Do serum CA 19-9 and CA 125 levels predict the severity of HCV-related liver fibrosis?

To study the value of measurement of serum tumor markers CA 19-9 and CA 125 as predictors of severity of liver fibrosis in patients with chronic hepatitis C. Fifty patients with chronic hepatitis C were recruited from the Hepatology and Gastroenterology Department at Ain Shams University Hospital. They were 31 men and 19 women, with ages ranging from 18 to 50 years. Participants were subjected to full clinical examination, liver function tests, viral markers [hepatitis B surface antigen, hepatitis C virus antibody], a fetoprotein, autoimmune markers, assay of serum levels of CA 19-9 and CA 125, abdominal ultrasonography, and ultrasound-guided liver biopsy. Histopathological examination for staging of liver fibrosis was performed using the Ishak scoring system. There was a highly significant positive correlation between serum levels of CA 19-9 and CA 125 and the stage of liver fibrosis [P<0.01]. There was also a difference in the mean values of serum CA 19-9 among different stages of liver fibrosis. Similar differences were seen for CA 125. The best cut-off value for CA 19-9 in predicting severe liver fibrosis and cirrhosis [stages 5, 6] was found to be 33.87 U/ml with sensitivity of 93.8% and specificity of 88.2%, whereas the best cut-off value for CA 125 in predicting severe liver fibrosis and cirrhosis [stages 5, 6] was found to be 25 U/ml with sensitivity of 93.8% and specificity of 82.4%. Combined elevation of CA 19-9 and CA 125 above the cut-off value showed less sensitivity [87.5%] than that of each of CA 19-9 [93.8%] and CA 125 [93.8%], and a better specificity [88.24%] than that of CA 19-9 [88.2%] and CA 125 [82.4%]. Serum CA 19-9 and CA 125 may be used as noninvasive markers of severe hepatitis C virus-related liver fibrosis. This needs to be validated by more studies

Relationship between insulin resistance, liver fibrosis and steatosis in non-diabetic non-obese chronic hepatitis C patients

Relationship between HCV and DM was documented in several studies. HCV through pro-inflammatory cytokines causes insulin resistance. Steatosis in HCV is a well known pathological feature. Interest in the last decade was turned into the possible link between insulin resistance and Steatosis and their effect on fibrosis progression was to study relationships between fibrosis, inflammation, Steatosis and insulin resistance in HCV patients. This study was conducted on 80 patients with HCV and 20 healthy controls. Participants were subjected to clinical examination, laboratory investigations [liver and kidney function tests, hepatitis markers, fasting glucose, insulin, and serum lipids], HOMA score estimation, BMI calculation and abdominal ultrasonography. Patients underwent liver biopsy and qualitative PCR for HCV RNA. showed higher HOMA score and fasting insulin levels in HCV patients than controls. A strong positive correlation was found between insulin resistance, fasting insulin levels and liver fibrosis in HCV patients. No correlation was found between insulin resistance and neither BMI nor age of patients. Prevalence of Steatosis in HCV patients biopsies was 93.75%. Significant correlation was found between fibrosis and Steatosis, and between insulin resistance and Steatosis. detection and treatment of insulin resistance in chronic hepatitis C patients are recommended to improve outcome of patients and decrease rate of progression of fibrosis

Portal hypertensive gastropathy; the role of helicobacter pylori infection

This study was conducted on 60 patients, 54 men and 6 women, aged 30 to 65 years [mean 42.1] with chronic liver disease and portal hypertension as evidenced by the presence of esophageal varices. In addition, 20 patients, 15 men and 5 women, aged 25 to 68 years [mean 39.3] having non-ulcer dyspepsia and no evidence of chronic liver disease were admitted as a controls. All patients were subjected to full clinical assessment, liver function tests, abdominal ultrasonographic examination, and upper gastrointestinal endoscopy. All patient's group had endoscopic evidences of portal gastropathy. Multiple antral biopsies were taken from all patients and controls and sujected for hisopathological examination to assess the presence of portal gastropathy, the degree of H.pylori colonization, the presence and the degree of inflammatory gastritis. The results showed high prevalence of H.pylori in both patients and controls. However, the grade of colonization was significantly higher in patient's group. The majority of patients [95%] showed histological manifestations of both portal gastropathy and inflammatory gastritis. On the other hand, 65% of the controls had no gastritis, and all showed no evidence of portal gastropathy. The severity of gastritis and gastric erosions was significantly correlated to the degree of H.pylori colonization. The latter was not correlated to the presence of variceal bleeding nor to occerrence of encephalopathy. It was concluded that, gastric mucosa of patients with portal hypertension is not inhospitable for H.pylori and in contrast H.pylori infection is more likely to be associated with more colonization and gastric mucosal lesions