Position statement on the use of albumin in liver cirrhosis.

Cirrhosis is characterised by a prolonged asymptomatic period in which the inflammation persists, increasing as the disease progresses. Characteristic of this is the increase in pro-inflammatory cytokines and pro-oxidant molecules which are determining factors in the development of multiple organ dysfunction. In the early development of cirrhosis, splanchnic arterial vasodilation, activation of vasoconstrictor systems (renin-angiotensin-aldosterone) and the sympathetic nervous system (noradrenaline) bring about bacterial translocation and systemic dissemination via portal circulation of bacterial products, and molecular patterns associated with damage, which exacerbate the systemic inflammation present in the patient with cirrhosis. Albumin is a molecule that undergoes structural and functional changes as liver damage progresses, affecting its antioxidant, immunomodulatory, oncotic and endothelial stabilising properties. Our knowledge of the properties of albumin reveals a molecule with multiple treatment options in patients with cirrhosis, from the compensated then decompensated phases to multiple organ dysfunction. Its recognised uses in spontaneous bacterial peritonitis, post-paracentesis circulatory dysfunction, acute kidney injury and hepatorenal syndrome are fully validated, and a treatment option has opened up in decompensated cirrhosis and in acute-on-chronic liver disease.

Effect of Antiviral Agents on Atherosclerosis in Patients with Chronic Hepatitis C.

BACKGROUND: Chronic hepatitis C is an independent risk factor for atherosclerosis and is associated with cardiovascular events. Mechanisms include inflammatory cytokines, endothelial dysfunction, and increased oxidative stress. AIM OF THE STUDY: The objective was to evaluate the response of carotid atherosclerosis to treatment with direct-antiviral agents. METHODS: We developed a prospective cohort study that included patients with chronic hepatitis C treated with direct-acting antiviral agents (DAAs), without cardiovascular disease, diabetes mellitus, significative chronic kidney disease or coinfections. Clinical characteristics, laboratory values and carotid ultrasound to measure carotid intima-media thickness (CIMT) and look for established atherosclerosis were performed at baseline and 3 months after completing treatment with DAAs. RESULTS: A total of 24 patients were included. The mean age was 60 years and 79% were women. The prevalence of smoking was 41.7%, obesity 25% and hypertension 20.8%. Age, arterial hypertension, genotype, AST, glomerular filtration rate and cirrhosis were significantly associated with established carotid atherosclerosis. After treatment with DAAs, an overall significant reduction of C-reactive protein (CRP) levels was found (p = 0.004). A trend towards reduction of significant CIMT (>0.9 mm) (20.8 vs. 8.3%, RR 1.18, IC 95% 0.75-1.86, p = 0.29) and a statistically significant resolution of atherosclerotic plaque (45.8 vs. 41.7% RR 0.09, IC 95% 0.01-0.63, p = 0.001) was found. CONCLUSIONS: Treatment of chronic hepatitis C with DAAs decrease carotid thickening, atheromatous plaques, and inflammatory markers like CRP. More studies are needed to confirm this finding and its impact on long-term cardiovascular outcomes.