Complication Of Liver Cirrhosis Research Articles

Gut microbiome and metabolome signatures in liver cirrhosis-related complications.

Shifts in the gut microbiota and metabolites are interrelated with liver cirrhosis progression and complications. However, causal relationships have not been evaluated comprehensively. Here, we identified complication-dependent gut microbiota and metabolic signatures in patients with liver cirrhosis. Microbiome taxonomic profiling was performed on 194 stool samples (52 controls and 142 cirrhosis patients) via V3-V4 16S rRNA sequencing. Next, 51 samples (17 controls and 34 cirrhosis patients) were selected for fecal metabolite profiling via gas chromatography mass spectrometry and liquid chromatography coupled to time-of-flight-mass spectrometry. Correlation analyses were performed targeting the gut- microbiota, metabolites, clinical parameters, and presence of complications (varices, ascites, peritonitis, encephalopathy, hepatorenal syndrome, hepatocellular carcinoma, and deceased). Veillonella bacteria, Ruminococcus gnavus, and Streptococcus pneumoniae are cirrhosis-related microbiotas compared with control group. Bacteroides ovatus, Clostridium symbiosum, Emergencia timonensis, Fusobacterium varium, and Hungatella_uc were associated with complications in the cirrhosis group. The areas under the receiver operating characteristic curve (AUROCs) for the diagnosis of cirrhosis, encephalopathy, hepatorenal syndrome, and deceased were 0.863, 0.733, 0.71, and 0.69, respectively. The AUROCs of mixed microbial species for the diagnosis of cirrhosis and complication were 0.808 and 0.847, respectively. According to the metabolic profile, 5 increased fecal metabolites in patients with cirrhosis were biomarkers (AUROC > 0.880) for the diagnosis of cirrhosis and complications. Clinical markers were significantly correlated with the gut microbiota and metabolites. Cirrhosis-dependent gut microbiota and metabolites present unique signatures that can be used as noninvasive biomarkers for the diagnosis of cirrhosis and its complications.

Chinese consensus on the management of liver cirrhosis.

Liver cirrhosis, characterized by diffuse necrosis, insufficient regeneration of hepatocytes, angiogenesis, severe fibrosis, and the formation of pseudolobules, is a progressive, chronic liver disease induced by a variety of causes. It is clinically characterized by liver function damage and portal hypertension, and many complications may occur in its late stage. Based on the updated practice guidelines, expert consensuses, and research advances on the diagnosis and treatment of cirrhosis, the Chinese Society of Gastroenterology of Chinese Medical Association established the current consensus to standardize the clinical diagnosis and management of liver cirrhosis and guide clinical practice. This consensus contains 43 statements on the etiology, pathology and pathogenesis, clinical manifestations, major complications, diagnosis, treatment, prognosis, and chronic disease control of liver cirrhosis. Since several practice guidelines and expert consensuses on the complications of liver cirrhosis have been published, this consensus emphasizes the research progress of liver cirrhosis itself.

Serum Branched-Chain Amino Acids and Long-Term Complications of Liver Cirrhosis: Evidence from a Population-Based Prospective Study.

The role of serum branched-chain amino acids (BCAAs) in long-term liver cirrhosis complication events remains unclear. We aimed to evaluate the associations between serum BCAAs and the risk of liver-related events. We included a total of 64,005 participants without liver cirrhosis complication events at baseline from the UK Biobank. Cox proportional hazards regression models were utilized to estimate multivariable hazard ratios (HRs) and 95% CIs for the incidence of liver cirrhosis complication events, adjusting for potential confounders, including sociodemographic and lifestyle factors. Relationships between serum BCAAs and liver cirrhosis complications were examined using nonparametrically restricted cubic spline regression. During a median follow-up of 12.7 years, 583 participants developed liver cirrhosis complication events. The multivariable Cox regression model suggested that total BCAAs (HR = 0.88, 95% CI 0.82-0.95), serum leucine (HR = 0.88, 95% CI 0.81-0.95), serum isoleucine (HR = 0.88, 95% CI 0.82-0.96), and serum valine (HR = 0.87, 95% CI 0.82-0.96) were all independent protective factors for liver cirrhosis complications after adjustment for sociodemographic and lifestyle factors. Cox models with restricted cubic splines showed U-shaped associations between serum valine and liver cirrhosis complication incidence. Serum total BCAA and isoleucine concentrations might reduce the risk of liver cirrhosis complications by raising the risk of (type 2 diabetes mellitus) T2DM. Lower serum BCAA levels exacerbate the long-term risk of liver cirrhosis complications. Future studies should confirm these findings and identify the biological pathways of these associations.

Fructooligosaccharides reverses hepatic vascular dysfunction and dysbiosis in rats with liver cirrhosis and portal hypertension.

Portal hypertension leads to lethal complications in liver cirrhosis. Oxidative stress induced hepatic vascular dysfunction, which exaggerated vasoconstriction and increases hepatic vascular resistance (HVR). Gut dysbiosis further exacerbates portal hypertension. Fructooligosaccharides are prebiotics with potent antioxidant effect. This study aimed to evaluate the roles of fructooligosaccharides in portal hypertension-related vascular dysregulation and gut microbiome. Sprague-Dawley rats received bile duct ligation to induce cirrhosis or sham operation as controls. The rats then randomly received fructooligosaccharides or vehicle for 4 weeks. Experiments were performed on the 29th day after operations. Fructooligosaccharides did not affect portal pressure. Interestingly, fructooligosaccharides significantly attenuated HVR (p = .03). Malondialdehyde, an oxidative stress marker, reduced significantly in the liver in fructooligosaccharides-treated group. In addition, superoxide dismutase and trolox equivalent antioxidant capacity increased in the treatment group. On the other hand, vasodilatation-related protein expressions, GTPCH and phospho-eNOS, enhanced significantly. Fructooligosaccharides had no adverse vasodilatation effects on splanchnic vascular system or porto-systemic collateral systems. Locomotor function was not affected by fructooligosaccharides. Faecal microbiota analysis showed that Negativicutes, Selenomonadales and Lactobacillus salivarius reduced in the fructooligosaccharides-treated group. In conclusion, fructooligosaccharides attenuate hepatic vascular dysfunction in cirrhotic rats via at least partly, ameliorate of dysbiosis and oxidative stress.

Analysis of factors related to recanalization of portal vein thrombosis in liver cirrhosis: a retrospective cohort study

BackgroundPortal vein thrombosis (PVT) is a common complication of liver cirrhosis, yet there are fewer studies about predictors of PVT recanalization. We aimed to further explore the predictors of recanalization in cirrhotic PVT to facilitate accurate prediction of patients’ clinical status and timely initiation of appropriate treatment and interventions. To further investigate the benefits and risks of anticoagulant therapy in cirrhotic PVT patients.MethodsA retrospective cohort study of patients with cirrhotic PVT in our hospital between January 2016 and December 2022, The primary endpoint was to analyze predictors of PVT recanalization by COX regression. Others included bleeding rate, liver function, and mortality.ResultsThis study included a total of 82 patients, with 30 in the recanalization group and 52 in the non-recanalization group. Anticoagulation therapy was the only independent protective factor for portal vein thrombosis recanalization and the independent risk factors included massive ascites, history of splenectomy, Child-Pugh B/C class, and main trunk width of the portal vein. Anticoagulation therapy was associated with a significantly higher rate of PVT recanalization (75.9% vs. 20%, log-rank P < 0.001) and a lower rate of PVT progression (6.9% vs. 54.7%, log-rank P = 0.002). There was no significant difference between different anticoagulation regimens for PVT recanalization. Anticoagulation therapy did not increase the incidence of bleeding complications(P = 0.407). At the end of the study follow-up, Child-Pugh classification, MELD score, and albumin level were better in the anticoagulation group than in the non-anticoagulation group. There was no significant difference in 2-year survival between the two groups.ConclusionAnticoagulation, massive ascites, history of splenectomy, Child-Pugh B/C class, and main portal vein width were associated with portal vein thrombosis recanalization. Anticoagulation may increase the rate of PVT recanalization and decrease the rate of PVT progression without increasing the rate of bleeding. Anticoagulation may be beneficial in improving liver function in patients with PVT in cirrhosis.

Non Invasive Assessment of Pulmonary Artery Pressure in Children with Portal Hypertension

Abstract Background Pulmonary artery hypertension is a complication of liver cirrhosis with Portal Hypertension (PHT). It has been mentioned in case reports or small series of children. Fewinformation known on its prevalence and long-term survival in childhood liver disease. This study will assess the Pulmonary Atery Pressure (PAP) in children with PHT in Pediatric Hepatologyclinic, Ain Shams University Children Hospital in order to identify clinical characteristics of Porto PH and its prevalence among those children. Aim of the Work To assess the PAP using Echocardiography in children with PHT who attend Pediatric Hepatology clinic, Ain Shams University Children Hospital. Patients and Methods This case-control study was conducted on thirty patients enrolled from Pediatric Hepatology clinic, Ain Shams University Children Hospital in a period of one year from June 2021 to June 2022 according to inclusion criteria : history of hematemesis and melena, clinical examination: Splenomegaly, dilated anterior abdominal wall vessels, ascites ± firm hepatomegaly and imaging: Ultrasonography (US) /color Doppler-US (CDUS): Splenomegaly, presence of Porto collateral vessels and ascites. This information will be completed with data on liver size, echo texture, and margins which can suggest underlying cirrhosis, portal vein diameter, portal blood flow velocity, direction of blood flow in portal vein with age ranging from 1 to 16 years with median (IQR) of 8 (4.5-12) years; they were 11 females (36.7%) and 19 males (63.3%) and thirty healthy matched age and sex as a control group. Results In our study, MPAP was 9.79 ± 2.21 mmHg (7.2-18.2 mmHg). Statistically, there was statistically significant increase in the level of TR velocity, TR PG, RVSP and MPAP in patients with PHT than control group with p-value &amp;lt;0.001, 0.001; 0.001 and &amp;lt;0.001; respectively. Also, there was statistically significant increase in the percentage of patients with abnormal TR PG and patients with elevated systolic PAP in patients with PHT (20.0%) than control group (0.0%) with p-value = 0.010 and 0.010; respectively. Also, there was statistically significant decrease in the level of PA acceleration time (ms) in patients with PHT than control group with p-value &amp;lt;0.001. Also, there was statistically significant increase in the level of PAEDP (mmHg) and LA (cm) in patients with PHT than control group with p-value &amp;lt;0.001 and 0.014; respectively. In our studied group of patients we did not found any of them has PH despite the higher parameters of their Echo studies and that needs follow up of those patients. So the prevalence of PH in those patients is 0%. Conclusion PHT is an important risk factor of development of PH in children. Transthoracic echocardiography can be reliably used as an initial non-invasive, safe and reliable modality for the assessment of pulmonary artery hypertension in children, and can obviate the need of right heart catheterization in some patients, especially those with mild PHT.

Serum Prolactin as a Marker of the Severity of Liver Cirrhosis in a Tertiary Hospital in India: A Cross-Sectional Study.

In India, cirrhosis is becoming a growing concern, leading to an unmet need for new non-invasive markers to assess the severity of liver disease. Serum prolactin is one such marker. To determine the association between serum prolactin, the severity of liver cirrhosis, and its complications such as ascites, hepatic encephalopathy, and esophageal varices. This cross-sectional study involved 117 patients with liver cirrhosis. They were evaluated for some complications such as ascites, esophageal varices, and hepatic encephalopathy, as well as for severity by using the Child-Turcotte-Pugh (CTP) score. Serum prolactin levels were measured, and their relationship with both the severity and complications of liver cirrhosis was determined. A P value of < 0.05 was considered significant. The mean age of the patients was 48.3 ± 12.08 years, and the majority (80.3%) were males. Seventy-one percent of the patients had elevated serum prolactin levels (>19.40 ng/mL). Elevated serum prolactin was found in approximately 95.0% and 86.8% of patients with hepatic encephalopathy and ascites, respectively. The median serum prolactin levels were significantly associated with esophageal varices grades (P = 0.043) and hepatic encephalopathy (P < 0.001). The sensitivity and specificity of serum prolactin for predicting severe CTP scores were 81.6% and 91.2%, respectively, with a diagnostic accuracy of 87.2%. On multivariate regression analysis, ascites (AOR = 3.8, 95%CI = 1.29-10.98, P = 0.015), hepatic encephalopathy (AOR = 6.1, 95%CI = 0.68-53.78, P = 0.012), CTP class B (AOR = 5.9, 95%CI = 1.39-24.68, P = 0.016), and CTP class C (AOR = 13.4, 95%CI = 2.25-82.21, P = 0.004) were significantly associated with elevated serum prolactin levels. There was a significant association between serum prolactin levels and CTP classes, esophageal varices, ascites, and hepatic encephalopathy in patients with liver cirrhosis.

Pathophysiology and therapeutic options for cirrhotic portal hypertension.

Portal hypertension represents the primary non-neoplastic complication of liver cirrhosis and has life-threatening consequences, such as oesophageal variceal bleeding, ascites, and hepatic encephalopathy. Portal hypertension occurs due to increased resistance of the cirrhotic liver vasculature to portal blood flow and is further aggravated by the hyperdynamic circulatory syndrome. Existing knowledge indicates that the profibrogenic phenotype acquired by sinusoidal cells is the initial factor leading to increased hepatic vascular tone and fibrosis, which cause increased vascular resistance and portal hypertension. Data also suggest that the phenotype of hepatic cells could be further impaired due to the altered mechanical properties of the cirrhotic liver itself, creating a deleterious cycle that worsens portal hypertension in the advanced stages of liver disease. In this Review, we discuss recent discoveries in the pathophysiology and treatment of cirrhotic portal hypertension, a condition with few pharmacological treatment options.

Risk factors for renal impairment after liver transplantation in Mongolia: a retrospective single-center study.

Renal impairment (RI) is a frequent complication of liver cirrhosis and is associated with increased mortality and morbidity. Liver transplantation (LT) serves as an effective treatment method for patients with cirrhosis who have impaired renal function. However, renal function often declines after LT, influenced by various factors. This study aimed to investigate the factors contributing to RI following LT in our cases. We analyzed the demographic data, preoperative and perioperative parameters, and postoperative outcomes of patients who underwent LT at the First Central Hospital of Mongolia from September 2011 to December 2022. Renal function was assessed by measuring the glomerular filtration rate using the Cockcroft-Gault creatinine clearance formula pretransplantation and at 24 hours, 72 hours, 7 days, 14 days, and 28 days post-LT. Several factors increased the risk of RI among recipients. These included female sex (odds ratio [OR], 3.06; 95% confidence interval [CI], 1.58-5.91), Child-Turcotte-Pugh (CTP) scores of B and C (OR, 4.23; 95% CI, 0.92-19.41 and OR, 7.68; 95% CI, 1.67-35.30, respectively), preoperative continuous renal replacement therapy (CRRT; OR, 5.86; 95% CI, 1.1-31.21), and a high graft-to-recipient weight ratio (GRWR; OR, 3.45; 95% CI, 1.23-9.63). Additionally, the survival rates for recipients with RI post-LT were 93.4% at 1 year and 78.1% at 3 years. Female sex, a high CTP score, preoperative CRRT, and high GRWR were identified as risk factors for RI after LT in Mongolia.

Evaluation of QT prolongation in children with cirrhosis and its association with the severity of liver diseases

Summary: Introduction: Prolongation of the QT interval in an electrocardiogram (ECG) is seen in more than 60% of adults with advanced cirrhosis. According to careful research, people with cirrhosis who have their QT intervals prolonged had worse survival rates, more severe disease symptoms, and faster development of their condition. Considering the importance of predicting complications of liver cirrhosis in children and the limited number of studies related to the relationship between prolonged QT and the severity of liver disease in children, in this study, prolonged QT in children with liver cirrhosis and its relationship with the severity of liver disease was investigated. Methods: In the present study, children under 18 years of age with liver cirrhosis were evaluated in the list of liver transplants referred to Abu Ali Sina Organ Transplantation Hospital in Shiraz between 2019 and 2021. QT was calculated based on two pediatric cardiologists‘ 12-lead ECG from liver transplant surgery. Results: In this study, 130 patients with liver cirrhosis with an average age of 7.05±5.34 years were evaluated. The average length of the QT segment was reported as 397±31milliseconds. Only 4 (3%) had a long QT segment in all the studied patients. The comparison of the Meld/ Peld criterion and Child criterion in the two groups of regular QT and prolonged QT showed that the mean of both criteria was signifi cantly longer in the standard QT group (P = 0.018, P = 0.038). Also, prolonged QT showed a signifi cant relationship with the cause of liver cirrhosis (P = 0.003). Conclusion: Our study is one of the fi rst to examine the relationship between QT and severity of cirrhosis in children. Based on the results of this study, prolonged QT is associated with severity of liver disease. Key words: liver – cirrhosis – children – long QT – fi brosis

Pay attention to the diagnosis and treatment of "easily neglected" complications in liver cirrhosis

Managing cirrhosis complications is an important measure for improving patients' clinical outcomes. Therefore, in order to provide a complete disease assessment and comprehensive treatment, improve quality of life, and improve the prognosis for patients with cirrhosis, it is necessary to pay attention to complications such as thrombocytopenia and portal vein thrombosis in addition to common or severe complications such as ascites, esophagogastric variceal bleeding, hepatic encephalopathy, and hepatorenal syndrome. The relevant concept that an effective albumin concentration is more helpful in predicting the cirrhosis outcome is gradually being accepted; however, the detection method still needs further standardization and commercialization.

Reply: Regarding the use of decision curve analysis in predicting long-term complications of liver cirrhosis.

Reply: Regarding the use of decision curve analysis in predicting long-term complications of liver cirrhosis.

A new model of portal vein thrombosis in rats with cirrhosis induced by partial portal vein ligation plus carbon tetrachloride and intervened with rivaroxaban

Background and aimsPortal vein thrombosis (PVT) is a common complication of liver cirrhosis that can aggravate portal hypertension. However, there are features of both PVT and cirrhosis that are not recapitulated in most current animal models. In this study, we aimed to establish a stable animal model of PVT and cirrhosis, intervene with anticoagulant, and explore the related mechanism.MethodsFirst, 49 male SD rats received partial portal vein ligation (PPVL), and 44 survival rats were divided into 6 groups: PPVL control group; 4-week, 6 -week, 8-week, and 10-week model group; and the rivaroxaban (RIVA)-treated group. The rats were intoxicated with or without carbon tetrachloride (CCl4) for 4–10 weeks. Seven normal rats were used as the normal controls. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and parameters for blood coagulation were all assayed with kits. Liver inflammation, collagen deposition and hydroxyproline (Hyp) levels were also measured. The extrahepatic macro-PVT was observed via portal vein HE staining, etc. The intrahepatic microthrombi was stained via fibrin immunohistochemistry. The portal blood flow velocity (PBFV) and diameter were detected via color Doppler ultrasound. Vascular endothelial injury was evaluated by von Willebrand Factor (vWF) immunofluorescence. Fibrinolytic activity was estimated by western blot analysis of fibrin and plasminogen activator inhibitor-1 (PAI-1).ResultsAfter PPVL surgery and 10 weeks of CCl4 intoxication, a rat model that exhibited characteristics of both cirrhosis and extra and intrahepatic thrombi was established. In cirrhotic rats with PVT, the PBFV decreased, both factors of pro- and anti-coagulation decreased, but with relative hypercoagulable state, vascular endothelial injured, and fibrinolytic activity decreased. RIVA-treated rats had improved coagulation function, increased PBFV and attenuated thrombi. This effect was related to the improvements in endothelial injury and fibrinolytic activity.ConclusionsA new rat model of PVT with cirrhosis was established through partial portal vein ligation plus CCl4 intoxication, with the characteristics of macrothrombi at portal veins and microthrombi in hepatic sinusoids, as well as liver cirrhosis. Rivaroxaban could attenuate PVT in cirrhosis in the model rats. The underlying mechanisms of PVT formation in the rat model and pharmacological action of rivaroxaban are related to the regulation of portal blood flow, coagulant factors, and vascular endothelial cell function.

Liver sinusoidal endothelial cells contribute to portal hypertension through collagen type IV-driven sinusoidal remodeling.

Portal hypertension (PHTN) is a severe complication of liver cirrhosis and is associated with intrahepatic sinusoidal remodeling induced by sinusoidal resistance and angiogenesis. Collagen type IV (COL4), a major component of basement membrane, forms in liver sinusoids upon chronic liver injury. However, the role, cellular source, and expression regulation of COL4 in liver diseases are unknown. Here, we examined how COL4 is produced and how it regulates sinusoidal remodeling in fibrosis and PHTN. Human cirrhotic liver sample RNA sequencing showed increased COL4 expression, which was further verified via immunofluorescence staining. Single-cell RNA sequencing identified liver sinusoidal endothelial cells (LSECs) as the predominant source of COL4 upregulation in mouse fibrotic liver. In addition, COL4 was upregulated in a TNF-α/NF-κB-dependent manner through an epigenetic mechanism in LSECs in vitro. Indeed, by utilizing a CRISPRi-dCas9-KRAB epigenome-editing approach, epigenetic repression of the enhancer-promoter interaction showed silencing of COL4 gene expression. LSEC-specific COL4 gene mutation or repression in vivo abrogated sinusoidal resistance and angiogenesis, which thereby alleviated sinusoidal remodeling and PHTN. Our findings reveal that LSECs promote sinusoidal remodeling and PHTN during liver fibrosis through COL4 deposition.

Assessment of single and combined administration of ubiquinone and lactoferrin on histopathology, ultrastructure, oxidative stress, and WNT4 expression gene induced by thioacetamide on hepatorenal system of adult male rats

BackgroundHepatorenal syndrome is a life-threatening medical complication of liver cirrhosis. Hepatic cirrhosis is commonly accompanied by rapid failure of renal functions. Thioacetamide (TAA) is a potent hepatotoxin and a class 2-type carcinogen. Ubiquinone (Coq10) and lactoferrin (LF) are potent antioxidants with antifibrotic and antiinflammatory effects. However, whether Coq10 and LF reduce the hepatorenal injury induced by TAA remains unclear. Here, we investigated the potential protective effect of both/or Coq10 and LF in ameliorating TAA-induced hepatorenal injury and the role of WNT4 gene expression in detecting TAA-induced renal injury in rats. Seventy healthy and mature male Sprague Dawley rats, weighting (200 g ± 20 g) and aging (4–6) weeks were randomly divided into seven groups (n = 10): control, Coq10, LF, TAA, TAA + Coq10, TAA + LF, and TAA + Coq10 + LF. The hepatorenal injury was induced through intraperitoneal (i.p.) injection of TAA (150 mg/kg/twice/weekly) for nine weeks. Coq10 (10 mg/kg/day) and LF (200 mg/kg/day) were orally administered for nine weeks.ResultsTAA induced marked hepatorenal damage, evident by the significant increase in the alanine aminotransferase (ALT), aspartate transaminase (AST), serum creatinine (SCr) activities, and the blood urea nitrogen (BUN) level. Besides, the significant increases in concentrations of malondialdehyde (MDA) and nitric oxide (NOx) together with significant decreases in the activities of catalase (CAT) and superoxide dismutase (SOD). The histopathological analysis of the TAA group showed obvious fibrosis, steatosis, and inflammation of the hepatic parenchyma as well as severe glomerular and tubular damage of the renal parenchyma. In addition, TAA induced marked ultrastructural alterations and up-regulation in the expression of the WNT4 gene in the kidney. Meanwhile, the biochemical, histopathological, and ultrastructural alterations were significantly decreased with significant down-regulation in the expression of WNT4 in the groups exposed to TAA and treated with Coq10 and LF.ConclusionOur data suggested that Coq10 and LF could have protective effects on TAA hepatorenal damage, through improving the hepatic and renal functions, reduction of oxidative stress, structural and ultrastructural alterations, besides down-regulation in the expression of WNT4.

Impact of sarcopenia on variceal rebleeding in patients after endoscopic therapy: a multicenter retrospective cohort study based on propensity score matching

Background Sarcopenia is a common complication of liver cirrhosis and can be used for predicting dismal prognostic outcomes. This study aimed to evaluate the role of sarcopenia in rebleeding and mortality of liver cirrhosis patients after endoscopic therapy. Methods The liver cirrhosis patients who received endoscopic treatment were enrolled. Propensity score matching (PSM) was used to overcome selection bias. Two-year rebleeding episodes and mortality after endoscopic therapy were recorded. Results A total of 109 (32.4%) sarcopenia patients were reported. Before PSM, the frequency of rebleeding was significantly higher in the sarcopenia group relative to the non-sarcopenia group (41.3% vs. 15.9%, p < 0.001). Moreover, the multivariable analysis revealed that sarcopenia (p < 0.001, HR:2.596, 95% CI 1.591–4.237) was independently associated with a 2-year rebleeding episode. After PSM, the sarcopenia group exhibited an increased rebleeding rate as compared with non-sarcopenia group (44.4% vs. 15.3%, p < 0.001). According to multivariable analysis, sarcopenia (p < 0.001, HR:3.490, 95% CI 1.756–6.938) was identified as a significant predictor for 2-year rebleeding. Conclusion Sarcopenia was significantly associated with a high 2-year rebleeding rate in liver cirrhosis patients after endoscopic treatment. Therefore, the precise evaluation of a patient’s nutritional status, including sarcopenia becomes mandatory before endoscopic treatment.

A randomized controlled trial of a postdischarge nursing intervention for patients with decompensated cirrhosis.

Few randomized trials have evaluated the effect of postdischarge interventions for patients with liver cirrhosis. This study assessed the effects of a postdischarge intervention on readmissions and mortality in patients with decompensated liver cirrhosis. We conducted a randomized controlled trial at a specialized liver unit. Adult patients admitted with complications of liver cirrhosis were eligible for inclusion. Participants were allocated 1:1 to standard follow-up or a family-focused nurse-led postdischarge intervention between December 1, 2019, and October 31, 2021. The 6-month intervention consisted of a patient pamphlet, 3 home visits, and 3 follow-up telephone calls by a specialized liver nurse. The primary outcome was the number of readmissions due to liver cirrhosis. Of the 110 included participants, 93% had alcohol as a primary etiology. We found no significant differences in effects in the primary outcomes such as time to first readmission, number of patients readmitted, and duration of readmissions or in the secondary outcomes like health-related quality of life and 6- and 12-month mortality. A post hoc exploratory analysis showed a significant reduction in nonattendance rates in the intervention group (RR: 0.28, 95% CI: 0.13-0.54, p=0.0004) and significantly fewer participants continuing to consume alcohol in the intervention group (p=0.003). After 12 months, the total number of readmissions (RR: 0.76, 95% CI: 0.59-0.96, p=0.02) and liver-related readmissions (RR: 0.55, 95% CI: 0.36-0.82, p=0.003) were reduced in the intervention group. A family-focused postdischarge nursing intervention had no significant effects on any of the primary or secondary outcomes. In a post hoc exploratory analysis, we found reduced 6-month nonattendance and alcohol consumption rates, as well as reduced 12-month readmission rates in the intervention group.

SURGICAL MANAGEMENT FOR BLEEDING FROM ESOPHAGUS VARICOSE VEINS

Portal hypertension and bleeding from varicose veins of the esophagus and stomach due to portal hypertension are the most dangerous and threatening complications of liver cirrhosis (6,7). The mortality rate from ongoing bleeding is about 4-8% (6,8,11). 20% of patients with acute bleeding die within 6 weeks compared with other complications (6,8,11). Mortality from rebleeding in patients with decompensated stages of liver cirrhosis reaches up to 78% (7). Currently, there are a number of different methods for the treatment of portal hypertension complicated by bleeding from varices of the esophagus and stomach (VES), including both endovascular interventions and endoscopic treatment. Many surgical methods have been developed to reduce pressure in the portal vein and prevent re-bleeding. But these operations have their limitations. Minimally invasive methods for bleeding from VES include endoscopic sclerotherapy, endoscopic ligation, endovascular transjugular intrahepatic portosystemic shunt, endovascular percutaneous transhepatic embolization of gastroesophageal varices and other combined methods. Surgical practice has proven that treatment results and patient survival are much better with delayed and especially with planned surgical interventions. At the same time, in the last decade, preference has been given to indirect portocaval anastomoses, and recently many adherents of the Sugiura operation have appeared (3,10,13). Thanks to the joint efforts of gastroenterologists, radiologists and surgeons in the treatment of bleeding from the esophagus with portal hypertension, gastrointestinal endoscopy and invasive diagnostic and therapeutic radiographic methods have acquired significant importance. Transendoscopic sclerotherapy of VRV has become particularly widespread. Recurrence of hemorrhages is possible in approximately 10% of cases, which is not much higher than the best results of surgical treatment (1,6,11), and complications (mediastenitis, pyothorax, bleeding, stenosis) develop in only 2% of patients (3).

Awareness of Atherosclerosis and Cardiovascular Events Among Undergraduate Healthcare Professionals

The word atherosclerosis consists of two parts: atherosis (accumulation of fats accompanied by several macrophages) and sclerosis (fibrosis layer comprising smooth muscle cells. The presence of hyperlipaemia is the major risk issue factor for coronary artery disease. In 2016 advances in atherosclerosis research were focused on the discovery and validation of newly targeted genetics and mechanistic connection to atherothrombotic heart diseases. The Survey on awareness about the risk factors and complications of liver cirrhosis among college students was conducted using a Google form link. We have distributed our survey among 100 college students. Pie charts and Bar diagrams were used to represent output variables. Results showed that the knowledge of cardiovascular 54.00 % said No and 46.00 % said yes. Stroke caused due to lack of blood supply to 44.00 % said heart, 50.00 % said brain, and 6.00 % said I don’t know. These findings conclude that the majority of the population is unaware of the risk factors such as obesity, LDL, and family history, which lead to the development of atherosclerosis, but only a few populations are aware of stress, smoking, coronary heart attack, cholesterol, sleep apnea, HDL, work pressure, physical activity, heart disease, and coronary disease that leads to atherosclerosis.

Transplantace jater pro deficit alfa-1-antitrypsinu

Summary: Alpha-1-antitrypsin deficiency (AATD) is an autosomal codominant genetic condition which manifests with lung emphysema at young age and with liver disease. A point mutation in the SERPINA1 gene, which encodes 1-antitrypsin (AAT), causes a defective secondary structure of the protein, which subsequently accumulates in the endoplasmic reticulum of hepatocytes and is not transported into the blood and body fluids. Deficiency of AAT, which inhibits neutrophil elastase in the lung, thus allows proteolytic damage to the connective tissue of the lung, leading to the development of emphysema. Liver disease is caused by the accumulation of the mutant AAT in liver cells, contributing to proteotoxic liver injury that can lead to liver cirrhosis. Liver transplantation (LT) is the only curative method; after LT, the recipient has the phenotype of the donor organ and normal serum AAT concentrations. The indication for LT should be considered in all patients with AATD and end-stage liver disease. The patients should be referred to the transplant centre when severe complications of liver cirrhosis, such as variceal bleeding, ascites, encephalopathy, and hepatorenal syndrome. In patients with hepatocellular carcinoma, LT represents an optimal treatment modality in the case of an early, unresectable tumour. The timing of LT is crucial; LT should be performed before the patient develops life-threatening complications of end-stage liver disease. LT should be considered in patients of Child-Pugh classification B and C and MELD score of 15 points or higher. Survival of patients after LT for AADT is excellent. Key words: 1-antitrypsin – 1-antitrypsin deficiency – liver cirrhosis – end-stage liver disease – hepatocellular carcinoma – live transplantation