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Elderly patients show increased incidence of multiple organ dysfunction in acute pancreatitis possibly due to bacterial translocation. This is associated with increased susceptibility to infections in older people. Several reports have related this increased susceptibility to a proinflammatory status called inflammaging, which decreases the capacity of the immunological system to respond to antigens. Cellular senescence also contributes to this low-grade chronic inflammation in older subjects. We discuss here the effect of ageing on systemic inflammation, focusing on that induced by acute pancreatitis and some of the mechanisms involved. It is important to understand the immunological changes in the elderly to adjust treatment strategies in order to reduce the morbidity and mortality associated with acute pancreatitis and other conditions that lead to systemic inflammation.

Summary. Non-alcoholic fatty liver disease (NAFLD) encompasses the whole spectrum of steatosis, nonalcoholic steatohepatitis (NASH), and NASH-related cirrhosis (NASH/Cir). Although molecular advances have been made in this field, the pathogenesis of NAFLD is not completely understood. The gene expression profiling associated to NASH/Cir was assessed, in an attempt to better characterize the pathways involved in its etiopathogenesis. Methods: In the first step, we used cDNA microarray to evaluate the gene expression profiles in normal liver (n=3) and NASH/Cir samples (n=3) by GeneSifter™ analysis to identify differentially expressed genes and biological pathways. Second, tissue microarray was used to determine immunohistochemical expression of phosphorylated mTOR and 4E-BP1 in 11 normal liver samples, 10 NASH/Cir samples and in 37 samples of cirrhosis of other etiologies to further explore the involvement of the mTOR pathway evidenced by the gene expression analysis. Results: 138 and 106 genes were, respectively, up and down regulated in NASH/Cir in comparison to normal liver. Among the 9 pathways identified as significantly modulated in NASH/Cir, the participation of the mTOR pathway was confirmed, since expression of cytoplasmic and membrane phosphomTOR were higher in NASH/Cir in comparison to cirrhosis of other etiologies and to normal liver. Conclusions: Recent findings have suggested a role for the cellular “nutrient sensor” mTOR in NAFLD and the present study corroborates the participation of this pathway in NASH/Cir. Phospho-mTOR evaluation might be of clinical utility as a potential marker for identification of NASH/Cir in cases mistakenly considered as cryptogenic cirrhosis owing to paucity of clinical data.

La falla hepática fulminante (FHF) es definida como el comienzo súbito de encefalopatía, coagulopatía e ictericia en un individuo que se encontraba en condiciones normales de salud. La falla hepática fulminante termina en un deterioro progresivo de múltiples órganos con un impacto dramático en el cerebro. El edema cerebral severo es un hallazgo frecuente que, finalmente, conlleva a hipertensión intracraneal y a la muerte. El manejo de pacientes con FHF apunta principalmente a prevenir o reversar el incremento de la presión intracraneal, asociada con el tratamiento de soporte para la falla de otros órganos. El tratamiento definitivo para pacientes con FHF es el trasplante de hígado. Este artículo tiene como objetivo presentar una aproximación práctica al cuidado anestésico e intraoperativo para el manejo de pacientes con FHF. Fulminant hepatic failure (FHF) is defined by sudden onset of encephalopathy, coagulopathy and jaundice in an otherwise normal individual. Fulminant hepatic failure results in progressive multi-organ failure with a dramatic impact in the brain. Severe cerebral edema is a frequent finding that ultimately lead to intracranial hypertension and death. The management of patients with FHF is aimed mainly in prevent or reversing increased intracranial pressure associated with support treatment for other failing organs. The definitive treatment for patients with FHF is liver transplantation. This article aims to present a practical approach to anesthesia care and intraoperative management of patients with FHF.