Absence Of Cirrhosis Research Articles

Interspecies transcriptomic comparison identifies a potential porto-sinusoidal vascular disorder rat model suitable for invivo drug testing.

Porto-sinusoidal vascular disorder (PSVD) involves a group of rare vascular liver diseases of unknown aetiology that may lead to the development of portal hypertension and its life-threatening complications. Its pathophysiology is not well understood, and animal models described to date do not fully recapitulate human disease. We developed three different PSVD rat models by either immunosensitization (repetitive intraportal LPS or intramuscular spleen extract injections) or toxic (Selfox: combination of FOLFOX and a selenium-enriched diet) treatment and characterized them at haemodynamic, histological, biochemical and transcriptional levels. We compared these results to human data. All three models developed significant portal hypertension, while only the LPS and the Selfox models displayed PSVD-specific and nonspecific histological alterations in the absence of cirrhosis. Transcriptional comparison between rat models and human data showed that both LPS and Selfox models recapitulate the main transcriptional alterations observed in humans, especially regarding haemostasis, oxidative phosphorylation and cell cycle regulation. Reproducibility and feasibility was higher for the Selfox model. The Selfox rat model faithfully reproduces the main alterations described in PSVD. Its use as a preclinical model for drug testing in progressing PSVD can be a significant step forward towards the development of new therapeutic targets for this rare condition.

A Narrative Review on Non-Cirrohotic Portal Hypertension: Not All Portal Hypertensions Mean Cirrhosis.

Non-cirrhotic portal hypertension (NCPH), also known as idiopathic non-cirrhotic portal hypertension (INCPH) and porto-sinusoidal vascular disorder (PSVD), is a rare disease characterized by intrahepatic portal hypertension (IPH) in the absence of cirrhosis. The precise etiopathogenesis of IPH is an area of ongoing research. NCPH diagnosis is challenging, as there are no specific tests available to confirm the disease, and a high-quality liver biopsy, detailed clinical information, and an expert pathologist are necessary for diagnosis. Currently, the treatment of NCPH relies on the prevention of complications related to portal hypertension, following current guidelines of cirrhotic portal hypertension. No treatment has been studied that aimed to modify the natural history of the disease; however, transjugular intrahepatic porto-systemic shunt (TIPS) placement, shunt and liver transplantation are considerable symptomatic options. In this review, we discuss the heterogeneity of NCPH as well as its etiopathogenesis, clinical presentation and management issues. Starting from the assumption that portal hypertension does not always mean cirrhosis, cooperative studies are probably needed to clarify the issues of etiology and the possible genetic background of this rare disease. This knowledge might lead to better treatment and perhaps better prevention.

Presence of underlying cirrhosis is associated with increased in-hospital mortality and length of stay following pancreatoduodenectomy

BackgroundPatient- and hospital-level factors associated with outcomes following pancreatoduodenectomy (PD) are well established. However, despite theoretical disruption in hepatopetal flow, the impact of cirrhosis on in-hospital mortality following PD is not well-studied. The objective of this study was to evaluate in-hospital mortality, length of stay (LOS), and post-discharge disposition in patients with cirrhosis undergoing PD. MethodsA retrospective analysis of the National Inpatient Sample (January 2002–August 2015) was conducted identifying patients undergoing PD. Using previously validated ICD-9-CM codes, patients were stratified into presence and absence of cirrhosis. Factors associated with in-hospital mortality following PD were analyzed adjusting for patient- and hospital-level factors. Following PD were analyzed after adjusting for patient- and hospital-level factors. ResultsIn 16,344 patients that underwent PD, 203 (1.2 %) patients had underlying cirrhosis prior to resection. Overall in-hospital mortality following PD was significantly worse in the cirrhosis cohort (11.3 % vs. 3.6 %, p < 0.001). Patients with underlying cirrhosis were less likely to be discharged home (73.9 % vs. 83.2 %, p < 0.001) and had a longer median LOS (12.0 vs. 10.0 days, p = 0.001). ConclusionThe presence of underlying cirrhosis is associated with increased in-hospital mortality, longer LOS, and decreased likelihood of home discharge following PD. Given the prohibitive risks, PD should not be performed in patients with underlying cirrhosis.

Association between gut-derived endotoxins and porto-sinusoidal vascular disorder with portal hypertension.

Porto-sinusoidal vascular disorder (PSVD) is characterised by lesions involving portal veins and sinusoids in absence of cirrhosis with an unclear pathophysiology. However, its association with immunodeficiency, bowel disorders and abdominal bacterial infections supports the role of altered intestinal permeability and gut-derived endotoxins. The study aimed at assessing the association between serological markers of increased intestinal permeability, pro-aggregating/procoagulant state and liver injury in PSVD and portal hypertension. Thirty-three patients with biopsy-proven PSVD and portal hypertension and 33 healthy subjects were submitted to a venous blood sampling for the measurement of zonulin and lipopolysaccharides (LPS) as markers of intestinal permeability, of s-Glycoprotein VI, sP-selectin, ADAMTS13 and von Willebrand factor (vWF), as markers of platelet aggregation and microvascular inflammation, factor VIII and F1 + 2 as markers of hypercoagulability. In 17 PSVD patients, histomorphological and immunohistochemical study on liver biopsies was performed. Compared with controls, PSVD patients had higher levels of LPS, zonulin, vWF, factor VIII and sP-selectin, F1 + 2. ADAMTS13 was reduced. Serum LPS correlated with zonulin, sP-selectin, FVIII and vWF. At histological analysis, PSVD specimens had increased LPS localisation, toll-like receptor-4(TLR4)-positive macrophages and platelet number compared with samples from healthy liver donors. TLR4+ macrophage number correlated with portal inflammation and fibrosis. Sinusoid dilation and capillarisation were observed. PSVD biopsies showed signs of biliary damage and reduced ductular reaction without alteration in Sox9+ cell population. PSVD patients display an altered intestinal permeability and endotoxemia correlated to a pro-aggregating/procoagulant state; histologically, PSVD was associated with increased TLR4+ cell involvement and platelet clumps within sinusoids. Our study suggests that LPS-TLR4 pathway could contribute to the pathophysiological basis of PSVD with portal hypertension.

Risk factors of low-level viremia in chronic hepatitis B patients receiving Entecavir monotherapy: a retrospective cohort study.

Low-level viremia (LLV), a special case of poor response to antiviral therapy, has become a focus of liver disease research; however, most studies have focused on poor response to antiviral therapy, and little attention has been paid to LLV. Therefore, this study aimed to investigate the factors influencing LLV in patients with chronic hepatitis B (CHB) receiving entecavir (ETV) monotherapy. Clinical data of CHB patients receiving ETV treatment for at least 1year at the outpatient department of the Affiliated Hospital of Xuzhou Medical University from November 2018 to June 2020 were collected. Patients were divided into LLV (180 cases) and sustained virological response (SVR) groups (337 cases) according to the hepatitis B virus (HBV) DNA load at the end of the observation period. Demographic features and laboratory markers were also examined. Univariate and multivariate logistic regression analyses were performed to examine factors influencing LLV in patients receiving long-term ETV monotherapy. Significant differences were noted between the LLV and SVR groups in terms of age, sex, presence or absence of cirrhosis, HBeAg positivity rate, baseline HBV DNA load, and baseline HBsAg level before treatment. Multivariate logistic regression analysis showed that baseline HBeAg status, HBV DNA load, and HBsAg quantification were pretreatment risk factors for LLV in long-term ETV antiviral therapy. CHB patients with a high HBV DNA load, high HBsAg quantification, and positive HBeAg results tend to have a high risk of LLV despite long-term ETV antiviral treatment and should be dynamically monitored.

INVESTIGATING THE RELATIONSHIP BETWEEN HEPCIDIN LEVELS AND CIRRHOSIS IN PATIENTS WITH CHRONIC LIVER DISEASE

Iron is an important element in the human body, and hepcidin is a crucial protein that plays a major role in regulating its levels. This protein is particularly important in patients with Chronic Liver Disease (CLD), and its complex interactions with other biomarkers need to be explored further, especially when differentiating between patients with and without liver cirrhosis. In this study, 200 CLD patients with CLD were divided into two groups based on the presence or absence of cirrhosis. The study aimed to investigate the correlation between hecidin levels, serum ferritin, and other iron-related parameters using advanced biochemical assays. The research was conducted over 24 months at a prestigious hepatology research facility. The study found that 65% of patients with cirrhosis had higher Hepcidin levels than those without cirrhosis. Additionally, there was a significant positive correlation between hecidin concentrations and serum ferritin levels, particularly in cirrhosis patients. The findings suggest that hepcidin could play a crucial role in diagnosing and treating CLD, especially in patients with cirrhosis. The multifaceted interactions of hepcidin in patients with cirrhosis could lead to a better understanding of the pathophysiology of CLD.

Outcomes of Patients with Acute Hepatotoxicity Caused by Mushroom-Induced Poisoning.

This study aimed to investigate the characteristics of severe hepatitis (SH), acute liver injury (ALI), and acute liver failure (ALF) in patients with mushroom-induced hepatotoxicity. Data of patients between 2010 and 2019 were retrospectively reviewed. Twenty-four patients with mushroom-induced hepatotoxicity were included and divided into 3 groups: SH, ALI, and ALF. SH was defined as transaminase level ≥10 times ULN, international normalized ratio (INR) ≤1.5, and the absence of hepatic encephalopathy (HE). ALI was defined as INR > 1.5, presumed acute illness onset, and the absence of HE. ALF was diagnosed based on the presence of HE of any degree, with INR > 1.5, presumed acute illness onset, and the absence of cirrhosis. The mean age of the patients was 51.6 years; 13 (54.2%) were female. At admission, 18 patients (75%) had SH, 5 (21%) had ALI, and 1 (4.1%) had ALF. During follow-up, 6 of the 18 SH (33%) patients progressed to ALI and 2 of the 5 ALI (40%) patients progressed to ALF. No progression to ALI or ALF was observed in the 8 SH cases with a baseline MELD score of <15. One patient with grade 4 HE died (4.1%). None underwent liver transplantation. The survival was 100% in the ALI and SH groups. A MELD score of <15 at admission may be used as a predictor of no progression to ALI or ALF in patients with SH. However, since 40% of ALI cases may progress to ALF, these cases should be followed up in a tertiary care center that is equipped to perform liver transplantation and advanced therapies.

Clinico-histological and molecular features of hepatocellular carcinoma from nonalcoholic fatty liver disease.

Patients with nonalcoholic fatty liver disease (NAFLD) continue to increase with the epidemics of obesity, and NAFLD is estimated to become the most prevalent etiology of hepatocellular carcinoma (HCC). Recently, NAFLD-HCC has been recognized to have clinico-histologically and molecularly distinct features from those from other etiologies, including a lower incidence rate of HCC and less therapeutic efficacy to immune checkpoint inhibitors (ICIs). Consistent with the clinical observations that up to 50% of NAFLD-HCC occurs in the absence of cirrhosis, the imbalance of pro- and antitumorigenic hepatic stellate cells termed as myHSC and cyHSC can contribute to the creation of an HCC-prone hepatic environment, independent of the absolute fibrosis abundance. Immune deregulations by accumulated metabolites in NAFLD-affected livers, such as a fatty-acid-induced loss of cytotoxic CD4 T cells serving for immune surveillance and "auto-aggressive" CXCR6+ CD8 T cells, may promote hepatocarcinogenesis and diminish therapeutic response to ICIs. Steatohepatitic HCC (SH-HCC), characterized by the presence of fat accumulation in tumor cells, ballooned tumor cells, Mallory-Denk body, interstitial fibrosis, and intratumor immune cell infiltration, may represent a metabolic reprogramming for adapting to a lipid-rich tumor microenvironment by downregulating CPT2 and leveraging its intermediates as an "oncometabolite." Genome-wide analyses suggested that SH-HCC may be more responsive to ICIs given its mutual exclusiveness with β-catenin mutation/activation that promotes immune evasion. Thus, further understanding of NAFLD-specific hepatocarcinogenesis and HCC would enable us to improve the current daily practice and eventually the prognoses of patients with NAFLD.

Porto-sinusoidal vascular disorder (PSVD): Application of new diagnostic criteria in a multicenter cohort of patients

Background and aimThe term porto-sinusoidal vascular disorder (PSVD) was recently proposed to replace that of idiopathic non-cirrhotic portal hypertension (INCPH) to describe patients with typical histological lesions in absence of cirrhosis, irrespective of the presence/absence of portal hypertension (PH), and new diagnostic criteria were defined. The study aimed to compare the applicability between the diagnostic criteria of PSVD and those of INCPH. Materials and methods53 patients affected by PSVD were enrolled. Biochemical, clinical, ultrasound and histological data, the presence and type of associated diseases were recorded in a database. According to the new criteria, histological data and signs of PH were divided into specific and non-specific. Percutaneous and transjugular biopsies were compared to establish the usability of the two methods for diagnostic purposes. ResultsIn 85% of the patients the diagnosis of PSVD was obtained by applying the first criterion (25 had specific histological signs with specific signs of PH); one patient presented with specific histological signs but no PH. In 8 patients the diagnosis was obtained by applying the second criterion. 19% of patients had portal vein thrombosis. Finally, the prevalence of the various histological lesions was similar between the patients submitted to percutaneous and transjugular liver biopsy. ConclusionsThe study confirms that the diagnostic criteria of PSVD lead to the inclusion of a greater number of patients than INCPH.

Predictors for Liver Cirrhosis in Patients with Hepatitis C Virus: A Cross-Sectional Study

Background: Cirrhosis is one of the most critical health problems with a great economic burden on the health system. Objectives: This study evaluated cirrhosis predictors in patients with hepatitis C virus (HCV). Methods: A total of 608 patients with HCV were included in the present study within 2011 and 2017 and divided into two groups based on the presence and absence of cirrhosis. Demographic and laboratory data (e.g., blood group, aspartate transaminase (AST), alanine transaminase (ALT), prothrombin time (PT), platelet count, anti-HCV antibodies, and virus level count) were collected by referring to patients’ files and compared between the two groups. Predictive factors were determined using the regression model. Results: In this study, 85 patients (13.9%) had liver cirrhosis. Univariate analysis showed that hepatic enzymes AST, ALT, platelet count, PT, partial thromboplastin time, international normalized ratio, and HCV ribonucleic acid levels in cirrhosis patients were significantly higher than in non-cirrhosis patients (P &lt; 0.05). Adjusted logistic regression analysis showed age &lt; 45 years (adjusted odds ratio (ORAdj): 1.11, P = 0.028), male gender (ORAdj: 2.08, P = 0.023), co-infection with hepatitis B virus (HBV) infection (ORAdj: 2.58, P = 0.001), and alcohol consumption (ORAdj: 1.87, P = 0.001) were predictive factors for cirrhosis in patients with HCV Conclusions: This study showed that in patients with hepatitis C, age &gt; 45 years, male gender, alcohol consumption, and co-infection with HBV significantly increased the risk of liver cirrhosis.

Resection Margin Width Does Not Influence the Prognosis of Solitary Hepatocellular Carcinoma After Anatomic Resection: A Real-World Study from China.

The influence of resection margin (RM) width on the prognosis of solitary hepatocellular carcinoma (HCC) following anatomical resection (AR) has yet to be determined. Therefore, we conducted a real-world study to identify the optimal RM width and assess its impact on the outcomes of solitary HCC patients undergoing AR. The data pertaining to patients diagnosed with solitary HCC who underwent AR between December 2012 and December 2015 were retrospectively collected. The optimal cutoff value for the width of the RM was determined using X-tile software. The Kaplan-Meier method was utilized to compare the overall survival (OS) and disease-free survival (DFS) between the narrow and wide RM groups. Additionally, propensity score matching (PSM) was performed to minimize potential bias in the data. Of the 1033 patients who met the inclusion criteria, 293 (28.4%) were categorized into the narrow RM group (≤4 mm) and 740 (71.6%) into the wide RM group (> 4mm). Before and after PSM, there were no significant differences in OS and DFS between the two groups (before PSM: OS, HR=0.78, P=0.071; DFS, HR=0.95, P=0.620; after PSM: OS, HR=0.77, P=0.150; DFS, HR=0.90, P=0.470). Multivariate analysis demonstrated that RM width was not an independent risk factor for DFS and OS both before and after PSM (all P>0.05). However, subgroup analyses revealed that patients with ALBI grade 1, absence of cirrhosis, and AJCC stage II significantly benefited from wide RM in OS (all P< 0.05). Similarly, patients without HBV infection and absence of cirrhosis also exhibited significant benefits from wide RM in DFS (both P< 0.05). In patients with solitary HCC undergoing AR, the width of the RM does not appear to have a significant impact on their prognosis. However, in certain selected patients, a wider RM may confer benefits.

Cystic fibrosis liver disease in children - A review of our current understanding.

Cystic fibrosis is the second most common genetic disease in infancy. It is the result of a mutated channel protein, the CFTR, which secretes chloride ions, fluidifying secretions. Recent improvements in the treatment have increased life expectancy in these patients. Nevertheless, liver involvement remains the third cause of death. Unfortunately, our understating of the physiopathology is still deficient. Biliary obstruction secondary to the presence of thick secretions is considered to lead to cirrhosis. However, treatment with ursodeoxycolic acid has not changed the natural history. Furthermore, the presence of portal hypertension in the absence of cirrhosis cannot be explained. Recently, the role of CFTR as modulator of immune tolerance has been proposed, which could explain the presence of a persistent portal inflammation leading to fibrosis, and the gut-liver axis would also have a role in disease presentation and progression.

Incidence of hepatocellular carcinoma in nonalcoholic fatty liver disease without cirrhosis or advanced liver fibrosis.

HCC can develop in the absence of cirrhosis in patients with NAFLD. We aimed to estimate the incidence of HCC in patients with NAFLD with and without cirrhosis or advanced liver fibrosis. We performed a cohort study to determine the incidence of HCC in patients with NAFLD identified by the International Classification of Diseases 9/10 codes in the electronic health records of a US health care system between 2004 and 2018. The incidence of HCC was stratified by the presence or absence of cirrhosis and by the Fibrosis-4 index (FIB-4) at the time of HCC diagnosis. Of 47,165 patients with NAFLD aged 40-89 years, 981 (2.1%) developed HCC (mean follow-up 3.4y). Among patients with HCC, 842 (85.8%) had cirrhosis, while 139 (14.2%) did not. Of the 139 patients with HCC without cirrhosis-related diagnostic codes, 26 (2.7%) had FIB-4 >2.67 (advanced fibrosis likely), whereas 43 (4.4%) had FIB-4 < 1.30 (excluding advanced fibrosis). The annual incidence of HCC in patients with NAFLD with and without cirrhosis was 23.6 and 1.1 per 1000 person-years, respectively. Among patients without cirrhosis, the annual incidence of HCC was 2.8 per 1000 person-years with FIB-4 >2.67 and 0.7 per 1000 person-years with FIB-4 <1.30. Patients with NAFLD and cirrhosis were 31.8 times (95% CI, 23.3-43.4) more likely to develop HCC than those without cirrhosis and FIB-4 <1.30, after adjustment for age and sex. Patients with NAFLD without cirrhosis nor advanced fibrosis have a low incidence of HCC.

Baseline Predictors of the Long-Term Insufficient Biochemical Response in Patients with Autoimmune Hepatitis: A Single Center Experience.

The treatment response criteria in autoimmune hepatitis (AIH) have been recently updated. This study aimed to assess treatment responses in 39 (16 males) patients with AIH confirmed by histology. Prednisone added to azathioprine or mycophenolate was the most frequent first-line treatment. Serum alanine aminotransferase (ALT) levels were periodically checked for a median of 45 months. Eight (20.5%) patients presented 4 weeks non-response (NR). Baseline lower multiples of ALT above the upper normal limit (UNL) (p = 0.005), Ishak liver fibrosis score > 3 (p = 0.029), and less frequent confluent necrosis > 2 (p < 0.001) were independent predictors of NR. 24 (61.5%) patients achieved complete biochemical response (CBR) at six months. Ishak liver fibrosis score ≤ 3 (p < 0.001), lobular eosinophilic infiltrate (p < 0.001), and ≥50% decrease in serum ALT levels at week 4 (p < 0.001) were independent predictors of CBR. In addition, the GLUCRE score, derived from the multiplication of serum creatinine (mg/dL) and glucose (mg/dL) levels, were identified. A baseline GLUCRE value > 100 strongly predicted CBR failure (p = 0.003) at a follow-up greater than 12 months. In conclusion, the absence of cirrhosis and a ≥50% UNL decrease in serum ALT levels were independent predictors for CBR. A baseline GLUCRE score may help identify patients maintaining longer CBR.

Noncirrhotic portal hypertension misdiagnosed as liver cirrhosis: A rare case

Noncirrhotic portal hypertension misdiagnosed as liver cirrhosis: A rare case

Evaluation of Response to High-Dose Intravenous Vitamin K Administration.

Essential to the coagulation pathway, vitamin K (phytonadione) is used to correct clotting factor deficiencies and for reversal of warfarin-induced bleeding. In practice, high-dose intravenous (IV) vitamin K is often used, despite limited evidence supporting repeated dosing. This study sought to characterize differences in responders and nonresponders to high-dose vitamin K to guide dosing strategies. This was a case-control study of hospitalized adults who received vitamin K 10 mg IV daily for 3 days. Cases were represented by patients who responded to the first dose of IV vitamin K and controls were nonresponders. The primary outcome was change in international normalized ratio (INR) over time with subsequent vitamin K doses. Secondary outcomes included factors associated with response to vitamin K and incidence of safety events. The Cleveland Clinic Institutional Review Board approved this study. There were 497 patients included, and 182 were responders. Most patients had underlying cirrhosis (91.5%). In responders, the INR decreased from 1.89 at baseline (95% CI = [1.74-2.04]) to 1.40 on day 3 (95% CI = [1.30-1.50]). In nonresponders, the INR decreased from 1.97 (95% CI = [1.83-2.13]) to 1.85 ([1.72-1.99]). Factors associated with response included lower body weight, absence of cirrhosis, and lower bilirubin. There was a low incidence of safety events observed. In this study of mainly patients with cirrhosis, the overall adjusted decrease in INR over 3 days was 0.3, which may have minimal clinical impact. Additional studies are needed to identify populations who may benefit from repeated daily doses of high-dose IV vitamin K.

Serum zinc levels in cancer patients are low and difficult to elevate when complicated by liver cirrhosis: A retrospective study.

In this study, we analyzed blood zinc concentration in patients with various cancer types and the degree of improvement in relation to the underlying disease following treatment with zinc preparations. Serum zinc levels of 530 cancer patients whose blood zinc levels were measured at our hospital from 2016 to 2021 were retrospectively examined in accordance with the primary disease. Changes in zinc levels were analyzed in 155 patients whose zinc levels had been measured on 2 or more occasions in accordance with whether they had received zinc preparations. In addition, the concentration course of zinc before and after zinc formulation administration in 73 patients was examined in accordance with the presence or absence of liver cirrhosis complications. Mean serum zinc levels were below normal in all carcinomas measured, and zinc levels were significantly lower in cirrhosis-hepatocarcinoma cases than in other primary disease cases. Furthermore, serum zinc levels in patients who did not receive zinc preparations decreased significantly over time. In patients who received zinc preparations, the elevated levels of zinc after treatment were significantly lower in patients with cirrhosis than in those without cirrhosis. There was a weak inverse correlation between pre-dose zinc concentration and increased zinc concentration in patients with cirrhosis. In the analysis of covariance, the presence of liver cirrhosis was predominantly correlated with elevated zinc per dose. In summary, serum zinc levels in cancer patients are low and especially low in cancer patients with liver cirrhosis compared with those without cirrhosis after the administration of zinc preparations.

Prognostic role of platelet lymphocyte ratio (PLR) among patients with hepatocellular carcinoma undergoing liver transplantation

Abstract Background Hepatocellular carcinoma (HCC) is the fifth most common cancer worldwide, but it is so aggressive that is the third most common cause of cancer related death. We aim to study the role of PLR in prognosis of HCC and to see if it can be a predictor of overall survival and disease free survival among HCC patients that received liver transplantation in our centre. Patients and Methods This is a single centre retrospective analysis of prospectively collected data. The study was carried out in liver transplant institute of Inonu University, Malatya, Turkey. Consecutive patients that received liver transplantation for HCC and survive for at least 90 days post transplantation were included in the study. Data was collected regarding age, gender, presence or absence of cirrhosis, cause of cirrhosis, number of nodules, maximum size of the tumour, preoperative PLR, pre-transplant GGT, type of transplant, presence or absence of microvascular invasion, overall survival and disease free survival. The study was censored on June 2022. Data was analyzed using SPSS version 25. Results Platelet lymphocyte ratio was found to be significantly associated with some poor prognostic factors of HCC in our patients. We found that PLR is significantly associated with maximum tumour diameter (MTD) and total tumor diameter (TTD) with p= &lt;0.0001 and 0.0016 respectively. Univariate analysis revealed that PLR is a predictor of worse DFS or OS but when subjected to multivariate analysis, we found that PLR is not an independent predictor of OS and DFS. Conclusion Platelet lymphocyte ratio is associated with poor prognostics feature of hepatocellular carcinoma.

Clinical characteristics of hospitalized patients with metabolic-associated fatty liver disease-related liver cancer: data from a single center, 2010-2019.

Metabolic-associated fatty liver disease (MAFLD) has become an important cause of liver cancer. The current understanding of MAFLD-related liver cancer is not sufficient, however. The objective of this study was to investigate the clinical and metabolic characteristics of inpatients with MAFLD-related liver cancer. This is a cross-sectional investigation. An investigation was conducted to collect the cases of hepatic malignant tumor hospitalized in Beijing Ditan Hospital, Capital Medical University from 1 January 2010 to December 31 2019. The basic information, medical history, laboratory examination results, and imaging examination results of 273 patients diagnosed with MAFLD-related liver cancer were recorded. The general information and metabolic characteristics of patients with MAFLD-related liver cancer were analyzed. In total, 5958 patients were diagnosed with hepatic malignant tumor. Among them, liver cancer due to other causes accounted for 6.19% (369/5958), MAFLD-related liver cancer was diagnosed in 273 cases of them. From 2010 to 2019, MAFLD-related liver cancer showed an increasing trend. Among 273 patients with MAFLD-related liver cancer, 60.07% were male, 66.30% were ⩾60 years old, and 43.22% had cirrhosis. The 273 patients were comprised by 38 patients with evidence of fatty liver and 235 patients without evidence of fatty liver. There was no significant difference in the proportions of sex, age, overweight/obesity, type 2 diabetes, and the presence of ⩾2 metabolic-related factors between the two groups. In the group without evidence of fatty liver, 47.23% patients had cirrhosis, which was significantly higher than 18.42% in the group with evidence of fatty liver (p < 0.001). MAFLD-related liver cancer should be considered in liver cancer patients with metabolic risk factors. Half of MAFLD-related liver cancer occurred in the absence of cirrhosis.

Porto-sinusoidal vascular disease: a new definition of an old clinical entity.

Porto-sinusoidal vascular disease (PSVD) is defined as a vascular liver disease characterized by the absence of cirrhosis and the presence of characteristic histological features, with or without the presence of portal hypertension (PH). Half of the patients with PSVD also have associated disease that may contribute to the development of PSVD. Patients usually remain asymptomatic until complications of PH arise. Variceal bleeding and portal vein thrombosis are major complications associated with PSVD. The treatment is focused on managing complications of PH, mainly through primary prophylaxis of variceal bleeding and treatment of portal vein thrombosis. Currently, there is insufficient evidence to support the use of anticoagulants for thrombosis prevention in these patients. Despite the increase of recognition of PSVD, further research is needed to enable early disease diagnosis, establish optimal screening methods, and develop strategies to slow down disease progression.