Univariate analysis of patients taking β-blockers showed an association of PVT with grade of esophageal varices (p < 0.01), CP class (p < 0.02), AST (p < 0.03), ALT and albumin (p < 0.02), PLT count and PLT/LD (p < 0.03), longitudinal diameter of the spleen (p < 0.005), ascites (p < 0.05), portal vein (p < 0.0001) and NSBB (OR 8.1; 95% CI 1.7-38.8).
GGT and AST showed discrimination between abstinence and recent drinking in patients with cirrhosis, including those without ascites, when appropriate (and for GGT, sex-specific) limits were used.
In addition, VEGF-induced Nectin-2 suppression in peritoneal endothelium may support an increase in vascular permeability leading to ascites production.
Ascites and plasma concentration of VEGF was also measured in cirrhotic patients with (n = 15) and without (n = 10) spontaneous bacterial peritonitis (SBP).
Evaluation of endothelial permeability finally showed a VEGF-dependent regulation via Claudin 5 suggesting a mechanism for the development of ascites in ovarian cancer patients.
In a PEL xenograft mouse model that showed profuse ascites, bevacizumab suppressed ascites formation completely, indicating the critical role of VEGF for PEL fluid retention.
This study was designed to investigate whether different vascular endothelial growth factor (VEGF) genotypes are associated with ascites formation in cirrhotic patients.
Expression of vascular endothelial growth factor by human renal cancer cells enhances angiogenesis of primary tumors and production of ascites but not metastasis to the lungs in nude mice.
Vascular endothelial growth factor (VEGF) augments tumor growth by inducing neovascularization and may stimulate ascites formation by increasing vascular permeability.
The diagnosis of this disease requires a high clinical index of suspicion and should be considered in the differential of ascites with a lymphocyte predominance and serum-ascitic albumin gradient of <1.1 mg/dl.
Pearson correlation analysis was performed for related postoperative indexes, and a diagnostic evaluation was performed using the receiver operating characteristic (ROC) of postoperative indexes.Differences in age, body mass index (BMI), portal vein hypertension, bile duct cancer, total bilirubin, alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (GGT), operation time, cumulative portal vein occlusion time, intraoperative blood volume, residual liver volume (RLV)/entire live rvolume, ascites volume at postoperative day (POD)3, supplemental albumin amount at POD3, hospitalization time after operation, and the prothrombin activity (PTA) were statistically significant.
Univariate analysis of patients taking β-blockers showed an association of PVT with grade of esophageal varices (p < 0.01), CP class (p < 0.02), AST (p < 0.03), ALT and albumin (p < 0.02), PLT count and PLT/LD (p < 0.03), longitudinal diameter of the spleen (p < 0.005), ascites (p < 0.05), portal vein (p < 0.0001) and NSBB (OR 8.1; 95% CI 1.7-38.8).
Polymorphism in all studied cytokine genes was correlated with recurrence, and interval to recurrence (>12 or < or =12 months post-OLT), and clinical (ascites, Child-Pugh score and death), biochemical parameters of recurrent HCV (serum alanine aminotransferase (ALT)), INR, albumin, bilirubin), and virological parameters (HCV genotype and load).
Factors associated with mortality included ascites (odds ratio [OR] 4.95, confidence interval [CI] 1.64-14.93, P = 0.005), previous cardiac surgery (OR 3.68, CI 1.46-9.26, P = 0.006), partially dependent or fully dependent functional status (OR 2.51, CI 1.12-5.56, P = 0.02), albumin <3 (OR 2.49, CI 1.18-5.29, P = 0.01), and American Society of Anesthesiologist class >3 (OR 2.10, CI 1.10-4.46, P = 0.05).
The IL-6 was elevated in ascites fluid versus baseline plasma levels (<i>p</i> = 0.003), and there were diminished levels of TNF-<i>α</i> in ascites fluid versus baseline plasma levels (<i>p</i> = 0.001).<i>Discussion</i>.