Hepatitis C virus (HCV) infection is associated with increased thrombotic risk. Several mechanisms are involved including direct endothelial damage by the HCV virus, with activation of tissue factor, altered fibrinolysis and increased platelet aggregation and activation. In advanced stages, chronic HCV infection may evolve to liver cirrhosis, a condition in which alterations in the portal microcirculation may also ultimately lead to thrombin activation, platelet aggregation, and clot formation. Therefore in advanced HCV liver disease there is an increased prevalence of thrombotic phenomena in portal vein radicles. Increased thrombin formation may activate hepatic stellate cells and promote liver fibrosis. In addition, ischemic changes derived from vascular occlusion by microthrombi favor the so called parenchymal extinction, a process that promotes collapse of hepatocytes and the formation of gross fibrous tracts. These reasons may explain why advanced HCV infection may evolve more rapidly to end-stage liver disease than other forms of cirrhosis.

We report increased values of fibroblast growth factor 23 (FGF-23) and soluble α Klotho in cirrhotic alcoholics. Both molecules are associated with liver function impairment, and with some cardiovascular risk factors such as diabetes, hypertension, increased body fat, left ventricular hypertrophy and atrial fibrillation independently of serum creatinine.

Alcoholic hepatitis is associated with high short-term mortality. Although not included in prognostic scores, lipid peroxidation plays an outstanding role in its pathogenesis. We found that malondialdehyde levels showed a better prognostic accuracy than the usually employed scores. Therefore, it should be included in the prognostic evaluation of these patients.

Hyperhomocysteinemia has been described in alcoholics and may be related to brain atrophy, a reversible condition with an obscure pathogenesis. We studied 59 patients and found that liver function derangement, vitamin B12 and homocysteine levels are all independently related to brain atrophy assessed by computed tomography, although we found no association between these parameters and cognitive alterations.

This study was performed in order to analyze the relationships between hair zinc, lead, and cadmium with the kind of diet consumed (by recall of the diet consumed the previous 14 days), living area (urban or rural), tobacco smoking, and body mass index (BMI) among 419 individuals of the Canary Archipelago. Median values and interquartile range were 43 μg/g (18.50-132.50) for zinc, 4.09 μg/g (2.19-8.38) for lead, and 0.128 μg/g (0.05-0.30) for cadmium. We observed that hair zinc was markedly elevated among those consuming fish more frequently and, to a lesser amount, among those who consumed meat frequently, among those living in urban areas, and among those with BMI over 25 kg/m(2), keeping a significant relationship with BMI. Hair lead was also higher among fish consumers, showed a trend to higher values among inhabitants of urban areas, and was lower among obese individuals. Hair cadmium was higher among those who consumed less vegetables and fruits. By multivariate analysis, introducing the variables meat, fish, and vegetable consumption, urban/rural; sex; age; and BMI values, we observed that fish consumption (beta = 0.15) was the only variable independently associated to higher zinc levels; fish consumption (beta = 0.15) and meat consumption (beta = 0.17) were related to high cadmium levels, whereas meat consumption was significantly associated to higher hair lead levels (beta = 0.15). Therefore, we conclude that hair zinc, cadmium, and lead seem to depend more heavily on dietary habits than on tobacco consumption or living in rural or urban areas.

No abstract

No abstract

No abstract