Background Hepatorenal syndrome-acute kidney injury (HRS-AKI) is an event that occurs in chronic liver disease (CLD) and is associated with high morbidity and mortality. Terlipressin, a vasopressin analog, is used for the treatment of portal hypertension-related gastrointestinal (GI) bleeding and is found to be effective in the management of HRS-AKI. Continuous infusion of terlipressin maintains a high mean arterial pressure while reducing adverse events. It is better tolerated and equally effective at lower doses than intravenous boluses in patients with HRS-AKI. Aim of the study This study aimed to evaluate the safety and efficacy of terlipressin infusion at the rate of 4 mg/day in the treatment of HRS-AKI. Methods This retrospective study included patients who had HRS-AKI according to the modified International Club of Ascites (ICA) definition. Patients were started on a continuous intravenous infusion. The included patients received terlipressin 1 mg stat followed by a 4 mg infusion over 24 hours, and the infusion was continued until specific response criteria were met or for a maximum of seven days. Results In total, 136 patients were included in this study. The mean age of the study group was 45 years, the mean Child-Turcotte-Pugh (CTP) score was 11, the mean model for end-stage liver disease (MELD) score was 30, and the mean serum creatinine was 2.46 mg/dl. A response to treatment in the form of reduction of serum creatinine was observed in 94 (69.1%) patients, 30 (22%) patients showed no response, and worsening of creatinine was seen in 12 (8.8%) patients. The mean duration of hospital stay was 7.6 days, the mean serum creatinine was 1.17 mg/dl at the end of treatment, and the mean CTP and MELD scores in treatment responders were nine and 27, respectively. A total of 29 (21.3%) of 136 patients had adverse events during the terlipressin infusion therapy.  Conclusion Terlipressin infusion has sustained effects on splanchnic hemodynamics with fewer and less severe adverse events than intravenous bolus doses. Terlipressin infusion at a dose of 4 mg/day appeared to be well tolerated, with similar outcomes to that of 2 mg/day with a significantly lower albumin dose. These findings emphasize the importance of optimizing treatment protocols, particularly those favoring infusion methods, to enhance efficacy and minimize adverse effects.

Alcoholic liver disease (ALD) is a broad category of disorders that begin with liver injury, lead to liver fibrosis, and ultimately conclude in alcohol-induced liver cirrhosis, the most chronic and irreversible liver damage. Liver fibrosis (LF) is a common pathological characteristic observed in most chronic liver inflammatory conditions that involve prolonged inflammation. In this review, we have summarized ethanol-mediated hepatic stellate cell (HSCs) activation and its role in liver fibrosis progression. We highlight important molecular mechanisms that are modulated by ethanol, play a role in the activation of HSCs and the progression of liver fibrosis and identifying potential targets to ameliorate liver fibrosis.

Cruveilhier-Baumgarten syndrome presents a rare manifestation of portal hypertension characterized by a portosystemic shunt through a dilated paraumbilical vein, typically accompanied by classical signs such as caput medusae and a venous hum. We report a compelling case of a 41-year-old male presenting with portal hypertension, exhibiting clinical and radiological features of Cruveilhier-Baumgarten syndrome but notably lacking the characteristic venous hum. Clinical examination revealed moderate splenomegaly with prominent dilated veins and venous thrill but no caput medusae. Laboratory investigations indicated thrombocytopenia and esophageal varices on upper GI endoscopy. Imaging studies confirmed portal hypertension with findings consistent with Cruveilhier-Baumgarten syndrome, including a dilated paraumbilical vein and splenic artery aneurysms, along with the unexpected absence of a venous hum. Despite the classical radiological features, our patient did not present with hematemesis, possibly attributed to the presence of paraumbilical veins. This case highlights the diagnostic challenges and atypical presentations of Cruveilhier-Baumgarten syndrome, emphasizing the importance of comprehensive clinical evaluation and imaging modalities in its diagnosis and management. Management strategies primarily focus on addressing portal hypertension and underlying liver disease. This case underscores the need for further research to elucidate the varied clinical presentations and pathophysiology of Cruveilhier-Baumgarten syndrome variants, enhancing our understanding and management of this rare entity.

BACKGROUND: Autoimmune hepatitis (AIH) is uncommon and predominantly affects females. Data on AIH from India are scanty. We retrospectively analyzed the spectrum and outcome of adults with AIH and compared it between male and female patients.
METHODS: AIH was diagnosed using a simplified AIH score. For suspected seronegative AIH, the revised score was used. Standard therapies for AIH and portal hypertension were administered and response was assessed at six months. Relapse rates and five-year mortality were also evaluated.
RESULTS: Of the 157 patients with AIH, 85 (male: female 25: 60) were included in the study. The median age at diagnosis was 46 (interquartile range (IQR) 32-55.5) years in males vs 45 (IQR 34.2-54) years in females (p=0.91). A similar proportion of male and female patients presented with cirrhosis, acute severe AIH, or AIH-related acute on chronic liver failure (ACLF); Extra-hepatic autoimmune diseases were less common in male patients (16% vs 35.5% p=0.02). Other laboratory and histological features were comparable in both groups. During the median follow-up period of 51 months (IQR 45-67 months). The biochemical and clinical response at six months were seen in 64% of male patients and 63.3% of female patients (p= 0.57). Of patients, 75% relapsed in the male AIH group (12 of 16 patients) after initial remission compared to 42% in the female group (p=0.02). Five-year mortality was 14.1%, and no patient developed hepatocellular carcinoma.
CONCLUSIONS: Male and female patients with AIH have similar clinical, biochemical, and histological profiles. More male patients relapsed after an initial response to therapy.

Objectives This study aimed to identify the causes, clinical characteristics, and 28-day in-hospital mortality predictors in patients with acute-on-chronic liver failure (ACLF). Methods A cross-sectional study enrolled sixty-four patients aged 18-70 years with acute-on-chronic liver failure. The study was conducted at the Gastroenterology Department, Lahore General Hospital. The study classified ACLF according to the criteria of the European Association for the Study of the Liver - Chronic Liver Failure (EASL-CLIF). Patients were followed for 28 days for mortality outcomes. The outcomes between Survivor and Non-survivor groups were compared using the Chi-Square/Fisher\'s Exact Test for categorical variables and the Mann-Whitney U test for continuous variables. Results In this study, age and duration of chronic liver disease were not significantly different between survivors and non-survivors. The etiology of liver disease and ACLF causes had no impact on 28-day mortality. Non-survivors had lower mean arterial pressure, and higher mortality was linked with lower Glasgow Coma Scale scores, upper gastrointestinal bleeding, and Grade IV hepatic encephalopathy. Significant differences in bilirubin, serum creatinine, urea, and C-reactive protein levels were observed at 28 days. Survival rates were highest with single organ failure (35.94%) and decreased with multiple organ failures. The overall survival rate was 51.56%. Predictive validity for mortality was assessed using the Area Under the Curve (AUC), with Child-Turcotte-Pugh (CTP) at 0.679, Model for End-Stage Liver Disease (MELD) at 0.819, and Chronic Liver Failure-Sequential Organ Failure Assessment (CLIF-SOFA) at 0.771. Conclusion This study concludes that in acute-on-chronic liver failure, factors like age, gender, and disease etiology do not significantly predict 28-day mortality. Key mortality indicators include clinical parameters such as lower Glasgow Coma Scale scores, hepatic encephalopathy Grade IV, and laboratory findings like elevated bilirubin and serum creatinine. The MELD score is the most compelling prognostic tool.

UNASSIGNED: Chronic liver disease (CLD) is one of the important causes of morbidity and mortality in our country, and since the damage to the liver is irreversible, we have to look for many severity markers or predictors for the prognosis of the patient. In this study, we have tried to correlate the level of serum uric acid (UA) with the severity of CLD presented as a Child-Pugh score.
UNASSIGNED: A cross-sectional observational study was conducted at Vijayanagar Institute of Medical Science (VIMS), Ballari, Karnataka, from October 2015 to June 2017 in the Department of General Medicine. Fifty patients diagnosed with CLD, aged between 18 and 65 years, of either gender, were enrolled in the study. Serum UA levels were measured, and liver function and coagulation parameters were assessed. A statistical analysis was performed to evaluate the association between serum UA levels, liver function test, and coagulation parameters.
UNASSIGNED: In our study, the mean serum UA level was 6.52 mg/dl and was raised in patients with CLD in correlation to its severity. Alcoholic liver disease (ALD) was the most common etiology for CLD (80%) followed by hepatitis B (Hep B) virus infection (12%) and hepatitis C (Hep C) virus infection (6%). Serum UA levels increased as the Child-Turcotte-Pugh (CTP) score increased. The mean UA level in CTP class C was 8.29 mg/dl. Various parameters such as serum aspartate aminotransferase (AST), alanine transaminase (ALT), alkaline phosphatase, total bilirubin, international normalized ratio (INR), calcium, and albumin were significantly associated with serum UA levels in CLD patients.
UNASSIGNED: The correlation between rising blood UA levels and the Child-Pugh score shows that UA estimate may be a valid and affordable indicator for assessing the extent of liver cirrhosis in CLD.

OBJECTIVE: Hepatocellular carcinoma (HCC) affects millions of people each year and is associated with high mortality and morbidity. Sarcopenia, a condition of muscle wasting, and decreased muscle performance is common among aging adults, and is associated with poor clinical outcomes. Individuals with HCC and chronic liver disease (CLD) are at high risk of sarcopenia because of the adverse effects of chronic inflammation, endocrine dysfunction, and hyperammonemia on muscle metabolism and adequate nutrition. Our aim is to review the clinical relationship between HCC and sarcopenia, and the assessment and management of these patients.
METHODS: A narrative review based on a literature search using PubMed. Keywords related to HCC and sarcopenia were used to identify relevant articles, primarily those published 2018-2023. The information was synthesized to provide a narrative review focused on the most recent literature.
UNASSIGNED: Sarcopenia frequently co-exists with HCC and increases risk for adverse clinical outcomes such as symptom burden, quality of life (QoL), survival, and side effects of antineoplastic therapy. Tools are available to screen, assess and manage patients with HCC, and although there is no specific pharmacologic agent approved for sarcopenia in the United States, multimodal therapy is feasible in daily practice. Comprehensive management by an interdisciplinary team should include nutritional counseling, an exercise regimen and control of symptoms affecting nutrition and function.
CONCLUSIONS: Sarcopenia has adverse effects on prognosis and tolerability of surgical and medical therapy in HCC. Patients with CLD and/or HCC would benefit from early identification, assessment, and therapeutic intervention. Management should be comprehensive, interdisciplinary, and include both pharmacologic and non-pharmacologic treatments. Further research is needed to identify individual agents that may mitigate muscle wasting and trials are needed to evaluate the benefit of multimodal therapy in HCC.

It is well established that direct oral anticoagulants (DOACs) are the cornerstone of anticoagulant strategy in atrial fibrillation (AF) and venous thromboembolism (VTE) and should be preferred over vitamin K antagonists (VKAs) since they are superior or non-inferior to VKAs in reducing thromboembolic risk and are associated with a lower risk of intracranial hemorrhage (IH). In addition, many factors, such as fewer pharmacokinetic interactions and less need for monitoring, contribute to the favor of this therapeutic strategy. Although DOACs represent a more suitable option, several issues should be considered in clinical practice, including drug-drug interactions (DDIs), switching to other antithrombotic therapies, preprocedural and postprocedural periods, and the use in patients with chronic renal and liver failure and in those with cancer. Furthermore, adherence to DOACs appears to remain suboptimal. This narrative review aims to provide a practical guide for DOAC prescription and address challenging scenarios.

Chronic liver disease (CLD) is a persistent public health burden, with over one billion cases reported worldwide. In most cases, the progression of CLD is slow and undulating with end-stage liver disease developing at variable time points depending on the underlying etiology of the disease. The concept of reversibility or halting progression to end stage liver disease is recent and various medications are in the pipeline which influence the progression of CLD. Non-invasive tests for monitoring of CLD may have the potential to avoid the morbidity and mortality related to invasive procedures. However, their applicability and validation in pediatrics requires further development and a coordinated effort by large pediatric liver centres. Recent advances in metabolomics and modern molecular technologies have led to an understanding of the interaction between gut microbiome liver axis and gut dysbiosis contributing to liver diseases. In the future, modifying the gut microbiome has the potential to change the outcome and significantly reduce the morbidity associated with CLD. This article focuses on newer modalities and concepts in the management of CLD, which may help develop strategies to prevent its progression to end-stage liver disease and associated morbidity/mortality.

Background Zinc, an essential trace element, plays a vital role in cellular metabolism, and the liver is the main organ responsible for its metabolism. Because serum zinc levels are found to be lowered in chronic liver diseases, it has been hypothesized to be a precipitating factor for the development of hepatic encephalopathy. Methodology This prospective, observational study included patients with decompensated cirrhosis of the liver who were admitted to the medical intensive care unit of a tertiary care institute in northern India between September 2021 and April 2023. The diagnosis was based on history and detailed clinical examination. The serum zinc levels of patients were estimated using atomic absorption spectrometry at admission and compared to that of healthy controls. Serum zinc levels were correlated with the severity of liver disease and hepatic encephalopathy among the cases. Results A total of 100 cases of decompensated cirrhosis of the liver and 50 healthy controls were included. The mean serum zinc level of the cases was 40.5 ± 10.0 µg/dL which was significantly lower than the mean serum zinc level (104.0±9.1 µg/dL) of controls (p < 0.0001). Serum zinc level was significantly lower in patients with higher grades of hepatic encephalopathy (p = 0.000). Similarly, serum zinc level was significantly reduced among patients with higher Child-Pugh and Model for End-stage Liver Disease scores. Conclusions Serum zinc level is significantly reduced in patients with decompensated cirrhosis of the liver, and lower serum zinc level is associated with the increased severity of the disease and higher grades of hepatic encephalopathy. In patients with decompensated cirrhosis of the liver, maintenance of adequate serum zinc levels may prevent hepatic encephalopathy.