Hepatic Viral Infection Research Articles

Tristetraprolin Family Members and Processing Bodies: A Complex Regulatory Network Involved in Fatty Liver Disease, Viral Hepatitis and Hepatocellular Carcinoma

Chronic liver diseases, such as those encountered with obesity, chronic/abusive alcohol consumption or viral infections, represent not only major public health concerns with limited therapeutic options but also important risk factors for the onset of hepatocellular carcinoma (HCC). Deciphering the molecular traits underlying these disorders is of high interest for designing new and effective treatments. The tristetraprolin (TTP) family members are of particular importance given their ability to control the expression of a wide range of genes involved in metabolism, inflammation and carcinogenesis at the post-transcriptional level. This regulation can occur within small cytoplasmic granules, namely, processing bodies (P-bodies), where the mRNA degradation occurs. Increasing evidence indicates that TTP family members and P-bodies are involved in the development of chronic liver diseases and cancers. In this review, we discuss the role of this regulatory mechanism in metabolic-dysfunction-associated steatotic liver disease (MASLD), alcohol-related liver disease (ALD), hepatic viral infections and HCC.

Dynamic role of exosomal long non-coding RNA in liver diseases: pathogenesis and diagnostic aspects.

Liver disease has emerged as a significant health concern, characterized by high rates of morbidity and mortality. Circulating exosomes have garnered attention as important mediators of intercellular communication, harboring protein and stable mRNAs, microRNAs, and long non-coding RNAs (lncRNA). This review highlights the involvement of exosomal lncRNA in the pathogenesis and diagnosis of various liver diseases. Notably, exosomal lncRNAs exhibit therapeutic potential as targets for conditions including hepatic carcinoma, hepatic fibrosis, and hepatic viral infections. An online screening process was employed to identify studies investigating the association between exosomal lncRNA and various liver diseases. Our study revealed a diverse array of lncRNAs carried by exosomes, including H19, Linc-ROR, VLDLR, MALAT1, DANCR, HEIH, ENSG00000248932.1, ENST00000457302.2, ZSCAN16-AS1, and others, exhibiting varied levels across different liver diseases compared to normal liver tissue. These exosomal-derived lncRNAs are increasingly recognized as pivotal biomarkers for diagnosing and prognosticating liver diseases, supported by emerging evidence. However, the precise mechanisms underlying the involvement of certain exosomal lncRNAs remain incompletely understood. Furthermore, the combined analysis of serum exosomes using ENSG00000258332.1, LINC00635, and serum AFP may serve as novel and valuable biomarker for HCC. Clinically, exosomal ATB expression is upregulated in HCC, while exosomal HEIH and RP11-513I15.6 have shown potential for distinguishing HCC related to HCV infection. The lack of reliable biomarkers for liver diseases, coupled with the high specificity and sensitivity of exosomal lncRNA and its non-invasive detection, promotes exploring their role in pathogenesis and biomarker for diagnosis, prognosis, and response to treatment liver diseases.

Female patients with hepatitis B may exhibit a reduced risk of breast cancer: A review of NHANES data.

Hepatic viral infections and breast cancer (BC) constitute major global health challenges, yet the interconnection between these hepatic infections and BC continues to be ambiguous. Conducting a comprehensive evaluation of the link between hepatitis virus infection and the incidence of BC and leveraging data from the National Health and Nutrition Examination Survey covering the period from 1999 to March 2022, we utilized logistic regression and subgroup analysis, among other methodologies, to execute a cross-sectional investigation. The univariate logistic regression analysis elucidates that individuals classified as non-Hispanic White exhibit a markedly higher incidence of BC at 2.620 (95% confidence interval [CI], 1.117-7.676; P = .045); moreover, advanced age at 1.063 (95% CI, 1.036-1.093; P < .001), elevated educational attainment at 1.962 (95% CI, 1.17-3.366; P = .012), and higher income levels at 2.835 (95% CI, 1.303-7.439; P = .017) emerge as significant predisposing factors for BC. In contrast, a greater number of live births significantly diminishes the risk of BC, reducing the incidence to 81.1% with each additional birth. Pertaining to hepatitis and vaccination status, our analysis distinctly demonstrates that only hepatitis B at 0.110 (95% CI, 0.018-0.353; P = .002) bears a significant inverse relationship with BC risk, suggesting a protective effect. The multivariate logistic regression analysis further reveals a negative association between hepatitis B infection and BC incidence, whereas hepatitis B vaccination shows a positive correlation with the disease incidence. After adjusting for all covariates, model 3 delineates odds ratios (95% CI) as follows: 0.14 (0.02-0.50; P = .009) and 1.92 (0.99-3.62; P = .046). Our investigation uncovers that within the general populace, there exists an inverse correlation between hepatitis B infection and BC incidence; in addition, the administration of the hepatitis B virus vaccine is potentially positively associated with the prevalence of BC.

Profile of Homosexuals, Bisexuals, and Transgender People in Kinshasa, the Democratic Republic of the Congo: A Cross-Sectional Study

&amp;lt;i&amp;gt;Introduction&amp;lt;/i&amp;gt;: It has been established that homosexuality plays a considerable role in the persistence of the Human Immunodeficiency Virus (HIV), Hepatitis B Virus (HBV), and Hepatitis C Virus (HCV) infections, but data related to their extent remains paradoxically fragmentary. &amp;lt;i&amp;gt;Objectives&amp;lt;/i&amp;gt;: This study aimed to determine the prevalence and determinants of viral infection (Human Immunodeficiency Virus and hepatic viral infections) among homosexuals, bisexuals, and transgenders in Kinshasa, Democratic Republic of the Congo. &amp;lt;i&amp;gt;Methods&amp;lt;/i&amp;gt;: Between February 1 and March 30, 2022, an analytical cross-sectional study was conducted among Kinshasa&amp;apos;s homosexual, bisexual, and transgender populations. The snowball method was used to choose participants from homosexuals’ organisations. Sociodemographic information and the prevalence of viral infections (HIV, HBV, and HCV) were included as study parameters. The determinants of viral infections were found using multivariate logistic regression. &amp;lt;i&amp;gt;Results&amp;lt;/i&amp;gt;: A total of 555 participants (mean age: 28.5±7.8 years, unmarried: 44.9%) were enrolled. Human immunodeficiency virus, hepatitis B, and hepatitis C infection rates were, respectively, 31.5%, 6.3%, and 9.7% prevalent. HIV-HCV, HIV-HBV, and HIV-HBV-HCV coinfection rates were 4.7%, 4.1%, and 0.7%, respectively. HIV and HBV infection had the same risk factors namely piercing, incarceration, prostitution, and non-condom usage. HCV infection was more pronounced among individuals with piercing, STIs and a previous occurrence of jaundice. &amp;lt;i&amp;gt;Conclusion&amp;lt;/i&amp;gt;: In Kinshasa, HIV, HBV, and HCV infections were widespread among homosexuals, bisexuals, and transgender people. Actions targeting LBGTs are essential to reduce HIV, HCV and HBV infections transmission in the community.

The association between hepatic viral infections and cancers: a cross-sectional study in the Taiwan adult population

BackgroundHepatitis B (HBV) and hepatitis C (HCV) viruses are diseases of global public health concern and are associated with liver cancer. Recent studies have revealed associations between hepatic viral infections and extrahepatic cancers. This study aimed to explore the associations between hepatitis B and C viruses and cancer at baseline in the Taiwan Biobank database while controlling for a wide range of confounding variables.MethodsIn a cross-sectional study of adults aged > 20 years, we compared the distribution of demographic factors, lifestyle, and comorbidities between viral and nonviral hepatic groups using the chi-square test. Univariate and multivariate logistic regressions were performed to observe the associations between hepatitis B and C viral infections and cancers by estimating the odds ratio (OR) and 95% confidence interval (CI). Multivariate regression analysis was adjusted for sociodemographic factors, lifestyle, and comorbidities.ResultsFrom the database, 2955 participants were identified as having HCV infection, 15,305 as having HBV infection, and 140,108 as the nonviral group. HBV infection was associated with an increased likelihood of liver cancer (adjusted OR (aOR) = 6.60, 95% CI = 3.21–13.57, P < 0.001) and ovarian cancer (aOR = 4.63, 95% CI = 1.98–10.83, P = 0.001). HCV infection was observed to increase the likelihood of liver cancer (aOR = 4.90, 95% CI = 1.37–17.53, P = 0.015), ovarian cancer (aOR = 8.50, 95% CI = 1.78–40.69, P = 0.007), and kidney cancer (aOR = 12.89, 95% CI = 2.41–69.01, P = 0.003).ConclusionOur findings suggest that hepatic viral infections are associated with intra- and extrahepatic cancers. However, being cross-sectional, causal inferences cannot be made. A recall-by-genotype study is recommended to further investigate the causality of these associations.

Activation of the PPARγ/NF-κB pathway by A-MPDA@Fe3O4@PVP via scavenging reactive oxygen species to alleviate hepatic ischemia-reperfusion injury.

Hepatic ischemia-reperfusion injury (IRI) is a common pathological process during hepatectomy and liver transplantation and the two primary reasons for hepatic IRI are reactive oxygen species (ROS)-mediated oxidative stress and excessive inflammatory responses. Herein, a novel antioxidant nanodrug (A-MPDA@Fe3O4@PVP) is prepared by employing L-arginine-doped mesoporous polydopamine (A-MPDA) nanoparticles as the carrier for deposition of ultra-small ferric oxide (Fe3O4) nanoparticles and further surface modification with polyvinylpyrrolidone (PVP). A-MPDA@Fe3O4@PVP not only effectively reduces the aggregation of ultra-small Fe3O4, but also simultaneously replicates the catalytic activity of catalase (CAT) and superoxide dismutase (SOD). A-MPDA@Fe3O4@PVP with good antioxidant activity can rapidly remove various toxic reactive oxygen species (ROS) and effectively regulate macrophage polarization in vitro. In the treatment of hepatic IRI, A-MPDA@Fe3O4@PVP effectively alleviates ROS-induced oxidative stress, reduces the expression of inflammatory factors, and prevents apoptosis of hepatocytes through immune regulation. A-MPDA@Fe3O4@PVP can further protect liver tissue by activating the PPARγ/NF-κB pathway. This multiplex antioxidant enzyme therapy can provide new references for the treatment of IRI in organ transplantation and other ROS-related injuries such as fibrosis, cirrhosis, and bacterial and hepatic viral infection.

Activated Gab1 drives hepatocyte proliferation and anti-apoptosis in liver fibrosis via potential involvement of the HGF/c-Met signaling axis.

Chronic liver diseases are caused by hepatic viral infection, chemicals, and metabolic stress. The protein Grb2-associated binder 1 (Gab1) binds to various growth factor receptors, and triggers cell differentiation/survival signaling pathways. To identify signaling molecules involved in the progression of liver diseases, we performed reverse-phase protein microarray (RPMA)-based screening of hepatocytes isolated from humanized mice after acute HCV infection. Acute viral infection in humanized liver mice significantly decreased the level of hepatocyte p-Gab1. Moreover, hepatoma cells upon HCV infection decreased Gab1 mRNA at later times of infection (D3 to D5) and p-Gab1 level was inversely related to the production of TGF-β. In contrast, the level of p-Gab1 was increased in CCL4-induced fibrotic liver. Hepatoma cells showed elevation of p-Gab1, along with an increase in STAT3 and ERK activation, upon treatment with HGF (ligand of HGF receptor/c-Met) and CCL4. In Gab1 knockdown hepatoma cells, cell proliferative signaling activity was reduced but the level of activated caspase-3 was increased. These findings suggest that hepatocyte Gab1 expression may play a role in promoting liver fibrosis progression by triggering ERK activation and inhibiting apoptosis. It implies that the Gab1-mediated signaling pathway would be a promising therapeutic target to treat chronic liver diseases.

The association between hepatic viral infections and cancers: A cross-sectional study in the Taiwan adult population

The association between hepatic viral infections and cancers: A cross-sectional study in the Taiwan adult population

HIV and liver disease.

Liver-related diseases are associated with the high levels of morbidity and mortality in people living with HIV. Between 13% and 18% of all-cause mortality in HIV-infected patients involves a liver-related damage, this being one of the main causes of death not related to acquired immunodeficiency syndrome (AIDS). People living with HIV, even when the disease is under control, are more likely to develop pathologies and complications of a liver-related origin than the general population, both due to common causes such as alcoholism, non-alcoholic fatty liver disease, hepatic viral infections and ageing, in addition to specific HIV-related processes such as antiretroviral treatment toxicity and liver damage inherent to HIV infection. On the other hand, some antiretroviral drugs may have a beneficial effect in reversing liver fibrosis in patients with HIV and chronic liver disease. This paper reviews the main risk factors associated with liver disease in people living with HIV and the role of antiretroviral therapy (ART) in this disease.

Non-Classical HLA Class 1b and Hepatocellular Carcinoma.

A number of studies are underway to gain a better understanding of the role of immunity in the pathogenesis of hepatocellular carcinoma and to identify subgroups of individuals who may benefit the most from systemic therapy according to the etiology of their tumor. Human leukocyte antigens play a key role in antigen presentation to T cells. This is fundamental to the host's defense against pathogens and tumor cells. In addition, HLA-specific interactions with innate lymphoid cell receptors, such those present on natural killer cells and innate lymphoid cell type 2, have been shown to be important activators of immune function in the context of several liver diseases. More recent studies have highlighted the key role of members of the non-classical HLA-Ib and the transcript adjacent to the HLA-F locus, FAT10, in hepatocarcinoma. The present review analyzes the major contribution of these molecules to hepatic viral infection and hepatocellular prognosis. Particular attention has been paid to the association of natural killer and Vδ2 T-cell activation, mediated by specific HLA class Ib molecules, with risk assessment and novel treatment strategies to improve immunotherapy in HCC.

Liver infarctions as the first manifestation of antiphospholipid antibody syndrome in pregnancy: a case report

BackgroundThe differential diagnosis of abdominal pain in pregnant women is broad. Liver diseases as the origin of abdominal pain in pregnancy are rare, and severe forms occur in less than 0.1% of pregnancies. Some disorders, such as hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome and preeclampsia, are unique to pregnancy, while others, such as antiphospholipid antibody syndrome, may manifest in pregnancy but have consequences beyond the current pregnancy. All of them require prompt identification and treatment.Case presentationA 27-year-old Caucasian woman who was 15+1 weeks pregnant reported to the emergency department twice due to stabbing right-upper-quadrant abdominal pain. Initial laboratory testing revealed mild leukocytosis and slightly elevated liver enzymes. On second presentation, the patient was febrile and had an increased C-reactive protein concentration. Over the course of the next days, nonhemolytic anemia and thrombocytopenia emerged with elevated liver enzymes. Coagulation studies also revealed a prolongation of activated partial thromboplastin time. Magnetic resonance imaging showed nonspecific alterations in the right liver lobe, possibly corresponding to infection or infarction. A hepatic viral infection was ruled out. At that time, the most likely diagnosis was cholangitis with liver abscess formation, and antibiotic therapy was started. Further worsening of the anemia and thrombocytopenia, development of proteinuria, together with a miscarriage on the fourth day of hospitalization resulted in the tentative diagnosis of (triple-positive) antiphospholipid antibody syndrome, which was confirmed 12 weeks after the initial investigation. Treatment consisted of prompt anticoagulation with heparin and later on with a vitamin K antagonist as well as high-dose glucocorticoid therapy. There was no need for intravenous immunoglobulin therapy or plasma exchange, although we suspected a catastrophic form of antiphospholipid antibody syndrome due to infarctions of the liver, placenta, and possibly kidneys (proteinuria). The outcome was favorable.ConclusionWe report a 27-year-old pregnant woman whose abdominal pain was caused by liver infarctions as the first manifestation of catastrophic antiphospholipid antibody syndrome. The antiphospholipid antibody syndrome was possibly secondary to hitherto clinically silent systemic lupus erythematosus since the antinuclear antibodies were increased later on. Hydroxychloroquine therapy was initiated to prevent antiphospholipid antibody syndrome recurrence in a future pregnancy.

Increased Circulating T Follicular Helper Cells Induced via IL-12/21 in Patients With Acute on Chronic Hepatitis B Liver Failure.

ObjectivesT Follicular helper (Tfh) cells, recognized as a distinct CD4+ T cell subset, mediate the development of long-lived humoral immunity via B cell activation/differentiation. Tfh cells play an important role during hepatic viral infection, but its role in hepatitis B virus-related acute on chronic liver failure (HBV-ACLF) remains to be explored.Materials and MethodsThe frequency of Tfh cells, serum pro-inflammatory cytokine (IL-12, IL-21, IL-17 and TNF) levels and IgG/M levels were investigated in HBV-ACLF (n = 36), serious chronic hepatitis B (n = 21), moderate chronic hepatitis B patients (n = 32) and healthy control (HC) subjects (n = 10).ResultsCirculating Tfh cells were significantly increased in HBV-ACLF patients compared to other groups, correlating well with MELD score. However, the frequency of Tfh cells decreased in ameliorated HBV-ACLF patients. Furthermore, serum IL-12 and IL-21 levels were higher in HBV-ACLF patients, compared to other groups. Naïve CD4+ T cells from HC subjects differentiate into Tfh cells following treatment with HBV-ACLF patients’ serum, a process that can be blocked by IL-12/21 neutralizing antibodies. Tfh cells induced by HBV-ACLF patient’s serum promoted the proliferation and IgG production of B cells in vitro. Moreover, circulating CD19+ B cells, serum and liver IgG/M levels were significantly higher in HBV-ACLF patients, compared to other groups.ConclusionsOur data demonstrated that there was a high frequency of Tfh cells and high levels of serum IL-12/21 in HBV-ACLF patients. Naïve CD4+ T cells differentiate into Tfh cells in the presence of HBV-ACLF patients’ serum rich in IL-12/21, which can be blocked by neutralizing IL-12/21 antibodies. These data may provide useful insights for both clinical and basic research in the treatment of HBV-ACLF.

ELEVATED LIVER ENZYMES IN PATIENTS WITH ACUTE CHOLECYSTITIS

Liver damage in patients with gallstones is thought to be the result of chronic extra hepatic large bile duct obstruction with or without repeated episodes of cholangitis and may ultimately progress to secondary biliary cirrhosis (11).Hepatic viral infection is by no means the only cause of acute hepatitis (Chen etal, 2007). One sitting in which there may be an acute inflammation of the liver parenchyma is the presence of common bile duct stones and cholangitis

Autophagy and liver cancer.

Autophagy is a highly conserved catabolic process that degrades cytosolic proteins and organelles via formation of autophagosomes that fuse with lysosomes to form autolysosomes, whereby autophagic cargos are degraded. Numerous studies have demonstrated that autophagy plays a critical role in the regulation of liver physiology and homeostasis, and impaired autophagy leads to the pathogenesis of various liver diseases such as viral hepatitis, alcohol associated liver diseases (AALD), non-alcoholic fatty liver diseases (NAFLD), and liver cancer. Recent evidence indicates that autophagy may play a dual role in liver cancer: inhibiting early tumor initiation while promoting progression and malignancy of already formed liver tumors. In this review, we summarized the progress of current understanding of how hepatic viral infection, alcohol consumption and diet-induced fatty liver diseases impair hepatic autophagy. We also discussed how impaired autophagy promotes liver tumorigenesis, and paradoxically how autophagy is required to promote the malignancy and progression of liver cancer. Understanding the molecular mechanisms underlying how autophagy differentially affects liver cancer development and progression may help to design better therapeutic strategies for prevention and treatment of liver cancer.

Post-transplantation Outcomes in Patients with PA or MMA: A Review of the Literature.

IntroductionLiver transplantation is recognised as a treatment option for patients with propionic acidemia (PA) and those with methylmalonic acidemia (MMA) without renal impairment. In patients with MMA and moderate-to-severe renal impairment, combined liver–kidney transplantation is indicated. However, clinical experience of these transplantation options in patients with PA and MMA remains limited and fragmented. We undertook an overview of post-transplantation outcomes in patients with PA and MMA using the current available evidence.MethodsA literature search identified publications on the use of transplantation in patients with PA and MMA. Publications were considered if they presented adequate demographic and outcome data from patients with PA or MMA. Publications that did not report any specific outcomes for patients or provided insufficient data were excluded.ResultsSeventy publications were identified of which 38 were full papers. A total of 373 patients underwent liver/kidney/combined liver–kidney transplantation for PA or MMA. The most typical reason for transplantation was recurrent metabolic decompensation. A total of 27 post-transplant deaths were reported in patients with PA [14.0% (27/194)]. For patients with MMA, 18 post-transplant deaths were reported [11% (18/167)]. A total of 62 complications were reported in 115 patients with PA (54%) with cardiomyopathy (n = 12), hepatic arterial thrombosis (HAT; n = 14) and viral infections (n = 12) being the most commonly reported. A total of 52 complications were reported in 106 patients with MMA (49%) with viral infections (n = 14) and renal failure/impairment (n = 10) being the most commonly reported.ConclusionsLiver transplantation and combined liver–kidney transplantation appears to benefit some patients with PA or MMA, respectively, but this approach does not provide complete correction of the metabolic defect and some patients remain at risk from disease-related and transplantation-related complications, including death. Thus, all treatment avenues should be exhausted before consideration of organ transplantation and the benefits of this approach must be weighed against the risk of perioperative complications on an individual basis.

Key features and homing properties of NK cells in the liver are shaped by activated iNKT cells

The contribution of natural killer (NK) cells to the clearance of hepatic viral infections is well recognized. The recently discovered heterogeneity of NK cell populations renders them interesting targets for immune interventions. Invariant natural killer T (iNKT) cells represent a key interaction partner for hepatic NK cells. The present study addressed whether characteristics of NK cells in the liver can be shaped by targeting iNKT cells. For this, the CD1d-binding pegylated glycolipid αGalCerMPEG was assessed for its ability to modulate the features of NK cells permanently or transiently residing in the liver. In vivo administration resulted in enhanced functionality of educated and highly differentiated CD27+ Mac-1+ NK cells accompanied by an increased proliferation. Improved liver homing was supported by serum-derived and cellular factors. Reduced viral loads in a mCMV infection model confirmed the beneficial effect of NK cells located in the liver upon stimulation with αGalCerMPEG. Thus, targeting iNKT cell-mediated NK cell activation in the liver represents a promising approach for the establishment of liver-directed immune interventions.

Crosssectional Assessment of Bone Mass Density in Adults with Hepatitis B Virus and Hepatitis C Virus Infection

Osteoporosis is one of the major complications in chronic hepatitis B virus (HBV) and hepatitis C (HCV) infection. However, few studies had examined the relationship between hepatic viral infection with bone loss. Our aim was to investigate the association between hepatic viral infection with bone mineral density (BMD) in a cross-sectional study. Participants who attended the health examinations at the Tri-Service General Hospital (TSGH), Taiwan, were enrolled in the study. Diagnosis of viral hepatitis was confirmed by the serum viral markers of hepatitis B surface antigen (HBsAg) and anti-HCV, and BMD measurement was performed by the bone densitometry. Subjects were divided into four groups by the presence of viral markers. The association between hepatic viral infection and BMD was examined by a multivariate linear regression model. HBV infection was inversely associated with BMD after full adjusting with β values of −0.17 (95% CI: −0.29, −0.05) (p < 0.05). The relationship remained significant in males (β = −0.16, 95% CI = −0.31, −0.01) (p < 0.05). In subjects with body mass index less than 30 HBV infection was associated with reduced BMD (β = −0.16, 95% CI = −0.29, −0.02) (p < 0.05). However, HCV infection was only associated with an increase in BMD in patients with BMI less than 30 (β = 0.17, 95% CI = 0.21, 0.32) (p < 0.05). Chronic HBV infection was significantly associated with reduced BMD in males. The impact of viral hepatitis on bone health deserves further investigation for the potential pathophysiological mechanisms.

Frequency of Hepatotropic Viruses Leading To Deranged Liver Function Tests in Renal Transplant Recipients.

The preferred modality for renal replacement therapy is renal transplantation. Marked improvements in early graft survival and long-term graft function have made renal transplantation a more cost-effective alternative to dialysis. The presence of liver disease in the posttransplant period adversely affects graft function and survival. Determining the cause of deranged liver function tests can be helpful in treating the underlying cause, leading to improved graft survival and overall quality of life in patients after renal transplant. Here, we determined the frequency of hepatotropic viral infections leading to deranged liver function tests in renal transplant recipients. Our study included 132 patients with deranged liver function tests who had undergone renal transplant within the past 6 months. Reactivity and nonreactivity of hepatotropic viruses leading to deranged liver function tests were recorded. Average age of patients was 37.17 ± 8.75 years. There were 84 male (63.64%) and 48 female (36.36%) patients. Rates of hepatitis C virus antibodies and hepatitis B surface antigen were 62.88% (83/132) and 37.12% (49/132), respectively, whereas no patients had hepatitis E virus immunoglobulin M antibodies or hepatitis A virus immunoglobulin M antibodies. Among the hepatotropic viral infections leading to deranged liver function tests in renal transplant recipients, hepatitis B virus accounted for a small fraction. In contrast, hepatitis C virus was highly prevalent in transplant recipients who developed deranged liver function tests. Renal transplant recipients with hepatic viral infections have worse patient and allograft survival after transplant compared with noninfected renal transplant recipients. We recommend that transplant candidates be screened for hepatitis B and C virus infection, thus allowing increased graft survival and improved quality of life in renal transplant recipients.

Nonalcoholic Fatty Liver Disease and Weight Loss

Nonalcoholic fatty liver disease(NAFLD)refers to hepatic steatosis without other known causes such as alcohol abuse or hepatic virus infection. NAFLD has become a chronic disease worldwide,and its prevalence is constantly growing. Hepatic insulin resistance caused by obesity results in the deposition of triglycerides in the liver,promoting the occurrence and development of NAFLD. Weight loss is the only safe and effective method for NAFLD. Lifestyle intervention plays a cornerstone role in treating NAFLD;however,most patients can not achieve and maintain the ideal body weight by lifestyle intervention alone. Glucagon-like peptide-1 receptor agonist and metabolic surgery are promising treatments for NAFLD.

Differential Diagnosis of Hepatic Necrosis Encountered at Autopsy.

The liver is subject to a variety of extrinsic and intrinsic insults that manifest with both specific and nonspecific patterns of necrosis. In the autopsy setting, these patterns are often encountered as incidental findings or even causes of death. There are several etiologies of hepatic necrosis, including toxins, drug injuries, viral infections, ischemic injuries, and metabolic disease, all of which possess overlapping gross and histologic presentations. Nonetheless, patterned necrosis in the context of clinical and demographic history allows for the forensic pathologist to develop a differential diagnosis, which may then be pruned into a specific or likely cause. The aim of the following review is to elucidate these patterns in the context of the liver diseases from which they arise with the goal developing a differential diagnosis and ultimate determination of etiology. Acad Forensic Pathol. 2018 8(2): 256-295.