Diabetic patients with chronic hepatitis C virus response compared to non diabetics when treated with directly acting antiviral therapy.

BACKGROUND AND STUDY AIMS: Hepatitis C virus (HCV) impairs glucose homoestasis, thus influences its clinical picture and prognosis. This study aimed at evaluating Diabetes mellitus (DM) on Egyptian patients with chronic hepatitis C (CHC), and its impact on their virologic response when treated with directly acting antiviral (DAA) medications. PATIENTS AND METHODS: Adult patients with CHC were divided into 2 groups; Diabetic patients, and Non diabetic patients serving as control group. All patients were subjected to thorough clinical evaluation, basic biochemical laboratory tests including fasting blood glucose/glycosylated haemoglobin (HbA1C), and virologic assay. They were treated with various combined DAAs, and were monitored during, at and after end of treatment. RESULTS: Diabetic patients constituted 9.85 % of CHC, and had generally worse laboratory tests (significantly higher transaminases, platelet count, Fib4 and hepatic steatosis) than non diabetic patients, and a less sustained virologic response (SVR) (significantly in Sofosbuvir (SOF) + pegylated interferon (PegIFN) + ribavirin (RBV), SOF + RBV, SOF + daclatasvir (DAC)). Although DM did not play a significant influence on SVR, yet Fib4 and SOF + RBV + PEG-IFN were significant factors affecting SVR among diabetics, while female gender and viraemia were significant factors affecting SVR among non diabetics. Hepatic fibrosis and SOF/RBV significantly influenced SVR in both groups. CONCLUSIONS: Diabetic patients with CHC have worse liver biochemical profile, yet DM per se did not influence the virologic response to DAAs, however, some factors played roles in affecting SVR among them.

Wavelet-based Computationally-Efficient Computer-Aided Characterization of Liver Steatosis using Conventional B-mode Ultrasound Images.

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 manufacturer-independent 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 human liver image data, the best classifier exhibited 92.5% accuracy, 93.0% sensitivity, 91.0% specificity, and the classification time was reduced from 0.660 s to 0.146 s. This technique can be useful for developing computationally-efficient and manufacturer-independent noninvasive CAD systems for fatty liver detection.

Evaluation of fluvastatin in combination with the standard of care therapy (PEG-IFN/Ribavirin) in Egyptian patients with hepatitis C virus.

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.

Plasma proteosome level as a potential marker for hepatocellular carcinoma.

BACKGROUND AND STUDY AIMS: Hepatocellular carcinoma (HCC) is a fatal malignancy. Effective curative surgery is achieved when HCC is detected earlier. Proteosomes, the main non-lysosomal proteolytic structures organising the cellular mechanisms of cleaving proteins, can be considered a tumour marker in many kinds of malignancies. The aim of this study was to assess the plasma proteosome level in HCC and cirrhosis and, accordingly, evaluate its potential diagnostic ability in the detection of HCC in cirrhosis. PATIENTS AND METHODS: This study included 60 patients, divided into two groups: the HCC group and the liver cirrhosis group. Twenty normal subjects served as a control group. Serum levels of proteosome and alpha-foetoprotein (AFP) were measured using the enzyme-linked immunosorbent assay (ELISA) technique. RESULTS: Plasma proteosome levels were significantly higher in patients with HCC and in patients with cirrhosis without HCC when compared to controls individually (p>0.002 and p>0.001, respectively) but did not reach a significant differentiating level between them (area under curve (AUC)=0.641, p=0.061). Moreover, the plasma proteosome level was not correlated with the severity of HCC by the Milan criteria or with AFP level. In addition, it was not significantly related to laboratory or Child-Pugh scoring. Moreover, the combined use of plasma proteosome level and AFP measurements for the diagnosis of HCC was not effective. CONCLUSIONS: In this study, the plasma proteosome level was comparably recorded in both patients with cirrhosis and patients with HCC (mean value±standard deviation were 5.796±1.46 and 7.176±2.48µgml(-1), respectively), not reaching a significant differentiating level between them, although predictability of HCC using the plasma proteosome level was significant (p=0.017).