- Email: [email protected]
169 CARVEDILOL OR PROPRANOLOL IN PORTAL HYPERTENSION? A RANDOMIZED CLINICAL TRIAL
POSTERS extent of LE, patients were dichotomized into a high or low LE group and analyzed in regard to liver, cardiocirculatory and renal functions. Results: Cardiac MRI demonstrated hyperdynamic left ventricular function and a patchy pattern of LE of the myocardium to a variable extent (range 2–62%) in all patients. There were no significant differences in MELD, Child–Pugh score or the left ventricular ejection fraction nor in the response to dobutamin stress between the high and low LE groups. However, patients showing high LE had a higher cardiac index and alcoholic liver cirrhosis was more often the underlying disease (p < 0.05). Biomarkers of myocardial stress were elevated. And while NT-proBNP and c-Troponin-T showed no differences, PLGF and sFLT1 were lower in the high LE group. There was a higher morbidity and mortality in the high LE group in patients undergoing liver transplantation. Conclusion: Cardiac MRI shows myocardial involvement in patients with ELD. The hyperdynamic circulation in portal hypertension may be an important factor in the development of cirrhotic cardiomyopathy. Larger prospective trials are warranted to confirm the association with severity and outcome of liver disease and to test the predictive power of MRI for patients listed for liver transplantation. 167 CLINICAL PROFILE AND OUTCOME OF PATIENTS WITH CHRONIC LIVER DISEASE AND LEPTOSPIRA INFECTION D.K. Chhina1 , O. Goyal2 , P. Goyal2 , R. Kumar1 , R.S. Chhina2 . 1 Dept of Microbiology, 2 Dept of Gastroenterology, DMC and Hospital, Ludhiana, India E-mail: [email protected] Background and Aim: Epidemics of leptospirosis have been reported from all over the world. However, there is no data regarding clinical profile and outcome of patients of chronic liver disease (CLD) who get leptospira infection. Hence, this study was undertaken. Methods: Data of serologically confirmed cases of leptospirosis (positive IgM anti-leptospira antibody by ELISA), admitted from Jan to Dec 2008 was evaluated. Patients were divided into 2 groups – CLD and non-CLD groups. ‘Good outcome’ was defined as recovery and discharge from hospital; while ‘poor outcome’ was defined as non-survival or leaving against medical advice in a sick condition. Statistical analysis was done using Fisher’s exact test and Student’s unpaired t test. Results: Leptospirosis was diagnosed in 216 patients, of which 124 (57.4%) had underlying CLD. The mean age in CLD and nonCLD groups was 46.7±11.3 years and 45.3±16.8 years respectively. Significantly more number of patients in CLD group presented with jaundice (95.2% v/s 71.7%; p = 0.0001), while significantly fewer patients had history of fever (72.8% v/s 50.8%; p = 0.0001). Mean creatinine value was significantly higher in the non-CLD group (3.0±2.7 v/s 2.3±2.0; p = 0.029). However, the number of patients with renal involvement (62.1% v/s 65.2%), and pulmonary involvement (30.6% v/s 43.5%) was not significantly different in the 2 groups. The mean values of bilirubin, albumin and INR were significantly higher, while that of AST, ALT, ALP and platelets were significantly lower in the CLD group. CLD was associated with poor outcome in more number of patients (33.9 % v/s 21.7 %, p = 0.06). Factors predicting poor outcome in the CLD group were – presence of renal failure, pulmonary involvement, requirement of dialysis and artificial ventilation, leucocytosis and high bilirubin levels. Conclusions: CLD is a risk factor for leptospirosis. Patients with CLD and leptospirosis present more commonly with jaundice, rather than fever, and have a poorer outcome as compared to patients without CLD. Factors which predict poor outcome are – renal failure, pulmonary involvement, requirement of dialysis and artificial ventilation, leucocytosis, and high bilirubin levels.
168 EVALUATION OF THE FUNCTIONAL CCL2 PROMOTER POLYMORPHISM -2518A>G AS RISK FACTOR FOR SPONTANEOUS BACTERIAL PERITONITIS AND DEATH IN DECOMPENSATED LIVER CIRRHOSIS 1 F. Grunhage ¨ , B. Appenrodt2 , M. Gentenmann2 , L. Thyssen2 , S. Schwartz2 , T. Sauerbruch2 , F. Lammert1 . 1 Medical Department II, Saarland University Hospital, Homburg, 2 Department of Internal Medicine I, University Hospital Bonn, Bonn, Germany E-mail: [email protected] Background: Factors influencing the development of spontaneous bacterial peritonitis (SBP) are poorly understood. We have shown that mutations in the nucleotide-binding oligomerization domain containing-2 (NOD2) gene are associated with both SBP and death in patients with liver cirrhosis (Appenrodt B et al. Hepatology in press). Clinical and experimental data also suggest that peritoneal macrophages contribute to the control of SBP via the chemokine CCL2 (MCP-1). Recently it was proposed that a functional promoter variant in the CCL2 gene is associated with SBP in patients with alcoholic cirrhosis (Gable ¨ E et al. Z Gastroenterol 2008;46A). We therefore aimed to replicate this finding in a larger cohort of patients with decompensated liver cirrhosis. Patients and Methods: We recruited 145 patients with liver cirrhosis and ascites and recorded the development of SBP and survival. SBP was defined as presence of PMN count >250 cells/mL or positive bacterial culture from ascitic fluid. All individuals were genotyped for the CCL2 promoter polymorphism -2518A>G using dye fluorescent labelled probes in a real-time PCR-based genotyping assay. Results: The majority of our patients presented with ascites due to alcoholic liver cirrhosis (62%) or chronic viral hepatitis (17%), all other aetiologies were less common. As expected, the majority of patients presented with advanced liver disease, with 94% of the patients classifying for Child–Pugh scores B or C. In total, 50 patients (34.4%) died. The median follow-up time was 98 days (range 1– 938). Employing PMN cell count larger than 250 cells/mL and/or bacterial growth in culture as diagnostic criteria, 48 patients (33%) and 20 patients (14%) were diagnosed with SBP, respectively. Allele frequencies of the -2518A>G variant did not differ between patients with and without SBP regardless of the definition. In addition, we did not detect an association with CCL2 genotypes. Finally, we could not detect differences in survival between carriers of the rare allele or specific genotypes. Overall, the CCL2 genotype distribution was consistent with Hardy-Weinberg-equilibrium. Conclusion: In contrast to NOD2 variants, our study does not support the previously reported association of chemokine variants and SBP in patients with decompensated liver cirrhosis. 169 CARVEDILOL OR PROPRANOLOL IN PORTAL HYPERTENSION? A RANDOMIZED CLINICAL TRIAL L. Hobolth1 , S. Møller2 , H. Grønbæk3 , S. Keiding4 , F. Bendtsen1 , E. Feldager1 . 1 Department of Gastroenterology, 2 Department of Clinical Physiology and Nuclear Medicine, Hvidovre University Hospital, Hvidovre, 3 Department of Medicine, 4 PET Center, Aarhus University Hospital, Aarhus, Denmark E-mail: [email protected] Background: Propranolol is used in primary and secondary prevention of variceal bleeding; however, up to 60% of patients respond inadequately. Carvedilol is a non-selective beta-blocker with intrinsic anti-alpha1 -adrenergic activity with a potentially greater effect on hepatic venous pressure gradient (HVPG). Aims: 1. To compare the long-term efficacy of carvedilol and propranolol in patients with portal hypertension.
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POSTERS 2. To assess whether the acute response to oral propranolol predicts the long-term response to these drugs. Methods: Thirty-eight patients with cirrhosis and HVPG ≥12 mmHg were included. The HVPG was measured at baseline and 90 minutes after an oral dose of 80 mg propranolol. Following randomisation, 17 patients received propranolol (mean dose 122.4 mg/day) and 21 carvedilol (mean dose 14.0 mg/day) titrated according to pulse and blood pressure response. After 12 weeks, HVPG-measurements were repeated. Results: Acute HVPG-response to propranolol was significant −19.3±12.8% (p < 0.01). Long-term treatment with propranolol and carvedilol decreased HVPG −12.5±16.7% (p < 0.01) and −18.7±16.7% (p < 0.01), respectively, with no significant difference between the two treatment-regimens (p = 0.26). The frequency of long-term responders (HVPG decrease ≥20% or to <12 mmHg) was 41% (propranolol) versus 62% (carvedilol) (p = 0.20). There were no significant differences in DMAP, DGFR or Dweight during treatment. Using receiver operating characteristic curve analysis, the acute decrease in HVPG could not discriminate between patients with or without long-term effect of carvedilol (area under the curve (AUC) 0.54, p = 0.8). In the propranolol group the discrimination was better but still insignificant (AUC 0.73, p = 0.13). The acute decrease in HVPG of ≥12 % after oral propranolol was the best cutoff value to predict the long-term response, with a sensitivity and specificity of 71% and 78%, respectively. Neither the threshold of 12 % nor the traditional of 20% could significantly discriminate between long-term responders or non-responders (p = 0.13 and p = 0.11, respectively). Conclusion: This randomized clinical trial shows no significant difference in the portal pressure-lowering effects of carvedilol and propranolol after 12 weeks of treatment. The acute response to propranolol might be a useful diagnostic tool to predict the longterm effect of propranolol but not of carvedilol. 170 HEPATOGENOUS DIABETES MELLITUS IN LIVER CIRRHOSIS: RELATIONSHIP WITH PORTAL PRESSURE AND VARICEAL HEMORRHAGE M.Y. Kim1 , S.K. Baik1 , C.S. Won1 , J.W. Byun1 , H.J. Park1 , H.J. Choi1 , Y.O. Jang1 , S.Y. Park1 , Y.H. Kwon1 , D.J. Kim2 , J.H. Kim2 , G.J. Cheon3 , Y.D. Kim3 , S.J. Lee4 , D.H. Choi4 . 1 Department of Internal Medicine and Institute of Basic Medical Science, Yonsei University Wonju College of Medicine, Wonju, 2 Department of Internal Medicine, Hallym University College of Medicine, Chuncheon, 3 Department of Internal Medicine, Kangneung Asan Hospital, Ulsan University College of Medicine, Kangneung, 4 Department of Internal Medicine, Kangwon National University College of Medicine, Chuncheon, Republic of Korea E-mail: [email protected] Background and Aim: Diabetes related with liver disease, so called hepatogenous diabetes mellitus (HDM) is frequent in cirrhotic patients. However, few studies were done about the clinical impact of HDM for cirrhosis and its complications. The present study aimed to evaluate the relationship of HDM with portal hypertension and variceal bleeding as well as its prevalence. Methods: From July 2007 to December 2008, 75gm oral glucose tolerance test (OGTT), insulin resistance (IR) were evaluated for 195 cirrhotic patients (M:F = 164:31, 53.0±10.2 years) who had no history of diabetes mellitus. IR was calculated with the formula HOMA-IR = [fasting insulin (mIU/mL) × fasting glucose (mg/dL)]/405. In addition, upper endoscopy for varix, radiological image studies, hepatic venous pressure gradient (HVPG) and serologic tests were undertaken. Results: The prevalence of HDM in cirrhosis was 54.9% (107/194). Among them, 62.9% needed to be taken OGTT for diagnosis because they did not show any abnormality in the fasting glucose test. S74
The presence of HDM showed significant correlation with high Child–Pugh’s score, variceal hemorrhage and high HVPG (P < 0.05). In multivariate analysis, Child–Pugh’s score showed significant relationship with HDM (odds ratio = 1.43, 95% Confidential Interval: 1.005–2.038). In addition, variceal bleeder within recent 6 months showed significantly higher glucose level at 2 hour in OGTT compared to non-bleeder (P < 0.05). However, fasting glucose level showed no difference between them. The mean HOMA-IR was 2.6±2.1 and 16.9% (33 patients) showed high IR (HOMA-IR ≥4). High IR was implicated with high HVPG and variceal bleeding (P < 0.05). However, high IR showed no significant correlation with Child–Pugh’s score, MELD score and etiology of cirrhosis (P > 0.05). Conclusion: More than 50% of cirrhotic patients showed HDM in OGTT. HDM and high IR have significant relationship with severe portal hypertension and variceal bleeding. Especially, postprandial hyperglycemia which is characteristics of HDM showed significant relationship with variceal bleeding. 171 PORTAL HYPERTENSIVE GASTROPATHY CORRELATE WITH PORTAL HYPERTENSION AND PROGNOSIS IN LIVER CIRRHOSIS M.Y. Kim1 , S.K. Baik1 , C.S. Won1 , J.W. Byun1 , H.J. Park1 , J.S. Park1 , S.Y. Park1 , Y.H. Kwon1 , Y.D. Kim2 , G.J. Cheon2 . 1 Department of Internal Medicine and Institute of Basic Medical Science, Yonsei University Wonju College of Medicine, Wonju, 2 Department of Internal Medicine, Kangneung Asan Hospital, Ulsan University College of Medicine, Kangneung, Republic of Korea E-mail: [email protected] Backgrounds: Portal hypertensive gastropathy (PHG) is a common endoscopic finding in patients with liver cirrhosis; however, the relationship between PHG and portal hypertension is controversial. Furthermore, nothing is known regarding the correlation between PHG and prognosis in patients with liver cirrhosis. Methods: The hepatic venous pressure gradient (HVPG), endoscopic PHG grade, Child–Pugh score, and model for end-stage liver disease (MELD) score were assessed at baseline and were followed prospectively in 331 cirrhotic patients (284 males, 85.8%; mean age, 52.16±9.05 years) from January 2001 to April 2009. The relationship between PHG with HVPG and survival was investigated. The degree of PHG was assessed according to a modified grading system proposed by the Baveno III meeting on portal hypertension: PHG was considered mild when a pink, mosaic-like mucosal pattern with no signs of red or black-brown spots was present; PHG was considered severe when a mosaic-like mucosal pattern with red point lesions and/or cherry red spots, or black-brown spots was present. Results: In univariate analysis, Child–Pugh’s score, MELD score, HVPG, spleen sized, platelet count and esophageal variceal grade were correlated with the severity of PHG. However, in multivariate analysis, only HVPG was significantly higher in patients with severe PHG than in those with mild or no PHG (absent, 4.9±1.7 mmHg; mild, 10.7±4.1 mmHg; severe, 15.6±4.6 mmHg; P < 0.001). During follow-up, 28 patients (8.5%) died from liver-related disease. In a Kaplan–Meier analysis, severe PHG showed a significantly shorter expected survival time than absent or mild PHG (median survival time, 77.6±9.6 months in severe PHG; log-rank test, P = 0.048). Conclusions: PHG was associated with portal hypertension severity and prognosis in patients with liver cirrhosis.
Journal of Hepatology 2010 vol. 52 | S59–S182
168 EVALUATION OF THE FUNCTIONAL CCL2 PROMOTER POLYMORPHISM -2518A>G AS RISK FACTOR FOR SPONTANEOUS BACTERIAL PERITONITIS AND DEATH IN DECOMPENSATED LIVER CIRRHOSIS 1 F. Grunhage ¨ , B. Appenrodt2 , M. Gentenmann2 , L. Thyssen2 , S. Schwartz2 , T. Sauerbruch2 , F. Lammert1 . 1 Medical Department II, Saarland University Hospital, Homburg, 2 Department of Internal Medicine I, University Hospital Bonn, Bonn, Germany E-mail: [email protected] Background: Factors influencing the development of spontaneous bacterial peritonitis (SBP) are poorly understood. We have shown that mutations in the nucleotide-binding oligomerization domain containing-2 (NOD2) gene are associated with both SBP and death in patients with liver cirrhosis (Appenrodt B et al. Hepatology in press). Clinical and experimental data also suggest that peritoneal macrophages contribute to the control of SBP via the chemokine CCL2 (MCP-1). Recently it was proposed that a functional promoter variant in the CCL2 gene is associated with SBP in patients with alcoholic cirrhosis (Gable ¨ E et al. Z Gastroenterol 2008;46A). We therefore aimed to replicate this finding in a larger cohort of patients with decompensated liver cirrhosis. Patients and Methods: We recruited 145 patients with liver cirrhosis and ascites and recorded the development of SBP and survival. SBP was defined as presence of PMN count >250 cells/mL or positive bacterial culture from ascitic fluid. All individuals were genotyped for the CCL2 promoter polymorphism -2518A>G using dye fluorescent labelled probes in a real-time PCR-based genotyping assay. Results: The majority of our patients presented with ascites due to alcoholic liver cirrhosis (62%) or chronic viral hepatitis (17%), all other aetiologies were less common. As expected, the majority of patients presented with advanced liver disease, with 94% of the patients classifying for Child–Pugh scores B or C. In total, 50 patients (34.4%) died. The median follow-up time was 98 days (range 1– 938). Employing PMN cell count larger than 250 cells/mL and/or bacterial growth in culture as diagnostic criteria, 48 patients (33%) and 20 patients (14%) were diagnosed with SBP, respectively. Allele frequencies of the -2518A>G variant did not differ between patients with and without SBP regardless of the definition. In addition, we did not detect an association with CCL2 genotypes. Finally, we could not detect differences in survival between carriers of the rare allele or specific genotypes. Overall, the CCL2 genotype distribution was consistent with Hardy-Weinberg-equilibrium. Conclusion: In contrast to NOD2 variants, our study does not support the previously reported association of chemokine variants and SBP in patients with decompensated liver cirrhosis. 169 CARVEDILOL OR PROPRANOLOL IN PORTAL HYPERTENSION? A RANDOMIZED CLINICAL TRIAL L. Hobolth1 , S. Møller2 , H. Grønbæk3 , S. Keiding4 , F. Bendtsen1 , E. Feldager1 . 1 Department of Gastroenterology, 2 Department of Clinical Physiology and Nuclear Medicine, Hvidovre University Hospital, Hvidovre, 3 Department of Medicine, 4 PET Center, Aarhus University Hospital, Aarhus, Denmark E-mail: [email protected] Background: Propranolol is used in primary and secondary prevention of variceal bleeding; however, up to 60% of patients respond inadequately. Carvedilol is a non-selective beta-blocker with intrinsic anti-alpha1 -adrenergic activity with a potentially greater effect on hepatic venous pressure gradient (HVPG). Aims: 1. To compare the long-term efficacy of carvedilol and propranolol in patients with portal hypertension.
Journal of Hepatology 2010 vol. 52 | S59–S182
S73
POSTERS 2. To assess whether the acute response to oral propranolol predicts the long-term response to these drugs. Methods: Thirty-eight patients with cirrhosis and HVPG ≥12 mmHg were included. The HVPG was measured at baseline and 90 minutes after an oral dose of 80 mg propranolol. Following randomisation, 17 patients received propranolol (mean dose 122.4 mg/day) and 21 carvedilol (mean dose 14.0 mg/day) titrated according to pulse and blood pressure response. After 12 weeks, HVPG-measurements were repeated. Results: Acute HVPG-response to propranolol was significant −19.3±12.8% (p < 0.01). Long-term treatment with propranolol and carvedilol decreased HVPG −12.5±16.7% (p < 0.01) and −18.7±16.7% (p < 0.01), respectively, with no significant difference between the two treatment-regimens (p = 0.26). The frequency of long-term responders (HVPG decrease ≥20% or to <12 mmHg) was 41% (propranolol) versus 62% (carvedilol) (p = 0.20). There were no significant differences in DMAP, DGFR or Dweight during treatment. Using receiver operating characteristic curve analysis, the acute decrease in HVPG could not discriminate between patients with or without long-term effect of carvedilol (area under the curve (AUC) 0.54, p = 0.8). In the propranolol group the discrimination was better but still insignificant (AUC 0.73, p = 0.13). The acute decrease in HVPG of ≥12 % after oral propranolol was the best cutoff value to predict the long-term response, with a sensitivity and specificity of 71% and 78%, respectively. Neither the threshold of 12 % nor the traditional of 20% could significantly discriminate between long-term responders or non-responders (p = 0.13 and p = 0.11, respectively). Conclusion: This randomized clinical trial shows no significant difference in the portal pressure-lowering effects of carvedilol and propranolol after 12 weeks of treatment. The acute response to propranolol might be a useful diagnostic tool to predict the longterm effect of propranolol but not of carvedilol. 170 HEPATOGENOUS DIABETES MELLITUS IN LIVER CIRRHOSIS: RELATIONSHIP WITH PORTAL PRESSURE AND VARICEAL HEMORRHAGE M.Y. Kim1 , S.K. Baik1 , C.S. Won1 , J.W. Byun1 , H.J. Park1 , H.J. Choi1 , Y.O. Jang1 , S.Y. Park1 , Y.H. Kwon1 , D.J. Kim2 , J.H. Kim2 , G.J. Cheon3 , Y.D. Kim3 , S.J. Lee4 , D.H. Choi4 . 1 Department of Internal Medicine and Institute of Basic Medical Science, Yonsei University Wonju College of Medicine, Wonju, 2 Department of Internal Medicine, Hallym University College of Medicine, Chuncheon, 3 Department of Internal Medicine, Kangneung Asan Hospital, Ulsan University College of Medicine, Kangneung, 4 Department of Internal Medicine, Kangwon National University College of Medicine, Chuncheon, Republic of Korea E-mail: [email protected] Background and Aim: Diabetes related with liver disease, so called hepatogenous diabetes mellitus (HDM) is frequent in cirrhotic patients. However, few studies were done about the clinical impact of HDM for cirrhosis and its complications. The present study aimed to evaluate the relationship of HDM with portal hypertension and variceal bleeding as well as its prevalence. Methods: From July 2007 to December 2008, 75gm oral glucose tolerance test (OGTT), insulin resistance (IR) were evaluated for 195 cirrhotic patients (M:F = 164:31, 53.0±10.2 years) who had no history of diabetes mellitus. IR was calculated with the formula HOMA-IR = [fasting insulin (mIU/mL) × fasting glucose (mg/dL)]/405. In addition, upper endoscopy for varix, radiological image studies, hepatic venous pressure gradient (HVPG) and serologic tests were undertaken. Results: The prevalence of HDM in cirrhosis was 54.9% (107/194). Among them, 62.9% needed to be taken OGTT for diagnosis because they did not show any abnormality in the fasting glucose test. S74
The presence of HDM showed significant correlation with high Child–Pugh’s score, variceal hemorrhage and high HVPG (P < 0.05). In multivariate analysis, Child–Pugh’s score showed significant relationship with HDM (odds ratio = 1.43, 95% Confidential Interval: 1.005–2.038). In addition, variceal bleeder within recent 6 months showed significantly higher glucose level at 2 hour in OGTT compared to non-bleeder (P < 0.05). However, fasting glucose level showed no difference between them. The mean HOMA-IR was 2.6±2.1 and 16.9% (33 patients) showed high IR (HOMA-IR ≥4). High IR was implicated with high HVPG and variceal bleeding (P < 0.05). However, high IR showed no significant correlation with Child–Pugh’s score, MELD score and etiology of cirrhosis (P > 0.05). Conclusion: More than 50% of cirrhotic patients showed HDM in OGTT. HDM and high IR have significant relationship with severe portal hypertension and variceal bleeding. Especially, postprandial hyperglycemia which is characteristics of HDM showed significant relationship with variceal bleeding. 171 PORTAL HYPERTENSIVE GASTROPATHY CORRELATE WITH PORTAL HYPERTENSION AND PROGNOSIS IN LIVER CIRRHOSIS M.Y. Kim1 , S.K. Baik1 , C.S. Won1 , J.W. Byun1 , H.J. Park1 , J.S. Park1 , S.Y. Park1 , Y.H. Kwon1 , Y.D. Kim2 , G.J. Cheon2 . 1 Department of Internal Medicine and Institute of Basic Medical Science, Yonsei University Wonju College of Medicine, Wonju, 2 Department of Internal Medicine, Kangneung Asan Hospital, Ulsan University College of Medicine, Kangneung, Republic of Korea E-mail: [email protected] Backgrounds: Portal hypertensive gastropathy (PHG) is a common endoscopic finding in patients with liver cirrhosis; however, the relationship between PHG and portal hypertension is controversial. Furthermore, nothing is known regarding the correlation between PHG and prognosis in patients with liver cirrhosis. Methods: The hepatic venous pressure gradient (HVPG), endoscopic PHG grade, Child–Pugh score, and model for end-stage liver disease (MELD) score were assessed at baseline and were followed prospectively in 331 cirrhotic patients (284 males, 85.8%; mean age, 52.16±9.05 years) from January 2001 to April 2009. The relationship between PHG with HVPG and survival was investigated. The degree of PHG was assessed according to a modified grading system proposed by the Baveno III meeting on portal hypertension: PHG was considered mild when a pink, mosaic-like mucosal pattern with no signs of red or black-brown spots was present; PHG was considered severe when a mosaic-like mucosal pattern with red point lesions and/or cherry red spots, or black-brown spots was present. Results: In univariate analysis, Child–Pugh’s score, MELD score, HVPG, spleen sized, platelet count and esophageal variceal grade were correlated with the severity of PHG. However, in multivariate analysis, only HVPG was significantly higher in patients with severe PHG than in those with mild or no PHG (absent, 4.9±1.7 mmHg; mild, 10.7±4.1 mmHg; severe, 15.6±4.6 mmHg; P < 0.001). During follow-up, 28 patients (8.5%) died from liver-related disease. In a Kaplan–Meier analysis, severe PHG showed a significantly shorter expected survival time than absent or mild PHG (median survival time, 77.6±9.6 months in severe PHG; log-rank test, P = 0.048). Conclusions: PHG was associated with portal hypertension severity and prognosis in patients with liver cirrhosis.
Journal of Hepatology 2010 vol. 52 | S59–S182