ABSTRACT
Hepatic encephalopathy (HE) is a neuropsychiatric and motor disorder, resulting from hepatic failure. It is one of the main manifestations of chronic liver disease and the cardinal presentation of acute liver failure. Its presence and severity are the main prognostic determinants among these patients. It is frequent in advanced chronic liver disease (30-45 percent) and in patients with TIPS (transjugular intrahepatic portosystemic shunt) (10-50 percent). Its pathogenesis is complex and it has multiple components, including ammonia, inflammatory cytokines, benzodiazepine- and manganese-like components, which alter the function of the neuronal cell. Its management requires identification and treatment of the precipitating factors, and ruling out other causes of mental status alteration. The majority of the therapies are aimed at reducing ammonia load in the intestine, such as non absorbable disaccharides (lactulose), antibiotics (neomycin, metronidazole and currently, rifaximin) and other, whose role has yet to be established. Severe encephalopathy is considered an indicator for liver transplantation. This article will analyze mainly hepatic encephalopathy in cirrhotic patients, its classification, etiopathogeny and current management.
La encefalopatía hepática (EH) es un síndrome neuropsiquiátrico y motor, que resulta de una disfunción hepática. Es una de las manifestaciones principales de la enfermedad hepática crónica y la presentación cardinal en la falla hepática aguda. Su presencia y gravedad son uno de los mayores determinantes pronósticos en estos pacientes. Es frecuente en enfermedad hepática crónica avanzada (30-45 por ciento)y en portadores de shunt postosistémico transyugular intrahepático (TIPS) (10-50 por ciento). Su patogénesis es compleja y tiene múltiples componentes, incluyendo el amonio, citoquinas inflamatorias, compuestos que semejan a benzodiacepinas y manganeso, que causan alteración funcional de la célula neuronal. El manejo requiere identificar y tratar los factores precipitantes, además de excluir otras causas de alteración del estado mental. La mayoría de las terapias están dirigidas a reducir la carga de amonio en el intestino, tales como los disacáridos no absorbibles (lactulosa), antibióticos (neomicina, metronidazol y actualmente rifaximina) y otros cuyo rol está por establecerse. La encefalopatía grave es considerada un indicador para trasplante hepático. En este artículo analizaremos principalmente la encefalopatía hepática en pacientes con cirrosis, su clasificación, etiopatogenia y manejo actual.
Subject(s)
Humans , Hepatic Encephalopathy/physiopathology , Hepatic Encephalopathy/therapy , gamma-Aminobutyric Acid , Ammonia/metabolism , Anti-Bacterial Agents/therapeutic use , Liver Cirrhosis , Portasystemic Shunt, Transjugular Intrahepatic/adverse effects , Hepatic Encephalopathy/classification , Hepatic Encephalopathy/metabolism , Lactulose/therapeutic use , Manganese/metabolism , Rifamycins/therapeutic use , Severity of Illness IndexABSTRACT
Background: Epidemiological differences suggest that treatments for H. pylori eradication should be locally validated. Aim: To perform a cost benefit study of different treatment options for H. pylori infection. Patients and methods: One hundred and sixty-seven patients with active duodenal ulcer and H. pylori infection who completed a 2-week treatment with one of the following regimens were included: famotidine plus amoxycillin plus metronidazole (FAM), omeprazole plus amoxycillin plus tinidazole (OAT) or lansoprazole plus clarithromycin plus amoxycillin in 3 (LAC1) or 2 (LAC2) daily doses. We compared efficacy, adverse effects and cost. Results: Eradication rate was 74.6, 72.9, 96.4 y 91.7 percent for FAM, OAT, LAC1 and LAC2 respectively (p<0.05). Direct cost ranged from US$ 50 for FAM to US$ 220 for LAC1. A decision analysis was carried out in a model including direct and indirect costs and considering retreatment with antibiotics after the first treatment failure and one-year treatment with H2-blockers in case of a second failure. FAM was selected as the most cost-effective option, with an estimated cost of about US$ 300 ñ 148 per patient. However, cost associated to LAC2 was very similar (US$ 320 ñ 58) and the lower standard deviation suggests less variation. Sensitivity analyses, considering reasonable fluctuation in parameters such as eradication rate, cost and follow-up period suggest that a regimen containing a proton pump inhibitor, clarithromycin and amoxycillin may be the most cost-effective treatment. Conclusions: These results should be confirmed in other settings, specially in ordinary clinical practice, far from clinical research