ABSTRACT: This study was undertaken to evaluate an image processing method for assessing liver fibrosis in conventional computed tomography (CT) scans in patients with chronic hepatitis C. Two cohorts (designated "estimation," n = 34; and "validation," n = 107) of chronic hepatitis C patients were assessed using digitized conventional helical CT. Weighted CT mean fibrosis (Fibro-CT) was calculated as a nonlinear weighted mean F-score for each sample. Fibrosis was defined according to Scheuer on the F0 to F4 scale by 2 pathologists blinded regarding the Fibro-CT data. Fibrosis according to Fibro-CT correlated with histology-determined fibrosis (r = 0.69; P < 0.001) and with increasing F-stage: F0 = 0.23 +/- 0.39; F1 = 0.90 +/- 0.99; F2 = 1.41 +/- 0.94; F3 = 2.79 +/- 0.55; F4 = 3.15 +/- 0.35 [analysis of variance: P < 0.0001). The receiver operating characteristics curve to diagnose significant fibrosis (>/=F2) was 0.83; 95% confidence interval (95%CI), 0.75 to 0.91; and, to diagnose advanced fibrosis (>/=F3), was 0.86, 95%CI: 0.80 to 0.93. The correlation between Fibro-CT and fibrosis was higher in patients with homogeneous distribution of fibrosis than in patients with heterogeneous distribution (r = 0.77 versus r = 0.43; P < 0.05). CONCLUSION: Optical digital analysis of CT images of the liver is effective in determining the stage and distribution of liver fibrosis in chronic hepatitis C. In patients with homogeneous fibrosis distribution, the correlation between Fibro-CT and histology was better than in patients with heterogeneous distribution. Fibro-CT is a simple to use, readily available, and useful method for the diagnosis of fibrosis in patients with chronic hepatitis C.
Hepatology 03/2008; 47(3):810-6. · 11.66 Impact Factor
ABSTRACT: To determine whether the different tumour necrosis factor alpha (TNF-alpha) promoter gene polymorphisms are involved in the development of steatosis in chronic hepatitis C.
One hundred and thirty patients (89 men and 41 women; mean age 42.5 +/- 12.3 years) with chronic hepatitis C were included. Insulin resistance was measured according to the Homeostasis model assessment (HOMA IR). Serum leptin levels were also obtained and the body mass index and fat mass were calculated. Liver biopsy was carried out in all the patients, and steatosis was measured as one of four stages (0 to 3): stage 0, no steatosis; stage 1, < 25% of hepatocytes with steatosis; stage 2, 25-50%; and stage 3, > 50%. DNA samples were obtained in order to describe the polymorphisms at the TNF-alpha promoter gene position.
Fifty-nine of the 130 (45.38%) patients had different degrees of steatosis, while 71/130 (54.62%) were not steatosic. Six of the 59 (10.2%) patients with steatosis presented mutations at the -238 position of the TNF-alpha promoter region, while 5/71 (7.0%) patients without steatosis also showed mutations at this position (P=NS). Seventeen of the 59 (28.8%) steatosic patients showed a mutation at the -308 position, while 16/71 (22.5%) without steatosis also had this mutation (P=NS). Insulin resistance, beta cells reserve, insulin and leptin levels showed no differences between patients with or without mutations at the promoter region of the TNF-alpha gene.
TNF-alpha mutations do not seem to play any role in the development of steatosis in chronic hepatitis C.
European Journal of Gastroenterology & Hepatology 08/2004; 16(8):761-5. · 1.76 Impact Factor
ABSTRACT: Hepatic steatosis (HS) has been related to obesity and fibrosis in chronic hepatitis C (CHC). The aim of this study was to determine the role of leptin system in HS development.
Patients (n = 131) with biopsy-proven CHC, positive HCV RNA, and raised ALT were enrolled. Body mass index, percentage of body fat by skin fold measurement, and bioelectrical impedance analysis was calculated and serum leptin concentration measured. Intrahepatic HCV RNA, HS, necroinflammatory activity, and fibrosis were determined in liver biopsy tissue.
HS was present in 63 patients (48.1%). Steatosis was evident in 32 of 91 patients (35.2%) infected with genotype 1 and in 22 of 27 patients (81.5%) with genotype 3a (p < 0.001). In patients infected by genotype 3a, HS correlated significantly with intrahepatic HCV RNA load (r = 0.78; p < 0.001). However, in genotype 1, HS was associated with host factors such as leptin, body mass index, percentage of body fat, and visceral obesity. Multivariate analysis showed genotype (OR = 11.54, 95% CI = 1.13-117.14, p = 0.038), leptin levels (OR = 1.09, 95% CI = 1.03-1.17, p = 0.008) and fibrosis (OR = 9.86, 95% CI = 2.11-5.86, p = 0.03) as independent variables of HS development.
Hepatic steatosis was related to genotype, fibrosis degree, and serum leptin levels. Genotype 3 seems to have a viral specific steatogenic effect. Leptin seems to be a link between obesity and steatosis development in CHC genotype 1-infected patients.
The American Journal of Gastroenterology 05/2003; 98(5):1135-41. · 7.28 Impact Factor