International Journal of Hepatology最新文献

Background: In recent years, inflammation-based scoring systems have been reported to predict survival in Hepatocellular Carcinoma (HCC). The aim of our study was to validate combined preoperative Neutrophil-to-Lymphocyte ratio (NLR)-Platelet-to-Lymphocyte ratio (PLR) in predicting overall survival (OS) and recurrence free survival (RFS) in patients who underwent curative resection for HCC.

Methods: We conducted a retrospective study of HCC patients underwent liver resection with curative intent from January 2010 to December 2013. Receiver-operating characteristic (ROC) curve analysis was used to determine the optimal cut-off values for NLR and PLR. Patients with both NLR and PLR elevated were allocated a score of 2; patients showing one or neither of these indices elevated were accorded a score of 1 or 0, respectively.

Results: 132 patients with a median age of 66 years (range 18-87) underwent curative resection for HCC. Overall morbidity was 30.3%, 30-day mortality was 2.3%, and 90-day mortality was 6.8%. At a median follow-up of 24 months (range 1-88), 25% patients died, and 40.9% had recurrence. On multivariate analysis, elevated preoperative NLR-PLR was predictive of both OS (HR 2.496; CI 1.156-5.389; p=0.020) and RFS (HR 1.917; CI 1.161-3.166; p=0.011). The 5-year OS was 76% for NLR-PLR=0 group, 21.7% for the NLR-PLR=1 group, and 61.1% for the NLR-PLR=2 group, respectively. The 5-year RFS was 39.3% for the NLR-PLR=0 group, 18.4% for the NLR-PLR=1 group, and 21.1% for the NLR-PLR=2 group, respectively.

Conclusion: The preoperative NLR-PLR is predictive of both OS and RFS in patients with HCC undergoing curative liver resection.

Background and Aims. Hepatocellular carcinoma is a major cause of cancer death worldwide, accounting for over half a million deaths per year. Its incidence varies with geographic locations and the type of etiologic factors. In Ethiopia, unidentified causes of liver disease are of sizeable proportion. Recent studies have shown an association of H. pylori infection with different spectrums of chronic liver disease. This study was conducted at St. Paul's Hospital Millennium Medical College in Ethiopia and assesses liver cancer and the association with H. pylori infection. Method. A prospective case-control study conducted on patients with chronic liver disease presenting with a suspicious liver lesion and diagnosed to have HCC in the Gastrointestinal (GI) Clinic of St. Paul's Hospital MMC from Dec 30, 2016, to Nov 1, 2017 G.C. Descriptive surveys on clinical history and physical examination and laboratory profiles were obtained, and the clinical course of the patients including the type of treatment was followed prospectively. Control cases were taken from adult patients without evidence of liver disease in the internal medicine clinic coming for routine evaluation. After collection data were analyzed using SPSS version 23 and associations were assessed using chi-square test. Binary logistic regression was used to assess the association of HCC with different variables and H. pylori infection. All variables with p-value <0.05 were considered as statistically significant. Results. One hundred twenty patients were analyzed with equal representation of cases and controls. The majority of patients with HCC were male with a mean age of 36 years. Older age adjusted Odds Ratio (AOR) (95%CI, p-value) 1.07(1.03-1.09, <0.001), viral hepatitis B (AOR) (95%CI, p-value) 6.19 (1.92-19.93, 0.002), and H. pylori infection (AOR) (95%CI, p-value) 5.22 (2.04-13.31, <0.001) were statistically significantly associated with HCC. Conclusion. H. pylori infection is associated with HCC in this case-control study. This study supports the emerging evidence of H. pylori association with other extra-gastric manifestations.

Background: The features of the portal hypertension enteropathy (PHE) vary from mild mucosal changes to varices with or without bleeding. The prevalence and the development are not fully understood.

Aim: Our aim is to examine the prevalence and the different manifestations of PHE using video capsule endoscopy (VCE).

Methods: It is a single center retrospective study of patients with cirrhosis, who had VCE. Based on the published literature, we divided the PHE lesions into vascular lesions and mucosal lesions.

Results: Of the 100 patients with cirrhosis that had a VCE study, the mean age was 62.82 years. Male gender was predominant (64%), while Caucasians represented 82% of the cohort. The most common etiology of cirrhosis was chronic alcohol abuse followed by chronic hepatitis C virus and nonalcoholic steatohepatitis. VCE detected small bowel lesions in 71% of the patients while the features of PHE were found in 65% from the total cohort. AVMs and inflammatory changes were the most common findings, followed by bleeding. More than 50% of the lesions were vascular in nature. The risk of finding PHE in decompensated cirrhosis is twice that in compensated cirrhosis. Forty-five patients had negative EGD exam for any active bleeding, esophageal varices, portal hypertensive gastropathy, or gastric varices. Of these, 69% had features of PHE in their VCE.

Conclusions: VCE detected small bowel lesions in 71% of our cohort. There is a high prevalence of PHE in decompensated cirrhosis. Vascular lesions are the most common finding in the small bowel of this population.

Background: The pathophysiology of nonalcoholic fatty liver disease (NAFLD) is related to unhealthy lifestyles that combine sedentary lifestyle, hypercaloric diets, excessive saturated fats, refined carbohydrates, and high intake of fructose as a food additive to various processed products. Both the broader recognition of the disease and the additional efforts to elucidate the NAFLD pathogenesis have led to an increase in animal models in recent years. Objective. This review was performed to provide better understanding of the association between the NAFLD and animal models.

Methods: The search in the literature occurred before May of 2018 in the PUBMED database.

Results: Most studies investigating the influence of diet on liver fat content have been performed using a high-calorie diet that leads to a significant increase in fat content in the liver.

Conclusion: The findings of this review show that diet is one of the factors that predisposes to the appearance of NAFLD and that the studies presented a wide variety of designs.

Aims: To describe the prevalence of significant liver fibrosis by ultrasound-based vibration-controlled transient elastography (VCTE; FibroScan®) and to identify the determinants of significant liver fibrosis in Thai chronic hepatitis B patients.

Methods: A cross-sectional study of consecutive chronic hepatitis B patients performed VCTE and followed up at Rajavithi Hospital, Bangkok, Thailand, was conducted between 1 January, 2013, and 31 December, 2016. Liver fibrosis was defined as minimal (METAVIR F0-1) by VCTE < 7.2 kPa and significant (METAVIR F2-4) by VCTE ≥ 7.2 kPa. VCTE assessments and medical records were retrospectively reviewed. The prevalence and determinants of significant liver fibrosis were analyzed.

Results: A total of 206 eligible patients were included; 120 patients (58.3%) were female. The mean age was 50 years (SD 12.4 years), and 32.5% had a body mass index ≥ 25. The prevalences of minimal (F 0-1) and significant fibrosis (F2-4) were 74.3% and 25.7%, respectively. The prevalence of hepatitis B e antigen negative (HBeAg -ve) was 83%. The median serum hepatitis B virus viral load was 4,340 IU/mL (range 20-271,883,036). Significant determinants of significant fibrosis (F2-4) were male gender (aOR 3.24 [95%CI: 1.36-7.72]) and high aspartate transaminase (AST) level (aOR 5.71 [95%CI: 2.03-16.04]).

Conclusion: Around one-quarter of the Thai patients with chronic viral hepatitis B had significant liver disease defined by VCTE, requiring further evaluation for specific treatment for hepatitis B virus. Determinants of significant liver fibrosis were male gender and high AST level.

Backgrounds: The aim of this study was to appraise the relationship between serum fragmented cytokeratin-18(CK-18), controlled attenuation parameter (CAP), and liver steatosis assessed by ultrasound (US) in nonalcoholic fatty liver disease (NAFLD) patients.

Methods: Patients who underwent abdominal US were recruited, followed with measurement of CAP using Fibroscan^® and serum fragmented CK-18 using enzyme-linked immunosorbent assay. The degree of liver steatosis assessed by US was categorized into mild (S1), moderate (S2), and severe (S3).

Results: A total of 109 patients were included in our study. CAP and fragmented CK-18 level were significantly correlated with liver steatosis grade with r_s = 0.56 and 0.68, p=0.001, respectively. NAFLD Fibrosis Score was poorly correlated with liver steatosis grade (r_s=-0.096, p=0.318). Using fragmented CK-18 level, area under receiver operating characteristic (AUROC) curves for S≥2 and S≥3 were excellent (0.82 and 0.84, respectively). Using CAP, AUROC curves for detection of S≥2 and S≥3 were good (0.76, 0.77, respectively). We also proposed cut-off value of CAP to detect S≥2 and S≥3 to be 263 and 319db/m, respectively, and fragmented CK-18 level to detect S≥2 and S≥3 (194 and 294 U/L, respectively).

Conclusions: Both the fragmented CK-18 level and the CAP, but not NAFLD Fibrosis Score, were well correlated with hepatic steatosis grade as assessed by US.

Background and aims: Both paracetamol (PA) and phenacetin (PH) are analgesic and antipyretic agents. Part of phenacetin therapeutic activity is attributed to its metabolism into paracetamol. Paracetamol causes direct hepatic oxidative stress damage. The present study aimed to investigate the possible damaging effects of both PA and PH, when used in therapeutic doses, on rat liver and to compare the antioxidant and hepatoprotective effects of N-acetylcysteine (NAC), N-acetyl-methionine (NAM), and N-acetylglucosamine (NAG) against PA- or PH-induced hepatic damage.

Methods: 90 male Wistar albino rats (120-140 gm) were undertaken, categorized randomly into 9 groups of 10 rats each, and administered by gavage for 2 weeks with DMSO 1% (controls), PA, PA+NAC, PA+NAM, PA+NAG, PH, PH+NAC, PH+NAM, and PH+NAG. Biochemical assays of malondialdehyde (MDA), nitric oxide (NO), reduced glutathione (GSH), total thiols, and alpha-fetoprotein (AFP) in liver homogenates and serum assays of ALT, AST, 8-hydroxy guanine (8-OH-Gua), and AFP were done. Also histopathological examinations of liver tissues in various groups were done.

Results: PA and PH cause significant increase in hepatic levels of MDA, NO, and AFP and serum ALT, AST, and 8-OH-Gua levels, with significant decrease in hepatic GSH and total thiols. NAG and NAC significantly improve the PA- and PH-induced hepatic and blood, biochemical, and histopathological disturbances, respectively.

Conclusions: Both PA and PH induce oxidative stress in rat liver within their therapeutic doses. NAG and NAC in pharmacological doses can antagonize the oxidative damaging effect of both PA and PH.

Background: Direct-acting antiviral (DAA) drugs have been highly effective in the treatment of chronic hepatitis C (CHC) infection. We aim to evaluate the treatment response of Sofosbuvir based DAA in CHC patients with compensated liver cirrhosis as limited data exists in the real-world community setting.

Methods: All the CHC patients with compensated liver cirrhosis treated with Sofosbuvir based DAAs between January 2014 and December 2017 in a community clinic setting were retrospectively analyzed. Pretreatment baseline patient characteristics, treatment efficacy with the sustained virologic response at 12 weeks posttreatment (SVR12), and adverse reactions were assessed.

Results: One hundred and twelve patients with CHC infection and concurrent compensated cirrhosis were included in the study. Black patients represented the majority of the study population (64%). Eighty-seven patients were treated with Ledipasvir/Sofosbuvir (LDV/SOF) ±Ribavirin and 25 patients were treated with Sofosbuvir/Velpatasvir (SOF/VEL). Overall, SVR 12 after treatment was achieved in 90% in patients who received one of the two DAA regimens (89.7% in LDV/SOF group and 92% in SOF/VEL group). SVR 12 did not vary based on age, sex, body mass index, baseline HCV viral load, HCV/HIV coinfection, type of genotype, and prior treatment status. Apart from a low platelet count, there were no other factors associated with a statistical difference in SVR 12(p=0.002) between the two regimens. Fatigue (35%) was the most common adverse effect and no patients discontinued treatment due to adverse effects.

Conclusion: In the community care setting, Sofosbuvir based DAAs are safe, effective with high overall SVR, and well tolerated in patients with CHC patients with compensated liver cirrhosis.

Aim: Nonalcoholic steatohepatitis (NASH) is the consequence of insulin resistance, fatty acid accumulation, oxidative stress, and lipotoxicity. We hypothesize that an increase in the inflammatory adipokine NOV decreases antioxidant Heme Oxygenase 1 (HO-1) levels in adipose and hepatic tissue, resulting in the development of NASH in obese mice.

Methods: Mice were fed a high fat diet (HFD) and obese animals were administered an HO-1 inducer with or without an inhibitor of HO activity to examine levels of adipose-derived NOV and possible links between increased synthesis of inflammatory adipokines and hepatic pathology.

Results: NASH mice displayed decreased HO-1 levels and HO activity, increased levels of hepatic heme, NOV, MMP2, hepcidin, and increased NAS scores and hepatic fibrosis. Increased HO-1 levels are associated with a decrease in NOV, improved hepatic NAS score, ameliorated fibrosis, and increases in mitochondrial integrity and insulin receptor phosphorylation. Adipose tissue function is disrupted in obesity as evidenced by an increase in proinflammatory molecules such as NOV and a decrease in adiponectin. Importantly, increased HO-1 levels are associated with a decrease of NOV, increased adiponectin levels, and increased levels of thermogenic and mitochondrial signaling associated genes in adipose tissue.

Conclusions: These results suggest that the metabolic abnormalities in NASH are driven by decreased levels of hepatic HO-1 that is associated with an increase in the adipose-derived proinflammatory adipokine NOV in our obese mouse model of NASH. Concurrently, induction of HO-1 provides protection against insulin resistance as seen by increased insulin receptor phosphorylation. Pharmacological increases in HO-1 associated with decreases in NOV may offer a potential therapeutic approach in preventing fibrosis, mitochondrial dysfunction, and the development of NASH.

Background: Newer oral anticoagulants (NOACs) are being utilized increasingly for the treatment of venous thromboembolism (VTE). NOAC use is the standard of care for stroke prophylaxis in nonvalvular atrial fibrillation and treatment of acute VTE involving extremities and pulmonary embolism. In contrast, most guidelines in the literature support the treatment of acute portal vein thrombosis (PVT) with low molecular weight heparin (LMWH) and vitamin K antagonists (VKA). Literature evaluating NOAC use in the treatment of acute portal vein thrombosis is sparse. This review focuses on the safety and efficacy of the use of NOACs in the treatment of acute PVT in patients, with or without concomitant cirrhosis, based on the most recent data available in the current literature.

Methods: A systematic review was conducted through a series of advanced searches in the following medical databases: PubMed, BioMed Central, Cochrane, and Google Scholar. Keywords utilized were as follows: NOAC, DOAC (direct oral anticoagulants), portal vein thrombosis, rivaroxaban, apixaban, dabigatran, and edoxaban. Articles related to newer anticoagulant use in patients with portal vein thrombosis were included.

Results: The adverse events, including bleeding events (major and minor) and the failure of anticoagulation (propagation of thrombus or recurrence of PVT), are similar between the NOACs and traditional anticoagulants for the treatment of acute PVT, irrespective of the presence of cirrhosis.

Conclusions: Newer oral anticoagulants are safe and efficacious alternatives to traditional anticoagulation with low molecular weight heparin and vitamin K antagonists in the treatment of acute portal vein thrombosis with or without cirrhosis.