losartan-potassium and Liver-Cirrhosis--Alcoholic

Patients with liver cirrhosis have a complex haemostasis disturbance including thrombocytopenia and abnormal bleeding time. Erythropoietin is the primary stimulator for erythrocyte production and also induces megakaryocyte formation. In healthy men erythropoietin increased platelet count and platelet reactivity.. As patients with liver cirrhosis often undergo invasive procedures, we were interested to study whether erythropoietin could improve platelet function in addition to thrombocytopenia.. In total, 22 thrombocytopenic (platelet counts < 120 g/L) patients with alcoholic liver cirrhosis received either 100 IE/kg erythropoietin or placebo on days 1, 3 and 5 in a 2:1 randomized, placebo-controlled double-blind fashion. Platelet counts and platelet reactivity (activator-stimulated expression of P-selectin on platelets measured by flow cytometry) were determined on study days 1, 3, 5 and 9.. Median platelet count was 80 g/L which is borderline for major elective surgical interventions. Baseline values were not different between groups (P > 0.05). Treatment with erythropoietin increased platelet count by 25% (P = 0.01) and platelet reactivity twofold (P < 0.01) vs. baseline. The increase in platelet count vs. baseline was more pronounced in patients with platelet counts <80 g/L. No significant effect was observed in the placebo group.. Treatment with erythropoietin significantly increased platelet counts and platelet reactivity in patients with alcoholic liver cirrhosis. Preoperative treatment with erythropoietin is therefore expected to yield higher platelet levels and better platelet function.

Topics: Adult; Bleeding Time; Blood Platelets; Double-Blind Method; Erythropoietin; Female; Humans; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Platelet Count; Reticulocyte Count; Reticulocytes; Thrombocytopenia

Erythropoietin (EPO) is produced in the liver during fetal life, but after birth the production shifts to the kidneys. The liver maintains a production capacity of 10% of the total EPO-production, but can be up-regulated to 100%. Previous studies have demonstrated both elevated and reduced concentrations of EPO in cirrhosis. Increased EPO concentrations could be expected due to anemia, hypoxia, renal hypoperfusion, or EPO-mediated hepatoprotective mechanisms. In contrast, poor hepatic production capacity may cause reduced EPO concentrations in cirrhosis. In the present paper we aimed to study hepatic and renal venous concentrations of EPO in relation to the severity of the disease.. We included 24 patients with alcoholic cirrhosis and eight age-matched healthy controls. All had a full catheterization performed with the determination of EPO concentrations in the hepatic, renal and femoral veins and artery. All patients were clinically, biochemically, and hemodynamically characterized.. The median arterial EPO concentrations in the cirrhotic patients and controls were 7.1 mIU/mL (range 3.5-179) and 7.2 mIU/mL (range 3.8-15.3), respectively. In the patient group we found no significant correlations to stage of disease of hemodynamic derangement.. We found no significant differences in EPO concentrations across the liver, kidney, or peripheral circulation in the patient or control groups; and no significant correlations to clinical, biochemical, or hemodynamic characteristics. This suggests that hepatic EPO synthesis is not enhanced in cirrhosis, but larger scale studies are needed to clarify this question.

Topics: Adult; Aged; Aged, 80 and over; Biomarkers; Case-Control Studies; Erythropoietin; Female; Femoral Artery; Femoral Vein; Hepatic Artery; Humans; Liver; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Renal Artery

We report the case of a patient with alcoholic liver cirrhosis and generalized atherosclerosis who rapidly developed erythrocytosis. Concomitantly we documented a significative and progressive increase of serum Erythropoietin (Epo) and a small focus of hepatocellular carcinoma (HCC) never diagnosed before. Even in absence of immunohistochemical and/or biomolecular evidence of Epo production in the neoplastic tissue we think the hypothesis of the paraneoplastic syndrome may be the most likely both for the strict temporal relationship between the observation of the neoplastic lesion and the appearance of polycythemia and for the absence of all other known causes of erythrocytosis. Objection to this hypothesis: 1) ectopic production of Epo during HCC has been usually described in large neoplastic lesions 2) liver cirrhosis by itself may be accompanied by increased Epo levels 3) an intratumoral hypoxia with compensatory production of Epo may have occurred 4) generalized vasculopathy could have determined renal hypoxia with greater local production of Epo.

Topics: Aged; Aged, 80 and over; Carcinoma, Hepatocellular; Erythropoietin; Fatal Outcome; Humans; Liver Cirrhosis, Alcoholic; Liver Neoplasms; Male; Neoplasm Proteins; Polycythemia

Topics: Aged; Carcinoma, Hepatocellular; Erythrocyte Count; Erythropoietin; Hepatorenal Syndrome; Humans; Liver Cirrhosis, Alcoholic; Liver Neoplasms; Male; Paraneoplastic Syndromes; Polycythemia

Topics: Anemia; Blood Transfusion, Autologous; Colorectal Neoplasms; Costs and Cost Analysis; Erythropoietin; Humans; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Preoperative Care; Recombinant Proteins