Higher Hepatic Venous Pressure Gradient Research Articles

Dissociation in hepatic vein pressure gradient, liver stiffness measurement and complications in histological subtypes of porto-sinusoidal vascular disease

Background and aimsPortosinusoidal vascular disease (PSVD) is a broad term encompassing varied histological patterns with changes in portal tracts and sinusoids without cirrhosis. We aimed to assess whether there is...

Risk factors associated with failure of endoscopic combined treatment to prevent varices rebleeding in patients with liver cirrhosis

ABSTRACT Background The aim of this study is to investigate risk factors associated with gastroesophageal variceal rebleeding after endoscopic combined treatment. Research design and methods Patients who had liver cirrhosis and underwent endoscopic treatment to prevent variceal rebleeding were retrospectively recruited. Hepatic venous pressure gradient (HVPG) measurement and CT examination of portal vein system were performed before endoscopic treatment. Endoscopic obturation for gastric varices and ligation for esophageal varices were performed simultaneously at the first treatment. Results One hundred and sixty-five patients were enrolled, and after the first endoscopic treatment, recurrent hemorrhage occurred in 39 patients (23.6%) during 1-year follow-up. Compared to the non-rebleeding group, HVPG was significantly higher (18 mmHg vs.14 mmHg, P = 0.024) and more patients had HVPG exceeding 18 mmHg (51.3% vs.31.0%, P = 0.021) in the rebleeding group. No significant difference was found in other clinical and laboratory data between two groups (P > 0.05 for all). By a logistic regression analysis, high HVPG was the only risk factor associated with failure of endoscopic combined therapy (OR = 1.071, 95%CI, 1.005–1.141, P = 0.035). Conclusions The poor efficacy of endoscopic treatment to prevent variceal rebleeding was associated with high HVPG. Therefore, other therapeutic options should be considered for the rebleeding patients with high HVPG.

The natural history of patients with compensated cirrhosis and elevated hepatic venous pressure gradient.

Portal hypertension is a major complication of liver cirrhosis. Hepatic venous pressure gradient (HVPG) appears to be one of the best surrogates of clinical outcomes. However, the utility of elevated HVPG in predicting subsequent clinical decompensation is unclear. We analyzed 410 patients who underwent HVPG assessment between 2014 and 2018. Of these, we identified and analyzed 20 patients with HVPG >12 mmHg without evidence of clinical decompensation (defined as ascites, non-bleeding esophageal varices or bleeding esophageal varices, hepatic encephalopathy, hepato-pulmonary syndrome, or hepatic hydrothorax). Additionally, we compared this group to 40 randomly selected cirrhotic patients with HVPG >12 mmHg with signs of clinical decompensation. Clinical events were subsequently assessed (mean = 33 months) after HVPG measurement. Patients with high HVPG without evidence of clinical decompensation had significantly lower model for end stage liver disease (MELD) scores (8 ± 4) compared to decompensated patients (13 ± 8, P = 0.05). HVPG measurements were similar in compensated (17 ± 6 mmHg) and decompensated (18 ± 4 mmHg) patients. Over follow-up for 33 months, 8/20 compensated patients had a decompensating event and neither MELD (8 and 8, respectively) nor HVPG (17 mmHg and 18 mmHg, respectively) differentiated patients who remained compensated vs. those that decompensated. Serum albumin at the time of HVPG measurement was significantly higher in patients who remained compensated than those with a decompensating event (3.5 g/dL vs. 2.6 g/dL, respectively, P = 0.05). A small, unique, population of cirrhotic patients with substantially elevated HVPG appear to remain free of complications over long term follow-up.

Hepatic venous pressure gradient in sinusoidal obstruction syndrome: Diagnostic value and link with histological lesions

Background & AimsLiver sinusoidal obstruction syndrome (SOS) is a well-established complication of myeloablative conditioning regimens used in hematopoietic stem cell transplantation. Hepatic venous pressure gradient (HVPG) >10 mmHg was described as an accurate diagnostic tool for SOS in the 1990s. However, epidemiology and presentation of SOS have dramatically changed. Moreover, elementary histological lesions influencing HVPG are unknown.MethodsWe retrospectively analyzed the charts of all patients who underwent transjugular liver biopsy with HVPG measurement for a clinical suspicion of SOS at our center. Two expert pathologists unaware of the presence or absence of SOS reviewed all liver samples and graded elementary histological lesions according to a semi-quantitative scoring defined a priori.ResultsOut of the 77 included patients, the 30 patients with SOS had higher HVPG than the 47 patients without SOS (median 14 mmHg [IQR 10-18], vs. 6 mmHg [3-9], respectively p <0.001). HVPG >10 mmHg had a specificity of 78% and a positive predictive value of 66% for the diagnosis of SOS. However, almost 40% of the patients with SOS had an HVPG ≤10 mmHg. HVPG correlated with sinusoidal congestion (r = 0.57; p = 0.001) and hepatocyte necrosis (r = 0.42; p = 0.02), but not with other lesions.ConclusionEven though HVPG is higher in patients with SOS, low HVPG values do not rule out SOS. Thus, HVPG cannot be used alone, and should be combined with transjugular liver biopsy, for the diagnosis of SOS.Lay summaryHepatic venous pressure gradient >10 mmHg has been described as an accurate tool for the diagnosis of liver sinusoidal obstruction syndrome after hematopoietic stem cell transplantation. This study shows that the sensitivity and specificity of hepatic venous pressure gradient measurement for sinusoidal obstruction syndrome are insufficient, so that liver pressure measurement should be combined with a liver biopsy in this setting.

Correlation between hepatic venous pressure gradient and portal venous pressure gradient in hepatitis B cirrhosis with different hepatic veins anatomy

PurposeThe hepatic venous pressure gradient (HVPG) has been employed as the gold standard for indicating the portal venous pressure gradient (PPG) in the diagnosis of portal hypertension (PHT). However, little has been reported on whether the HVPG can accurately estimate the PPG in patients with hepatic vein collateral shunts. We aimed to explore the correlation between the HVPG and the PPG in hepatitis B cirrhosis patients with different hepatic vein anatomies. MethodsA total of 461 hepatitis B cirrhosis patients with portal hypertension (PHT) who were treated with a transjugular intrahepatic portosystemic shunt (TIPS) between January 2016 and June 2020 were included. All patients underwent various venous pressure measurements and balloon-occluded compression hepatic venography during the TIPS operation. Agreements were evaluated by Pearson’s correlation and the Bland–Altman method. Disagreements were assessed by paired t tests. ResultsThe correlation coefficient (r) values (P < 0.001) between the HVPG and the PPG of the early (151 patients, 32.8 %), middle (73 patients, 15.8 %), late (46 patients, 10.0 %), portal vein (151 patients, 32.8 %), and no lateral branch development groups (40 patients, 8.7 %) were 0.373, 0.487, 0.569, 0.690, and 0.575, respectively; the determination coefficient (R2) values were 0.139, 0.238, 0.323, 0.475, and 0.330, respectively. According to the Bland–Altman method, agreement was the greatest in the portal vein development group, with the 95 % limits of agreement (95 % LoA, mean differences ± 1.96 SD) being the smallest. The differences were statistically significant (P < 0.05). ConclusionThe correlation between the HVPG and the PPG is the worst in early lateral branch development, followed by middle development, and the influence of lateral branches becomes significantly reduced in late development. Hepatic venous collateral formation is a vital factor for underestimation of the HVPG, which is the most accurate predictor of PPG in patients with portal vein development. Patients with no collateral channel development in the hepatic vein have a higher HVPG than PPG, which is an important reason for overestimation of the HVPG.

Erectile Dysfunction in Cirrhosis: Its Prevalence and Risk Factors

Erectile dysfunction (ED) is common in men with cirrhosis. The aim of this study was to assess the prevalence of ED and the factors associated with ED in men with cirrhosis. 400 men with cirrhosis [Child-Turcotte-Pugh (CTP) class A, 44.0%; CTP class B, 41.0%; and CTP class C, 15.0%] having high Karnofsky performance score, and living in a stable monogamous relationship with a female partner were included in the study. International Index of Erectile Function (IIEF) questionnaire, and Short-Form (36) Health Survey (SF-36) were used to assess erectile function and the health-related quality of life (HRQOL), respectively. ED was found in 289 (72.3%) patients. Patients with ED reported significantly lower SF-36 scores across all the eight domains of SF-36 (i.e., physical functioning score, role physical score, bodily pain score, general health perception score, vitality score, social functioning score, role emotional score, and mental health score); physical component summary score, and mental physical component summary score, compared with those without ED. On multivariate analysis, factors associated with ED were older age, longer duration of cirrhosis, CTP-C (vs. CTP-A), higher hepatic venous pressure gradient (HVPG), presence of generalized anxiety disorder (GAD), presence of major depression, and lower appendicular skeletal muscle index measured by dual-energy X-ray absorptiometry (DEXA ASMI). ED is common in men with cirrhosis, and men with ED have poor HRQOL compared with those without ED. Older age, longer duration of cirrhosis, CTP-C (vs. CTP-A), higher HVPG, presence of GAD, presence of major depression, and lower DEXA ASMI are associated with ED.

Clinical Outcomes in Patients with Advanced Chronic Liver Disease and Hepatic Venous Pressure Gradient ≤ 10mm Hg.

Clinically significant portal hypertension (CSPH), defined as hepatic venous pressure gradient (HVPG) ≥ 10mmHg predicts clinical decompensation (CD) in cirrhosis. A proportion of cirrhosis patients have HVPG 6-10mmHg. Their natural history is largely unknown. Consecutive patients with advanced chronic liver disease (aCLD) [histological cirrhosis(n = 196) or liver stiffness measurement (LSM) > 15kPa(n = 65)] and HVPG 6-10mmHg were included. Primary objective was to study their natural course and patterns of CD. We also analyzed the predictors of CD at presentation and on follow-up and response to carvedilol. Of 261patients with HVPG 6-10mmHg,129(49.4%) had CD at first presentation; 78(29.9%) had single and 51(19.5%) had ≥ 2CD. The most common CDs wereascites(n = 77) and jaundice(n = 65).A baseline HVPG ≥ 8mmHg was independently associated with greater risk of CD [HR:1.7; p-0.002, AUROC:0.85(95%CI-0.81-0.91)]. New CD developed in 14.4% patients with compensated aCLD (median duration-23.1months). Despite comparable baseline HVPG, patients developing new CD had higher HVPG on follow-up(15.3 ± 3.7 vs. 8 ± 2.1mmHg; p < 0.001). Baseline LSM > 26.6kPa, portosystemic shunt and serum albumin independently predicted newCD.Overall HVPG response to carvedilol(n = 60)was 23.3%, independent of baseline CD and HVPG. Five-year mortality was higher with ≥ 2CD compared to single or no CD (23.5, 10 and 3%, respectively; p < 0.001). Nearly one-half of aCLD patients with HVPG 6-10mmHg had CD, justifying the need to redefine CSPH. Interventions to reduce portal pressure in patients with HVPG ≥ 8mmHg might improve long-term outcomes.

Severe Protein-Calorie Malnutrition-Associated Hepatic Steatosis in a Woman Who Had Roux-en-Y Gastric Bypass for Morbid Obesity Thirteen Years Ago

Hepatic steatosis is common in everyday liver pathology practice. There are many etiologies leading to hepatic steatosis. These etiologies include metabolic syndrome, alcohol, medications, monogenetic disease, infectious diseases, and malnutrition. Correct diagnosis of underlying etiology through clinicopathological correlation is key to adequate treatment and optimal outcome for the patient. In this case report, we describe severe protein-calorie malnutrition as an etiology for hepatic steatosis in a middle-aged woman who presented with lethargy, low body mass index (15.8 kg/m2), abdominal distention and bilateral lower extremity edema, hyperammonemia, and hypoalbuminemia, 13 years after Roux-en-Y gastric bypass for morbid obesity. Laboratory tests revealed hyperammonemia, hypoalbuminemia, and low ceruloplasmin levels. Hemodynamic measurement demonstrated high hepatic venous pressure gradient of 12 mm Hg. Transjugular liver biopsy showed moderate macrovesicular steatosis, mild siderosis, and abundant lipofuscin but no evidence of fibrosis, cirrhosis, or steatohepatitis. This patient was treated with lactulose and enteral feeding, however, the patient died of progressive liver failure 3 weeks after admission. We also review relevant literature to help diagnose protein-calorie malnutrition (kwashiorkor) and hepatic steatosis as a possible late complication of Roux-en-Y gastric bypass. In patients with hepatic steatosis, encephalopathy, hyperammonemia and portal hypertension, malnutrition should be considered as an etiology and diagnosed with a synthesis of clinical, pathological, and laboratory information. Kwashiorkor is a severe disease and should be treated promptly as it may be fatal as in our case.

Clinical Decompensation and Outcomes in Patients With Compensated Cirrhosis and a Hepatic Venous Pressure Gradient ≥20 mm Hg.

Hepatic venous pressure gradient (HVPG) of ≥10 mm Hg predicts clinical decompensation (CD) in compensated cirrhosis. A proportion of cirrhotic patients at presentation have high HVPG (≥20 mm Hg) and are compensated. The natural history, spectrum of CD, and mortality in this group is largely unknown. Consecutive compensated cirrhotic patients with HVPG ≥6 mm Hg (n = 741) were followed up for 3-6 months for the development of any CD. Patients were classified based on the baseline HVPG (6 to <12 mm Hg [low HVPG, Gr.A, n = 163], 12 to <20 mm Hg [intermediate HVPG, Gr.B, n = 437] and ≥20 mm Hg [high HVPG, Gr.C, n = 141]). We analyzed the predictors of first CD, HVPG response to carvedilol, and mortality in these groups. CD developed in 217 (29.3%) patients during a mean follow-up of 1.6 ± 0.4 years, and those who developed CD had higher baseline HVPG (17.02 ± 4.79 vs 14.28 ± 4.86; P < 0.001). First CD was seen earlier (1.3 ± 0.7 years vs 1.5 ± 0.6 years and 1.6 ± 0.5 years, P = 0.02) and more frequently (44.7% vs 11% and 31.1%, P < 0.01) in high HVPG groups compared with low and intermediate HVPG groups, with higher mortality rates. Patients in the high HVPG group compared with the low HVPG group more often had NASH-cirrhosis (35.5% vs 19.6%; P 0.001), higher liver stiffness values (45.06 ± 20.46 vs 20.09 ± 5.47 kPa, P < 0.001), and lower platelet counts (113.37 ± 72.57 vs 151.7 ± 87.30/cmm, P < 0.001). Patients with HVPG ≥12 mm Hg received carvedilol, and a repeat HVPG performed in a proportion after 9.3 ± 2.4 months showed response (≥20% reduction in HVPG or <12 mm Hg) in 31.6% patients (Gr. B, 44.9% > Gr. C, 22.2%, P < 0.05). Baseline HVPG (HVPG ≥12 to <20 mm Hg [Hazard ratio: 2.73] and HVPG ≥20 mm Hg [Hazard ratio: 4.48], P < 0.001) independently predicted CD. HVPG ≥20 mm Hg in patients with compensated cirrhosis independently predicts early and more frequent CD and poor outcomes. These patients should be labeled as "high-risk compensated cirrhosis," and early and effective interventions to reduce portal pressure should be initiated to improve long-term outcomes.

Measurement of Exhaled Nitric Oxide in Cirrhotic Patients with Esophageal and Gastric Varices.

Background and aims. This study aimed to detect exhaled nitric oxide (eNO) level in cirrhotic patients and explore the correlation between eNO levels and the severity of cirrhosis. Methods. Patients were enrolled to analyze the relationship of eNO with noncirrhosis, cirrhosis, and complications of decompensated cirrhosis. We explored the potential predictive values of eNO in different states of cirrhosis. Results. The eNO levels were significantly increased in cirrhotic patients compared with noncirrhotic patients (14 (10–18) vs 8 (6–13) ppb, P < 0.001). The eNO level was increased in those with ascites (15 (14–22) vs 13 (10–18) ppb, P=0.026), with portal vein thrombosis (19.5 (11.75–22) vs 13.5 (10–17) ppb, P=0.032), or with the mucosal red-color sign of esophageal and gastric varices (EGV) (16.5 (10–21.75) vs 13 (10–14.75) ppb, P=0.041). Among cirrhotic patients undergoing hepatic venous pressure gradient (HVPG) measurement, the eNO level was significantly increased in the high-HVPG group (HVPG >12 mm Hg) compared with the low-HVPG group (6 mm Hg ≤ HVPG ≤ 12 mm Hg) (15 (11.75–19.25) vs 10 (8–14) ppb, P=0.011). Conclusions. The eNO level was increased in cirrhotic patients, especially in those complicated with ascites, portal vein thrombosis, mucosal red-color sign of varices, and high HVPG.

The Natural History of Advanced Fibrosis Due to Nonalcoholic Steatohepatitis: Data From the Simtuzumab Trials.

Progression of nonalcoholic steatohepatitis (NASH) is incompletely characterized. We analyzed data on longitudinal changes in liver histology, hepatic venous pressure gradient (HVPG), and serum markers of fibrosis in 475 patients with NASH with bridging fibrosis (F3) or compensated cirrhosis (F4) enrolled in two phase 2b, placebo-controlled trials of simtuzumab. The trials were terminated after 96 weeks because of lack of efficacy, so data from treatment groups were combined. Liver biopsies and HVPG measurements (only for patients with F4 fibrosis) were collected at screening and at weeks 48 and 96. Patients were assessed for Ishak fibrosis stage, hepatic collagen content and alpha-smooth muscle actin (by morphometry), NAFLD Activity Score (NAS), and serum markers of fibrosis. Associations with progression to cirrhosis (in patients with F3 fibrosis) and liver-related clinical events (in patients with F4 fibrosis) were determined. Progression to cirrhosis occurred in 22% (48/217) of F3 patients, and liver-related clinical events occurred in 19% (50/258) of patients with cirrhosis. Factors significantly associated with progression to cirrhosis included higher baseline values of and greater increases in hepatic collagen content, level of alpha-smooth muscle actin, and Enhanced Liver Fibrosis score. Similar factors, plus lack of fibrosis stage improvement (hazard ratio, 9.30; 95% confidence interval, 1.28-67.37), higher HVPG at baseline, and greater increase in HVPG over time, were associated with an increased risk of liver-related clinical events in patients with cirrhosis. Disease progression was not associated with the NAS at baseline or changes in NAS during treatment after adjustment for fibrosis stage. Conclusion: In patients with advanced fibrosis due to NASH, the primary determinant of clinical disease progression is fibrosis and its change over time.

&lt;p&gt;Combination of modified Sugiura technique and proximal splenorenal shunt for the management of portal vein thrombosis in noncirrhotic portal hypertension&lt;/p&gt;

Background: Noncirrhotic portal hypertension (NCPH) is a condition when a high hepatic venous pressure gradient with preserved liver functions and the absence of parenchymal dysfunction. NCPH with portal vein thrombosis (PVT) is a rare condition. Surgery aims to reduce portal vein flow and alter portal vein circulation.Case: A male, 59 years old, complained of blackish stool in the last 2 weeks and enlarged abdomen. Physical examination revealed anemia and melena with splenomegaly and ascites. Laboratory findings were anemia, normal hepatobiliary function, and no liver infection. Abdominal Doppler ultrasonography and contrast-enhanced abdominal computed tomography scan revealed ascites, splenomegaly, noncirrhotic liver, dilatation of portal vein, low portal vein peak velocity, and PVT. Esophagogastroduodenoscopy revealed esophageal varices grade 3 with a positive red color sign and cardia stomach varices. We performed a modified Sugiura technique through the left subcostal incision and proximal splenorenal shunt. The procedures of the modified Sugiura technique are splenectomy, devascularization, transection, and end-to-end anastomosis of the lower esophagus above the gastroesophageal junction, devascularization of the upper 2/3 of the lesser and greater curvatures of the stomach, and pyloroplasty. Portal circulation alteration used the proximal splenorenal shunt with end-to-side anastomosis of the splenic vein to left renal vein. At the one-year follow-up after surgery, his physical condition was better and there was no sign of complications.Conclusion: Devascularization procedure using a modified Sugiura technique is useful to treat and avoid rupture of esophageal varices. Portal circulation alteration using the proximal splenorenal shunt is a good choice. The treatment in NCPH utilizing the combination of modified Sugiura technique and the proximal splenorenal shunt is proper without complication.

Combined effect of hepatic venous pressure gradient and liver stiffness on long-term mortality in patients with cirrhosis.

Background/AimsBoth hepatic venous pressure gradient (HVPG) and liver stiffness (LS) are useful tools for predicting mortality in patients with cirrhosis. We investigated the combined effect of HVPG and LS on long-term mortality in patients with cirrhosis.MethodsWe retrospectively collected data from 103 patients with cirrhosis, whose HVPG and LS were measured between November 2009 and September 2013. The patients were divided into four groups according to the results of the HVPG and LS measurements. Long-term mortality and the risk factors for mortality were analyzed.ResultsOf the 103 patients, 35 were in group 1 (low HVPG and low LS), 16 in group 2 (high HVPG and low LS), 24 in group 3 (low HVPG and high LS), and 28 in group 4 (high HVPG and high LS). Over a median follow-up of 47.3 months, 18 patients died. The mortality rate of patients in group 4 was significantly higher than in the other three groups (vs. group 1, p = 0.005; vs. group 2, p = 0.049; vs. group 3, p = 0.004), but there were no significant differences in survival between groups 1, 2, and 3. In multivariable analyses, both HVPG and LS were identified as independent risk factors for mortality (hazard ratio [HR], 1.127, p = 0.018; and HR, 1.062, p = 0.009, respectively).ConclusionsIn patients with cirrhosis, those with concurrent elevation of HVPG and LS had the highest long-term mortality rates. However, when either HVPG or LS alone was elevated, mortality did not increase significantly.

Incidence and hemodynamic feature of risky esophageal varices with lower hepatic venous pressure gradient.

Background: To examine the incidence of cirrhosis patients with high-risk esophageal varices (EV) who show hepatic venous pressure gradient (HVPG) < 10 mmHg and to identify their hemodynamic features.Methods: This prospective study consisted of 110 cirrhosis patients with EV, all with the candidate for primary or secondary prophylaxis. Sixty-one patients had red sign, and 49 patients were bleeders. All patients underwent both Doppler ultrasound and HVPG measurement.Results: There were 18 patients (16.4%) with HVPG < 10 mmHg. The presence of venous-venous communication (VVC) was more frequent in patients with HVPG < 10 mmHg (10/18) than in those with HVPG ≥ 10 mmHg (19/92; p = 0.0021). The flow volume in the left gastric vein (LGV) and the incidence of red sign were higher in the former (251.9 ± 150.6 mL/min; 16/18) than in the latter (181 ± 100.5 mL/min, p = 0.02; 45/92; p = 0.0018). The patients with red sign had lower HVPG (13.3 ± 4.5) but advanced LGV hemodynamics (velocity 13.2 ± 3.8 cm/s; flow volume 217.5 ± 126.6 mL/min), whereas those without red sign had higher HVPG (16.2 ± 4.6, p = 0.001) but poorer LGV hemodynamics (10.9 ± 2.3, p = 0.002; 160.1 ± 83.1, p = 0.02).Conclusion: Patients with high-risk EV with HVPG < 10 mmHg showed 16.4% incidence. Although low HVPG may be underestimated by the presence of VVC, the increased LGV hemodynamics compensates for the severity of portal hypertension, which may contribute to the development of red sign.

Erectile dysfunction in cirrhosis is impacted by liver dysfunction, portal hypertension, diabetes and arterial hypertension.

BackgroundAlthough several risk factors for erectile dysfunction may be present in patients with cirrhosis, data on the actual prevalence and cause of erectile dysfunction is limited. The International Index of Erectile Function‐5 (IIEF‐5) is a well‐validated survey to determine the presence and severity of erectile dysfunction in men. We assessed (i) the prevalence and severity of erectile dysfunction, and (ii) risk factors for erectile dysfunction in patients with cirrhosis.MethodsIn this prospective study, erectile dysfunction was defined as: absent (>21 IIEF‐5‐points), mild (12‐21) and severe (5‐11). Patients with overt hepatic encephalopathy, active alcohol abuse, extrahepatic malignancy, previous urologic surgery, previous liver transplantation and severe cardiac conditions were excluded.ResultsAmong n = 151 screened patients, n = 41 met exclusion criteria and n = 30 were sexually inactive. Thus, a final number of n = 80 male patients with cirrhosis were included. Patient characteristics: age: 53 ± 9 years; model for end‐stage liver disease score (MELD): 12.7 ± 3.9; Child‐Pugh score (CPS) A: 30 (37.5%), B: 35 (43.8%), C: 15 (18.7%); alcohol: 38 (47.5%), viral: 25 (31.3%), alcohol/viral: 7 (8.8%) and others: 10 (12.5%). The presence of erectile dysfunction was found in 51 (63.8%) patients with 44 (55%) and 7 (8.8%) suffering from mild‐to‐moderate and moderate‐to‐severe erectile dysfunction. Mean MELD and hepatic venous pressure gradient (HVPG) were significantly higher in patients with erectile dysfunction (P = .021; P = .028). Child‐Pugh score C, MELD, creatinine, age, arterial hypertension, diabetes, low libido, low testosterone and high HVPG were associated with the presence of erectile dysfunction. Interestingly, beta‐blocker therapy was not associated with an increased risk. In multivariate models, arterial hypertension (OR: 6.36 [1.16‐34.85]; P = .033), diabetes (OR: 7.40 [1.31‐41.75]; P = .023), MELD (OR: 1.19 [1.03‐1.36]; P = .015) and increasing HVPG (n = 48; OR: 1.11 [1.002‐1.23]; P = .045) were independent risk factors for the presence of erectile dysfunction.ConclusionAbout two‐thirds of male patients with cirrhosis show erectile dysfunction. Severity of liver dysfunction, portal hypertension, arterial hypertension and diabetes were identified as risk factors for erectile dysfunction.

Effects of extremely high hepatic venous pressure gradient on short-term prognosis of endoscopic therapy in secondary prophylaxis for patients with gastroesophageal varices

Objective To evaluate effects of extremely high hepatic venous pressure gradient (HVPG) on the prognosis of endoscopic therapy in secondary prophylaxis for patients with gastroesophageal varices. Methods This was a single center prospective cohort study. From April 1st, 2013 to May 31st, 2015, patients with gastroesophageal varices and treated for secondary prophylaxis were enrolled and divided into extremely high HVPG group (HVPG≥20 mmHg, 1 mmHg=0.133 kPa) and non-extremely high HVPG group (HVPG<20 mmHg). After combination of endoscopic ligation and tissue glue treatment, one-year, two-year and three-year rebleeding rates and survival statuses were compared. Cox regression was performed for further analysis of prognosis factors related with rebleeding and survive. Results Eventually, 126 patients were enrolled and divided into extremely high HVPG group (32 cases) and non-extremely high HVPG group (94 cases). The one-year rebleeding rates of extremely high HVPG group and non-extremely high HVPG group were 37.9% (11/29) and 27.6% (24/87), respectively, and the difference was not statistically significant (χ2=1.105, P=0.293). The two-year rebleeding rate of extremely high HVPG group was significantly higher than non-extremely high HVPG group 51.7% (15/29) vs 29.9% (26/87), and the difference was statistically significant (χ2=4.539, P=0.033). And so was the three-year rebleeding rate, 51.7% (15/29) vs 29.9% (24/87), and the difference was statistically significant (χ2=4.539, P=0.033). The one-year, two-year and three-year survival rates of extremely high HVPG group and non-extremely high HVPG group were 92.6% (25/27) vs 94.0% (78/83), 85.2% (23/27) vs 94.0% (78/83), and 85.2% (23/27) vs 94.0% (78/83), and the differences between two groups were not statistically significant (all P>0.05). Single factor analysis showed that portal vein thrombosis was associated with rebleeding (hazard ratio (HR)=1.883, 95% confidence interval (CI) 1.015 to 3.492, P=0.045). No prognosis factors associated with survival were found. Conclusions Medium and long term rebleeding rate of the extremely high HVPG group is higher than that of the non-extremely high HVPG group. Extremely high HVPG does not affect the one-year prognosis of endoscopic therapy in secondary prophylaxis for patients with gastroesophageal varices. Key words: Hepatic venous pressure gradient; Esophageal and gastric varices; Secondary prophylaxis; Endoscopic therapy

Second prophylaxis of variceal bleeding in cirrhotic patients with a high HVPG

Objective: The hepatic venous pressure gradient (HVPG) could be used to stratify patients in different risk groups. No studies have reported the role of transjugular intrahepatic portosystemic shunt (TIPS) placement in a subgroup of patients with a high HVPG (≥20 mmHg) for secondary prophylaxis of variceal bleeding. This study was designed to evaluate the benefit of TIPS in cirrhotic patients with a high HVPG (≥20 mmHg) for rebleeding and survival.Material and methods: We included 46 cirrhotic patients with a history of variceal bleeding and a high HVPG (≥20 mmHg) admitted to our hospital between January 2013 and June 2014 (TIPS group). Patients were matched by Child-Pugh scores to patients in our historical cohort hospitalized for prophylaxis of variceal rebleeding between April 2011 and December 2012 (propranolol + EVL group). The end points included time to significant rebleeding from portal hypertensive sources, 1-year survival, and time to the occurrence of hepatic encephalopathy (HE).Results: The 1-year actuarial probability of remaining free of variceal rebleeding was significantly higher in the TIPS group than in the propranolol + EVL group (85% vs. 54%, p = 0.01). The 1-year survival rates were not different between the two groups (85% vs. 89%, p = 0.591). The 1-year actuarial probability of remaining free of HE was significantly lower in the TIPS group than in the propranolol + EVL group (67% vs. 91%, p = 0.003).Conclusions: TIPS was more effective than propranolol + EVL in preventing variceal rebleeding in cirrhotic patients with a high HVPG (≥20 mmHg). During the limited follow-up, survival was similar in the two groups.

Correlation of HVPG level with ctp score, MELD Score, ascites, size of varices, and etiology in cirrhotic patients.

Background/Aim:This study intends to determine the correlation of a patient's hepatic venous pressure gradient (HVPG) measurement with six factors: Child–Turcotte–Pugh (CTP) score, model for end-stage liver disease (MELD) score, presence of ascites, size of varices, presence of variceal bleeding, and an etiology of cirrhosis. The study also aims to identify the predictors of higher HVPG measurements that can indirectly affect the prognosis of cirrhotic patients.Patients and Methods:Thirty patients diagnosed with cirrhosis were enrolled prospectively and each patient's HVPG level was measured by the transjugular catheterization of the right or middle hepatic vein. The wedged hepatic venous pressure (WHVP) and free hepatic venous pressure (FHVP) were measured using a 7F balloon catheter. The HVPG level was calculated as the difference between the WHVP and FHVP measurements.Results:The mean HVPG level was higher in alcoholic than in nonalcoholic cirrhosis (19.5 ± 7.3 vs 15.2 ± 4.5 mm Hg, P = 0.13). The mean HVPG was also higher in bleeders compared with nonbleeders (18.5 ± 5.3 vs 10.7 ± 3.1 mmHg, P = 0.001). Patients with varices had a higher mean HVPG level than those without varices (17.4 ± 5.8 vs 11.7 ± 3.9 mmHg, P = 0.04). The difference among the three categories of varices (small, large, and no varices) was statistically significant (P = 0.03). In addition, the mean HVPG level was higher in patients with ascites than in those without ascites (18.7 ± 4.7 vs 11 ± 5.3 mmHg, P = 0.002), and it was significantly higher in patients in CTP class C (21.8 ± 5.5 mmHg) as compared with those in CTP class B (16.9 ± 2.9 mmHg) and CTP class A (10.5 ± 4.1 mmHg; P ≤ 0.001).Conclusion:HVPG levels were significantly higher in patients in CTP class C as compared with those in CTP classes A and B, thereby indicating that an HVPG measurement correlates with severity of liver disease. A high HVPG level signifies more severe liver disease and can predict the major complications of cirrhosis.

Hepatogenous Diabetes in Cirrhosis Is Related to Portal Pressure and Variceal Hemorrhage

The clinical impact and complications of hepatogenous diabetes (HD) on cirrhosis have not been elucidated. This study aimed to evaluate the relationship of HD with portal hypertension (PHT) and variceal hemorrhage and to assess the prevalence of HD. From July 2007 to December 2009, 75-g oral glucose tolerance test and insulin resistance (IR) were evaluated for 195 consecutive cirrhotic liver patients (M:F = 164:1, 53.0 ± 10.2 years) who had no history of diabetes mellitus. IR was calculated using the homeostasis model of assessment-insulin resistance (HOMA-IR) formula. Endoscopy for varices, hepatic venous pressure gradient (HVPG), and serologic tests were also conducted. HD was observed in 55.4 % (108/194) of the patients. Among them, 62.0 % required OGTT for diagnosis because they did not show an abnormal fasting plasma glucose level. The presence of HD showed a significant correlation with high Child-Pugh's score, variceal hemorrhage, and HVPG (p = 0.004, 0.002, and 0.019, respectively). In multivariate analysis, Child-Pugh's score (OR 1.43, 95 % CI 1.005-2.038) and HVPG (OR 1.15, 95 % CI 1.003-2.547) had significant relationships with HD. Patients with recent variceal hemorrhages (within 6 months) exhibited significantly higher glucose levels at 120 min in OGTT compared to patients without hemorrhages (p = 0.042). However, there was no difference in fasting glucose levels. The 120-min glucose level and HOMA-IR score were significantly and linearly correlated with HVPG (r (2) = 0.189, p < 0.001 and r (2) = 0.033, p = 0.011, respectively). HD and IR have significant relationships with PHT and variceal hemorrhage. Postprandial hyperglycemia in particular had a significant relationship with variceal hemorrhage.

Hepatic and systemic hemodynamic derangements predict early mortality and recovery in patients with acute‐on‐chronic liver failure

Acute-on-chronic liver failure (ACLF) is a clinical entity where there is a potential for reversibility of hepatic dysfunction once the acute hepatic insult resolves. The portal and systemic hemodynamics in ACLF patients to study its relevance in determining the clinical outcomes was studied. Clinical, laboratory, portal, and systemic hemodynamic assessments were done at admission and after 3 months. Standard medical care was given to all the patients. Fifty-seven patients with ACLF were enrolled, and they underwent baseline hepatic venous pressure gradient (HVPG) measurement. Twenty-six (46%) patients died during the 3-month follow-up. Presence of high HVPG and hepatic encephalopathy were found to be independent baseline predictors of mortality. Of the 31 surviving patients, 24 consented for a repeat HVPG. The baseline HVPG reduced from 16 (range 12-30) to 13 (range 6-21) mmHg; (P < 0.05). The reduction in HVPG correlated with clinical and biochemical recovery, and reduction in Child-Turcotte-Pugh score score (P < 0.05), while the aortic mean arterial pressure, cardiac index and systemic vascular resistance index improved significantly (< 0.05). Six (25%) patients developed upper gastrointestinal bleed; the median HVPG between bleeders and non-bleeders was not different possibly because of early onset of bleed (median 20 [15-45 days]). Baseline HVPG is an independent predictor of mortality in ACLF patients. The portal and systemic circulatory anomalies regress substantially by 90 days and correlate with clinical recovery. However, in the initial phase, the raised portal pressure predisposes these patients to high risk of variceal bleeding.