Thomas Jeffers

The changing landscape of hepatitis C virus therapy: focus on interferon-free treatment

Chronic hepatitis C (CHC) affects over 185 million individuals worldwide, approximately 3% of the world’s population. CHC can lead to quality of life impairment, cirrhosis, hepatocellular carcinoma (HCC), liver failure and liver-related death. While CHC has been associated with increases in HCC, liver-related mortality and all-cause mortality, being cured of CHC is associated with improvement in these outcomes. Older interferon-based regimens were complex and toxic and required 6–12 months of therapy, with cure rates averaging around 40–45% for HCV genotype 1. Newer interferon-free regimens are now available in the US, Europe, Japan and in other countries. These regimens have short durations, minimal side effects, low pill burden and efficacy approaching 90–100%. We may eventually see single-tablet regimens lasting no more than 4–6 weeks. This review will summarize the data regarding these interferon-free regimens, including Gilead’s Harvoni (sofosbuvir/ledipasvir), AbbVie’s Viekira Pak (paritaprevir/ritonavir/ombitasvir with dasabuvir), and Janssen’s Olysio (simeprevir) with sofosbuvir. Some practical considerations as we move into an interferon-free era will also be discussed, such as patient adherence and drug–drug interactions.

Independent Predictors of Mortality and Resource Utilization in Viral Hepatitis Related Hepatocellular Carcinoma

INTRODUCTION Hepatitis B (HBV) and C viruses (HCV) are important causes of hepatocellular carcinoma (HCC). Our aim was to assess mortality and resource utilization of patients with HCC-related to HBV and HCV. MATERIAL AND METHODS National Cancer Institutes Surveillance, Epidemiology and End Results (SEER)-Medicare linked database (2001-2009) was used. Medicare claims included patient demographic information, diagnoses, treatment, procedures, ICD-9 codes, service dates, payments, coverage status, survival data, carrier claims, and Medicare Provider Analysis and Review (MEDPAR) data. HCC related to HBV/HCV and non-cancer controls with HBV/HCV were included. Pairwise comparisons were made by t-tests and chisquare tests. Logistic regression models to estimate odds ratios (ORs) with 95% confidence intervals (CIs) were used. RESULTS We included 2,711 cases of HCC (518 HBV, 2,193 HCV-related) and 5,130 non-cancer controls (1,321 HBV, 3,809 HCV). Between 2001-2009, HCC cases related to HBV and HCV increased. Compared to controls, HBV and HCV patients with HCC were older, more likely to be male (73.2% vs 48.9% and 57.1% vs. 50.5%), die within one-year (49.3% vs. 20.3% and 52.2% vs. 19.2%), have decompensated cirrhosis (44.8% vs. 6.9% and 53.9% vs. 10.4%) and have higher inpatient (

139 CD45−CD34+ Circulating Progenitor Cells Levels Are Associated With the Presence of Coronary Artery Disease (CAD) in Patients With Nonalcoholic Fatty Liver Disease (NAFLD)

60.471 vs.

Tu2019 Role of Vitamin D in the Inflammatory Response of Morbidly Obese Patients With Non-Alcoholic Fatty Liver Disease (NAFLD)

47.223 and

Resource Utilization and Outcomes of Medicare Recipients With Chronic Hepatitis B in the United States

56.033 vs.

Tu1516 - Are Biomarkers for Cardiovascular Disease Increased in Patients with Nonalcoholic Fatty Liver Disease (NAFLD)?

41.005) and outpatient charges (

248 - Non-Targeted Metabolomics Profile can Differentiate Nonalcoholic Fatty Liver Disease (NAFLD) Patients with Coronary Artery Disease (CAD)

3,840 vs.

230 - Hepatokines, Metalloproteases and their Tissue Inhibitors Provide Predictive Assessment for Liver Fibrosis in Nonalcoholic Fatty Liver Disease

3,328 and

An exploratory study examining how nano-liquid chromatography–mass spectrometry and phosphoproteomics can differentiate patients with advanced fibrosis and higher percentage collagen in non-alcoholic fatty liver disease

3,251 vs.

Lower Levels of Hepatokines Angiopoietin-Like 4 and RBP-4 are Independently Associated with Non-Alcoholic Steatohepatitis (NASH)

2,096) (all P < 0.05). In two separate multivariate analyses, independent predictors of one-year mortality were older age, being male and the presence of decompensated cirrhosis. CONCLUSIONS The rate of viral hepatitis-related HCC is increasing. Mortality and resource utilization related to HBV and HCV-related HCC is substantial.INTRODUCTION Hepatitis B (HBV) and C viruses (HCV) are important causes of hepatocellular carcinoma (HCC). Our aim was to assess mortality and resource utilization of patients with HCC-related to HBV and HCV. MATERIAL AND METHODS National Cancer Institutes Surveillance, Epidemiology and End Results (SEER)-Medicare linked database (2001-2009) was used. Medicare claims included patient demographic information, diagnoses, treatment, procedures, ICD-9 codes, service dates, payments, coverage status, survival data, carrier claims, and Medicare Provider Analysis and Review (MEDPAR) data. HCC related to HBV/HCV and non-cancer controls with HBV/HCV were included. Pair-wise comparisons were made by t-tests and chi-square tests. Logistic regression models to estimate odds ratios (ORs) with 95% confidence intervals (CIs) were used. RESULTS We included 2,711 cases of HCC (518 HBV, 2,193 HCV-related) and 5,130 non-cancer controls (1,321 HBV, 3,809 HCV). Between 2001-2009, HCC cases related to HBV and HCV increased. Compared to controls, HBV and HCV patients with HCC were older, more likely to be male (73.2% vs 48.9% and 57.1% vs. 50.5%), die within one-year (49.3% vs. 20.3% and 52.2% vs. 19.2%), have decompensated cirrhosis (44.8% vs. 6.9% and 53.9% vs. 10.4%) and have higher inpatient (