BACKGROUND & AIMS: It is established that cirrhotic patients who respond to beta-blockers by lowering their hepatic venous pressure gradient (HVPG) to < or =12 mmHg or by > or =20% of the baseline values are protected from bleeding. However, it is not known whether the effect remains unchanged over the treatment period. METHODS: A group of 24 patients with cirrhosis and oesophageal varices, treated with beta-blockers+/-nitrates, good-responders on haemodynamic criteria, were followed for up to 76 months with sequential HVPG measurements. Another group of 16 patients was used for validation. RESULTS: HVPG worsened in 10 of the 24 patients during follow-up. Changes in HVPG correlated to concomitant changes in liver function parameters. Variceal bleeding occurred in four of the 10 patients whose HVPG had worsened (bleed; 3-21 months after the measured increase in HVPG) and in none of those with stable HVPG (p=0.02). Patients with increased HVPG also had shorter survival (p=0.05). Worsening of HVPG was an independent predictor of death, additive to Child-Pugh or MELD scores, in a time-dependent Cox's regression analysis. This relationship was confirmed in the validation group. CONCLUSIONS: Worsening HVPG during follow-up in patients who had initially been good-responders to medical treatment is related to worsening in hepatic function. The maintenance of a good haemodynamic response to medical treatment of portal hypertension is an excellent predictor of outcome in these patients.
Clinical significance of worsening portal hypertension during long-term medical treatment in patients with cirrhosis who had been classified as early good-responders on haemodynamic criteria
MERKEL, CARLO;BOLOGNESI, MASSIMO;AMODIO, PIERO;GATTA, ANGELO
2010
Abstract
BACKGROUND & AIMS: It is established that cirrhotic patients who respond to beta-blockers by lowering their hepatic venous pressure gradient (HVPG) to < or =12 mmHg or by > or =20% of the baseline values are protected from bleeding. However, it is not known whether the effect remains unchanged over the treatment period. METHODS: A group of 24 patients with cirrhosis and oesophageal varices, treated with beta-blockers+/-nitrates, good-responders on haemodynamic criteria, were followed for up to 76 months with sequential HVPG measurements. Another group of 16 patients was used for validation. RESULTS: HVPG worsened in 10 of the 24 patients during follow-up. Changes in HVPG correlated to concomitant changes in liver function parameters. Variceal bleeding occurred in four of the 10 patients whose HVPG had worsened (bleed; 3-21 months after the measured increase in HVPG) and in none of those with stable HVPG (p=0.02). Patients with increased HVPG also had shorter survival (p=0.05). Worsening of HVPG was an independent predictor of death, additive to Child-Pugh or MELD scores, in a time-dependent Cox's regression analysis. This relationship was confirmed in the validation group. CONCLUSIONS: Worsening HVPG during follow-up in patients who had initially been good-responders to medical treatment is related to worsening in hepatic function. The maintenance of a good haemodynamic response to medical treatment of portal hypertension is an excellent predictor of outcome in these patients.
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