Acute Alcoholic Liver Disease Research Articles

Protective Effects of Lycium ruthenicum Murray against Acute Alcoholic Liver Disease in Mice via the Nrf2/HO-1/NF-κB Signaling Pathway.

Acute alcoholic liver disease (ALD) resulting from short-term heavy alcohol consumption has become a global health concern. Moreover, anthocyanins have attracted much attention for their ability to prevent oxidation and inflammation. The present work evaluates the protective effects of Lycium ruthenicum Murray (LRM) against ALD and explores the possible underlying mechanism involved. The total anthocyanin content in LRM was 43.64 ± 9.28 Pt g/100 g dry weight. Mice were orally administered 50, 125, or 375 mg LRM/kg body weight (BW) for 21 days. On days 18-21, mice were orally administered 15 mL of ethanol/kg BW. Markers of liver damage, oxidative stress, and inflammation were examined. Furthermore, the modulatory effect of LRM on Nrf2/HO-1/NF-κB pathway molecules was evaluated through quantitative reverse transcription polymerase chain reaction (RT‒qPCR) and immunohistochemistry analyses. The difference between the groups indicated that LRM improved liver histopathology and the liver index, decreased aspartate transaminase, alanine transaminase, malondialdehyde, reactive oxygen species, IL-6, TNF-α, and IL-1β expression, but elevated superoxide dismutase, catalase, and glutathione-s-transferase levels. Moreover, LRM upregulated Nrf2 and Ho-1 but downregulated Nf-κb and Tnf-α genes at the transcript level. In summary, LRM alleviated ethanol-induced ALD in mice by reducing oxidative damage and associated inflammatory responses. LRM protects against ALD by reducing damage factors and enhancing defense factors, especially via the Nrf2/HO-1/NF-κB pathway. Thus, LRM has application potential in ALD prophylaxis and treatment.

Ethanol extracts of Isochrysis zhanjiangensis alleviate acute alcoholic liver injury and modulate intestinal bacteria dysbiosis in mice.

Alcoholic liver disease (ALD) is responsible for 3.3 million deaths per annum. Efficacious therapeutic modalities or drug treatments for ALD have not yet been found, so it is urgent to seek new agents for preventing ALD and its related disease. Many experiments have indicated that modulating the gut microbiota and regulating the toll-like receptor 4 (TLR4)/nuclear transcription factor-κB (NF-κB) inflammatory pathway can provide a new target for prevention and treatment of ALD. Marine microalgae have their natural metabolic pathways to synthesize various of bioactive compounds as promising candidates for hepatoprotection. In this study, we investigated ethanol extracts from Isochrysis zhanjiangensis (EEIZ) to evaluate their ability to alleviate acute alcoholic liver injury, regulate TLR4/NF-κB inflammatory pathway and modulate intestinal bacteria dysbiosis in mice for ALD treatment. In the acute ALD mouse model, EEIZ reduced levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, triacylglyceride, total cholesterol and low-density lipoprotein, while increasing the level of high-density lipoprotein. Besides, TLR4, myeloid differentiation factor 88, NF-κB and tumor necrosis factor-α expression levels in liver tissue were effectively downregulated by EEIZ. Furthermore, treatment with EEIZ enhanced intestinal homeostasis and significantly alleviated the damage caused by alcohol. EEIZ showed effective hepatoprotective activity against alcohol-induced acute liver injury in mice as it could alleviate hepatocyte damage, suppress the TLR4/NF-κB inflammatory pathway and regulate the intestinal flora structure. EEIZ could be a good candidate for preventing acute alcoholic liver injury. © 2024 Society of Chemical Industry.

Structural elucidation of an active polysaccharide from Radix Puerariae lobatae and its protection against acute alcoholic liver disease

Radix Pueraria lobata can be used as medicine and food, whose polysaccharide is one of the main bioactive ingredients. To explore the effect and mechanism of Pueraria lobata polysaccharide, a homogeneous and novel water-soluble polysaccharide (PLP1) was successfully isolated and purified from P. lobata by column chromatography in the current study. Structure analysis revealed that PLP1 (Mw = 10.43 kDa) was constituted of the residues including (1 → 4)-α-d-glucose and (1 → 4, 6)-α-d-glucose, which were linked together at a ratio of 5:1 and represented the main glycosidic units. In vitro experiments indicated that PLP1 exhibited a better free radical-scavenging ability than amylose and amylopectin, meanwhile in vivo experiments indicated that PLP1 effectively protected against liver injury in mice with acute ALD through significantly inhibiting oxidative stress to regulate lipid metabolism, increasing short-chain fatty acid production, and maintaining intestinal homeostasis by regulating intestinal flora. Taken together, our results illustrate that PLP1 can regulate intestinal microecology as a feasible therapeutic agent for protecting against ALD on the ground of the gut-liver axis, thus laying a theoretical foundation for the rational exploitation and utilization of P. lobata resources in the clinic.

The protective effect of Nostoc commune Vauch. polysaccharide on alcohol-induced acute alcoholic liver disease and gut microbiota disturbance in mice.

In recent years, the incidence of alcoholic liver disease (ALD) has gradually increased, the development of ALD is attached great attentions. Nostoc commune Vauch. polysaccharide (NCVP) is beneficial to maintain the gut health, but the protective effect of NCVP on the liver has not been reported yet. To study the protective effect and the underlying mechanisms of NCVP on ALD, a mouse model of acute ALD was established. We built an acute ALD mouse model and explored the protective effect of NCVP through the detection of cytokines, histological examination, determination of short chain fatty acids, and 16S rRNA analysis of gut microbiota. NCVP had hepatoprotective effects on acute alcohol-induced mice by improving antioxidant capacity, reducing oxidative stress and the serum cytokine levels (IL-1β, IL-6, and TNF-α). Simultaneously, histopathological changes in liver indicated that NCVP could inhibit local hepatocyte necrosis, cytoplasmic vacuolation and inflammatory cell infiltration induced by alcohol. NCVP also increased the level of total short-chain fatty acids of acute ALD mice. In addition, NCVP could significantly decrease the Firmicutes/Bacteroidetes ratio and the abundance of Patescibacteria, Helicobacter, and Actinomycetes and increase the abundance of Lachospiraceae, Prevotellaceae-UCG-003, Lactobacillaceae, and Desulfovibrio. Our study proved that NCVP had in vivo hepatoprotective effect on acute ALD mice and provided scientific evidences that NCVP might be a promising drug candidate for the prevention and treatment of ALD.

Hepatoprotective Effect of Albumin Peptide Fractions from Corn Germ Meal against Alcohol-Induced Acute Liver Injury in Mice.

Acute alcoholic liver disease can cause serious liver damage. This study reports on the hepatoprotective effect of albumin peptide fractions from corn germ meal (MW < 1 kDa) (APF4) on acute alcohol hepatic damage in mice. In the mice model, the results indicated that APF4 at a dose of 800 mg/kg/bw could markedly boost alcohol metabolism, which was shown in the reduced duration of the loss of the righting reflex; the reduced level of blood alcohol concentration (BAC), cytochrome P450 2E1 (CYP2E1), alanine aminotransferase (ALT), aminotransferase (AST), triglycerides (TG), and malondialdehyde (MDA) (p < 0.01); the enhanced activity of aldehyde dehydrogenase (ALDH); and the superoxide dismutase (SOD) and glutathione (GSH) levels being increased by up to 84.02% and 193.22% (p < 0.01) compared to the control group. The antioxidant capability and lipid peroxidation inhibition activity of APF4 may be responsible for its protective effect against liver damage induced by alcohol. The findings suggested that APF4 had the hepatoprotective property against liver damage induced by alcohol.

Compound Probiotic Ameliorates Acute Alcoholic Liver Disease in Mice by Modulating Gut Microbiota and Maintaining Intestinal Barrier.

Alcoholic liver disease (ALD) is a worldwide health threaten lack of effective treatment. Gut dysbiosis and concomitant augmented intestinal permeability are strongly implicated in the pathogenesis and progression of ALD. Research on the protective effect of probiotics on ALD is limited, and more effective intestinal microecological regulators and the related mechanisms still need to be further explored. In the present study, the protective effects and mechanisms of a compound probiotic against acute alcohol-induced liver injury in vivo were explod. It was showed that the compound probiotic ameliorated liver injury in acute ALD mice and stabilized the levels of ALT, AST, and TG in serum. The compound probiotic reversed acute alcohol-induced gut dysbiosis and maintained the intestinal barrier integrity by upregulating the production of mucus and the expression of tight junction (TJ) proteins and thus reduced LPS level in liver. Meanwhile, the compound probiotic reduced inflammation level by inhibiting TLR4/NF-κB signaling pathway and suppressed oxidative stress level in liver. Furthermore, the compound probiotic alleviated liver lipid accumulation by regulating fatty acid metabolism-associated genes and AMPK-PPARα signaling pathway. Noteworthy, fecal microbiota transplantation (FMT) realized comparable protective effect with that of compound probiotic. In conclusion, present study demonstrates the beneficial effects and underlying mechanism of the compound probiotic against acute alcohol-induced liver injury. It provides clues for development of novel strategy for treatment of ALD.

The Protective Effects of Corn Oligopeptides on Acute Alcoholic Liver Disease by Inhibiting the Activation of Kupffer Cells NF-κB/AMPK Signal Pathway.

Alcohol can cause injury and lead to an inflammatory response in the liver. The NF-κB/AMPK signaling pathway plays a vital role in regulating intracellular inflammatory cytokine levels. In this study, corn oligopeptides (CPs), as the research objects, were obtained from corn gluten meal, and their regulation of the activation of the Kupffer cell NF-κB/AMPK signal pathway induced by LPS was investigated. Results showed that ALT, AST, and inflammatory cytokines in mice serum after the administration of CPs at 0.2, 0.4, and 0.8 g/kg of body weight displayed a distinct (p < 0.05) reduction. On the other hand, the CPs also inhibited the expression of recognized receptor CD14 and TLR4, down-regulated P-JNK, P-ERK, and P-p-38, and thus inhibited inflammatory cytokine levels in Kupffer cells (KCs). Furthermore, four kinds of dipeptides with a leucine residue at the C-terminus that might exhibit down-regulated inflammatory cytokines in the NF-κB/AMPK signaling pathway functions were detected using HPLC-MS/MS. These results indicated that CPs have a potential application value in acute alcoholic liver disease.

Targeting Thyroid Hormone/Thyroid Hormone Receptor Axis: An Attractive Therapy Strategy in Liver Diseases.

Thyroid hormone/thyroid hormone receptor (TH/TR) axis is characterized by TH with the assistance of plasma membrane transporters to combine with TR and mediate biological activities. Growing evidence suggests that TH/TR participates in plenty of hepatic metabolism. Thus, this review focuses on the role of the TH/TR axis in the liver diseases. To be specific, the TH/TR axis may improve metabolic-associated fatty liver disease, hepatitis, liver fibrosis, and liver injury while exacerbating the progression of acute liver failure and alcoholic liver disease. Also, the TH/TR axis has paradoxical roles in hepatocellular carcinoma. The TH/TR axis may be a prospecting target to cure hepatic diseases.

Roxadustat, a Hypoxia-Inducible Factor 1α Activator, Attenuates Both Long- and Short-Term Alcohol-Induced Alcoholic Liver Disease.

Alcoholic liver disease (ALD) is a worldwide healthcare problem featured by inflammation, reactive oxygen species (ROS), and lipid dysregulation. Roxadustat is used for chronic kidney disease anemia treatment. As a specific inhibitor of prolyl hydroxylase, it can maintain high levels of hypoxia-inducible factor 1α (HIF-1α), through which it can further influence many important pathways, including the three featured in ALD. However, its effects on ALD remain to be elucidated. In this study, we used chronic and acute ALD mouse models to investigate the protective effects of roxadustat in vivo. Our results showed that long- and short-term alcohol exposure caused rising activities of serum transaminases, liver lipid accumulation, and morphology changes, which were reversed by roxadustat. Roxadustat-reduced fatty liver was mainly contributed by the reducing sterol-responsive element-binding protein 1c (SREBP1c) pathway, and enhancing β-oxidation through inducing peroxisome proliferator-activated receptor α (PPARα) and carnitine palmitoyltransferase 1A (CPT1A) expression. Long-term alcohol treatment induced the infiltration of monocytes/macrophages to hepatocytes, as well as inflammatory cytokine expression, which were also blocked by roxadustat. Moreover, roxadustat attenuated alcohol caused ROS generation in the liver of those two mouse models mainly by reducing cytochrome P450 2E1 (CYP2E1) and enhancing superoxidase dismutase 1 (SOD1) expression. In vitro, we found roxadustat reduced inflammation and lipid accumulation mainly via HIF-1α regulation. Taken together, our study demonstrates that activation of HIF-1α can ameliorate ALD, which is contributed by reduced hepatic lipid synthesis, inflammation, and oxidative stress. This study suggested that roxadustat could be a potential drug for ALD treatment.

Fermented milk of cheese-derived Lactobacillus delbrueckiisubsp.bulgaricus displays potentials in alleviating alcohol-induced hepatic injury and gut dysbiosis in mice

An isolate of Lactobacillus delbrueckii subsp. bulgaricus (L. bulgaricus L7) with robust antioxidant capacity was screened from traditional fermented Xinjiang cheese. Here, we focused on evaluating the effect of L. bulgaricus fermented milk on acute alcoholic liver disease prevention using a mice model, with glutathione treated mice as positive control. The results showed that both fermented milk and glutathione feeding could relieve alcohol-induced oxidative stress and inflammatory responses significantly. However, fermented milk feeding seemed to hold more promise in restoring gut dysbiosis relative to glutathione. Enhanced abundance of potential pathogens, Porphyromonas sp. and Enterococcus sp., induced by alcohol was considerably attenuated by additional feeding of fermented milk. Different scenario was firstly observed when additionally fed with glutathione in this study, showing remarkably increased abundance of Bacteroides sp. and Enterococcus sp. Our results suggested the more robust capability of L. bulgaricus fermented milk in restoring alcohol-induced gut dysbiosis relative to glutathione, indicating its potential protective effects on alcohol-induced hepatic injury.

Extracts of Dracocephalum tanguticum Maxim Ameliorate Acute Alcoholic Liver Disease via Regulating Transcription Factors in Mice.

Alcoholic liver disease (ALD) caused by excessive drinking is a health and economic concern worldwide. Given the high morbidity, mortality, and the progressive nature of ALD, finding effective interventions is essential. Previous studies have confirmed that edible food plants and their bioactive compounds exert a protective effect against ALD. Dracocephalum tanguticum Maxim (DTM) is one of the important traditional Tibetan medicines in China with the effect of clearing away liver heat, used for the treatment of hepatitis. In this study, the DTM chloroform extract (DtM-C), ethyl acetate extract (DtM-E), and n-butanol extract (DtM-B) were obtained by ethanol extraction combined with fractional extraction. Acute ALD was induced in mice given intragastric ethanol. Serum and liver biochemical markers were detected by ELISA. Liver histological observation, Oil Red O, and Masson’s trichrome staining were performed. Liver injury cells were induced by ethanol. The cell vitality was detected by using MTT colorimetry. The expressions of Nrf2, NF-κB, STAT3, AP-1, CREB, HIF-1α, HO-1, NQO-1, GSTA1, IKB2, and Keap1 were detected by real-time polymerase chain reaction (PCR) to elucidate the mechanism of hepatoprotective effect, and the results were verified by using Western blot. The results of serum liver function indicators (ALT, AST, and ADH), serum hepatic lipid indicators (TC, TG, HDL-C, and LDL-C), and lipid peroxidation indicators (ADH, MDA, SOD, CAT, and GSH-Px) in liver tissue and liver histological observation showed that DtM-E could improve liver function, alleviate fatty degeneration, edema, cell necrosis, and liver fibrosis caused by alcohol. DtM-E also increased the vitality of EtOH-induced liver injury cells, upregulated the mRNA expression of Nrf2, HO-1, NQO-1, and GSTA1, while downregulated the expression of Keap-1, p65, and NF-κB. Western blot results were consistent with PCR. The results suggest that DtM-E has a protective effect against ALD in vitro and in vivo, and its mechanism of action may be related to the activation of Nrf2/Keap-1 and inhibition of the P65/NF-κB signaling pathways.

Rosa rugosa polysaccharide attenuates alcoholic liver disease in mice through the gut-liver axis

In the present work, the protective effect of polysaccharide from Rosa rugosa (RRP) on acute alcoholic liver disease (ALD) was investigated. The viscera index, liver function and H&E staining results showed that RRP had a protective effect on ALD mice. RRP can increase activities of SOD, GSH, GSH-Px and decrease the content of NO, MDA in ALD mice. At the same time, the serum levels of IL-6, IL-1β and TNF-α were decreased in ALD mice treated with RRP. Our results suggested that RRP significantly prevented alcohol-induced hepatotoxicity as the concentration rises. In this study, 16S rRNA sequencing technology was used to explore the effect of RRP on the gut microbiota in ALD mice. It was found that RRP can reduce the pathogenic Gammaproteobacteria and Patescibacteria but increase the beneficial gut Firmicute and Lachnospira, thereby maintain the relative stability of the gut microbiota by adjusting the gut-liver axis. This research not only opens up a new idea for the research on the efficient utilization of resources and physiological activity of Rosa rugosa, but also provides theoretical references for the search and development of natural liver-protecting drugs.

Multiple Roles of Black Raspberry Anthocyanins Protecting against Alcoholic Liver Disease.

This study aimed to investigate the protective effect of black raspberry anthocyanins (BRAs) against acute and subacute alcoholic liver disease (ALD). Network analysis and docking study were carried out to understand the potential mechanism. Thereafter, the serum biochemical parameters and liver indexes were measured, the histopathological changes of the liver were analyzed in vivo. The results showed that all tested parameters were ameliorated after the administration of BRAs with alcohol. Meanwhile, there was increased protein expression of NF-κB and TGF-β in extracted livers, which was associated with hepatitis and hepatic fibrosis. Furthermore, BRAs and cyanidin-3-O-rutinoside exhibited cytotoxic effects on t-HSC/Cl-6, HepG2, and Hep3B and induced the apoptosis of HepG2 cells; downregulated the protein expression level of Bcl-2; upregulated the level of Bax; and promoted the release of cytochrome C, cleaved caspase-9, cleaved caspase-3, and cleaved PARP in HepG2 cells. In addition, the antioxidant activity of BRAs was tested, and the chemical components were analyzed by FT-ICR MS. The results proved that BRAs exert preventive effect on ALD through the antioxidant and apoptosis pathways.

Sedum emarginatum and its polysaccharide have a therapeutic effect on alcoholic liver disease in mice

Objective: To explore the therapeutic effect of Sedum emarginatum (SE) and its polysaccharide on alcoholic liver disease. Methods: First, we ground fresh SE to obtain homogenate, and then test the effect of SE on a mouse model of acute alcoholic fatty liver disease (AFLD). Kunming female mice were given intragastric administration of alcohol once every 12 hours to induce AFLD, three times in total, and the mice received ethanol and SE at the same time. The mice were sacrificed 4 hours after the last alcohol administration, and serum and liver were collected for testing. We found that SE was effective and then carried out subsequent experiments. The dried SE powder was extracted under heating and reflux by different polar solvents: petroleum ether, ethyl acetate, methanol and water. The extracting solution were heat and concentrated to obtain an extract. The water part was purified to obtain polysaccharide. We tested the therapeutic effect of each part of SE in a mouse model of early alcoholic hepatitis (AH). Mice were given 5 g/kg of alcohol every 12 hours, a total of 9 times, and lipopolysaccharide (LPS) was injected intraperitoneally at the 36 h and 84 h. After 4 hours of the last gavage, the mice were sacrificed. The serum and liver tissue were used to tested relevant biochemical indexes. Results: SE had a certain reversal effect on the increase of serum triglycerides caused by alcohol, and it had a better effect on the accumulation of lipid droplets in liver tissues. Oil red O staining proved this result. In the second acute experiment, the mortality rate of the animal in the model group was 7/12, and the mortality rate in each treatment group was 1/8, 1/7, 4/8, and 1/8. In all parts, the crude polysaccharide did not significantly reverse the increase of serum triglyceride levels in early AH, but it could significantly alleviate the increase of inflammatory foci and steatosis in liver tissue. The transmission electron microscopy result indicates that the crude polysaccharide component has a certain protective effect on mitochondrial damage caused by alcohol. Conclusion: SE can reduce fatty liver and hyperlipidemia caused by alcohol, and its polysaccharide can reduce liver inflammation in the early alcoholic hepatitis by protecting mitochondron.

Increase in the incidence of alcoholic pancreatitis and alcoholic liver disease in Iceland: impact of per capita alcohol consumption

Objective: To analyze the incidence of acute alcoholic pancreatitis and of severe alcoholic liver disease (ALD) and its association with per capita alcohol consumption with identification of both alcoholic cirrhosis (AC) and severe alcoholic hepatitis (AH), in a population-based setting.Methods: A search was undertaken in diagnoses database for diagnostic codes in order to find patients hospitalized with incident acute alcoholic pancreatitis (AP) and alcoholic liver disease in Iceland in 2001–2015. Diagnoses were verified in all patients who were retrospectively reviewed. Those with ALD had either AC or AH. Alcohol sales during the study period were obtained from Statistics Iceland.Results: Overall, 273 patients with acute AP, mean age at diagnosis 50 (14) years, 74% males and 159 patients with ALD, mean age 57 (11) years, 73% males, were identified. Mean per capita alcohol consumption was 6.95 (0.4) liters and increased by 21% over the study period. The annual incidence of AP increased from 4.2 per 100.000 to 9.5 and ALD from 1.6 to 6.1 per 100.000. Trend analysis showed a significant annual increase of 7% (RR 1.07, 95%CI 1.04–1.10) for AP and an annual increase of 10.5% (RR 1.10, 95%CI 1.06–1.15) for ALD. The increase was only significant in males.Conclusions: Increase per capita alcohol consumption over a 15 year study period was associated with an increase in the incidence of severe alcoholic liver disease and alcohol-related acute pancreatitis in males but not in females.

Camel milk modulates ethanol-induced changes in the gut microbiome and transcriptome in a mouse model of acute alcoholic liver disease

Morbidity and mortality as a result of liver disease are major problems around the world, especially from alcoholic liver disease (ALD), which is characterized by hepatic inflammation and intestinal microbial imbalance. In this study, we investigated the hepatoprotective effects of camel milk (CM) in a mouse model of acute ALD and the underlying mechanism at the gut microbiota and transcriptome level. Male Institute of Cancer Research mice (n = 24; Beijing Weitong Lihua Experimental Animal Technology Co. Ltd., China) were divided into 3 groups: normal diet (NC); normal diet, then ethanol (ET); and normal diet and camel milk (CM), then ethanol (ET+CM). Analysis of serum biochemical indexes and histology revealed a reduction in hepatic inflammation in the ET+CM group. Sequencing of 16S rRNA showed that CM modulated the microbial communities, with an increased proportion of Lactobacillus and reduced Bacteroides, Alistipes, and Rikenellaceae RC9 gut group. Comparative hepatic transcriptome analysis revealed 315 differentially expressed genes (DEG) in the ET+CM and ET groups (150 upregulated and 165 downregulated). Enrichment analysis revealed that CM downregulated the expression of inflammation-related (ILB and CXCL1) genes in the IL-17 and tumor necrosis factor (TNF-α) pathways. We conclude that CM modulates liver inflammation and alleviates the intestinal microbial disorder caused by acute alcohol injury, indicating the potential of dietary CM in protection against alcohol-induced liver injury.

Relationship between metabolic and immunological disorders in experimental acute tetrachlomethane, ischemic and alcoholic liver disease

The aim of this study was to investigate the relationship of metabolic and immunological disorders in acute tetrachlomethane, ischemic and alcoholic liver damage modelled in adult Wistar male rats weighing 120-160 g. After evaluation of metabolic and immunological parameters at the local and systemic levels, and correlation analysis was used to establish the relationship between the dynamics of the indicators against the background of experimental pathology models. The close correlation between the studied immune and metabolic parameters recognized for the tetrachlomethane, ischemic and alcoholic liver damage shows the existing "tension" between the indicators of immune and metabolic status. Such close correlation between the studied immunological and metabolic parameters at the system and local levels can serve to assess the severity of the disease, its prognosis, treatment effectiveness and preventive measures.

Front Cover: The Preventative Effects of Procyanidin on Binge Ethanol‐Induced Lipid Accumulation and ROS Overproduction via the Promotion of Hepatic Autophagy

Mol. Nutr. Food Res. 2019, 63, 1801255 DOI: 10.1002/mnfr.201801255 Owing to their health promotion function, the procyanidins have long been employed as dietary supplements. In article number 1801255, Kaiping Wang and co-workers find that the dimer procyanidin may alleviate acute alcoholic liver disease via the activation of hepatocyte autophagy, providing novel insight into a strategy to fight against alcoholic liver disease.

ASSESSMENT OF CLINICAL PROFILE OF PATIENTS WITH ALCOHOLIC LIVER DISEASE

Background: Alcohol consumption affects both mental and physical function of the body and hence called as “dual disease” because it has mentioned in etiology of morbidity in both the components of the body. According to the reports of World Health Organization there were more than 150 million people worldwide has indulged with alcoholism.&#x0D; Material &amp; Methods: The present prospective study was conducted at department of general medicine of our tertiary care hospital. 100 Patients who were diagnosed as acute onset alcoholic liver disease were enrolled from outdoor and from ward by simple random sampling.&#x0D; Results: The most common clinical feature recorded among study participants was of nausea and vomiting seen in 46 (92%) of patients, which was followed by jaundice reported among 43 (86%) of patients. Hepatomegaly was reported among 37 (74%) of patients, which was followed by signs of liver failure reported among 30 (60%) patients, followed by anorexia reported among 29 (58%) of patients. Splenomegaly was reported among 17 (34%) of patients, fever was reported among 13 (26%) of patients, abdominal pain was reported among 12 (24%) of cases and ascites was reported among 8 (16%) study participants.&#x0D; Conclusion: We concluded from the present study that larger quantities of alcohol consumption for a longer duration of time result in high morbidity and mortalities. Alcoholic liver disease is not only a medical burden but also a social burden which leads to frequent hospitalization and unwanted out of pocket expenditure.&#x0D; Key words: alcoholic liver disease, liver cirrhosis, hepatomegaly.

Severe acute alcoholic hepatitis and liver transplant: A never-ending mournful story.

Severe acute alcoholic liver disease (SAAH) unresponsive to medical therapy shows one-year-mortality rates of up to 90%. Most transplant centers request six months of alcohol abstinence prior to transplantation, the so-called “6-month rule.” This regulation is not based on strong evidence, repeatedly making it a topic of controversial debates. The majority of patients with SAAH will die before fulfilling the 6-month rule. Therefore, liver transplantation (LT) protocols are becoming more flexible towards the rigid abstinence regulation, especially concerning SAAH patients. We conducted a literature review regarding LT in SAAH and its outcomes, including post-transplant mortality and recidivism. We studied available data on PubMed from 2011 and onwards whilst including articles dealing with genetic components, medical therapy and historic snapshots of alcoholism. Emerging studies recommend LT in SAAH not responding to medical therapies even without realizing the required abstinence period, since the majority of these patients would die within 6 months. SAAH without response to medical therapy has one-year-mortality rates of up to 90%. The 6-month rule is not based on strong evidence and is repeatedly a topic of controversial debates. There is genetic linkage to alcoholism and medical therapy is not as effective as estimated, yet. The 6-months-regulation has not shown to evidently decrease the risk of recidivism post-LT, which is a lifesaving treatment in SAAH patients. Insisting on rigid sobriety rules results in excluding patients with a low risk of recidivism from being transplanted. Moreover, the genetic linkage of alcoholism must be recognized.