Study of the correlation between; nitric oxide profile, degree of liver injury and structural vascular changes of the gastric mucosa in chronic hepatitis C virus related liver diseases

Nitric oxide [NO] plays an important role in HCV associated hepatic dysfunction and in the pathogenesis of portal hypertension. This study was designed to correlate serum nitrite and nitrate levels with the degree of liver injury and gastric mucosal changes in HCV patients at different stages of the disease. 80 HCV infected patients were classified equally into 4 groups; chronic hepatitis C, Child A, B and C cirrhosis groups. 20 healthy subjects were allocated as a control group. For all patients, serum nitrite and nitrate levels, HCV RNA and liver test profile were evaluated. Liver biopsies for chronic hepatitis C and Child-A cirrhotic patients were obtained for grading, staging and expression of interferon gamma [INF- gamma] and pentosidine. Esophagogastrodudenoscopy to evaluate the degree of portal hypertensive gastropathy [PHG] and expression of vascular endothelial growth [VEGF] by histopathology. Serum NO profile was significantly higher in all HCV infected patients than healthy subjects. A significant correlation between IFN-gamma expression and both of serum NO and viral load. Also, hepatic pentosidine expression was correlating with staging and fibrosis. Also both of serum NO and gastric VEGF were over expressed and correlating with the degree of PHG. In HCV infected patients, serum NO was significantly overexpressed and correlating with the severity of chronic liver disease. Our study supports the role of direct viral cytopathic effect in HCV patients because of the significant correlation of viral load with both of serum NO and hepatic IFN-gamma expression. Pentosidine might be considered a marker of oxidative stress and fibrosis in chronic HCV liver disease

reparative role of CD34[+] cells in human nephropathies

Stem cells are defined by the two properties of self renewal and pleuripotency. In different adult tissues, they generate new cells either continuously or in response to injury depending on local factors in the surrounding microenvironment which direct their line of differentiation. Circulating stem cells frequently engraft into the kidney and differentiate into renal parenchymal cells [tubular epithelial cells, podocytes, mesangial cells and fib roast]. This study included 36 human renal biopsies of different types of glomerulonephritis to determine the role of stem cells in the repair process of glomerulonephritis. Renal biopsies were stained immunohistochemically with monoclonal anti - CD34 antibodies, the stem cell marker as well as alpha SMA, Vimentin, Proliferating Cell Nuclear Antigen [PCNA], Insitu End Labeling [ISEL], CD68. Positivity was evaluated using a point counting technique in the glomeruli and by counting individual positive cells per HPF [X400] in the interstitium. To rule out the endothelial nature of positive cells, double staining for factor IIX related antigen and CD31 was done. CD34 positive cells were detected in the glomerular mesangial areas with peripheral accentuation suggestive of a visceral epithelial distribution, tubular epithelial cells [cytoplasmic in 3/36 cases and in the luminal border of the rest of the cases] as well as in isolated cells in the renal interstitium, these cells also double stained for alpha SMA. CD34 positivity was counted in the glomeruli [3.05 +/- 0.58], tubules [6.38 +/- 2.58] and for interstitial areas [9.76 +/- 2.34]. Significant positive correlation between glomerular CD34 and glomerular regeneration ratio was found. These results imply the presence and may be a role for stem cells in the repair process of glomerulonephritis