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Treatment of hepatitis C virus has been vastly transformed by the arrival of all-oral, interferon-free, direct-acting antiviral regimens. Despite the high rate of success with these agents, a small portion of treated patients fail therapy and the emergence of viral resistance is the most common cause of treatment failure. Given the error-prone hepatitis C virus polymerase, baseline resistance-associated substitutions (RASs) may be present before direct-acting antiviral exposure. Clinicians need to understand the role of baseline RAS testing and the settings and manner in which the treatment regimens need to be customized based on the presence of RASs.

Introduction Liver transplantation (LT) remains the gold standard for treatment of end-stage liver disease. Given the increasing number of liver transplantation in females of reproductive age, our aim was to conduct a systematic review and meta-analysis evaluating pregnancy outcomes after LT. Methods MEDLINE, Embase, and Scopus databases were searched for relevant studies. Study selection, quality assessment, and data extraction were conducted independently by 2 reviewers. Estimates of pregnancy-related outcomes in LT recipients were generated and pooled across studies using the random-effects model. Results A comprehensive search identified 1,430 potential studies. Thirty-eight studies with 1,131 pregnancies among 838 LT recipients were included in the analysis. Mean maternal age at pregnancy was 27.8 years, with a mean interval from LT to pregnancy of 59.7 months. The live birth rate was 80.4%, with a mean gestational age of 36.5 weeks. The rate of miscarriages (16.7%) was similar to the general population (10%-20%). The rates of preterm birth, preeclampsia, and cesarean delivery (32.1%, 12.5%, and 42.2%, respectively) among LT recipients were all higher than the rates for the general US population (9.9%, 4%, and 32%, respectively). Most analyses were associated with substantial heterogeneity. Discussion Pregnancy outcomes after LT are favorable, but the risk of maternal and fetal complications is increased. Large studies along with consistent reporting to national registries are necessary for appropriate patient counseling and to guide clinical management of LT recipients during pregnancy.

Hepatitis B virus (HBV) is the most common cause of chronic hepatitis and end-stage liver disease worldwide. Untreated, chronic hepatitis B acquired early in life results in cirrhosis, liver failure, or hepatocellular carcinoma in up to 40% of individuals. Until recently, the options for a patient who had end-stage hepatitis B cirrhosis were severely limited, but during the past 15 years great strides have been made in prevention and treatment of hepatitis B cirrhosis. This article reviews recent advances in the understanding of the natural history, prevention, and medical management of HBV-related end-stage liver disease.

Background/ Aims: Portal vein thrombosis (PVT) in patients with liver cirrhosis is usually associated with hepatocellualar carcinoma. The pathogenesis of non-malignant PVT in cirrhotics has not been specifically studied and risk factors of PVT in this group of patients are still poorly understood. The aim of this study was to ascertain the prevalence and the significance of hyperhomocyteinemia among other risk factors in the development of PVT in cirrhotic patients. Patients and methods: Fifty two subjects were included in this study. Forty two cirrhotic patients; among them 21 had PVT and 21 had liver cirrhosis without PVT. Ten healthy subjects were included as controls. Plasma levels of homocysteine, antithrombin III, protein C and protein S were measured. Factor V Leiden was determined and methylenetetrahydrofolate reductase (MTHFR) C677T gene mutation was detected. Results: Our results revealed that plasma levels of protein C, protein S and antithrombin III were lower in cirrhotic patients with PVT than in those without PVT and controls. Plasma homocysteine level was higher among cirrhotics with PVT compared to those without PVT and controls. Factor V Leiden was detected only in 10% of controls and in 9.52% of cirrhotics with and without PVT whereas MTHFR gene mutation TT (homozygous) was detected in 23.81% of cirrhotics with PVT and not found in other groups. Conclusion: Heyperhomocyteinemia could be considered as a newly recognized risk factor for PVT in cirrhotic patients and should be routinely measured particularly when the etiology of PVT is unclear. These results could be clinically important due to the readily available therapy of folate, vitamin B6 and B12 supplementation that may reduce homocysteine and prevent further thrombotic complications.