without cirrhosis is different: GAVEs are often discovered by chance in patients with cirrhosis, because endoscopy is routinely performed for portal hypertension. Anemia is rare in these patients, whereas noncirrhotic patients with GAVE undergo endoscopy for anemia as a result of GAVE. This selection bias must be kept in mind in noncirrhotic patients, In the second part of their letter, Gostout and Carpenter suggest that GAVE and severe portal hypertensive gastropathy (PHG) could not be different entities because the differences could only be attributed to different causal factors. In fact, we think that this subtle reasoning does not change the fact that the characteristics of the two syndromes are different. Another argument for the difference is the lack of description of abnormalities similar to PHG in patients without portal hypertension, whereas GAVEs are described in such patients. We agree that other causal factors play a role in the pathogenesis of GAVE. Thus, we have recently observed that antral motility was significantly different in cirrhotic patients with or without GAVE)
PAUL CAL]~S JEAN-LOUIE PAVEN Services d'Hgpato-GastroentCrologie Centre Hospitalier Universitaire dAngers et de Toulouse-Purpan 59033 Angers Cgdex 01, France 1. Cal~s 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 1 9 9 3 ; 3 4 : 5 5 8 - 5 6 1 . 2. Audeguy P, Payen JL, Benouna A, Obertif F, Voigt JJ, Crou~ A, et al. Syndrome d'ectasies vasculaires antralos: caract6ristiques particuli~res chez le malade cirrhotique et histoire naturelle. Gastroenterol Clin Biol 1995;19:102. 3. Charneau J, Petit R, Cal~s P, Dauver A, Boyer J. Antral motility in patients with cirrhosis with or without antral vascular ectasia. Gut (in press).
Effects of purified Clostridium difficile toxin A in the animal intestine of the rat in vivo. Natural Toxins 1 9 9 3 ; 1 : 3 6 9 - 3 7 5 . 3. Cassuto J, Jodal M, Tuttle R, R, Lungren O. On the role of intramural nerves in the pathogenesis of cholera toxin-induced intestinal secretion. Scand J Gastroenterol 1 9 8 1 ; 1 6 : 3 7 7 - 3 8 4 . 4. Cassuto J, Jodal M, Lungren O. The effects of nicotinic and muscarinic receptor blockade on cholera toxin induced intestinal secretion in rats and cats. Acta Physiol Scand 1 9 8 2 ; 1 1 4 : 5 7 3 - 5 7 7 . 5. Pothoulakis C, Castagliuolo I, LaMont JT, Jaffer A, O'Keane JC, Snider RM, Leeman SE. CP-96,345, a substance P antagonist, inhibits rat intestinal responses to Clostridium difficile toxin A but not cholera toxin, Proc Natl Acad Sci USA 1 9 9 4 ; 9 1 : 9 4 7 - 9 5 1 .
Portal Hypertensive Vasculopathy and Mucosal Vascular Ectasias Dear Sir: The recent article by Payen et al. entitled "Severe Portal Hypertensive Gastropathy and Antral Vascular Ectasia Are Distinct Entities in Patients With Cirrhosis" is of interest) The authors examined the clinical and histological differences between cirrhotic patients with portal hypertension who have two different endoscopic patterns of vasculopathy: portal hypertensive gastropathy and gastric antral vascular ectasia. They found that refractory gastrointestinal bleeding develops more often in patients with endoscopic antral vascular ectasia (watermelon stripe or diffuse red spots) than in patients with endoscopic portal hypertensive gastropathy (mosaic pattern and red spots usually present in the gastric body and fundus). Our experience is similar. Significantly, it is often difficult to control bleeding in patients who have only mild to moderate portal hypertension and the endoscopic pattern of antral vascular ectasia. In this circumstance, neither shunting nor endoscopic ablation controls bleeding and therapy relies largely on pharmacological reduction of splanchnic blood flow; results are frequently less than satisfactory. Although we agree that the two endoscopic patterns of vasculoparhy in patients with portal hypertension have prognostic significance, we find that it is more important from the therapeutic point of view to determine whether patients bleeding from antral vascular ectasia have portal hypertension. 2'3 The patients without portal hypertension are usually elderly women who also have atrophic gastritis affecting the proximal stomach and in whom bleeding may be successfully controlled by endoscopic ablation of the mucosal vascular lesions. In addition to noting clinical differences between patients with portal hypertension and different endoscopic patterns ofvasculopathy, the authors describe histological differences in biopsy specimens from areas of endoscopic antral vascular ectasia compared with areas of endoscopic portal hypertensive gastropathy. On the basis of both the clinical and histological differences, the authors conclude that, in the setting of portal hypertension, endoscopic antral vascular ectasia and endoscopic portal hypertensive gastropathy represent distinct entities. We disagree with this conclusion. We have found that the histological alterations in the antral mucosa are the same in patients with endoscopic antral vascular ectasia irrespective of whether they have portal hypertension. Because the histological changes are the same in antral vascular ectasia irrespective of portal pressure and different in patients with portal hypertension depending on the endoscopic pattern, we believe it is likely that the observed differences are the result of other factors, probably factors specific to the antrttrn, such as motility or mucosal prolapse. Indeed, the authors report that 14 patients (64%) with the endoscopic pattern of severe portal hypertensive gastropathy also had the antral vascular ectasia, as shown endoscopically and on biopsy. This also suggests that the endoscopic and histological manifestations of portal hypertension in the gastric mucosa are hetero-
CORRESPONDENCE 333
geneous in appearance, the differences probably relate to coexisting factors and do not necessarily indicate the presence of distinct and separate entities. CHRISTOPHER J. GOSTOUT HERSCHEL A. CARPENTER Mayo Clinic and Mayo Foundation 200 First Street S. W. Rochester, Minnesota 55905 1. Payen J-L, Cal~s P, Voigt JJ, Barbe S, Pilette C, Dubuisson L, Desmorat H, Vinel J-P, Kervran A, Chayvialle J-A, Pascal J-P. Severe portal hypertensive gastropathy and antral vascular ectasia are distinct entities in patients with cirrhosis. Gastroenterology 1995; 1 0 8 : 1 3 8 - 1 4 4 . 2. Viggiano TR, Gostout CJ. Portal hypertensive intestinal vasculopathy: a review of the clinical, endoscopic, and histopathologic features. Am J Gastroenterol 1 9 9 2 ; 8 7 : 9 4 4 - 9 5 3 . 3. Gostout CJ, viggiano TR, Ahlquist DA, et al. The clinical and endoscopic spectrum of the watermelon stomach. J Clin Gastroenterol 1992;15:256-263. Reply. The interesting letter from Drs. Gostout and Carpenter deserves several comments. In our experience, as in theirs, treatment aimed at decreasing the level of portal pressure is ineffective in patients with gastric antral vascular ectasia (GAVE). 1 Likewise, we recently compared a personal series of 85 patients with GAVE, 89% of whom had cirrhosis, to 77 detailed observations of the literature. 2 The following characteristics were more often found in noncirrhotic patients: female sex, anemia, and watermelon stomach. However, we must emphasize that the recruitment of patients with or without cirrhosis is different: GAVEs are often discovered by chance in patients with cirrhosis, because endoscopy is routinely performed for portal hypertension. Anemia is rare in these patients, whereas noncirrhotic patients with GAVE undergo endoscopy for anemia as a result of GAVE. This selection bias must be kept in mind in noncirrhotic patients, In the second part of their letter, Gostout and Carpenter suggest that GAVE and severe portal hypertensive gastropathy (PHG) could not be different entities because the differences could only be attributed to different causal factors. In fact, we think that this subtle reasoning does not change the fact that the characteristics of the two syndromes are different. Another argument for the difference is the lack of description of abnormalities similar to PHG in patients without portal hypertension, whereas GAVEs are described in such patients. We agree that other causal factors play a role in the pathogenesis of GAVE. Thus, we have recently observed that antral motility was significantly different in cirrhotic patients with or without GAVE)
PAUL CAL]~S JEAN-LOUIE PAVEN Services d'Hgpato-GastroentCrologie Centre Hospitalier Universitaire dAngers et de Toulouse-Purpan 59033 Angers Cgdex 01, France 1. Cal~s 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 1 9 9 3 ; 3 4 : 5 5 8 - 5 6 1 . 2. Audeguy P, Payen JL, Benouna A, Obertif F, Voigt JJ, Crou~ A, et al. Syndrome d'ectasies vasculaires antralos: caract6ristiques particuli~res chez le malade cirrhotique et histoire naturelle. Gastroenterol Clin Biol 1995;19:102. 3. Charneau J, Petit R, Cal~s P, Dauver A, Boyer J. Antral motility in patients with cirrhosis with or without antral vascular ectasia. Gut (in press).