Value of portal hemodynamics and hypersplenism in cirrhosis staging.

AIM: To determine the correlation between portal hemodynamics and spleen function among different grades of cirrhosis and verify its significance in cirrhosis staging. METHODS: The portal and splenic vein hemodynamics and spleen size were investigated by ultrasonography in consecutive 38 cirrhotic patients with cirrhosis (Child's grades A to C) and 20 normal controls. The differences were compared in portal vein diameter and flow velocity between patients with and without ascites and between patients with mild and severe esophageal varices. The correlation between peripheral blood cell counts and Child's grades was also determined. RESULTS: The portal flow velocity and volume were significantly lower in patients with Child's C (12.25+/-1.67 cm/s vs 788.59+/-234 mm/min, respectively) cirrhosis compared to controls (19.55+/-3.28 cm/s vs 1254.03+/-410 mm/min, respectively) and those with Child's A (18.5+/-3.02 cm/s vs 1358.48+/-384 mm/min, respectively) and Child's B (16.0+/-3.89 cm/s vs 1142.23+/-390 mm/min, respectively) cirrhosis. Patients with ascites had much lower portal flow velocity and volume (13.0+/-1.72 cm/s vs 1078+/-533 mm/min) than those without ascites (18.6+/-2.60 cm/s vs 1394+/-354 mm/min). There was no statistical difference between patients with mild and severe esophageal varices. The portal vein diameter was not significantly different among the above groups. There were significant differences in splenic vein diameter, flow velocity and white blood cell count, but not in spleen size, red blood cell and platelet counts among the various grades of cirrhosis. The spleen size was negatively correlated with red blood cell and platelet counts (r = -0.620 and r = -0.8.34, respectively). CONCLUSION: An optimal system that includes parameters representing the portal hemodynamics and spleen function should be proposed for cirrhosis staging.

Angiogenesis effect on rat liver after administration of expression vector encoding vascular endothelial growth factor D.

AIM: To verify the expressing efficiency and angiogenesis effect after administration of expression vector encoding for vascular endothelial growth factor D in normal and ischemic rat liver. METHODS: Ten female S-D rats were administrated with liver tissue dot injection of naked PCHO/hVEGF-D, 50 microg/dot, three dots for each. The same amount of physiological saline was used as control in the neighboring lobe. Fourteen S-D rats, using inflow occlusion of left lateral lobe, were divided into two groups, seven rats in each group. One was ischemic plasmid group, which received naked plasmid PCHO/hVEGF-D injection of 150 microg. The other received the equal amount of natural saline injection and designed as control. The expressions of hVEGF-D in mRNA and protein levels were identified by in situ hybridization and immunohistochemistry, respectively. Endothelial cells were labeled by the factor VIII immunohistochemistrically. The average number of peri-sinusoidal capillaries of each group was calculated and compared statistically 8 days after injection. RESULTS: A large amount of hVEGF-D in mRNA level was found in both normal and ischemic plasmid groups and but none in their corresponding control groups. The protein of hVEGF was also highly expressed in both normal and ischemic plasmid groups than in the controls. The mean number of capillaries under microscopy (X200) of the plasmid group and control was 10.2+/-2.78 vs 7.1+/-2.02 (P<0.05), and those of ischemic plasmid group and ischemic control were 7.43+/-1.72 vs 4.71+/-1.11 with statistical difference (P<0.05). CONCLUSION: The naked PCHO/hVEGF-D dot injection to normal, ischemic rat liver can produce comparatively high expression of hVEGF in both protein and mRNA levels, and prominently increase the number of new capillaries around hepatic sinuses. Therefore, it could be another ideal choice for the treatment of ischemic liver diseases.

Expressions of vascular endothelial growth factor in cirrhotic tissues and their relations to proto-oncogene c-fos, c-myc.

OBJECTIVE: To investigate the significance of vascular endothelial growth factor (VEGF) in the pathogenesis of liver cirrhosis and the correlation between VEGF and proto-oncogene c-fos and c-myc in cirrhotic liver. METHODS: The proteins of VEGF, c-fos, and c-myc were identified immunohistochemically in each tissue section of 53 cases of liver cirrhosis. The correlations between VEGF, c-fos and c-myc were analyzed. The levels of VEGF protein in different Child gradings were also compared. RESULTS: The proteins of VEGF were more highly expressed in Child A and B patients than in Child C patients and controls. The expressions of both c-fos and c-myc were not statistically significant between VEGF positive and negative patients. CONCLUSIONS: The protein level of VEGF can reflect the compensation status of cirrhosis patients and may act as an anti-cirrhotic factor. The proto-oncogene c-fos, c-myc and VEGF may have different mechanisms in the course of cirrhosis or hepatic tumorigenesis.