Indicator Of Portal Hypertension Research Articles

Genome-Wide Association Study Identifies New Risk Loci for Progression of Schistosomiasis Among the Chinese Population.

Schistosoma japonicum infections, which lead to local inflammatory responses to schistosome eggs trapped in host tissues, can result in long-term, severe complications. The development of schistosomiasis may result from a complex interaction between the pathogenic, environmental, and host genetic components. Notably, the genetic factors that influence the development of schistosomiasis complications are poorly understood. Here we performed a genome-wide association study on multiple schistosomiasis-related phenotypes of 637 unrelated schistosomiasis patients in the Chinese population. Among three indicators of liver damage, we identified two novel, genome-wide significant single-nucleotide polymorphisms (SNPs) rs34486793 (P = 1.415 × 10-8) and rs2008259 (P = 6.78 × 10-8) at locus 14q32.2 as well as a gene, PMEPA1, at 20q13.31 (index rs62205791, P = 6.52 × 10-7). These were significantly associated with serum levels of hyaluronic acid (HA). In addition, RASIP1 and MAMSTR at 19q13.33 (index rs62132778, P = 1.72 × 10-7) were significantly associated with serum levels of aspartate aminotransferase (AST), and TPM1 at 15q22.2 (index rs12442303, P = 4.39 × 10-7) was significantly associated with serum levels of albumin. In schistosomiasis clinical signs, ITIH4 at 3p21.1 (index rs2239548) was associated with portal vein diameter (PVD) class, an indicator of portal hypertension, and OGDHL at 10q11.23 (index rs1258172) was related to ascites grade. We also detected an increased expression of these six genes in livers of mice with severe schistosomiasis. Summary data-based Mendelian randomization analyses indicated that ITIH4, PMEPA1 and MAMSTR were pleiotropically associated with PVD class, HA and AST, respectively.

Role of platelet-albumin-bilirubin score in predicting re-bleeding after band ligation for acute variceal hemorrhage.

Platelet-albumin-bilirubin (PALBI) score was proposed by Roayaie et al with modification of previously studied albumin-bilirubin score to include platelet as an indicator of portal hypertension in 2015. Predictive value of this score was recently tested by Elshaarawy et al for re-bleeding in patients presenting with acute variceal hemorrhage. We did a similar study at our center (n = 170) to look at incidence of re-bleeding after band ligation defined as drop in 2 units of hemoglobin and witnessed melena or hematemesis within 2 wk of the procedure. We calculated PALBI scores for all patients based on lab values prior to the procedure. Of 25.3% had re-bleeding episodes, area under receiver operating characteristic curve for PALBI as predictor of re-bleeding was 0.601 (95% confidence interval: 0.502-0.699). PALBI score showed moderate accuracy at predicting re-bleeding in our population.

Low circulating chemerin levels correlate with hepatic dysfunction and increased mortality in decompensated liver cirrhosis

Nutritional status, infections, inflammation and extrahepatic organ dysfunction are critical factors for the progression of chronic liver disease. Chemerin is an immune-metabolically and chemotactically active adipokine and we hypothesized that it is associated with disease severity and prognosis in patients with advanced decompensated cirrhosis. Therefore, we measured serum concentrations of chemerin in a prospectively characterized cohort of 80 patients with decompensated cirrhosis and ascites and assessed the associations with markers of disease severity and short-term outcome at 28 days. In a subset of patients (n = 40), ascitic fluid chemerin was determined. Advanced liver disease was associated with decreased serum but not ascitic chemerin levels. Serum chemerin correlated with markers of hepatic function (total bilirubin, albumin, INR) and inversely correlated with indicators of portal hypertension (platelet count, gastrointestinal bleeding) but not with extrahepatic organ failure and systemic inflammation. Patients presenting with acute-on-chronic liver failure or infection did not exhibit altered serum or ascitic fluid chemerin concentrations. However, serum chemerin levels below 87 ng/ml predicted an increased risk for mortality or liver transplantation within 28 days independently of MELD and infections. We conclude that low serum chemerin is an independent adverse prognostic factor in patients with advanced decompensated cirrhosis.

Effects of Portal Hypertension on Gadoxetic Acid-Enhanced Liver Magnetic Resonance: Diagnostic and Prognostic Implications.

The aim of this study was to investigate the impact of portal hypertension (PH) on gadoxetic acid-enhanced liver magnetic resonance imaging (MRI) and assess diagnostic and prognostic implications in comparison to established imaging features of PH. Institutional review board-approved retrospective study of 178 patients (142 men; median age, 59.4 years) with chronic liver disease undergoing MRI and hepatic venous pressure gradient (HVPG) measurement between January 2008 and April 2015. Magnetic resonance imaging was assessed for established features of PH (splenic and portal vein diameters, portosystemic collaterals, ascites) and for features on 20 minutes delayed T1-weighted gadoxetic acid-enhanced MRI, that is, relative liver enhancement (RLE), biliary contrast excretion, or portal vein hyperintensity or isointensity (ie, portal vein hyperintensity sign, PVHS). Statistics encompassed linear regression, logistic regression, and survival analysis. There was an inverse correlation between HVPG and RLE (r = 0.18, P < 0.0001). On univariate analysis, clinically significant PH (ie, HVPG ≥ 10 mm Hg, n = 109) and severe PH (ie, HVPG ≥ 12 mm Hg, n = 99) were associated with delayed biliary contrast excretion (n = 33) and the PVHS (n = 74) (P < 0.01 for all). Multivariate analysis demonstrated significant associations between the PVHS and severe PH (odds ratio [OR], 3.33; P = 0.008), independently of spleen size (OR, 1.26; P = 0.002), portosystemic collaterals (n = 81; OR, 5.46; P = 0.0001), and ascites (n = 88; OR, 3.24; P = 0.006). Lower RLE and the PVHS were associated with lower 3-year, transplantation-free survival (hazards ratios, 0.98 and 3.99, respectively, P = 0.002 for all), independently of the Child-Pugh and Model for End-Stage Liver Disease scores. The presence of the PVHS on gadoxetic acid-enhanced MRI is an independent indicator of severe PH and may enable more accurate diagnosis. This feature and decreased hepatic contrast uptake may also comprise prognostic information.

Diagnosis of portal hypertension by transabdominal ultrasound

Portal hypertension is pathologic increase in portal venous pressure, with diversion of portal blood to the systemic circulation. The study was directed to measure as well as to compare the diameters of splenic, superior mesenteric and portal veins with their variation with respiration in normal subjects and in patients with portal hypertension. An analytic type of cross-sectional study was conducted at Radiology and Imaging Department of BIRDEM, Shahbag, Dhaka for one year (2011-12) among purposively selected 59 study subjects with chronic liver disease and portal hypertension, and 45 individuals without liver disease. Transabdominal ultrasonograpy of hepatobiliary system was carried out using computed sonography system with multiple probes having multiple frequency depending on physical built of the subjects. The diameters of selected veins were measured in the course of expiration and deep inspiration. In all control subjects, diameter variations of splenic vein and superior mesenteric vein were noted in the phases of respiration, the diameters increased during deep inspiration and decreased during deep expiration mean diameter and standard deviation of splenic vein and superior mesenteric vein were 6.95 ± 1.75 mm and 8.77 ± 2.06 mm respectively and during expiration they were 4.45 ± 1.24 mm and 5.66 ± 1.41 mm respectively. The difference in deep inspiratory and expiratory diameters had high statistical significance (p&lt;0.0001). Patients with portal hypertension diameter variation with breathing at the level of splenic and superior mesenteric veins was observed only in 5 (9.47%) cases. Diminished response of splenic and superior mesenteric veins with respiration in transabdominal ultrasonography is an indicator of portal hypertension. DOI: http://dx.doi.org/10.3329/bmjk.v47i1-2.22558 Bang Med J (Khulna) 2014; 47 : 21-24

Ascitic Fluid Analysis in the Differential Diagnosis of Ascites: Focus on Cirrhotic Ascites

Ascites is the pathologic accumulation of fluid within the peritoneal cavity. Because many diseases can cause ascites, in particular cirrhosis, samples of ascitic fluid are commonly analyzed in order to develop a differential diagnosis. The concept of transudate versus exudate, as determined by total protein measurements, is outdated and the use of serum-ascites albumin gradient as an indicator of portal hypertension is more accurate. Lactate dehydrogenase (LDH), vascular endothelial growth factor (VEGF), and other tumor markers can be helpful in distinguishing between malignant and benign conditions. Glucose and adenosine deaminase levels may support a diagnosis of tuberculous disease, and amylase level may indicate a diagnosis of pancreatitis. Given the specificity and sensitivity of laboratory results, accurate diagnosis should be based on both laboratory data and clinical judgment.

Spleen Stiffness Correlates with the Presence of Ascites but Not Esophageal Varices in Chronic Hepatitis C Patients

Although spleen stiffness has recently been identified as potential surrogate marker for portal hypertension, the relationship between spleen stiffness and portal hypertension has not been fully elucidated. We attempted to determine the relationship between the liver or spleen stiffness and the presence of ascites or esophageal varices by acoustic radiation force impulse (ARFI) imaging. A total of 33 chronic hepatitis C (CHC) patients (median age 68; range 51–84) were enrolled. We evaluated the relationship between the liver or spleen stiffness and indicators of portal hypertension as well as clinical and biochemical parameters. Fourteen healthy volunteers were used for validating the accuracy of AFRI imaging. The liver and spleen stiffness increased significantly with progression of liver disease. A significant positive correlation was observed between the liver and spleen stiffness. However, spleen stiffness, but not liver stiffness, was significantly associated with the presence of ascites (P < 0.05), while there was no significant association between the spleen stiffness and spleen index/presence of esophageal varices in CHC patients. The area under the receiver operating characteristic curve based on the spleen stiffness was 0.80. In conclusion, spleen stiffness significantly correlates with the presence of ascites but not esophageal varices in CHC patients.

Prevalence and Indicators of Portal Hypertension in Patients With Nonalcoholic Fatty Liver Disease

Little is known about the prevalence and severity of portal hypertension in patients with nonalcoholic fatty liver disease (NAFLD). We investigated the prevalence and noninvasive predictors of portal hypertension in patients with NAFLD. Signs of portal hypertension, including esophageal varices, splenomegaly, portosystemic encephalopathy, and ascites, were investigated in 354 patients with NAFLD. One hundred patients had portal hypertension at the time of NAFLD diagnosis (28.2%), 88 of these patients had septal fibrosis or cirrhosis (88%). Fibrosis stage correlated with presence (r = 0.41, P < .0001) and number of findings (r = 0.48, P = .006) of portal hypertension. Of the 204 patients with no or mild fibrosis (stages, 0-2), 12 patients had portal hypertension (6%); they had a significantly higher grade of steatosis, based on biopsy analysis, compared with the 192 patients without portal hypertension (94%). Thrombocytopenia, hyperbilirubinemia, cirrhosis, and obesity were associated independently with portal hypertension. Esophageal varices were found in 57 of the 128 patients undergoing endoscopic screening (44.5%) and were associated independently with thrombocytopenia, type 2 diabetes, and splenomegaly. Signs of portal hypertension were present in 25% of patients at the time of diagnosis of NAFLD; most had advanced fibrosis or cirrhosis. Portal hypertension can occur in a small proportion of patients with mild or no fibrosis and is associated with the extent of steatosis. Features of advanced liver disease and insulin resistance might identify patients with NAFLD and portal hypertension, and those expected to derive the most benefit from endoscopic screening for esophageal varices.

Prevalence and Indicators of Portal Hypertension in Patients With Nonalcoholic Fatty Liver Disease.

Prevalence and Indicators of Portal Hypertension in Patients With Nonalcoholic Fatty Liver Disease.

163. Congestion index: early indicator of portal hypertension in cystic fibrosis patients

163. Congestion index: early indicator of portal hypertension in cystic fibrosis patients

Plasma volume contraction in portal hypertension

The effect of blood volume contraction induced by a 4-week regimen of spironolactone (100 mg/day) or furosemide (40 mg/day) on the hepatic venous pressure gradient (HVPG), an indicator of portal hypertension, was evaluated in patients with cirrhosis and no ascites. In the spironolactone group (n = 15), HVPG decreased significantly from 16.5 +/- 0.9 mmHg (mean +/- S.E.M.) to 12.9 +/- 1.0 mmHg (P < 0.005) and total blood volume contracted significantly from 4338 +/- 231 ml to 4006 +/- 203 ml (n = 14, P < 0.01). Although the HVPG changes did not correlate significantly with changes in measured total blood volume or in simultaneously determined systemic haemodynamics, a significant inverse correlation (r = -0.74, P < 0.01, n = 12) was found between the HVPG change and posttreatment plasma aldosterone levels, attesting to the effectiveness of spironolactone therapy in lowering HVPG. In the furosemide group (n = 10), neither HVPG (13.7 +/- 0.3 mmHg vs. 13.6 +/- 0.9 mmHg) nor total blood volume (4961 +/- 153 ml vs. 4964 +/- 162 ml) declined significantly. These results show that long-term administration of spironolactone to patients with cirrhosis and no ascites produced a significant reduction in HVPG that may have been due to gradual, sustained volume contraction. Thus, spironolactone may prove to be an effective treatment for portal hypertension in cirrhosis without ascites.

Ultrasonographic investigation of respiratory influence on diameters of portal vessels in normal subjects.

In order to improve the basis for ultrasonographic studies of portal hypertension the normal diameters and respiratory variations in the portal vessels were measured in sixty-seven volunteers. In healthy subjects, measurements were made on the portal vein and its major tributaries. The respiratory variations were most prominent in the splenic vein, somewhat less in the superior mesenteric vein and least in the portal vein. There were no significant correlations to weight, age or height. The hypothesis that examinations performed after food intake would give more prominent respiratory variations had to be rejected but showed that the portal vein should be examined under defined conditions regarding alimentary status. The diameters alone of the portal vessels can probably not be used reliably as an indicator of portal hypertension while a respiratory variation of less than 30 per cent in the splenic vein should be considered pathologic and lead to further investigations.