No abstract available.

Ascites is the most common complication of liver cirrhosis, but its pharmacological management is unsatisfactory in some patients because of a lack of response to treatment with conventional diuretics. Patients with cirrhosis and ascites generally have increased non-osmotic secretion of vasopressin which participates in the pathogenesis of fluid retention. Vaptans are a new family of orally active drugs that increase urine volume by antagonizing specifically the vasopressin receptors in the principal cells of the collecting ducts that have been shown to correct dilutional hyponatremia effectively. They also seem to be promising in the management of ascites by reducing the increased extracellular fluid volume in conditions associated with water retention including liver cirrhosis. However, there is a paucity of information on whether vaptans might have beneficial effect in enhancing ascites reduction in patients with cirrhosis. This review addresses the pharmacological actions of vaptans, their clinical applications, and future potential roles in managing patients with liver cirrhosis and ascites.
Ascites ; Diuretics ; Extracellular Fluid ; Fibrosis ; Humans ; Hyponatremia ; Liver ; Liver Cirrhosis ; Receptors, Vasopressin ; Retention (Psychology) ; Vasopressins ; Water

Vertical transmission of hepatitis B virus (HBV) is the main source of chronic infection in Korea, an HBV-endemic area, and chronically infected people are at high risk of developing liver cirrhosis or hepatocellular carcinoma. Thus, preventing vertical transmission is an important step in eradicating or reducing the burden of chronic HBV infection. However, despite passive-active immunoprophylaxis provided to infants, up to 10% of infants born to highly viremic mothers still become infected with HBV. Therefore, antiviral treatments or management protocols to reduce vertical transmission should be considered for highly viremic mothers and infants born to these mothers. Additionally, in-depth discussions with the mothers about the risks, benefits, and limitations of the current published data are essential. This article reviews the potential mechanisms of vertical transmission and current intervention strategies to prevent vertical transmission of HBV.
Antiviral Agents ; Carcinoma, Hepatocellular ; Hepatitis B virus* ; Humans ; Infant ; Korea ; Liver Cirrhosis ; Mothers ; Pregnancy

Vertical transmission of hepatitis B virus (HBV) is the main source of chronic infection in Korea, an HBV-endemic area, and chronically infected people are at high risk of developing liver cirrhosis or hepatocellular carcinoma. Thus, preventing vertical transmission is an important step in eradicating or reducing the burden of chronic HBV infection. However, despite passive-active immunoprophylaxis provided to infants, up to 10% of infants born to highly viremic mothers still become infected with HBV. Therefore, antiviral treatments or management protocols to reduce vertical transmission should be considered for highly viremic mothers and infants born to these mothers. Additionally, in-depth discussions with the mothers about the risks, benefits, and limitations of the current published data are essential. This article reviews the potential mechanisms of vertical transmission and current intervention strategies to prevent vertical transmission of HBV.
Antiviral Agents ; Carcinoma, Hepatocellular ; Hepatitis B virus* ; Humans ; Infant ; Korea ; Liver Cirrhosis ; Mothers ; Pregnancy

Portal hypertension is responsible for most of the complications associated with liver cirrhosis, including variceal hemorrhage, ascites, and hepatic encephalopathy. It has become clear that a decrease in portal pressure can prevent or manage these serious complications. Until now, the pharmacotherapy of portal hypertension has focused on agents that reduce splanchnic blood flow, such as non-selective beta blockers and splanchnic vasoconstrictors. However, recent advances in the knowledge of the pathophysiology of portal hypertension have directed future treatment towards modulating the increased intrahepatic vascular resistance, in addition to managing the splanchnic circulation. Consequently, agents that modulate either the hyperdynamic circulation or angiogenesis are new therapeutic targets for managing portal hypertension. Several have been developed or are under investigation. To incorporate these pharmacologic approaches into clinical practice, data on patient-oriented outcomes are needed.
Ascites ; Hemorrhage ; Hepatic Encephalopathy ; Hypertension, Portal ; Liver Cirrhosis ; Portal Pressure ; Splanchnic Circulation ; Vascular Resistance ; Vasoconstrictor Agents

Portal hypertensive gastropathy (PHG) is a term used to define the endoscopic findings of gastric mucosa with a characteristic mosaic-like pattern with or without red spots, and a common finding in patients with portal hypertension. These endoscopic findings correspond to dilated mucosal capillaries without inflammation. The pathogenesis of PHG in not well known, but portal hypertension and some humoral factors seem to be crucial factors for its development. Pharmacological (e.g. propranolol), or interventional radiological (such as transjugular intrahepatic portosystemic shunt) procedures may be useful in preventing re-bleeding from PHG. The classic features of gastric antral vascular ectasia (GAVE) syndrome include red, often haemorrhagic lesions predominantly located in the gastric antrum which can result in significant blood loss. Although the pathogenesis of GAVE is not clearly defined, it seems to be a separate disease entity from PHG, because GAVE generally does not respond to a reduction of portal pressures. Endoscopic ablation (such as argon plasma coagulation) is the first-line treatment of choice. This review will focus on the incidence, clinical importance, etiology, pathophysiology, and treatment of PHG and GAVE syndrome in the setting of portal hypertension.
Esophageal and Gastric Varices/*diagnosis/etiology/therapy ; Gastric Antral Vascular Ectasia/*diagnosis/etiology/therapy ; Gastric Mucosa/metabolism/pathology ; Humans ; Hypertension, Portal/*complications ; Portasystemic Shunt, Transjugular Intrahepatic ; Vasodilator Agents/therapeutic use

No abstract available.
Female ; Humans ; Hypertension, Portal/*diagnosis ; Male ; *Portasystemic Shunt, Transjugular Intrahepatic

The goal of antiviral therapy for chronic hepatitis B virus (HBV) infection is to eliminate or suppress HBV with the aim of preventing the devastating complications of cirrhosis, hepatic failure, and hepatocellular carcinoma. Oral antiviral agents suppress but do not eradicate HBV, therefore long-term treatment is necessary to achieve the sustained suppression of viral replication. To optimize the treatment response, treatment should be initiated at an appropriate time with the best available drugs. The indications for treatment are generally based on HBeAg status, serum HBV-DNA level, serum alanine aminotransferase, and the severity of the liver disease. Patients with clinical evidence of active viral replication either with liver inflammation or potentially evolving to cirrhosis should be treated. Nowadays, lamivudine, adefovir, clevudine, telbivudine, entecavir, and tenofovir have been approved for chronic hepatitis B (CHB). Among these, tenofovir and entecavir are potent HBV inhibitors with a high genetic barrier to resistant mutants, so they are recommended by the current treatment guidelines as preferred first-line monotherapies. Failure of antiviral therapy for CHB results in a partial virological response and virological breakthrough, which are related to antiviral-resistant mutants. If genotypic resistance is confirmed, rescue therapy should be initiated, and the regimen should include a potent drug without cross-resistance to prior antiviral agents to minimize the risk of emergence of multiple drug-resistant mutants. This article reviews the current developments in oral antiviral agents, recommendations in CHB treatment guidelines, the medical insurance policy of Korea's National Health Insurance, and the optimal strategies for using these drugs in clinical practice.
Alanine Transaminase ; Antiviral Agents* ; Carcinoma, Hepatocellular ; Fibrosis ; Hepatitis B e Antigens ; Hepatitis B virus ; Hepatitis B, Chronic* ; Hepatitis, Chronic* ; Humans ; Inflammation ; Insurance ; Lamivudine ; Liver ; Liver Cirrhosis ; Liver Diseases ; National Health Programs ; Tenofovir ; Viruses