Standards of liver cirrhosis care in Central Australia.

Background: Liver cirrhosis and hepatocellular carcinoma (HCC) are highly prevalent in Australia's Northern Territory. Contributing factors include high levels of alcohol consumption, viral hepatitis and metabolic syndrome. Rural Aboriginal residents form a significant proportion of the Central Australian population and present a challenge to traditional models of liver care.

Hypomagnesaemia and its potential impact on thiamine utilisation in patients with alcohol misuse at the Alice Springs Hospital.

Introduction And Aims: Alcohol rapidly reduces thiamine among alcohol-dependent individuals. Poor diet and alcohol's impact on absorption, storage, activation and excretion of thiamine are thought to be the mechanisms. Previous literature identifies magnesium as an important cofactor in thiamine utilisation, which might also be compromised in alcohol dependent patients.

Controversies in and challenges to our understanding of hepatitis C.

Discovered in 1989, the hepatitis C virus (HCV) continues to cause significant morbidity and mortality world-wide despite a huge research commitment to defining and understanding the virus and the disease it causes. This paper discusses a number of areas where progress in the management of the HCV have not kept pace with the scientific understanding of the HCV. It is suggested that in the fields of HCV prevention and providing access to treatment, practice falls short of what could be achieved.

Pegylated interferon-alpha2beta in combination with ribavirin does not aggravate thyroid dysfunction in comparison to regular interferon-alpha2beta in a hepatitis C population: meta-analysis.

Background: Interferon (IFN) has been well documented to cause thyroid dysfunction, especially in high risk patients and when combined with ribavirin (RBV). There is very sparse data to assess if pegylated IFN will further aggravate the thyroid disease risk in comparison to regular IFN. The purpose of this study was to assess the risk of developing thyroid disease with pegylated IFN (pIFN) versus regular IFN (rIFN) therapy (in combination with RBV).

Role of ethanol in the regulation of hepatic stellate cell function.

Evidence has accumulated to suggest an important role of ethanol and/or its metabolites in the pathogenesis of alcohol-related liver disease. In this review, the fibrogenic effects of ethanol and its metabolites on hepatic stellate cells (HSCs) are discussed. In brief, ethanol interferes with retinoid metabolism and its signaling, induces the release of fibrogenic cytokines such as transforming growth factor beta-1 (TGFbeta-1) from HSCs, up-regulates the gene expression of collagen I and enhances type I collagen protein production by HSCs.

The spectrum of thyroid dysfunction in an Australian hepatitis C population treated with combination Interferon-alpha2beta and Ribavirin.

Background: The study aims to assess the pattern of thyroid response to combination Interferon-alpha2beta (IFN-alpha) and Ribavirin (RBV) anti-viral therapy in an Australian hepatitis C cohort. These include the prevalence of thyroid dysfunction (TD) including hyperthyroidism and hypothyroidism and their possible predictors, the common overall pattern of thyroid function tests whilst receiving therapy and TD outcomes, and the correlation with HCV status outcome.

Methods: A retrospective analysis of all medical records was performed to assess thyroid function in Hepatitis C Virus (HCV) patients who were treated at the Hunter Area hepatitis C treatment center between 1995 and March 2004.

The medical complications of alcohol use: understanding mechanisms to improve management.

The use of alcohol in a dependent or even a regular heavy pattern predisposes the drinker to a range of adverse consequences. These include a risk of direct harm from alcohol, including organ damage, mental health disorders and a range of social and legal problems associated with behaviours due to alcohol's effects. The range of organ damage associated with regular heavy alcohol consumption is well described.

Complementary and alternative medicine in the treatment of chronic liver disease.

Interest in and use of complementary and alternative medicines (CAM) in the treatment of chronic liver diseases has increased in the past decade. However, this has not been supported by a significant increase in sound clinical research evidence for their efficacy. The research literature is growing, providing improved knowledge on population use of CAM, possible mechanisms of action of a large range of complementary and alternative medications, and possible specific indications for these agents in patients with liver disease.

Factors associated with severity of hepatic fibrosis in people with chronic hepatitis C infection.

Objective: To determine factors associated with hepatic fibrosis development in people with chronic hepatitis C virus (HCV) infection.

Methods: As a requirement for access to interferon therapy through the S100 scheme in Australia, individual pretreatment demographic and clinical information was collected on 2986 patients from 61 hospital-based liver clinics from 1 October 1994 through 31 December 1996. Patients with both a hepatic fibrosis score and an estimated duration of HCV infection (910) were divided into 540 with no or minimal hepatic fibrosis (stage 0-1) and 370 with moderate to severe hepatic fibrosis (stage 2-3).

Molecular pathogenesis of T lymphocyte-induced liver injury in alcoholic hepatitis.

The development of alcohol-induced liver injury is, in part, a consequence of the immunological/inflammatory response that alcohol stimulates. The abnormalities of immune function in heavy drinkers have been documented well. Cytokines, especially TNF alpha, produced from macrophages/Kupffer cells, play a role in the induction of liver cell necrosis and apoptosis.

Lymphocyte-mediated liver injury in alcohol-related hepatitis.

The pathogenesis of alcohol-related liver disease (ALD) remains inadequately explained. Increasing alcohol intake is associated with an increased risk of ALD, but many heavy drinkers develop no liver damage. An explanation for ALD susceptibility requires theories that extend beyond a biochemical understanding of alcohol metabolism.