Challenges and Opportunities in Liver Cirrhosis
Diet, Gut Dysbiosis and Liver Cirrhosis and their Influence upon Hepatic Encephalopathy
Rosângela Passos de Jesus
Food, Nutrition and Health Postgraduate Programme, Federal University of Bahia, Brazil
Ramona Baqueiro Boulhosa
Municipal Department of Health, Salvador, Brazil
Lucivalda Magalhães Oliveira
Food, Nutrition and Health Postgraduate Programme, Federal University of Bahia, Brazil
Carla de Magalhães Cunha
Food, Nutrition and Health Postgraduate Programme, Federal University of Bahia, Brazil
Alexandre Nogueira Matos
Municipal Hospital of Salvador, Brazil.
Lourianne Nascimento Cavalcante
D’Or Institute for Research and Education, Salvador, Bahia, Brazil; Hospital São Rafael, Salvador, Bahia, Brazil; Gastro-Hepatology Service, Hospital Universitário Prof. Edgar Santos, Department of Medicine, Federal University of Bahia, Brazil.
Maria Gabriela Fernandes Dezan
Medicine and Health Postgraduate Programme, Federal University of Bahia, Brazil
Allain Amador Bueno
College of Health, Life and Environmental Sciences, University of Worcester
André Castro Lyra
D’Or Institute for Research and Education, Salvador, Bahia, Brazil; Hospital São Rafael, Salvador, Bahia, Brazil; Gastro-Hepatology Service, Hospital Universitário Prof. Edgar Santos, Department of Medicine, Federal University of Bahia, Brazil.
Abstract
Cirrhosis is the end stage of progressive liver fibrosis, resulted from chronic inflammation and liver injury. Early identification of risk factors and appropriate treatment for hepatic decompensation is paramount for positive health outcomes. In this review study, we revisited mechanisms associated with gut dysbiosis and intestinal hyperpermeability in advanced liver disease, and further discussed nutritional strategies for the management of dysbiosis in liver cirrhosis. In gut dysbiosis, proportionally lower concentrations of bacteria belonging to beneficial taxa such as Lachnospiraceae, Clostridiales, Ruminococcaceae and Veillonellaceae and others are observed, in relation to pathogenic taxa such as Enterobacteriaceae, Bacteroidaceae and others. Cirrhotic patients present decreased bowel motility, bacterial overgrowth and increased intestinal permeability. Dysbiosis may further exacerbate such conditions due to the ability of pathogenic bacteria to adhere to the epithelium, produce endotoxin, disrupt bile acid metabolism, activate the immune system and trigger inflammation, in a vicious cycle. The triad hepatic encephalopathy – cirrhosis – gut dysbiosis is an evident entity, and primary prevention as well as management strategies for those three conditions aim strongly at improving intestinal health by focusing on nutritional interventions. High-protein diets may be recommended for cirrhosis patients, and the protein source is a key factor to consider, and so are dietary fibre and carbohydrate compositions. Attention is given to reduce saturated fat intake. Supplementation with branched-chain amino acids, probiotics and prebiotics have also shown positive results.
Bernardo Times de Carvalho
Abstract
Hepato-splenic schistosomiasis is the most important etiology of non-cirrhotic portal hypertension. It represents a particular type of chronic liver disease, which presents unique characteristics that differentiate it from those found in cirrhosis. The relative preservation of liver parenchyma despite portal fibrosis was thought to yield a more benign course of hepato-splenic schistosomiasis in terms of synthetic dysfunction and late decompensations. However, a wide range of immunologic and vascular modifications is responsible for an otherwise progressive liver disease resulting in decompensated condition frequently undistinguished from hepatic cirrhosis. A predominant Th2 immune response type, in which a fibrogenic profile of cytokines and interleukins such as IL-13, provides an immune-inflammatory background that favors fibrosis and its progression. Intra-hepatic vascular changes with portal vein branch derangement and abnormal vascular proliferation also contribute to continued disarray of the liver architecture resulting in decompensated disease frequently undistinguished from hepatic cirrhosis. This article will review immunologic and pathophysiological aspects of hepato-splenic schistosomiasis that might explain disease progression and severity.
Nwe Ni Than, Dr.
Abstract
Metabolic dysfunction associated steatotic liver disease (MASLD) or previously known Non-alcoholic fatty liver disease (NAFLD) is a common condition with an estimated global prevalence of around 30%. It is becoming a public health concern due to its close association with type 2 diabetes mellitus and obesity. It is important to screen for those with inflammation and fibrosis to halt the progression to cirrhosis. Cirrhosis is associated with liver related complications and liver cancer. Currently, there are no targeted treatments for MASLD at this stage and most treatments are currently in clinical trials. The focus of treatment had been on managing underlying risk metabolic risk factors.
The purpose of this review to inform the readers of the change in the nomenclature from NAFLD to MASLD. This review will also focus on the background of MASLD, the pathogenesis as well as assessment and treatment of patients with MASLD.
Phillip Huang Chen
Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA
Steven-Huy Han
Pfleger Liver Institute, UCLA Medical Center, Los Angeles, CA; Greater Los Angeles VA Healthcare System, Los Angeles, CA
Abstract
Hepatitis B (HBV) in special populations within this article is considered as acute on chronic liver failure due to HBV, coinfection with Hepatitis C (HCV), Hepatitis D (HDV), or Human Immunodeficiency Virus (HIV), and HBV infection in patients who are in immunosuppressive states due to specific therapies and liver transplant recipients. Patients within these special populations are at higher risk of liver-related complications such as fibrosis, accelerated cirrhosis, acute on chronic liver failure, and/or development of hepatocellular carcinoma (HCC). Given their respective complex pathophysiology, specific treatment approaches are required for each population. With the introduction of effective antiviral HBV therapies over the past decade and the respective treatment options for the special population diseases, patient outcomes have seen improvement. With the advent of HCV direct antivirals, treatment of HBV-HCV coinfection has been more successful and consistently shown high rates of sustained virologic response. Treatment of HBV-HDV coinfection remains primarily as interferon-based, though new promising therapies have shown greater improvement in viral suppression. HBV-HIV coinfection has also shown promising results given overlapping mechanisms for treatment and specific regimens should be chosen to decrease risk of resistance. HBV reactivation in patients undergoing immunosuppressive therapies have been reported and guidelines recommend close monitoring and in certain cases, HBV antiviral therapy prophylaxis. With the effective HBV therapies, the perception of HBV as a contraindication for liver transplant has been diminishing and prolonged graft survival with effective antiviral therapies have shown promising outcomes.
Mukund Tinguria
Abstract
Celiac disease (CD) is an immune mediated disorder characterised by intolerance to glutens in certain grains like whet, barley, and rye. The exposure to gliadin protein component in the susceptible individuals leads to an inflammatory reaction damaging small bowel mucosa with progressive disappearance of intestinal villi. The damaged intestinal mucosa leads to malabsorption. The usual symptoms of celiac disease include diarrhea, steatorrhea, weight loss, fatigue, and abdominal pain. Diagnosis is based on clinical features, duodenal biopsy, elevated levels of anti-gliadin antibodies and response to gluten free diet. Contrary to common belief, celiac disease is a protein systemic disease rather than merely a pure digestive alteration. Celiac disease is closely associated with genes that code HLA -II antigens mainly of DQ2 and DQ8 classes, production of disease specific antibodies (i.e., endomysial antibodies), multiorgan involvement, comorbidity with other autoimmune diseases (shared autoimmunity), familial aggregation, and immune system dysregulation.
The clinical presentation of celiac disease can be variable. In mild form, patients can be almost asymptomatic whereas in the most severe form, the patients are at increased risk of life-threatening complications. Celiac disease has a well-known association with other autoimmune diseases such as autoimmune liver diseases (autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis), diabetes mellitus, autoimmune thyroid diseases, skin diseases such as dermatitis herpetiformis, rheumatoid arthritis, systemic lupus erythematosus, Sjogren’s syndrome, psoriasis, sarcoidosis, immune thrombocytopenic purpura, and pancreatitis. In addition, celiac disease may be associated with rare but potentially serious complications such as, collagenous sprue, ulcerative jejunoileitis, refractory celiac disease (RCD), enteropathy associated T-cell lymphoma, small bowel adenocarcinoma (SBA), hyposplenism, and cavitating mesenteric lymph node syndrome (CMLNS). The present article describes clinicopathologic features of these rare but serious complications of celiac disease.
