Journal of hepatology · 1998
Clinical vs haemodynamic response to drugs in portal hypertension.
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McCormick P A, Patch D, Greenslade L, Chin J, McIntyre N, Burroughs A K
Аннотация
BACKGROUND/AIMS: The combination of non-selective beta-blockers and nitrates is an effective therapy for the prevention of rebleeding from oesophageal varices. However, a significant number of patients fail to respond and have further haemorrhage. It has been suggested that measurement of the hepatic venous pressure gradient response to long-term drug therapy may allow early selection of non-responders. We aimed to test this hypothesis in 63 patients with cirrhosis and variceal bleeding treated with propranolol+/-isosorbide mononitrate.
METHODS: Hepatic venous pressure gradient was measured before and during treatment. Response was defined as a reduction of 20% or more in hepatic venous pressure gradient, or a fall in hepatic venous pressure gradient to 12 mmHg or less.
RESULTS: Forty-four patients were evaluable: 28 responders and 16 non-responders. Hepatic venous pressure gradient fell significantly in the responder group (17.5+/-0.5 mmHg vs 12.2+/-0.5 mmHg; p<0.01) but not in the non-responders (18.0+/-1.0 vs 17.9+/-1.2 mmHg; p=n.s.). Overall, there was no difference in rebleeding rates between the two groups: responders 43%, non-responders 25%. However, rebleeding was uncommon in compliant patients with alcoholic cirrhosis, in whom the hepatic venous pressure gradient fell to less than 12 mmHg (9%).
CONCLUSIONS: In this study a fall in hepatic venous pressure gradient of 20% was not a reliable predictor of clinical response. A threshold value of 12 mmHg was useful, but applied to relatively few patients.
METHODS: Hepatic venous pressure gradient was measured before and during treatment. Response was defined as a reduction of 20% or more in hepatic venous pressure gradient, or a fall in hepatic venous pressure gradient to 12 mmHg or less.
RESULTS: Forty-four patients were evaluable: 28 responders and 16 non-responders. Hepatic venous pressure gradient fell significantly in the responder group (17.5+/-0.5 mmHg vs 12.2+/-0.5 mmHg; p<0.01) but not in the non-responders (18.0+/-1.0 vs 17.9+/-1.2 mmHg; p=n.s.). Overall, there was no difference in rebleeding rates between the two groups: responders 43%, non-responders 25%. However, rebleeding was uncommon in compliant patients with alcoholic cirrhosis, in whom the hepatic venous pressure gradient fell to less than 12 mmHg (9%).
CONCLUSIONS: In this study a fall in hepatic venous pressure gradient of 20% was not a reliable predictor of clinical response. A threshold value of 12 mmHg was useful, but applied to relatively few patients.