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Editor,—Spahr and colleagues recently published a case series which described the poor response of a haemorrhage from gastric antral vascular ectasia (GAVE) to portal decompression by insertion of a transjugular intrahepatic portosystemic shunt (TIPS) (Gut1999;44:739–742). However, the authors' claim that this indicates the absence of a relation between GAVE and portal hypertension is seriously flawed. The failure of this condition to respond to portal decompression cannot exclude a primary role for portal hypertension in the pathogenesis of the disorder. Furthermore, this study would have been more informative if aortoportography—that is, superior mesenteric and splenic angiography with venous phase imaging, had been performed in order to determine the pattern of portosystemic shunting before and after TIPS insertion. The authors have not addressed the question of whether portosystemic shunts supply the vascular lesions of GAVE; it would have been helpful if they had performed angiography in at least some patients after the TIPS procedure to confirm that blood flow had been restored to the liver from all portal vein tributaries, as it cannot be assumed that normalisation of portal vein pressure will completely ablate all preformed portosystemic shunts. Finally, it was not stated whether splenic vein thrombosis was excluded in all patients. If present, this could have caused ongoing segmental portal hypertension which could not have been expected to respond to TIPS insertion.
It is evident from previous case series, which suggested that GAVE might occur without portal hypertension, that some did not exclude portal hypertension in their patients.1 A rigorous exclusion of portal hypertension would require liver biopsy and/or measurement of the portocaval pressure gradient, together with imaging of the portal venous system in order to exclude portal or splenic vein thrombosis. The importance of this is illustrated by the series of patients with GAVE after bone marrow transplantation, cited by Spahret al.2 In this series, all patients with available liver histology were found to have hepatic veno-occlusive disease, a well recognised cause of portal hypertension. A further link between GAVE and autoimmune disorders may be explained by extrahepatic or non-cirrhotic portal hypertension in some of those patients.1 3 The possible association of GAVE with chronic renal failure cited by Spahr et alpresumably refers to an early series of patients with diffuse haemorrhagic gastric lesions in the absence of any overt liver disease; however, these lesions would probably not be classified as GAVE by current criteria, therefore this association is questionable.1 4
Thus, the pathogenesis of this interesting disorder remains uncertain but the strong association of portal hypertension (whether overt or covert) with the majority of cases of GAVE means that this is likely to be a key contributory factor.
Editor,—We appreciate Dr Fisher's comments on our recent paper, in which we provided evidence against the role of portal hypertension in the pathogenesis of GAVE. Firstly, lowering or normalisation of portal pressure was not followed by improvement in either the endoscopic findings or the rate of transfusions needed for recurrent bleeding. In this case series, one patient had to be transfused repeatedly for five years despite a patent surgical end to side portocaval shunt (portocaval gradient 2 mm Hg). Furthermore, the degree of residual portal hypertension was not correlated with clinical and endoscopic evolution in patients treated by TIPS. Interestingly, the only patient that responded to TIPS still had an increased gradient after the treatment (14 mm Hg); in this patient, the favourable outcome of GAVE was parallelled by a noticeable improvement in liver function.
One study has suggested that arterioportography may have a diagnostic value in GAVE.1-1 However, typical findings were shown on the arterial phase (hypervascularisation of the antrum and early arteriovenous shunting), and none of our patients had a coeliac axis arteriogram. On direct portography, it was impossible to show dilated mucosal blood vessels in the antrum. In all non-responders, bleeding recurred despite a reversed portal blood flow observed after TIPS or surgical shunt. In addition, splenic vein thrombosis was not observed in any of our patients, obviously because such a finding would contraindicate TIPS, which is not a treatment of segmental portal hypertension. Therefore, we are still convinced that portosystemic shunting and liver function could both influence liver metabolism of the vasodilating substances that contribute to the pathogenesis of GAVE, whereas portal hypertension alone has no influence.
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