Alcoholic Liver Disease Patients Research Articles

Which patient should have preference for liver transplantation: ALD?

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Nutritional Support for Alcoholic Liver Disease.

Malnutrition is a common finding in alcohol use disorders and is associated with the prognosis of patients with alcoholic liver disease (ALD). These patients also frequently show deficiencies in vitamins and trace elements, increasing the likelihood of anemia and altered cognitive status. The etiology of malnutrition in ALD patients is multifactorial and complex and includes inadequate dietary intake, abnormal absorption and digestion, increased skeletal and visceral protein catabolism, and abnormal interactions between ethanol and lipid metabolism. Most nutritional measures derive from general chronic liver disease recommendations. Recently, many patients with ALD have been diagnosed with metabolic syndrome, which requires individualized treatment via nutritional therapy to avoid overnutrition. As ALD progresses to cirrhosis, it is frequently complicated by protein-energy malnutrition and sarcopenia. Nutritional therapy is also important in the management of ascites and hepatic encephalopathy as liver failure progresses. The purpose of the review is to summarize important nutritional therapies for the treatment of ALD.

THE SIGNIFICANCE OF TRANSAMINASES AND DERITIS RATIO FOR PREDICTING ALCOHOLIC LIVER DISEASE

Background: A signicant public health issue is alcoholic liver disease (ALD). At any stage of the disease, the Deritis ratio (AST/ALT) is more sensitive than other standard criteria in detecting biochemical abnormalities in ALD. This study's objective was to evaluate the importance of transaminases and the Deritis ratio as well as their potential prognostic value in alcoholic liver disease patients. Materials and Methods: It was a hospital-based retrospective study that used information kept in the Biochemistry department of Sri Venkateswara Medical College in Tirupati. Age, gender, total protein, albumin, AST, ALT, and AST/ALT ratio were the factors that was gathered. Descriptive statistics and hypothesis testing was analysed. Software tools EPI INFO and SPSS 23 was used to examine the data. Results: The percentage of ALD among the 50 patients was projected with 50 controls. Odds Ratio=3.2, p=0.0001, was 3.2 times more likely to develop above 40yrs of age. In ALD patients, the mean AST value (171.5 SD 94.46 IU/L) was substantially higher than the ALT value (85.12 SD 58.24 IU/L), resulting in a higher AST/ALT ratio (2.01 SD 0.58). When comparing the Deritis ratio in controls and cases, mean values are 0.78 with CI (1.02, 1.06) and 2.01 with CI (1.49, 1.69) respectively which showed higher signicance(p=0.001) in cases. An AST:ALT ratio >2 with CI (93.9%, 99.9%) was present in 96.9% of individuals with alcoholic liver disease. Each variable's mean value in cases was considerably higher than in controls (p 0.001). Conclusion: Due to its widespread use, ethanol consumption causes various liver illnesses, each of which is extremely serious. Equally crucial is to know its complication and to know its magnitude of impact. To grasp the extent of damage in alcoholic liver disease rationally, the assessment of the Deritis ratio is helpful.

Targetable Brg1-CXCL14 axis contributes to alcoholic liver injury by driving neutrophil trafficking.

Alcoholic liver disease (ALD) accounts for a large fraction of patients with cirrhosis and hepatocellular carcinoma. In the present study we investigated the involvement of Brahma-related gene 1 (Brg1) in ALD pathogenesis and implication in ALD intervention. We report that Brg1 expression was elevated in mouse models of ALD, in hepatocyte exposed to alcohol, and in human ALD specimens. Manipulation of Brg1 expression in hepatocytes influenced the development of ALD in mice. Flow cytometry showed that Brg1 deficiency specifically attenuated hepatic infiltration of Ly6G+ neutrophils in the ALD mice. RNA-seq identified C-X-C motif chemokine ligand 14 (CXCL14) as a potential target for Brg1. CXCL14 knockdown alleviated whereas CXCL14 over-expression enhanced ALD pathogenesis in mice. Importantly, pharmaceutical inhibition of Brg1 with a small-molecule compound PFI-3 or administration of an antagonist to the CXCL14 receptor ameliorated ALD pathogenesis in mice. Finally, a positive correlation between Brg1 expression, CXCL14 expression, and neutrophil infiltration was detected in ALD patients. In conclusion, our data provide proof-of-concept for targeting the Brg1-CXCL14 axis in ALD intervention.

Expression and functions of transient receptor potential channels in liver diseases.

Liver diseases constitute a major healthcare burden globally, including acute hepatic injury resulted from acetaminophen overdose, ischemia-reperfusion or hepatotropic viral infection and chronic hepatitis, alcoholic liver disease (ALD), non-alcoholic fatty liver disease (NAFLD) and hepatocellular carcinoma (HCC). Attainable treatment strategies for most liver diseases remain inadequate, highlighting the importance of substantial pathogenesis. The transient receptor potential (TRP) channels represent a versatile signalling mechanism regulating fundamental physiological processes in the liver. It is not surprising that liver diseases become a newly explored field to enrich our knowledge of TRP channels. Here, we discuss recent findings revealing TRP functions across the fundamental pathological course from early hepatocellular injury caused by various insults, to inflammation, subsequent fibrosis and hepatoma. We also explore expression levels of TRPs in liver tissues of ALD, NAFLD and HCC patients from Gene Expression Omnibus (GEO) or The Cancer Genome Atlas (TCGA) database and survival analysis estimated by Kaplan-Meier Plotter. At last, we address the therapeutical potential and challenges by pharmacologically targeting TRPs to treat liver diseases. The aim is to provide a better understanding of the implications of TRP channels in liver diseases, contributing to the discovery of novel therapeutic targets and efficient drugs.

Roles and correlations of TIM-3 and LAG-3 with cytokines and chemokines in alcoholic liver disease

BackgroundDysregulation of immune checkpoint regulators has been reported in alcoholic liver disease (ALD). This study was designed to assess the serum levels of cytokines and chemokines associated with ALD and uncover the possible disease correlations with the soluble TIM-3 and LAG-3. MethodsThe soluble TIM-3 and LAG-3 levels were measured by enzyme-linked immunoassay, and 14 cytokines and chemokines were measured using Luminex-based multiplex assay in 111 male ALD patients and 45 healthy controls (HCs). ResultsOur results showed that soluble TIM-3 was significantly increased (p < 0.001) while soluble LAG-3 was significantly decreased (p < 0.001) in ALD group compared to HCs. Among the 14 cytokines and chemokines assessed, granulocyte-colony stimulating factor (G-CSF) (p = 0.003) and interferon γ-induced protein (IP)-10 (p < 0.001) were significantly increased, while interleukin (IL)-4 (p = 0.005) and IL-12 (p40) (p = 0.001) were significantly decreased in the ALD group. Kaplan-Meier analysis showed that overall survival decreased in higher TIM-3 level individuals. ConclusionsOur results showed that TIM-3, LAG-3, and IP-10 appear to be important for clinical diagnosis of ALD and ALD severity and may represent potential therapeutic targets in ALD.

Gut microbiota might influence the risk of rejection after liver transplantation

IntroductionLiver transplantation is the only radical treatment option available for patients with end-stage chronic liver disease. However, severe post-transplant complications remain relevant, including acute graft rejection and infection. Thus, the impact of gut microbiota on the frequency of these complications is highly promising. Materials and methodsThis prospective, cohort, closed-label study included 24 adults who underwent liver transplantation. The mean age was 49.2 ± 13.4 years; Child-Turcotte-Pugh A, B, and C classes were distributed as follows: A: 8 (33.3%); B: 11 (45.8%); C: 5 (20.8%). Gut microbiota was evaluated using 16S RNA new-generation sequencing. Study registrationNCT04281797. ResultsAccording to etiological distribution, significant differences were observed in the number of Firmicutes (p = 0.03) and Chlorobi (p = 0.009) harbored by the patients of alcoholic liver disease. Similarly, the severity of hepatic decompensation varied significantly for patients harboring Chlorobi (p = 0.01) and coprothermobacterota (p = 0.03). The association between sarcopenia and the microbiota was not significant among all taxa (p>0.1). Acute graft rejection differences between groups were found: Protobacteria (p = 0.001); Chlamydiae (p = 0.02); Gammaproteobacteria (p = 0.01); Chloroflexia (p = 0.004); Chlamydiia (p = 0.01); Enterobacteriaceae (p = 0.001); and Candidatus Saccharibacteria (p = 0.04), the median of which was found to be lower in patients with an acute graft rejection episode. ConclusionsObtained results prove a reliable interaction between gut microbiota and the incidence of acute liver graft rejection in dominant taxa and Candidatus Saccharibacteria that had not yet been observed in patients with rejection episodes.

Comparison of patterns of alcohol consumption among patients of alcoholic liver disease with various presentations among South Asian population

Comparison of patterns of alcohol consumption among patients of alcoholic liver disease with various presentations among South Asian population

RAGE promotes dysregulation of iron and lipid metabolism in alcoholic liver disease

Alcoholic liver disease (ALD) is associated with hepatic inflammatory activation and iron overload. The receptor for advanced glycation end products (RAGE) is an important metabolic mediator during the development of ALD. The aim of this study was to determine the effect of RAGE on iron homeostasis in ALD. We found increased circulating transferrin, hepcidin and ferritin in ALD patients and positively correlated with RAGE level. RAGE knockout (RAGE−/−) and wild-type mice were subjected to chronic alcoholic feeding for 6 weeks to induce ALD, and RAGE inhibitor, iron chelator or lipid peroxidation inhibitor were administered. We showed that chronic alcohol administration triggered hepatic steatosis, inflammation, and oxidative stress, which were eliminated by deficiency or inhibition of RAGE. Surprisingly, pathways of hepatic iron metabolism were significantly altered, including increased iron uptake (Tf/TfR) and storage (Ferritin), as well as decreased iron export (FPN1/Hepcidin). In vitro experiments confirmed that RAGE had different effects on the mechanism of iron metabolism of hepatocytes and macrophages respectively. In conclusion, our data revealed preclinical evidence for RAGE inhibition as an effective intervention for alleviating alcohol-induced liver injury.

The Correlation Between Fibroscan and APRI Score in Non Alcoholic Fatty Liver Disease Patients for Assessing Liver Fibrosis Degree : A Literature Review

NAFLD or non alcoholic fatty liver disease is increasingly known as one of the main causes of chronic liver disease globally, growing rapidly linear with the increase of obesity, type 2 diabetes and metabolic syndromes. Liver fibrosis is key factor to predict the adverse reaction that caused by NAFLD. Liver biopsy is known for a long time to be the golden standard to diagnose liver fibrosis, but its high cost, and risky procedure is limiting its own benefit, therefore other diagnostic methods is developed. Transient elastography Fibroscan is the most accurate way to diagnose because the accuracy is similar with liver biopsy. Using ultrasound emiting probe to determine the stages of liver fibrosis. Simple diagnostic test using laboratory result is also developed, APRI score or AST/Platelet Ratio is a method that diagnose the existence and degree of liver fibrosis using result from simple blood tests. Significant positive correlations is found between Fibroscan and APRI result to diagnose the degrees of liver fibrosis on NAFLD patients from several study that conducted from different countries. Using them as a combination could avoid the needs to use liver biopsy to reduce cost and risk.

Expert consensus on the diagnosis and management of alcoholic liver disease

&lt;p&gt;Alcoholic liver disease (ALD) is a spectrum of liver injuries caused due to harmful use of alcohol. It is the primary cause of liver disease and is responsible for around 4% of mortality worldwide. ALD progresses from fatty liver to alcoholic hepatitis depending upon risk factors, such as continued alcohol consumption or comorbid liver diseases. Screening and diagnosis are suggested for patients with histological symptoms and in high-risk populations. Management of ALD includes strategies such as abstinence from alcohol consumption, nutrition therapy, pharmacological therapy, and liver transplantation, with alcohol abstinence being the most beneficial to reverse fatty liver conditions. Various novel treatment approaches having distinct mechanisms of action are also developed besides conventional corticosteroid therapy, which include microbiota-based precision medicine, monoclonal antibody therapy, hepatocyte regeneration therapy, epigenetic modulators, liver degeneration boosters, and targeting the gut-liver axis. Ursodeoxycholic acid (UDCA) has shown to benefit ALD patients with cholestasis by exerting biochemical improvements; hence, it can be considered as an adjunct therapy. National and regional advisory board meetings were conducted to discuss the current diagnostic and management techniques, including existing and novel pharmacological treatments available for ALD along with current clinical practices in India.&lt;/p&gt;

Lipid and renal profile in assessing the severity of alcoholic liver disease.

Lipid and Renal dysfunction in Alcoholic liver disease (ALD) patients occurs either due to multi-organ involvement or secondary to alcoholism. This study was conducted to evaluate the role of lipid and renal parameters in assessing the severity of progression of ALD. Sixty cases of ALD (two groups based on compensated and decompensated features) and thirty healthy controls for comparison were included. Lipid profile (Total Cholesterol, LDL, HDL and Triglycerides) and renal parameters (serum urea, creatinine and uric acid), total and direct bilirubin, total protein and albumin were measured using automated chemistry analyzer. There was a significant decrease in Total cholesterol ,LDL and HDL levels and increased triglycerides when compared to controls (mean of 128.4 ± 59 vs 155 ± 27.2, 77 ± 44.3 vs 97.4 ± 27.2, 28.3 ± 18 vs 39.5 ± 14.1 and 115.8 ± 70.4 vs 91 ± 38 mg/dL respectively). Lipid profile showed a linear decrease while progressing from compensated to decompensated ALD. Renal parameters revealed a statistically significant decrease in serum urea ,increased creatinine and uric acid levels when compared to controls (17.57±2.96 vs23.73±4.94, 1.12±0.55 vs0.88±0.16,6.60±1.32 vs 4.68±1.40 mg/dL respectively).Total cholesterol and HDL showed a linear decrease when ALD progresses. Serum uric acid showed an early increase in compensated stage of ALD. This study inferred that Total cholesterol, TGL, HDL and uric acid can be used for assessing the severity of progression of ALD.

Circulating Cytokines Reflect the Etiology-Specific Immune Environment in Cirrhosis and HCC.

Simple SummaryChronic liver diseases commonly cause severe scarring of the liver (cirrhosis) and liver cancer. The eventual progression of this scarring process to liver cancer is influenced by a variety of factors, including inflammatory cytokines (soluble mediators of cell communication). In order to increase our understanding of these mediators we studied them in the blood of patients with hepatitis B (HBV), hepatitis C (HCV), alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD) patients with liver cirrhosis. We studied more than a 100 cytokines in up to 400 patients. We discovered that patients with cirrhosis had a vast upregulation of a wide variety of immune mediators, which stimulated inflammation and were linked with tumor-promoting roles. In contrast to prevailing assumptions, each type of underlying liver disease exhibited a unique immune mediator profile in blood, which is likely to impact how we will study these markers in the future. Patients with HBV cirrhosis had the largest number of upregulated inflammation-inducing mediators, compared to HCV, ALD and NAFLD. Next, we related blood immune mediator levels with liver cancer. To do so, we studied cytokine profiles in patients with small tumors, thus, those qualified for surgical curative strategies. We observed unique sets of cytokines in serum in each liver cancer group, indicating a role for these mediators in detecting liver cancer. In conclusion, our findings underscore the impact of different liver diseases on circulating immune mediators. Future studies that aim to study them as diagnostic tools will need to correct for this important effect accordingly.Background and Aims: Chronic liver disease—from any etiology—can progress to fibrosis, cirrhosis and hepatocellular carcinoma (HCC). The progression of liver cirrhosis to the end stages of disease is influenced by a variety of factors, including inflammatory cytokines. We pursued a study of cytokine-mediated inflammatory responses in hepatitis B (HBV), hepatitis C (HCV), alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD) patients with liver cirrhosis. Methods: Immune profiles were determined through the serum multiplex profiling of >100 cytokines in a 188 cirrhotic patients, 35 healthy controls and 196 early-stage HCC patients. Results: Patients with liver cirrhosis exhibited a vast upregulation of proinflammatory cytokines (p < 0.0001), including those with pro-oncogenic features, when compared to healthy individuals. In contrast to prevailing assumptions, each etiological cause of cirrhosis exhibited a unique cytokine profile in blood. Regardless of antiviral therapy, HBV cirrhosis patients had the largest number of upregulated proinflammatory mediators, compared to HCV, ALD and NAFLD (p < 0.0001). To further evaluate the etiology-dependent modulation of cytokine response in relation to liver cancer, we studied cytokine profiles in early-stage HCC patients strictly stratified by underlying liver disease. We observed unique sets of differentially expressed cytokines in each cohort of early-stage HCC patients of different cirrhosis etiologies. Conclusions: Our findings, therefore, underscore the importance of stratification by the etiological cause of liver cirrhosis in immune-based studies.

DETERMINANTS OF SIGNIFICANT HEPATIC FIBROSIS IN TYPE 2 DIABETES PATIENTS WITH NON-ALCOHOLIC FATTY LIVER DISEASE IN SOUTH INDIA.

Introduction: Non-alcoholic fatty liver disease is more prevalent among type 2 diabetes(T2D). Apart from liver related morbidity and mortality, fatty liver is associated with increased risk for cardiovascular disease. Severity of hepatic brosis correlates with poor outcome. Early diagnosis and treatment will improve the quality of life. Transient elastography (TE) is a validated tool for assessment of severity of brosis. We estimate the proportion of patients with signicant brosis and its determinants using TE in south india. Methods: Hospital based prospective cross sectional study was conducted among type 2 diabetes patients with ultrasound abdomen reported as fatty liver over the study period of one year. Exclusion criteria was applied to rene the study population to asymptomatic non alcoholic fatty liver disease patients. TE examination was done and signicant hepatic brosis (≥ F2 = 7.1 to 8.7kpa) was correlated with various blood parameters and anthropometrics. Results: 140 patients were selected from 781 type 2 diabetes population. Proportion of signicant brosis (≥ F2) was 47.1 percent. All patients except one were either obese 59(89.4%) or overweight 6(9.1%) in the subgroup of signicant brosis. T2D patients with uncontrolled HbA1c levels had more signicant brosis (p = 0.02) than controlled patients. Liver enzymes (AST/ALT) and lipid prole measurements do not correlate with signicant brosis. Ultrasound abdomen imaging fails to detect signicant brosis in two third of cases (p=0.002). Conclusion: Nearly half of type 2 diabetes with NAFLD in south India had signicant hepatic brosis. Higher BMI (&gt; 30) and poor glycemic control were key determinants of signicant hepatic brosis. This subset of T2D patients warrant TE screening study

Do Non Alcoholic Fatty Liver Disease Patients Have more Severe Metabolic Syndrome

Background and goal: Alcohol-unrelated fatty liver disease (NAFLD) is a frequent type of chronic liver disease (CLD) that is rapidly spreading around the world. The study's primary goal is to evaluate the severity of metabolic syndrome in people with nonalcoholic fatty liver disease. Materials and methods: From January to July 2019, Shalimar Medical and Dental College in Lahore, Pakistan, conducted this cross-sectional study. Through the use of non-probability sampling, the data was gathered. 100 patients with hepatic cirrhosis provided the data. The participants in this study ranged in age from 20 to 60. For the serum examination of liver enzymes, blood was drawn. Results: A correlation between the severity of the metabolic syndrome and NAFLD was found in this study, which included data from 100 individuals with biopsy-proven NAFLD. The patients were 45.67 3.56 years old on average. Compared to the normal control (11,3.42), the ALT levels in the patients were 258.291.73, 79.6628.63, and 50.73 8.4 correspondingly. Patients with cirrhosis, alcoholic liver disease, and viral hepatitis all had considerably higher aspartate aminotransferase levels. The significant frequency elevated aminotransferases and of NAFLD in IR-obese adolescents, as well as the potential consequences for their health, are concluded. The strong connections between NAFLD and MetS encourage the screening for additional MetS co-morbidities.

EVALUATION OF LIVER FIBROSIS IN LIVER BIOPSY OF ALCOHOLIC LIVER DISEASE CASES, WITH RETICULIN STAIN AND CD31 IMMUNOSTAIN

Background: Alcoholic liver disease (ALD) remains a major cause of morbidity and mortality world - wide. Liver biopsy is the gold standard method to assess the presence of liver fibrosis , and is useful in determining the staging and severity of hepatic injury. To interpret Liver fibrosis in liver biopsies, Reticulin stain, and CD31,an immunohistochemical marker, which plays an important role in determining the degree of fibrosis in Alcoholic liver disease, were used in the evaluation of it. Methods: 50 Alcoholic Liver Disease patients, were evaluated for Liver fibrosis, with H&amp;E stain and Reticulin stain, and were correlated with the staging of Liver fibrosis with CD 31 immunostaining expression by statistical analysis. Results: Strong positive correlation with CD31 and Reticulin staining was seen among 34 cases (68%), moderate positive correlation in 8 cases (16%), mild positive correlation in 2 cases (4%), negative correlation in 6 cases (12%). Conclusion: The existence of strong correlation, between CD31 immunostaining and fibrosis seen with Reticulin stain, revealed that the immunohistochemical methods are very much applicable in assessing prognostic and therapeutic strategies.

Pattern recognition receptor CD14 gene polymorphisms in alcohol use disorder patients and its Influence on liver disease susceptibility.

BackgroundAlcohol use disorders (AUDs) leading to liver disease is major concern over other spectrum of disorder. Excessive alcohol consumption resulting in leaky gut syndrome is attributed to alcohol-induced liver injury through portal translocation of bacterial endotoxin. Susceptibility to alcoholic liver disease (ALD) in AUD patients could be dependent upon genes responsible for inflammation and alcohol metabolism. The pattern recognition receptor CD14 gene is a major player in endotoxin-mediated inflammation and susceptibility to ALD. This study investigated the genetic association of CD14 polymorphisms and other mechanisms relevant to altered inflammatory responses leading to ALD.MethodsPatients with alcohol use disorder with ALD (n = 128) and without liver disease (ALC, n = 184) and controls without alcohol use disorder (NALC, n = 152) from North India were enrolled. The CD4 gene polymorphisms in the North Indian population were evaluated by RFLP and sequencing. Secretory CD14 (sCD14), LBP, TLR4, MD2, TNFα, IL1b, IFNγ, IL6, IL10, and IL4 levels in serum were measured by ELISA among groups. The influence of polymorphisms on CD14 gene promoter activity and circulatory bacterial DNA level was determined.ResultsThe CD14 gene promoter and exonic region SNPs were found to be monomorphic, except for SNP rs2569190 for the North Indian population. The genetic association of SNP rs2569190(C/T) with the risk of developing ALD was found significant for TT genotype [ORTT, 95% CI = 2.19, 1.16–4.13 for ALD vs. ALC and OR, 2.09, 1.18–3.72 for ALD vs. NALC]. An increased sCD14 level was observed in AUD patients compared to NALC control. Increased levels of LBP, TLR4, TNFα, IL1β, IFNγ, and IL6 and reduced levels of MD2, IL10, and IL4 were observed among the ALD patients compared to the other two control groups. Elevated levels of pro-inflammatory and reduced levels of anti-inflammatory cytokines were observed in the risk genotype TT groups of ALD patients and the ALC group compared to NALC. Promoter activity was observed in the intronic region flanking SNPs and risk genotype can influence reporter activity, indicating CD14 gene expression.ConclusionEnhanced CD14 expression associated with inflammatory responses increases susceptibility to ALD in the TT genotype of AUD patients.

Endoplasmic reticulum-targeted inhibition of CYP2E1 with vitamin E nanoemulsions alleviates hepatocyte oxidative stress and reverses alcoholic liver disease

Alcoholic liver disease (ALD) is a global healthcare problem and socioeconomic issue that is primarily driven by chronic and/or excessive alcohol consumption. Upon alcohol exposure, parenchymal hepatocytes (HCs) up-regulate endoplasmic reticulum (ER)-localized monooxygenase Cytochrome P450 family 2 subfamily E member 1 (CYP2E1) to accelerate the metabolism of ethanol (EtOH), which concurrently exacerbates the production and accumulation of toxic metabolic intermediates, especially reactive oxygen species (ROS), playing a decisive role in the initiation and perpetuation of alcohol-induced liver injury. ALD patients without timely intervention may develop a spectrum of metabolic and functional disorders in the liver, including hepatic steatosis, hepatitis, fibrosis, and even cirrhosis. However, up to now, there have been no FDA-approved pharmacological or nutritional therapeutics for treating patients with ALD, and an effective amelioration of alcohol-induced hepatotoxicity with satisfactory biosafety is still demanding. In this study, antioxidant Vitamin E-incorporating nanoemulsions modified with ER-targetable small molecule p-dodecylbenzene sulfonamide (p-DBSN) was constructed to load and deliver CYP2E1 inhibitor Clomethiazole (CMZ) to the ER of HCs for site-specific inhibition, which displayed remarkable hepatoprotective effects against chronic alcohol exposure without off-target toxicity, both intravenously injected and orally administrated. Generally, our work may provide a promising nanoplatform for reversing ALD.

A STUDY OF HAEMATOLOGICAL ABNORMALITIES IN CHRONIC LIVER DISEASE IN AJMER REGION

Chronic liver disease refers to a disease of the liver, which had lasted more than six months. The disease process involves progressive destruction and regeneration of liver parenchyma leading to brosis and cirrhosis. This study evaluates the various hematological indices as these parameters are part of an inexpensive, easily accessible, and routinely performed test for almost all patients admitted to health facilities to nd out a correlation between variation in hematological parameters and the illness under study. This study is conducted in the department of Pathology J.L.N Medical College and Associated group of hospitals, Ajmer (Rajasthan) prospectively from July 2019 to June 2020 (one year). In our study, the mean age for chronic liver disease was 44.48±11.84 years and the highest incidence was seen between the age group of 41-50 years (4th decade). M: F ratio was 6:1. Alcohol has been implicated as the most common cause. In the case of non- alcoholic hepatitis B has been implicated as the most common cause. The most common anemia is normocytic normochromic anemia. Microcytic anemia is most common among women. Macrocytosis is almost common with alcoholics. The mean MCV, MCH and MCHC were signicantly higher in alcoholic chronic liver disease patients. Thrombocytopenia is present in more than 30% of patients. In chronic liver failure patients, most of them had abnormalities in hematological parameters. Hence with this study, all the chronic liver disease patients must be evaluated for hematological and should be monitored for any complications. Early treatment to correct these comorbidities can decrease mortality.

Diagnostic Role of Tumor Markers for Hepatocellular Carcinoma in Liver Transplantation Candidates: An Analysis Using the Korean Organ Transplantation Registry Database

BACKGROUND This study analyzed pretransplant alpha-fetoprotein (AFP) and proteins induced by vitamin K absence or antagonist-II (PIVKA-II) in liver transplantation (LT) candidates. MATERIAL AND METHODS A total of 3,273 LT recipients enrolled at the Korean Organ Transplantation Registry were divided according to hepatocellular carcinoma (HCC) status and background liver disease, and AFP and PIVKA-II were compared. RESULTS In all patients, the median AFP and PIVKA-II were 6.3 ng/mL and 29 mAU/mL in the viable-HCC group and 3.3 ng/mL and 35 mAU/mL, respectively, in the no-HCC group (P<0.001 for AFP and p=0.037 for PIVKA-II). In patients with hepatitis B virus infection, they were 6.0 ng/mL and 26 mAU/mL in the HCC group and 3.2 ng/mL and 21 mAU/mL in the no-HCC group, respectively (P<0.001 and P<0.001). In patients with hepatitis C virus infection, they were 10.7 ng/mL and 37 mAU/mL in the HCC group and 2.6 ng/mL and 21 mAU/mL in the no-HCC group, respectively (P<0.001 and P=0.117). In alcoholic liver disease patients, they were 5.2 ng/mL and 61 mAU/mL in the HCC group and 6.4 ng/mL and 75 mAU/mL in the no-HCC group, respectively (P<0.001 and P=0.419). In patients with other diseases, they were 7.1 ng/mL and 32 mAU/mL in the HCC group and 3.3 ng/mL and 28 mAU/mL in the no-HCC group, respectively (P<0.001 and P=0.822). CONCLUSIONS The results of the present study indicate that pretransplant serum AFP and PIVKA-II were highly variably expressed in LT candidates with end-stage liver diseases; therefore, their values should be cautiously interpreted because their role in HCC diagnosis is limited.