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Seminars in Liver Disease



ISSN: 0272-8087 (1098-8971)
Gastroenterology & Hepatology - Hepatology
Full APC costs for WUR authors (no discount)

Recent articles

1 show abstract
ATP-binding cassette subfamily B member 4 (ABCB4) is a phospholipid translocator at the canalicular membrane of the hepatocyte, which “flops” phosphatidylcholine into bile. Dysfunction of this transporter due to ABCB4 gene variants can cause liver diseases and has been called ABCB4 deficiency. Several diseases including progressive familial intrahepatic cholestasis type 3 (PFIC3), low phospholipid-associated cholelithiasis (LPAC), a subgroup of patients developing intrahepatic cholestasis of pregnancy (ICP), drug-induced liver injury and chronic cholangiopathy with biliary fibrosis and cirrhosis were attributed to ABCB4 deficiency and characterized in the past decade. LPAC and ICP are usually caused by monoallelic variants, whereas patients affected by PFIC3 are homozygous or compound heterozygous carriers of ABCB4 variants. Treatment with ursodeoxycholic acid is often effective, but as the more severe forms of ABCB4 deficiency progress, nevertheless, new diagnostic and therapeutic approaches are warranted. Current functional classifications for ABCB4 deficiency–associated mutations can guide the development of novel genotype–based targeted pharmacotherapies for these conditions. Recently, increasing evidence from genome-wide association studies is emerging on associations of ABCB4 variants with hepatobiliary malignancies.
2 show abstract
Autophagy actively participates in the physiological process of the liver. While the direct effect of autophagy may be limited to the sequestration and degradation of a selective cargo, its overall impact can be broad, affecting many more physiological processes regulated by the particular cargo. This review will discuss two aspects of the importance of autophagy in the liver: metabolic regulation in response to feeding and starvation, and pathological consequences in the absence of autophagy. These two aspects illustrate the homeostatic functions of autophagy in the liver, one in a more direct fashion, regulating the cellular nutrient supply, and the other in a more indirect fashion, controlling the pathological signaling triggered by the abnormal accumulation of cargos. Remarkably, the hepatic pathology in autophagy-deficient livers does not seem different from that presented in other chronic liver diseases. Autophagy deficiency can be a model for the study of the relevant molecular mechanisms.
3 show abstract
Activation of the hepatic unfolded protein response (UPR), a highly conserved cellular response to endoplasmic reticulum (ER) stress, is a firmly established feature of nonalcoholic fatty liver disease (NAFLD). ER stress is now widely accepted as both a cause and a consequence of hepatic steatosis. Moreover, the accumulation of hepatic lipids induces ER stress, which, in turn, disrupts hepatic lipid metabolism thus creating a vicious cycle that potentiates hepatic lipid accumulation. Additionally, there is interplay between the UPR and the inflammatory cascades associated with progressive nonalcoholic steatohepatitis. Understanding the molecular mechanisms by which the UPR regulates hepatic lipid metabolism and lipotoxic liver injury may lead to the identification of novel therapeutic targets for the treatment of NAFLD.
4 show abstract
TGR5 (GPBAR1) is a G protein–coupled receptor activated by primary and secondary bile acids, which is expressed in different nonparenchymal cells of the liver, such as sinusoidal endothelial cells, Kupffer cells, cholangiocytes as well as activated hepatic stellate cells. In liver, TGR5 modulates microcirculation, inflammation, regeneration, biliary secretion and proliferation as well as gallbladder filling. Absence of TGR5 renders mice more susceptible toward infectious, inflammatory, metabolic as well as cholestatic liver injuries. It is unknown whether TGR5 plays a role in the pathogenesis of human nonalcoholic steatohepatitis and cholestatic liver diseases such as primary sclerosing cholangitis and primary biliary cholangitis. However, overexpression of TGR5 has been detected in human intra- and extrahepatic cholangiocarcinoma as well as in cystic cholangiocytes, where the receptor promotes cell proliferation, anti-apoptosis as well as cyst growth. While TGR5 agonists may improve various aspects of metabolic, inflammatory, and cholestatic liver diseases, TGR5 inhibitors may attenuate disease progression in polycystic liver disease and cholangiocarcinoma.
5 show abstract
Macrophages are innate immune cells with diverse functions including clearing infectious agents, inducing inflammation and fibrosis, resolving fibrosis, and restoring tissue integrity. Liver macrophages consist of both resident Kupffer cells and infiltrating macrophages. They have heterogeneous highly plastic phenotypes, and they change their phenotypes rapidly in response to a diverse array of signals present in the injured or recovering liver. Cell death by apoptosis, necroptosis, or pyroptosis is a common response of liver macrophages to infectious and toxic insults. At the same time, the uptake of apoptotic and other dead cells, efferocytosis, is mediated by a series of dead cell receptors including MerTK, TIM4, and Stablin-1. These generate a critical signal that determines macrophage phenotype evolution. This review discusses the processes that lead to macrophage apoptosis and efferocytosis, and how these alter the course of liver diseases.
6 show abstract
Neuroendocrine tumors are slow-growing tumors and associated with prolonged overall survival even in the presence of untreated liver metastases. The presence of liver metastases may be responsible for severe symptoms with impairment of quality of life. Liver resection has been proposed to achieve better symptom control and/or improve overall survival, but this concerns less than 20% of patients with liver metastases. In addition, the chance to be really cured after liver resection is around 40%, which prompts consideration of liver transplantation as the only potential curative treatment. Time has come to move beyond the traditional debate around the best candidates and prognostic factors for liver transplantation. This review gives the opportunity to discuss new insights: (1) outcome of liver transplantation for neuroendocrine liver metastases as compared with hepatocellular carcinoma, (2) outcome of salvage liver transplantation as a secondary procedure after surgical resection of neuroendocrine liver metastases, (3) outcome of palliative liver transplantation for neuroendocrine liver metastases, and (4) the chance to be cured after liver transplantation for neuroendocrine liver metastases.
7 show abstract
Exertional heat stroke most commonly develops following prolonged levels of aerobic activity in a warm or humid environment. Hypoperfusion of the vital organs along with activation of the inflammasome can lead to progressive and potentially fatal multiorgan failure including acute liver failure. In the United States, herbal and dietary supplements that are marketed to improve performance, strength, and weight loss are increasingly being used by both amateur and professional athletes. Consumption of bodybuilding supplements that contain androgenic anabolic steroids can lead to adverse hepatic effects ranging from asymptomatic serum aminotransferase elevations to severe cholestatic hepatitis with prolonged jaundice. Various non-bodybuilding nutritional supplements that contain a mixture of botanicals, caffeine, and chemicals have also been associated with idiosyncratic hepatotoxicity. In particular, green tea extract derivatives that contain epigallocatechin gallate are hepatotoxic in animal models and have been associated with severe acute hepatocellular injury in humans.
8 show abstract
Immune checkpoint inhibition targeted against cytotoxic T-lymphocyte–associated antigen 4 (CTLA-4) and programmed cell death protein 1 (PD-1) has shown clinically significant survival benefit when used to treat multiple types of advanced cancer. These drugs have gained approval by the US Food and Drug Administration and their indications continue to increase. Checkpoint inhibitor therapy is associated with a unique side-effect profile characterized as immune-related adverse events (irAEs), which can result in significant morbidity and rarely mortality. Hepatotoxicity from checkpoint inhibitors is a less common irAE and often mild, while its incidence and severity vary based on the class and dose of checkpoint inhibitor, monotherapy versus combination therapy, and the type of cancer. Histological assessment of suspected irAEs is nonspecific and can show a variety of features. Hepatic irAEs can require discontinuation of checkpoint inhibitor therapy and treatment with immunosuppressive agents.
9 show abstract
Multikinase inhibitors with antiangiogenic properties used to be standard therapy for patients with advanced hepatocellular carcinoma (HCC). Recently, several antiangiogenic agents (lenvatinib, cabozantinib, and ramucirumab) have demonstrated antitumor activity for advanced HCC in randomized controlled trials. However, the landscape of drug development for HCC may change dramatically with the advent of immune checkpoint inhibitor therapy, particularly the anti–programmed cell death-1 (anti-PD1) agents. In addition, early-phase clinical trials of combination of anti–PD-1 and antiangiogenic agents have shown very promising anti-tumor activity in patients with advanced HCC. Therefore, the critical research questions at present are whether this combination strategy will be the next generation of standard therapy and which antiangiogenic agents will be the optimal partner for the combination. All of the 4 multikinase inhibitors for HCC (sorafenib, regorafenib, lenvatinib, and cabozantinib) have been reported to have immune modulatory effects. The authors systematically reviewed the pre-clinical evidence of their immune modulatory effects to explore whether these effects were mediated by angiogenesis inhibition or by other “off-target” effects on the tumor microenvironment. Studies of sorafenib comprised the majority (58 of the 71) of the research articles reviewed. Potentially beneficial effects on anti-tumor immunity may result from increased M1 polarization of macrophages and stimulation of CD8 T cell function. On the other hand, high dosage of the kinase inhibitors in pre-clinical models and hypoxia associated with angiogenesis may contribute to immune suppression in the tumor microenvironment. Sorafenib and other multikinase inhibitors may promote anti-tumor immunity through modulation of multiple immune cell types as well as the tumor microenvironment. The optimal immune modulatory dosage should be defined to facilitate design of future combination regimens.
10 show abstract
Acetaminophen (APAP) is one of the most popular and safe pain medications worldwide. However, due to its wide availability, it is frequently implicated in intentional or unintentional overdoses where it can cause severe liver injury and even acute liver failure (ALF). In fact, APAP toxicity is responsible for 46% of all ALF cases in the United States. Early mechanistic studies in mice demonstrated the formation of a reactive metabolite, which is responsible for hepatic glutathione depletion and initiation of the toxicity. This insight led to the rapid introduction of N-acetylcysteine as a clinical antidote. However, more recently, substantial progress was made in further elucidating the detailed mechanisms of APAP-induced cell death. Mitochondrial protein adducts trigger a mitochondrial oxidant stress, which requires amplification through a MAPK cascade that ultimately results in activation of c-jun N-terminal kinase (JNK) in the cytosol and translocation of phospho-JNK to the mitochondria. The enhanced oxidant stress is responsible for the membrane permeability transition pore opening and the membrane potential breakdown. The ensuing matrix swelling causes the release of intermembrane proteins such as endonuclease G, which translocate to the nucleus and induce DNA fragmentation. These pathophysiological signaling mechanisms can be additionally modulated by removing damaged mitochondria by autophagy and replacing them by mitochondrial biogenesis. Importantly, most of the mechanisms have been confirmed in human hepatocytes and indirectly through biomarkers in plasma of APAP overdose patients. The extensive necrosis caused by APAP overdose leads to a sterile inflammatory response. Although recruitment of inflammatory cells is necessary for removal of cell debris in preparation for regeneration, these cells have the potential to aggravate the injury. This review touches on the newest insight into the intracellular mechanisms of APAP-induced cells death and the resulting inflammatory response. Furthermore, it discusses the translation of these findings to humans and the emergence of new therapeutic interventions.
11 show abstract
Pruritus is a frustrating and sometimes debilitating symptom that commonly accompanies primary biliary cholangitis (PBC). The mechanism by which this symptom manifests remains elusive but extensive research has now shown that the itch is not just “weak pain” as had been the commonly held belief for decades. As this research now shines a light on the many diverse paths by which pruritus might be experienced, the necessity for a comprehensive approach to the symptom becomes clear. Understanding the interplay between the pathophysiology of PBC and delicately balanced neural circuitry is paramount to guiding the search for definitive treatment. Most relevant to providers today is the efficacy of currently available treatments and the side effects that may accompany them. Anion exchange resins, while remaining an important element in therapy, are no longer the only available medication to arrest pruritus. Rifampin, opioid antagonists, and other adjunctive therapies have quickly become a mainstay. Newer therapies such as the molecular adsorbent recycling system now also have a role in treatment. Increased recognition of these modalities may serve to alleviate the often debilitating pruritus experienced by patient suffering from PBC and might ultimately allow them to live more meaningful lives.
12 show abstract
Reliable biomarkers are of great clinical value in predicting cancer occurrence/recurrence, anticipating its detection at an asymptomatic stage, supporting the radiological diagnosis, stratifying patients for prognosis and proper therapy, and measuring the response to treatment. Despite the plethora of biomarkers proposed for hepatocellular carcinoma (HCC), the first one identified, α-fetoprotein (AFP), remains the most utilized. This article reviews the lights and shadows of AFP as a surveillance test for patients at risk of HCC, and as a diagnostic test for those with chronic liver disease and a suspected hepatic mass. Moreover, the article scrutinizes the large body of evidence supporting the prognostic relevance of AFP in patients undergoing both curative and palliative treatment of HCC and the growing importance attributed to this biomarker (as a static or a dynamic variable) in the selection of potential candidates for liver transplantation. In fact, the inclusion of AFP among transplant criteria would improve the ability of identifying poor candidates due to an unacceptable risk of HCC recurrence regardless of tumor burden, and of adopting flexible morphological selection criteria.
13 show abstract
Prediction of future hepatocellular carcinoma (HCC) risk in the sizable chronic liver disease population is an urgent unmet need to enable regular HCC screening for early detection. Germline deoxyribonucleic acid polymorphisms likely represent etiology-specific host factors that determine HCC susceptibility, including single nucleotide polymorphisms in EGF, IFNL3, MICA, and TLL1 in hepatitis C with or without active viral infection, and PNPLA3, TM6SF2, and MBOAT7 in metabolic liver diseases. Transcriptome-based prognostic liver signature in diseased liver tissue has been associated with long-term HCC risk in viral and metabolic etiologies. Transcriptomic signatures of hepatic injury and specific cell type such as aggregated lymphocytes also predict HCC development. Circulating factors such as proteins and their chemical modification, nucleotides, and metabolites may serve for less-invasive assessment of short- or long-term HCC risk. These biomarkers will enable individual HCC risk-based personalized clinical management for cost-effective early HCC detection and improvement of patient survival.
14 show abstract
Hepatocellular carcinoma (HCC) is a devastating and prevalent cancer with limited treatment options. Technological advances have enabled genetic screens to be employed in HCC model systems to characterize genes regulating tumor initiation and growth. Relative to traditional methods for studying cancer biology, such as candidate gene approaches or expression analysis, genetic screens have several advantages: they are unbiased, with no a priori selection; can directly annotate gene function; and can uncover gene–gene interactions. In HCC, three main types of screens have been conducted and are reviewed here: (1) transposon-based mutagenesis screens, (2) knockdown screens using RNA interference (RNAi) or the CRISPR/Cas9 system, and (3) overexpression screens using CRISPR activation (CRISPRa) or cDNAs. These methods will be valuable in future genetic screens to delineate the mechanisms underlying drug resistance and to identify new treatments for HCC.
15 show abstract
Statins, or 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, are widely used to treat hypercholesterolemia for primary and secondary prevention of cardiovascular disease. Statins inhibit HMG-CoA reductase, the rate-limiting step in cholesterol synthesis, and modulate the downstream signaling of the mevalonate pathway. In addition to the primary effect, the antitumor effect of statins can be associated with mevalonate pathway-mediated and nonmevalonate pathway-mediated mechanisms, which improve endothelial function and lead to proapoptotic, antiproliferative, antiinflammatory, and antifibrotic properties. Statins are implicated in the improvement of metabolic status. Statins are orally available and safely and widely used for long-term treatment; they represent a novel approach for the prevention and treatment for hepatocellular carcinoma (HCC). Although several observational studies and experimental studies have revealed the preventive and therapeutic potential of statins for HCC treatment, further prospective interventional studies and randomized control trials are warranted to confirm these observations.
16 show abstract
Endoplasmic reticulum (ER) stress is a major contributor to liver disease and hepatic fibrosis, but the role it plays varies depending on the cause and progression of the disease. Furthermore, ER stress plays a distinct role in hepatocytes versus hepatic stellate cells (HSCs), which adds to the complexity of understanding ER stress and its downstream signaling through the unfolded protein response (UPR) in liver disease. Here, the authors focus on the current literature of ER stress in nonalcoholic and alcoholic fatty liver diseases, how ER stress impacts hepatocyte injury, and the role of ER stress in HSC activation and hepatic fibrosis. This review provides insight into the complex signaling and regulation of the UPR, parallels and distinctions between different liver diseases, and how ER stress may be targeted as an antisteatotic or antifibrotic therapy to limit the progression of liver disease.
17 show abstract
Immune dysregulation and accumulation of leukocytes is a hallmark of adult chronic liver diseases. Progressive hepatic inflammation can lead to fibrosis and cirrhosis with a high risk of liver failure or hepatocellular cancer (HCC). Recent advances have been made in the treatment of liver disease including the development of highly effective antiviral therapy for hepatitis C and the potential of immunotherapy for HCC. Despite this, the majority of other chronic liver diseases including alcoholic liver disease, fatty liver disease, and cholestatic diseases do not respond to conventional anti-inflammatory therapies. Recent studies defining the organ-specific properties that contribute to resident immune activation and immune cell recruitment from the circulation in these conditions have identified novel hepatic inflammatory pathways, which are now being targeted in clinical trials. Further understanding of how the immune microenvironment is regulated within the liver and how disease-specific mechanisms alter this process will hopefully lead to combination therapies to prevent aberrant inflammation and also promote fibrosis resolution. In this review, we focus on the advances that have been made in identifying key components of the inflammatory pathway including the recognition of danger signals, the recruitment and retention of lymphocytes from the circulation, and the pathways that promote resolution.
18 show abstract
Failure to control variceal bleeding with current recommendations occurs in 10 to 20% of cases. This systematic review and meta-analysis analyzes the experience, results, and complications of “bridge” therapies for failure to control acute variceal bleeding: balloon tamponade and esophageal stents. The main outcomes assessed were failure to control bleeding and mortality in the short-term and medium-term follow-up, and adverse events. Balloon tamponade studies had a pooled rate of short-term failure to control bleeding of 35.5%, and adverse events in over 20% of cases; 9.7% resulting in death. Stenting failed to control bleeding in the short term and medium term in 12.7 and 21.5% of cases of severe or refractory variceal bleeding, respectively, despite stent migration in 23.8% of cases. Medium-term mortality rates were similar in both therapies. Although only one trial compared these treatments, the available evidence consistently supports that stents serve as a better and safer bridge therapy in refractory acute variceal bleeding.
19 show abstract
Here, the authors review the remarkable genetic discoveries that have illuminated the biology of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). The authors integrate genes associated with NAFLD and NASH into regulatory pathways to elucidate the disease pathogenesis. They review the evidence for molecular mediators of chronic liver damage, which suggests that convergent pathophenotypes, including inflammation and fibrosis, share common genetic modifiers. They further demonstrate that genes involved in the genetic susceptibility of NAFLD and NASH participate in cross-phenotype associations with diseases of the metabolic syndrome, including type 2 diabetes, obesity, and cardiovascular disease. However, immune-related loci associated with NAFLD and NASH exhibit some level of pleiotropy influencing disparate phenotypes, such as premature birth or sepsis. They finally focus on the translation of current genetic knowledge of NAFLD and NASH toward precision medicine. They provide evidence of genetic findings that can be leveraged to identify therapeutic targets.
20 show abstract
Occult hepatitis B infection (OBI) is a status of undetectable serum hepatitis B surface antigen (HBsAg) yet detectable serum and/or intrahepatic hepatitis B virus (HBV) DNA. Mutations in the preS1, preS2, and S regions of the HBsAg gene may result in undetectable HBsAg. OBI may either result from a self-limiting acute hepatitis, or in patients with chronic hepatitis B who achieved HBsAg seroclearance, which refers to the loss of detectability of serum HBsAg with or without antibody to HBsAg (anti-HBs) in chronic hepatitis B (CHB) patients. HBsAg seroclearance contributes to a significant proportion of population in seropositive OBI. Both spontaneous and antiviral treatment-induced HBsAg seroclearance rarely happens; yet both types of HBsAg seroclearance are durable. CHB patients who achieve HBsAg seroclearance generally have a favorable clinical course. There is still a low yet definite risk of HCC occurrence, particularly in male CHB patients who achieve HBsAg seroclearance after being 50 years old. Clinical implications of OBI include occurrence of cirrhosis and HCC, liver transplantation, blood products transfusion, hemodialysis, and so on. A potentially life-threatening condition would be OBI reactivation in patients during immunosuppression therapy, especially in the setting of intensified immunosuppression including in onco-hematological patients (those receiving hematopoietic stem cell transplantation and treated with the anti-CD20 monoclonal antibody [e.g., rituximab]). With more new insights into these two conditions, CHB patients who achieved HBsAg seroclearance generally have benign clinical course and good prognosis. Sensitive assay for serum HBV DNA should be considered to establish the presence of OBI in the clinical settings mentioned earlier, which will affect the management plan.
21 show abstract
Direct-acting oral anticoagulants (DOACs) have provided benefit in patients requiring anticoagulation for certain diseases by decreasing the burden of subcutaneous injections and the requirement for frequent monitoring through regular blood tests, to ensure adequacy of the therapeutic doses. Studies have demonstrated DOACs to be as safe, and in some instance safer, compared with traditional anticoagulants in the general population. However, the studies evaluating DOACs excluded patients with cirrhosis, a condition associated with an increased risk of developing portal vein thrombosis (PVT). Warfarin or low-molecular weight heparin are the standard-of-care treatment for acute PVT in cirrhosis, although there is enthusiasm in a paradigm shift switching to DOACs for the treatment of acute PVT in cirrhosis, particularly since the release of DOAC antidotes. This article reviews the current Food and Drug Administration-approved DOACs, hepatic metabolism of DOACs, pharmacokinetics of DOACs in patients with cirrhosis, safety of DOACs (including bleeding, hepatotoxicity, and pregnancy), current treatment guidelines for PVT in cirrhosis, and studies evaluating the use of DOACs in cirrhosis and for the treatment of PVT in cirrhosis. The potential use of DOACs for PVT primary prophylaxis in at-risk patients with cirrhosis and the possible antifibrotic effects of DOACs are also discussed.
22 show abstract
Authors: Patten ; Daniel A. ; Shepherd ; Emma L. ; Weston ; Christopher ; Shetty ; Shishir
Article URL: http://dx.doi.org/10.1055/s-0039-1688409
Citation: Semin Liver Dis ; : -
Publication Date: 2019-04-16T00:00:00+01:00
Journal: Seminars in Liver Disease

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Researchers from RUG, TU/e, UL, UM and UvA will receive a 25% discount on the Article Processing Charges that need to be paid by a first or corresponding author to publish open access in this journal.

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This deal is valid until 2019-12-31.

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Last updated: 2019-01-14


Journal Citation Reports (2017)

Impact factor: 4.167
Q1 (Gastroenterology & Hepatology (20/80))

Scopus Journal Metrics (2017)

SJR: 2.416
SNIP: 1.270
Impact (Scopus CiteScore): 0.446
Quartile: Q1
CiteScore percentile: 90%
CiteScore rank: 6 out of 58
Cited by WUR staff: 8 times. (2014-2016)

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