Liver Damage In Patients Research Articles

SIX1/EYA1 are novel liver damage biomarkers in chronic hepatitis B and other liver diseases.

BackgroundThis study aimed to investigate the clinicopathological significance of sine oculis homeobox homolog 1 (SIX1) and eyes absent 1 (EYA1) in patients with chronic hepatitis B (CHB) and other liver diseases.MethodsSIX1 and EYA1 levels were detected in human serum and liver tissues by enzyme linked immunosorbent assay (ELISA) and immunofluorescent staining method, respectively.ResultsThe serum SIX1 and EYA1 levels in 313 CHB patients were 7.24±0.11 and 25.21±0.51 ng/mL, respectively, and these values were significantly higher than those in 33 healthy controls (2.84±0.15 and 13.11±1.01 ng/mL, respectively; P<0.05). Serum SIX1 and EYA1 levels were also markedly increased in patients with numerous other liver diseases, including liver fibrosis, hepatocellular carcinoma, fatty liver disease, alcoholic liver disease, fulminant hepatic failure, autoimmune liver disease, and hepatitis C, compared to the healthy controls (P<0.05). Dynamic observation of these proteins over time in 35 selected CHB patients revealed that SIX1 and EYA1 serum levels increased over an interval. Immunofluorescent staining revealed that both SIX1 and EYA1 were only expressed in hepatic stellate cells (HSCs), and their increased expression was evident in CHB liver tissue.ConclusionsSIX1 and EYA1 are novel biomarkers of liver damage in patients of CHB and other liver diseases, with potential clinical utility.

A model to predict liver damage in patients with HBeAg-positive chronic HBV infection.

A model to predict liver damage in patients with HBeAg-positive chronic HBV infection.

Case of severe liver damage in COVID-19

The 2019 outbreak of coronavirus disease (COVID-19) caused by severe acute coronavirus 2 respiratory syndrome (SARS-CoV-2) has been a global concern since December 2019. Although most patients with COVID-19 have mild clinical manifestations, in about 5% of these patients the disease eventually progresses to severe lung injury or even multiple organ dysfunction. This situation presents various problems for hepatology. In the context of liver damage in patients with COVID-19, several key problems need to be addressed. For example, it is important to determine whether a SARS-CoV-2 can directly enter the liver, especially when it appears that ACE2 is marginally expressed in hepatocytes. In addition, the mechanisms underlying liver dysfunction in patients with COVID-19 are multifactorial and are associated with hyperinflammation, dysregulated immune responses, abnormal coagulation, and drugs. The article describes the potential pathogenesis of liver damage associated with COVID-19. Histopathological evidence suggests a marked disruption of the intrahepatic network of blood vessels secondary to systemic changes caused by a virus that can trigger a coagulation cascade and damage the endothelial layer of blood vessels. There is also a clinical case of polyethylene damage to the liver in a young man who led to death. Against the background of infection COVID-19 he developed massive thrombosis of the liver vessels, followed by the development of necrosis — fibrosis — cirrhosis — acute liver failure, which caused death.

Liver damage in patients with diabetes mellitus in the practice of a family doctor

This article presents information on the main pathological processes developing in the liver in diabetes mellitus. Non-alcoholic fatty liver disease (NAFLD) is an independent nosological unit that includes a spectrum of clinical and morphological changes in the liver parenchyma: steatosis (fatty degeneration) and non-alcoholic steatohepatitis (NASH), the natural course of which can lead to the development of terminal stages of the disease: cirrhosis and liver cancer. This article is devoted to the etiology, pathogenesis, clinical picture, diagnosis and treatment of fatty liver disease in patients with diabetes mellitus.

Novel PRKAG2 variant presenting as liver cirrhosis: report of a family with 2 cases and review of literature

BackgroundMutations in the PRKAG2 gene encoding the 5′ Adenosine Monophosphate-Activated Protein Kinase (AMPK), specifically in its γ2 regulatory subunit, lead to Glycogen storage disease of heart, fetal congenital disorder (PRKAG2 syndrome). These mutations are rare, and their functional roles have not been fully elucidated. PRKAG2 syndrome is autosomal dominant disorder inherited with full penetrance. It is characterized by the accumulation of glycogen in the heart tissue, which is clinically manifested as hypertrophic cardiomyopathy. There is little knowledge about the characteristics of this disease. This study reports a genetic defect in an Iranian family with liver problems using targeted-gene sequencing.Case presentationA 4-year-old girl presented with short stature, hepatomegaly, and liver cirrhosis. As there was no specific diagnosis made based on the laboratory data and liver biopsy results, targeted-gene sequencing (TGS) was performed to detect the molecular basis of the disease. It was confirmed that this patient carried a novel heterozygous variant in the PRKAG2 gene. The echocardiography was a normal.ConclusionA novel heterozygous variant c.592A > T (p.Met198Leu) expands the mutational spectrum of the PRKAG2 gene in this family. Also, liver damage in patients with PRKAG2 syndrome has never been reported, which deserves further discussion.

Highly activated TRAIL+ CD56bright NK cells are associated with the liver damage in HBV-LC patients

BackgroundChronic hepatitis B-related liver cirrhosis(HBV-LC)is the most common cirrhosis in China, which is characterized as liver damage and high mortality. We aim to investigate the characteristics of TRAIL+NK cells in patients with HBV-LC and their relationship with liver damage in patients with HBV-LC. MethodsThirty cases each of chronic hepatitis B (CHB), HBV-related compensated liver cirrhosis (HBV-CLC) and HBV-related decompensated liver cirrhosis (HBV-DLC) patients were recruited in this study. Thirty age‐and sex‐matched healthy individuals were recruited as healthy controls (HCs). NK cell phenotypes were determined using flow cytometry. Serum chemokine concentrations were ascertained using the CBA Flex set. Cell apoptosis was analyzed using the Annexin V-PE/7-AAD apoptosis Kit. ResultsCD56bright NK cells increased, but CD56dim NK cells reduced in HBV-LC patients. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) was mainly expressed on CD56bright NK cells. As the degree of liver damage increased, the frequency and activation of total TRAIL+NK cells and TRAIL+NK cell subsets continued to increase, especially in the HBV-LC patients. Furthermore, the difference in frequency and activation of total TRAIL+NK cells between the HBV-CLC and HBV-DLC groups was mainly due to the highly activation and increase of TRAIL+CD56bright NK cells. With the increasing degree of liver damage, CXCR3-associated chemokines (including CXCL9, CXCL10 and CXCL11) were constantly increased, particularly in the HBV-DLC group. The expression of CXCR3 on CD56bright NK cells was almost 100 % in all enrolled cohorts. CXCR3-associated chemokines were negatively correlated with liver function and positively correlated with fibrosis degree. TRAIL+CD56bright NK cells were negatively correlated with liver function, and positively correlated with fibrosis degree and CXCR3-associated chemokines. The apoptosis of K562 cells and hepatocytes was suppressed partially by the TRAIL-neutralizing antibodies. ConclusionsThe increase of CXCR3-related chemokines (including CXCL9, CXCL10 and CXCL11) might be related to the migration of TRAIL+ CD56bright NK cells to the liver. Highly activated TRAIL+ CD56bright NK cells were associated with the liver damage in HBV-LC patients. These findings may provide new perspectives and theoretical basis for future immunotherapy of HBV-LC patients.

Возможности ультразвуковой эластографии в оценке поражения печени при хронической сердечной недостаточности

The article presents the literature data on the possibilities of modern types of ultrasound elastography in hepatology and their application in various diffuse hepatic pathologies. The features and advantages of shear wave ultrasound elastography with elastometry are highlighted; the prognostic significance of this method in assessing the severity of hepatic fibrosis is presented. Among the publications, there are also noted the studies concerning the issues of elastography in cardiac liver damage in patients with chronic heart failure. The literature review showed that elastographic diagnostic methods are promising, since their sufficient informativeness was noted in the diagnosis of not only primary diffuse liver damage, but also in assessing the prognosis of the outcome of the disease. The most important advantages of elastography are speed and accessibility, non-invasiveness, possibility of primary diagnosis and assessment of the disease progression and the therapy effectiveness. At the same time, the possibilities of ultrasound elastography in general are still understudied and heir further study is relevant, especially the methods of two-dimensional elastography and shear wave elastometry for diagnosing cardiogenic liver damage in patients with chronic heart failure.

The clinical characteristics and underlying causes of liver damage in patients with COVID-19 infection: Retrospective analysis.

Objectives:2019-nCoV has become a global threat to human health. The primary objective of this study was to examine the hepatic damage in 2019-nCoV infected patients and the associated underlying causes.Methods:In this retrospective study, a total of 68 laboratory-confirmed and 20 suspected COVID-19 cases from 23rd January 2020 to 15th February 2020 were included. The study was conducted in The First People’s Hospital of Jingzhou, Hubei. SPSS version 23.0. was used for Statistical analysis using the Student’s t-test or Chi-square test. Data was analyzed for the clinical characteristics and underlying causes of liver damage. The outcomes were followed up until March 29, 2020.Results:Out of the 68 COVID-19 confirmed cases, 51 had an abnormal liver function, of which 15 had an abnormal liver function at the time of hospital admission. The relationship between the liver function and clinical prognosis of patients showed that the abnormal liver function was positively correlated with the severity of the infection (100% vs.70.2%, p=0.036). The proportion of patients with an elevated level of ALT and a depleted level of Albumin (ALB) were significantly lower in the COVID-19 suspected group than the confirmed group (5% vs. 50.9%, p=0.000; 10% vs. 35.8%, p=0.030, respectively). Besides, the utilization rate of lopinavir/ritonavir, azithromycin, and methylprednisolone in COVID-19 suspected patients were significantly lower than the confirmed patients (25% vs. 62.3%, p=0.004; 35% vs. 62.3%, p=0.037; 25% vs. 64.2%, p=0.003, respectively).Conclusions:Liver function anomalies are one of the common symptoms associated with the COVID-19 infection, where virus-replication in the liver cells, virus-induced inflammatory response, and administration of clinical medication could be the plausible reason.

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

CRP Levels in Viral Hepatitis: A Meta-Analysis Study

Context: Viral hepatitis is a common infectious disorder with a high degree of mortality. The host immunological feedback to the hepatitis virus is dim and unable to down-regulate and clear infection. C-reactive protein (CRP), an acute phase reactant synthesized by hepatocytes in response to inflammatory reactions, facilitates apoptosis and phagocytosis. An effort has been made in the current meta-analysis study to elucidate the relationship between CRP and hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. Methods: Eighteen published research articles on CRP levels of viral hepatitis patients were included in this study. A random-effects model was used to calculate the pooled mean level for CRP. Results: The pooled mean level of CRP hepatitis B and hepatitis C was 6.93 mg/L (95% CI: 3.04 - 10.81) and 2.31 mg/L (95% CI: 1.06 - 3.55), respectively. A high degree of variance was observed among the studies, with the I2 more than 90%. Conclusions: The pooled mean level of CRP was within the normal range in patients with hepatitis C; however, it was high in patients with hepatitis B. The pooled mean CRP level reported in this study can be useful to determine the level of liver damage in patients with viral hepatitis.

Correlation analysis of coagulation dysfunction and liver damage in patients with novel coronavirus pneumonia: a single-center, retrospective, observational study

Background The novel coronavirus disease 2019 (COVID-19) is currently breaking out worldwide. COVID-19 patients may have different degrees of coagulopathy, but the mechanism is not yet clear. We aimed to analyse the relationship between coagulation dysfunction and liver damage in patients with COVID-19. Methods A retrospective analysis of 74 patients with COVID-19 admitted to the First People’s Hospital of Yueyang from 1 January to 30 March 2020 was carried out. According to the coagulation function, 27 cases entered the coagulopathy group and 47 cases entered the control group. A case control study was conducted to analyse the correlation between the occurrence of coagulation dysfunction and liver damage in COVID-19 patients. Results Alanine aminotransferase (ALT) and aspartate aminotransferase (AST), markers of liver damage, were positively correlated with coagulopathy (p = 0.039, OR 2.960, 95% CI 1.055–8.304; and p = 0.028, OR 3.352, 95% CI 1.137–9.187). Alkaline phosphatase (ALP), γ-glutamyl transpeptidase (γ-GT), and total bilirubin (TBIL) were not statistically correlated with coagulopathy. According to the diagnosis and treatment plan, the included cases were classified into mild, moderate, severe, and critical. The results showed that the occurrence of coagulation dysfunction had no statistical correlation with the severity of COVID-19. Conclusion Coagulation dysfunction in patients with COVID-19 is closely related to liver damage. A longer course of the disease may cause a vicious circle of coagulopathy and liver damage. Clinicians need to closely monitor coagulation and liver function tests and to give prophylactic or supportive therapy when needed.

Tropism of COVID-19 to digestive organs. Features of damage and approaches to treatment

Coronavirus disease 2019 (COVID‑19) began in December 2019 in Wuhan, Hubei, People’s Republic of China. On March 11, 2020, COVID‑19 was recognized by the World Conservation Organization (WHO) as a pandemic. As of May 31, 2020, more than 6 million cases were recorded in almost all countries. The etiological factor of the disease is a new coronavirus of severe acute respiratory syndrome‑2 (SARS‑CoV‑2), which belongs to the genus β‑coronaviruses, as well as other already known pathogens of this family — SARS and coronavirus of Middle Eastern respiratory syndrome (MERS). About 350 thousand people died as a result of the disease. More than 2.5 million people have recovered. To date, it has been proven that SARS‑CoV‑2 can affect all organs and systems of the body (lungs — pneumonia, respiratory distress syndrome, brain — encephalitis, cardiovascular system, kidneys, gastrointestinal tract). The main clinical symptoms of COVID‑19 include: fever and other manifestations of the respiratory system (headache, rarely — runny nose, loss and/or change in taste and smell, dry cough, shortness of breath, chest pain, etc.), and also symptoms of the gastrointestinal tract (GI tract), such as loss of appetite, nausea and/or vomiting, diarrhea, abdominal pain, increased liver transaminases, exacerbation of chronic gastrointestinal diseases (inflammatory bowel disease, etc.). Data from Chinese studies have shown that SARS‑CoV‑2 RNA is present not only in airway material but also in faecal samples from infected patients. These data demonstrate the ability of SARS‑CoV‑2 to actively affect and replicate in the gastrointestinal tract, which is important for the choice of tactics for the diagnosis and treatment of the disease, as well as to prevent the spread of infection. Numerous studies have shown varying degrees of liver damage in patients infected with SARS‑CoV‑2. The COVID‑19 case studies did not pinpoint the exact cause of liver damage, and there is no clear evidence of an interaction between liver damage and COVID‑19. Research is ongoing. Due to the low level of awareness of physicians about the effects of COVID‑19 on the gastrointestinal tract, it is advisable to review existing data in order to increase the effectiveness of diagnosis, treatment and dynamic supervision of patients. This article discusses the effects of SARS‑CoV‑2 on the gastrointestinal tract. Particular attention is paid to liver damage in COVID‑19, as well as the impact of liver complications on the effectiveness of COVID‑19 treatment and prognosis.

Liver Chemistries in Patients With COVID-19 Who Were Discharged Alive or Died: A Meta-analysis.

Although abnormal liver chemistries are linked to a higher risk of coronavirus disease 2019 (COVID‐19)–related death, liver manifestations may be diverse and even confusing. Thus, we performed a meta‐analysis of published liver manifestations and described the liver damage in patients with COVID‐19 who died or discharged alive. We searched PubMed, Google Scholar, medRxiv, bioRxiv, the Cochrane Library, Embase, and three Chinese electronic databases through April 22, 2020. We analyzed pooled data on liver chemistries stratified by the main clinical outcome of COVID‐19, using a fixed or random‐effects model. In our meta‐analysis of 19 studies, which included a total of 4,103 patients, the pooled mean alanine aminotransferase and aspartate aminotransferase levels were, respectively, 31.7 IU/L and 51.0 IU/L in the patients with COVID‐19 who died and 27.7 IU/L and 32.9 IU/L in those discharged alive (both P < 0.0001). Compared with the patients discharged alive, those who died tended to have lower albumin levels but longer prothrombin time and higher international normalized ratio. Conclusion: In this meta‐analysis, according to the main clinical outcome of COVID‐19, we comprehensively describe three patterns of liver impairment related to COVID‐19: hepatocellular injury, cholestasis, and hepatocellular disfunction. The patients who died from COVID‐19 tended to have different liver chemistries from those discharged alive. Special caution should be given to the patients with a relatively higher index of liver chemistries.

Direct or Collateral Liver Damage in SARS-CoV-2-Infected Patients.

Liver injury can result from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection with more than one-third of COVID-19 patients exhibiting elevated liver enzymes. Microvesicular steatosis, inflammation, vascular congestion, and thrombosis in the liver have been described in autopsy samples from COVID-19 patients. Several factors, including direct cytopathic effect of the virus, immune-mediated collateral damage, or an exacerbation of preexisting liver disease may contribute to liver pathology in COVID-19. Due to its immunological functions, the liver is an organ likely to participate in the viral response against SARS-CoV-2 and this may predispose it to injury. A better understanding of the mechanism contributing to liver injury is needed to develop and implement early measures to prevent serious liver damage in patients suffering from COVID-19. This review summarizes current reports of SARS-CoV-2 with an emphasis on how direct infection and subsequent severe inflammatory response may contribute to liver injury in patients with and without preexisting liver disease.

Liver diseases in COVID-19: Etiology, treatment and prognosis.

In December 2019, a novel coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was identified in Wuhan, China causing coronavirus disease-2019 (COVID-19). Numerous studies have shown varying degrees of liver damage in patients infected with SARS-CoV-2. However, in previous case studies of COVID-19, the exact cause of liver injury has not been clearly elucidated, nor is there clear evidence of the interaction between liver injury and COVID-19. This study will analyze the causes of liver injury in COVID-19 and the influence of liver-related complications on the treatment and prognosis of COVID-19.

Platelet activation during chronic hepatitis B infection exacerbates liver inflammation and promotes fibrosis.

Recurrent hepatitis activity during chronic hepatitis B virus infection results in fibrosis and even hepatocellular carcinoma. It is still unclear what causes acute exacerbation. As platelets have recently been identified as a significant role in inflammation, we here investigated the role of platelets in mediating liver damage in patients with chronic hepatitis B virus infection. Platelet aggregation testing and flow cytometry were carried out to evaluate platelet activation status in 121 patients chronically infected with hepatitis B across different phases of the condition. The correlation between platelet aggregation rate and liver inflammation or liver fibrosis index was evaluated. To investigate the genesis of platelet activation, several serum cytokines were also assessed by MILLIPLEX microsphere-based multiplex cytokine assay. Active hepatitis patients showed a higher aggregation rate than others. Levels of CD62p, a marker of platelet activation, were also increased in this group of patients. Positive correlations between platelet aggregation rate and liver inflammation or liver fibrosis were also noted, indicating a significant role of platelet in the progression of liver disease. The level of tumor necrosis factor-alpha, which is known to trigger platelet activation, was markedly higher in the active hepatitis group (P < .005). Based on the findings in our study, platelet activation plays a vital role in the progression of chronic hepatitis B virus infection. Antiplatelet therapy may provide a new means of hepatitis B infection treatment.

Risk factors profile for liver damage in cardiac inpatients

Background/Aim. Liver damage, with potentially serious consequences, is not uncommon in hospitalized cardiac patients. The aim of our study was to determine the risk factor profile for liver damage in patients hospitalized from a deterioration of their acute or chronic cardiac illness. Methods. The study had observational case-control design with retrospective data collections from medical files of adult patients hospitalized in a tertiary health care center. The cases (n = 140) were subjects with novel liver injury (which emerged during hospital stay) and three control subjects were matched (age, date) for each case subject (n = 420). The primary outcome was hepatotoxicity (present or absent) and independent variables were proposed risk factors. Statistical analysis included descriptive methods, hypothesis testing and univariate and multivariate binary logistic regression, with p ? 0.05. Results. In the whole study population, there were 432 (77.1%) females and the mean age of patients was 64.1 years [standard deviation (SD) = 10.7, range 24?85 years]. The most common illnesses were coronary heart disease (n = 385), hypertension (n = 334) and arrhythmia (n = 115). Mean value of Charlson Comorbidity Index (CCI) score was 3.8 (SD=1.7; range 1-10) corresponding to estimated CCI 10-years survival rate of 54.4% (SD = 33.5%). In the group of cases, 114 (81.4%) of the patients had hepatocellular, 9 (6.4%) cholestatic and 17 (12.2%) mixed type of hepatic injury. Factors independently associated with hepatotoxic event were previous occasional alcohol intake odds ratio (OR) 96.47; 95% confidence interval (CI) 28.95?321.43; p &lt; 0.001), amiodarone (OR 3.70; 95% CI 1.82?7.53; p &lt; 0.001), enoxaparin (OR 3.29; 95% CI 1.79?6.05; p &lt; 0.001), obesity (OR 2.78; 95% CI 1.15? 6.71; p &lt; 0.023), atorvastatin (OR 2.67; 95% CI 1.33?5.38; p &lt; 0.006) and CCI total score (OR 1.89; 95% CI 1.53?2.34; p &lt; 0.001). Conclusion. Major factors associated with acute liver damage in patients hospitalized in cardiology ward of a tertiary health care institution were patient?s constitutional and habitual characteristics (occasional alcohol intake, obesity, CCI total score) and drugs with known hepatotoxic properties (amiodarone, enoxaparin, atorvastatin).

Fat and Sugar-A Dangerous Duet. A Comparative Review on Metabolic Remodeling in Rodent Models of Nonalcoholic Fatty Liver Disease.

Nonalcoholic fatty liver disease (NAFLD) is a common disease in Western society and ranges from steatosis to steatohepatitis to end-stage liver disease such as cirrhosis and hepatocellular carcinoma. The molecular mechanisms that are involved in the progression of steatosis to more severe liver damage in patients are not fully understood. A deeper investigation of NAFLD pathogenesis is possible due to the many different animal models developed recently. In this review, we present a comparative overview of the most common dietary NAFLD rodent models with respect to their metabolic phenotype and morphological manifestation. Moreover, we describe similarities and controversies concerning the effect of NAFLD-inducing diets on mitochondria as well as mitochondria-derived oxidative stress in the progression of NAFLD.

Vascular and Parenchymal Alterations of the Liver and Liver Surveillance in Patients Who Received Inotuzumab Ozogamicin As the Standard of Care for Relapse/Refractory Acute Lymphoblastic Leukemia

Vascular and Parenchymal Alterations of the Liver and Liver Surveillance in Patients Who Received Inotuzumab Ozogamicin As the Standard of Care for Relapse/Refractory Acute Lymphoblastic Leukemia

Hepatitis C virus clearance and less liver damage in patients with high cholesterol, low-density lipoprotein cholesterol and APOE ε4 allele.

BACKGROUNDCholesterol is related to improvements in the rate of sustained virological response and a robust immune response against the hepatitis C virus (HCV). APOE gene polymorphisms regulate cholesterol levels modifying the course of the HCV infection. The relationship between cholesterol, APOE alleles, and the outcome of HCV infection has not been evaluated in the admixed population of Mexico.AIMTo investigate the role of APOE -ε2, -ε3, and -ε4 alleles and the metabolic profile in the outcome of HCV infection.METHODSA total of 299 treatment-naïve HCV patients were included in this retrospective study. Patients were stratified in chronic hepatitis C (CHC) (n = 206) and spontaneous clearance (SC) (n = 93). A clinical record was registered. Biochemical tests were assessed by dry chemistry assay. APOE genotypes were determined using a Real-Time polymerase chain reaction assay.RESULTSTotal cholesterol, low-density lipoprotein cholesterol (LDL-c), triglycerides, and hypercholesterolemia were higher in SC than CHC patients as well as the frequency of the APOE ε4 allele (12.4% vs 7.3%). SC patients were overweight (54.8%). The ε4 allele was associated with SC (OR = 0.55, 95%CI: 0.31-0.98, P = 0.042) and mild fibrosis (F1-F2) in CHC patients (OR 0.091, 95%CI 0.01-0.75, P = 0.020). LDL-c ≥ 101.5 mg/dL (OR = 0.20, 95%CI: 0.10-0.41, P < 0.001) and BMI ≥ 26.6 kg/m2 (OR= 0.37, 95%CI: 0.18-0.76, P < 0.001) were associated with SC status; while ALT ≥ 50.5 IU/L was negatively associated (OR = 5.67, 95%CI: 2.69-11.97, P < 0.001).CONCLUSIONIn SC patients, the APOE ε4 allele and LDL-c conferred a protective effect in the course of the HCV infection in the context of excess body weight.