Soluble α-Klotho in Liver Cirrhosis and Alcoholism.

Aims And Background: Alpha Klotho is a transmembrane protein that serves as co-receptor for FGF23. Ectodomain of membrane bound α Klotho may be shed by membrane bound proteases (activated, among other factors, by tumor necrosis factor (TNF)-α) generating the soluble form of the protein (sKl) that functions as a hormone by itself. It modulates calcium influx into cells, blunts IGF-1/Insulin signaling, promotes synthesis of antioxidants, generally slows down tumor progression, delays cell senescence, is neuroprotective and promotes oligodendrocyte maturation and myelin synthesis, and muscle rejuvenation.

Handgrip strength and lean mass are independently related to brain atrophy among alcoholics.

Background: In neurodegenerative disorders or in normal aging humans a relationship between muscle mass and/or performance and brain volume was observed, that is not dependent on age or other confounding factors. The aim of the present study is to analyse the relationship between lean mass and handgrip strength in alcoholics, who frequently show brain and muscle atrophy.

Methods: It was included 101 male patients aged 58.

Soluble Klotho and Brain Atrophy in Alcoholism.

Aim: Fibroblast growth factor (FGF-23) and α-Klotho (Klotho) levels may be altered in inflammatory conditions, possibly as compensatory mechanisms. Klotho exerts a protective effect on neurodegeneration and improves learning and cognition. No data exist about the association of Klotho and FGF-23 levels with brain atrophy observed in alcoholics.

Lipid profile and bone mineral density in heavy alcoholics.

Background & Aims: Some studies have illustrated the association between serum lipid profile and bone mineral density (BMD) or fractures. None of these studies was performed among alcoholics, despite the fact that alcoholism may affect both bone mass and lipid metabolism. We here analyse the relationship of serum lipid profile with bone mass among a population of 280 heavy alcoholics (29 women).

Alpha Klotho and Fibroblast Growth Factor-23 Among Alcoholics.

Aims: Alcoholism may be a cardiovascular risk factor. Osteocyte derived molecules such as fibroblast growth factor 23 (FGF-23) and soluble α Klotho have recently been associated with cardiovascular disease, but their role in alcoholics is unknown. We here analyze the behavior of FGF23 and α Klotho in alcoholics.

[Metabolic syndrome and cardiovascular risk in diabetic population of El Hierro, Canary Islands].

Introduction: In the Canary Islands there is a high prevalence of vascular risk factors. Objective: To analyze the clinical characteristics of 300 patients with type 2 diabetes in El Hierro, in the Canary Islands. Methods: Patients were assessed at the Internal Medicine Unit of the hospital from 1982 to 2010, and followed up until December 2014 or until death.

Malondialdehyde as a Prognostic Factor in Alcoholic Hepatitis.

Aims: Alcoholic hepatitis is a severe complication of alcoholism, associated with high short-term mortality. Although pathogenesis remains obscure, it is generally accepted that lipopolysaccharide-induced cytokine secretion with further generation of reactive oxygen species (ROS) play outstanding roles. Prognosis is uncertain, and the usually employed prognostic scores do not include variables related to ROS generation.

Homocysteine, Liver Function Derangement and Brain Atrophy in Alcoholics.

Aims: Hyperhomocysteinemia may be involved in the development of brain atrophy in alcoholics. Its pathogenesis is multifactorial. In the present study, we analyse the relationship between homocysteine levels and brain atrophy, and the relative weight of co-existing factors such as liver function impairment, the amount of ethanol consumed, serum vitamin B12, B6, and folic acid levels on homocysteine levels and brain alterations in alcoholic patients.

Thrombin activation and liver inflammation in advanced hepatitis C virus infection.

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.

Adipokines, cytokines and body fat stores in hepatitis C virus liver steatosis.

Aim: To identify patients with or without liver steatosis and its severity in treatment-naïve patients affected by hepatitis C virus (HCV) infection.

Methods: We included 56 HCV infected patients, and assessed the amount of liver fat by histomorphometry, and its relationships with fat and lean mass at different parts of the body (by densitometry), hormones [insulin, homeostatic model assessment (HOMA)], adipokines (resistin, adiponectin, leptin), and cytokines (tumor necrosis factor α, interleukin-6).

Results: Although the intensity of liver steatosis is related to trunk fat mass and HOMA, 33% of patients showed no liver steatosis, and this finding was not related to body mass index or genotype.

Liver steatosis in hepatitis C patients.

There is controversy regarding some aspects of hepatitis C virus (HCV) infection-associated liver steatosis, and their relationship with body fat stores. It has classically been found that HCV, especially genotype 3, exerts direct metabolic effects which lead to liver steatosis. This supports the existence of a so called viral steatosis and a metabolic steatosis, which would affect HCV patients who are also obese or diabetics.

Bone changes in alcoholic liver disease.

Alcoholism has been associated with growth impairment, osteomalacia, delayed fracture healing, and aseptic necrosis (primarily necrosis of the femoral head), but the main alterations observed in the bones of alcoholic patients are osteoporosis and an increased risk of fractures. Decreased bone mass is a hallmark of osteoporosis, and it may be due either to decreased bone synthesis and/or to increased bone breakdown. Ethanol may affect both mechanisms.

Vitamin D, vascular calcification and mortality among alcoholics.

Aims: To analyze the relationship between low vitamin D levels and mortality among alcoholics.

Methods: One hundred twenty-eight alcoholic patients admitted to our hospital were followed up as outpatients. Nutritional status was evaluated measuring percentages of fat and lean mass in different body compartments.

Alcoholism: a systemic proinflammatory condition.

Excessive ethanol consumption affects virtually any organ, both by indirect and direct mechanisms. Considerable research in the last two decades has widened the knowledge about the paramount importance of proinflammatory cytokines and oxidative damage in the pathogenesis of many of the systemic manifestations of alcoholism. These cytokines derive primarily from activated Kupffer cells exposed to Gram-negative intestinal bacteria, which reach the liver in supra-physiological amounts due to ethanol-mediated increased gut permeability.

Serum sclerostin in hepatitis C virus infected patients.

Background: Sclerostin inhibits osteoblast functions, differentiations, and survival rates. As an endogenous inhibitor of the Wnt/β-catenin pathway, the sclerostin should be related to decreased bone masses, although several studies indicate opposite results. In addition, it may be related to insulin resistances and carbohydrate metabolisms, a relation shared with other markers of bone metabolisms, such as osteocalcin.

Antioxidant vitamins and brain dysfunction in alcoholics.

Aims: Alcohol induces cytokine secretion by Kupffer cells, which may exert also deleterious effects on distant organs, mediated in part by cytokine-derived increased production of reactive oxygen species (ROS). It is therefore important to assess antioxidant levels. The objective of this study is to analyse the relation of antioxidant vitamins with brain atrophy and cognitive dysfunction.

Iron and proinflammatory cytokines in chronic hepatitis C virus infection.

Steatohepatitis is a common finding in chronic hepatitis C virus (HCV) infection. As in other forms of steatohepatitis, oxidative damage may play an outstanding role. However, there are conflicting results relative to the role of iron on hepatic lipogenesis.

Relative and combined effects of selenium, protein deficiency and ethanol on hepatocyte ballooning and liver steatosis.

Oxidative damage plays a key role in alcohol-mediated liver alterations. Selenium, a potent antioxidant, is decreased in alcoholics. This study was conducted to analyse if the supplementation with selenium may alter liver changes in a murine model fed ethanol and/or a 2 % protein-containing diet, following the Lieber-DeCarli design.

Serum sclerostin in alcoholics: a pilot study.

Aims: Sclerostin is an endogenous inhibitor of the Wnt/β-catenin pathway secreted by osteocytes, which inhibits osteoblast function, differentiation and survival. As a consequence, sclerostin tends to decrease bone mass. Alcoholics frequently present osteoporosis, mainly due to decreased bone synthesis.

Bone alterations in hepatitis C virus infected patients.

Background And Aims: Most studies have shown that patients with chronic hepatitis C virus (HCV) infection are affected by osteoporosis. However, liver function impairment and deranged nutrition may both play a role in the bone alterations observed. In some works no osteoporosis was found, and some cases of osteosclerosis have been reported.

TH-1 and TH-2 cytokines in stable chronic alcoholics.

Unlabelled: In alcoholics, the activation of Kupffer cells by gram negative bacteriae leads to an inflammatory response and cytokine secretion, which in turn activate T-lymphocytes. Possibly, Th-1 lymphocytes are activated first, followed by a Th-2 response. Th-2 cytokines, especially interleukin (IL)-13 (scarcely studied in alcoholics), may be involved in the progression to chronic stages.

Changes in cytokine levels during admission and mortality in acute alcoholic hepatitis.

Cytokine levels are raised in acute alcoholic hepatitis. However, there are disparate results regarding the duration of altered plasma levels, and there are also discrepancies about the relation of changes during the first 15 days after admission with short-term (in-hospital) or long-term mortality. In 56 patients with acute alcoholic hepatitis we found that IL-8, IL-4, Interferon-γ (IFN-γ), malondialdehyde and C-reactive protein remained higher in patients than in 18 age- and sex-matched controls at admission, at the 7th day and at the 15th day after admission.