Value In Cirrhosis Research Articles

Coagulation factor XI in cirrhosis does not predict thrombo-hemorrhagic complications and hepatic decompensation

IntroductionFactor XI (FXI) is associated with thrombosis in patients without liver disease, but it alterations and prognostic value in cirrhosis are uncertain. Patients and methodsWe studied a prospective cohort of cirrhosis patients determining FXI and its association with portal vein thrombosis (PVT), bleeding, and hepatic decompensation/ACLF during 1-year follow-up. Odds ratios (OR) and 95 % CIs were calculated using logistic regression. ResultsWe included 183 patients (Child-Pugh [CP] A/B/C 57/59/57). FXI was reduced in cirrhosis, decreasing with CP stage (78 % [66–94] vs. 58 % [44–78] vs. 41 % [30–52] in CP A, B, and C, respectively; p < 0.001). FXI was correlated with MELD score (rho: -0.6, p < 0.001), INR (rho: -0.6, p < 0.001), and platelet count (rho: 0.4, p < 0.001). Sixteen patients (8.7 %) experienced PVT, which only predictor was baseline platelet count (OR: 0.94; CI95 %: 0.91–0.97, p < 0.001). Bleeding occurred in 7 patients (3.8 %). Cirrhosis severity, platelet count, fibrinogen, and FXI (60% vs. 78 %; p = 0.2) were comparable between bleeding and non-bleeding individuals. Finally, no association was found between FXI and hepatic decompensation/ACLF, which were predicted by lower albumin and platelet count, respectively. ConclusionFXI seems not to be responsible for thrombosis and cirrhosis progression. The lack of association between low FXI and bleeding events, however, indirectly opens to future studies evaluating FXI inhibitors in cirrhosis.

Pentraxin-3 is not related to disease severity in cirrhosis and hepatocellular carcinoma patients

The acute-phase protein pentraxin-3 (PTX3) is a component of the innate immune system. Inflammation and tissue injury increased PTX3 in the injured liver, and accordingly, circulating PTX3 was induced in patients with chronic liver diseases. In the present study, PTX3 protein was determined in systemic, hepatic, and portal vein plasma of patients with liver cirrhosis to assess a possible association between hepatic PTX3 release and extent of liver injury. However, PTX3 levels were not related to disease severity. Of note, portal PTX3 levels were higher than concentrations in the hepatic vein. PTX3 in the hepatic and portal veins was negatively correlated with factor V, antithrombin 3, and prothrombin time. PTX3 did neither correlate with C-reactive protein nor galectin-3 or resistin, whereby the latter two proteins are associated with hepatic injury. PTX3 levels were not changed in cirrhosis patients with ascites or varices and did not correlate with the hepatic venous pressure gradient. Likewise, serum PTX3 was not correlated with histological steatosis, inflammation, or fibrosis stage in patients with hepatocellular carcinoma (HCC). Moreover, PTX3 was not associated with tumor node metastasis classification in HCC. Above all, PTX3 increased in hepatic, portal, and systemic blood immediately after transjugular intrahepatic portosystemic shunt (TIPS). Higher PTX3 in portal than hepatic vein plasma and further increase after TIPS suggests that the liver eliminates PTX3 from the circulation. In summary, PTX3 is not of diagnostic value in cirrhosis and HCC patients.

A Comparative Study of Serum-Ascitic Fluid Albumin Gradient (SAAG) and Ascitic Fluid Total Protein (AFTP) as a Diagnostic Parameter in Patients Having Ascites

Ascites is a manifestation of various number of diseases and the aetiopathogenesis of ascites is varied. The differential diagnosis of ascites remains a clinical problem. Although cirrhosis is the cause of ascites in most patients (80%), approximately 20% have a cause other than liver disease. Approximately 5% of patient with ascites have more than one cause (i.e. ‘mixed’ ascites). The present study was conducted on 75 consecutive patients admitted to indoor wards, Department of Medicine, Mayo Institute of Medical Science, Barabanki (UP), between June 2015 to May 2016 of age group 18–70 years having clinical symptoms and signs of ascites. Samples of blood and ascitic fluid were obtained simultaneously. The aim of present study was to evaluate various parameters especially serum ascitic fluid albumin gradient in case of ascites in an Indian setting and to compare the SAAG with the AFTP levels in terms of usefulness in establishing a cause of ascites. In the present study value of SAAG was 1.56 ± 0.37 gm/dl (mean ± standard deviation) for patients with portal hypertension related ascites whereas for non-portal hypertension related ascites excluding cardiac ascites SAAG was 0.95 ±0.14 gm%. Corresponding values for cirrhosis and cardiac ascites were 1.6 ± 0.39 gm/dl and 1.44 ± 0.21 gm/dl respectively. It was observed that SAAG in cardiac ascites group (even though placed in non portal hypertension related ascites group based on absence of portal hypertension) resembled the SAAG of portal hypertension related ascites group. It was concluded from our present study that serum ascitic fluid albumin gradient(SAAG) is a better diagnostic parameter than ascitic fluid total protein (AFTP) in the patients having ascites. During the study we observed that SAAG has greater sensitivity and specificity values in comparision to AFTP for detection of portal hypertension related ascites.

Apparent diffusion coefficient (ADC) in liver fibrosis: Usefulness of normalized ADC using the spleen as reference organ

ObjectiveThe purpose of the current study was to determine the usefulness of the usage of the spleen as a reference organ to normalize liver ADC to improve the diagnostic performance of diffusion weighted imaging (DWI) for assessing liver fibrosis. Materials and methodsForty-nine subjects, 34 patients with liver disease and 15 control subjects were assessed with diffusion-weighted imaging. Liver ADC and normalized liver ADC (defined as the ratio of liver ADC to spleen ADC) were compared between patients and the control groups as well as among patients with different stages of fibrosis. Receiver operating characteristic (ROC) analysis was used to determine the performance of ADC and normalized liver ADC for prediction of liver fibrosis and cirrhosis. ResultsThere was no significant difference between spleen ADC values among patients in comparison to control (1.107±0.07×10−3mm2/s vs. 1.12±0.068×10−3mm2/s, p=0.998) or among patients with different stages of fibrosis (p=0.59–0.89). The mean liver ADC and mean normalized liver ADC values were significantly lower in patients with hepatic fibrosis compared to volunteers (P=0.01,<0.001 respectively), however liver ADC could not significantly differentiate different stages of fibrosis except between stages 0 and 4. The mean normalized liver ADC was significantly different between stage 0 and stages 2, 3, and 4 as well as between stage 1 and stage 4. In addition, it had a trend toward significance between stage 0 and 1, stage 2 and 4 as well as stage 3 and 4. Both liver ADC and normalized liver ADC had a significant negative correlation with the grade of fibrosis, however it was more powerful for normalized liver ADC in comparison to liver ADC (r=−0.694 vs. −0.361, p=0.01 vs. 0.05). ROC analysis showed higher performance using normalized liver ADC in comparison to liver ADC, with higher AUC, sensitivity, and specificity for detection of fibrotic stages ⩾2 (0.88, 92.5% and 76.2% Vs 0.72, 82.1%, and 57.1% respectively). The corresponding values for stages ⩾3 were 0.83, 100%, and 55% vs. 0.69, 77.3%, and 44.4% respectively), while the corresponding values for cirrhosis (stage 4) were 0.87, 81.8%, and 81.8% for normalized liver ADC vs. 0.74, 69.2%, 72.2%.for ADC liver. ConclusionThe utility of using the spleen as a reference organ could improve the diagnostic performance of ADC measurement for the diagnosis of liver fibrosis. The application of this technique for the evaluation of liver fibrosis is promising.

S13 * NONINVASIVE SCREENING FOR LIVER CIRRHOSIS IN ADDICTIVE PATIENTS * S13.1 * IS LIVER STIFFNESS THE NOVEL GOLD STANDARD TO ASSESS LIVER CIRRHOSIS?

S13 * NONINVASIVE SCREENING FOR LIVER CIRRHOSIS IN ADDICTIVE PATIENTS * S13.1 * IS LIVER STIFFNESS THE NOVEL GOLD STANDARD TO ASSESS LIVER CIRRHOSIS?

Noninvasive assessment of liver fibrosis

Noninvasive assessment of liver fibrosis

Portal pressure response has prognostic value in cirrhosis

Portal pressure response has prognostic value in cirrhosis

Reticuloendothelial system phagocytic activity in cirrhosis and its relation to bacterial infections and prognosis.

The reticuloendothelial system phagocytic activity, estimated by the plasma elimination rate constant of 99mtechnetium-sulfur colloid, was studied in 41 decompensated cirrhotics and 10 normal subjects. The results were related to the incidence and type of bacterial infections occurring during hospitalization and follow-up, and to survival. The elimination rate constant of 99mtechnetium-sulfur colloid was lower in cirrhotic patients (0.168 +/- 0.007) (means +/- S.E.) than in normal subjects (0.220 +/- 0.005) (p less than 0.01). Cirrhotics were divided into two groups. Group I (16 patients) and Group II (25 patients) had normal or reduced elimination rate constant of 99mtechnetium-sulfur colloid, respectively. Both groups were similar in relation to clinical and biochemical data, hepatic blood flow, and wedged hepatic venous pressure. However, the liver scan and the elimination rate constant of indocyanine green were more altered in Group II. Patients in Group II developed acute bacterial infections more frequently than did patients in Group I. During hospitalization (24 +/- 2 days), bacteremia occurred in six patients in Group II and in none in Group I (p less than 0.05). During follow-up (28 +/- 3 months), 5 patients in Group II and none in Group I developed bacteremia (p less than 0.05). The cumulative survival rate of Group I patients was higher (p less than 0.05) than that of Group II patients at 3 months (100 vs. 80%), 6 months (94 vs. 68%), 24 months (74 vs. 42%), and 48 months (68 vs. 34%). We suggest that decompensated cirrhotics with depressed reticuloendothelial system phagocytic activity are at great risk to acquire bacteremia, and that reticuloendothelial system phagocytic activity has prognostic value in cirrhosis.

Furosemide disposition in cirrhosis

Furosemide disposition after rapid intravenous injection (80 mg) was studied in 10 normal healthy subjects and eight patients with cirrhosis and ascites. In the cirrhotic patients the elimination half-life was modestly longer (81.0 +/- 8.0 min and 60.2 +/- 5.8 min). This prolongation was not associated with a difference in systemic clearance (156 +/- 7 ml/min in normal and 142 +/- 16 ml/min in cirrhotic subjects), rather it was a reflection of alterations in furosemide distribution. The steady-state volume of distribution was increased from 8.5 +/- 0.4 l in the healthy subjects to 12.1 +/- 1.3 l in the cirrhotic subjects; estimation in terms of unbound drug indicated an approximately 50% smaller value in cirrhosis. These observations were quantitatively consistent with the increased percentage of furosemide in plasma in the unbound form in the patients (10.2 +/- 1.0%) compared to in the normal subjects (4.0 +/- 0.1%). The 24-hr percentage urinary recovery of unchanged drug (58.8 +/- 2.8% and 53.1 6.5%) and the glucuronide metabolite (17.8 +/- 1.5 and 21.3 +/- 3.4) were on the same order in the normal and cirrhotic groups. The lack of major effects of cirrhosis on furosemide disposition suggests that changes in furosemide diuretic efficacy in such patients is a result of altered dynamic factors rather than altered disposition.