Hepatitis B in situ is a consequential entity which can be missed in clinical practice. It is a new clinical pattern of chronic HBV infection that considers HBV in liver biopsy and adds a new indication for antiviral therapy.
Hepatic steatosis occurs when lipids accumulate in the liver leading to steatohepatitis, which can evolve into cirrhosis and consequently may end with hepatocellular carcinoma. Several automatic classification algorithms have been proposed to detect liver diseases. However, some algorithms are manufacturer-dependent, while others require extensive calculations and consequently prolonged computational time. This may limit the development of real-time and manufacturerindependent computer-aided detection of liver steatosis. This work demonstrates the feasibility of a computationally-efficient and manufacturer-independent wavelet-based computer-aided liver steatosis detection system using conventional B-mode ultrasound (US) imaging. Seven features were extracted from the approximation part of the second-level wavelet packet transform (WPT) of US images. The proposed technique was tested on two datasets of ex-vivo mice livers with and without gelatin embedding, in addition to a third dataset of in-vivo human livers acquired using two different US machines. Using the gelatin-embedded mice liver dataset, the technique exhibited 98.8% accuracy, 97.8% sensitivity, and 100% specificity, and the frame classification time was reduced from 0.4814 s using original US images to 0.1444 s after WPT preprocessing. When the other mice liver dataset was used, the technique showed 85.74% accuracy, 84.4% sensitivity, and 88.5% specificity, and the frame classification time was reduced from 0.5612s to 0.2903 s. Using
Background/Aims: Cholesterol biosynthesis suppresses the replication of HCV-1b replicons, thus influencing hepatitis C virus (HCV) natural history. This study aimed at comparing the efficacy and safety of fluvastatin (FLV) as an adjuvant therapy to the standard of care (SOC) therapy, i.e., pegylated interferon (PEG-IFN) and ribavirin, for the treatment of HCV patients. Materials and Methods: Sixty HCV patients were enrolled and allocated to either group I, who received the triple therapy (fluvastatin + SOC), or group II, who received SOC; the duration for both treatments was 48 weeks. All patients were subjected to pretreatment liver biopsy and monthly biochemical tests (liver profile, CBC), and quantitative HCV-RNA test was performed at weeks 0, 4, 12, 48, and 72. Results: All virological responses were higher in group I than in group II, with no statistical difference. Group I showed no manifestations of hepatotoxicity. Conclusion: Fluvastatin yielded a borderline, significantly higher complete early virological response than SOC; therefore, it is a safe adjuvant to the SOC therapy.
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