Acute-on-chronic liver failure: the liver and portal haemodynamics

Mookerjee, Rajeshwar P.

doi:10.1097/mcc.0b013e328344a076

Cited by 43 publications

(35 citation statements)

References 67 publications

(46 reference statements)

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“…El óxido nítrico (NO), cuya producción es inducida por la inflamación y el estrés oxidativo, parece explicar la aparición de los trastornos circulatorios y renales presentes en la ACLF (10). Además, junto con las citoquinas proinflamatorias, se ha relacionado con la aparición de encefalopatía, gracias al efecto modulador que podría tener sobre las concentraciones de amonio (2).…”

Section: Disfunción Hepáticaunclassified

Falla hepática aguda sobre crónica

Guerra

Cardona

Grajales

et al. 2017

Rev. Colomb. Gastroenterol.

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ResumenLa falla hepática aguda sobre crónica (ACLF, del inglés Acuteon Chronic Liver Failure) comprende el deterioro agudo de la función hepática en un paciente que tiene de base una enfermedad hepática crónica de novo o conocida y desencadenada por diferentes factores precipitantes que pueden ser hepáticos o extrahepáticos. Dentro de las manifestaciones clínicas se encuentran: disfunción renal, encefalopatía hepática y falla orgá-nica multisistémica, que de no ser tratadas oportunamente se traducen en mal pronóstico. Se han utilizado varias puntuaciones para valorar la función hepática y el pronóstico de los pacientes. A pesar de que la falla orgánica multisistémica es una contraindicación para el trasplante hepático, este sigue siendo la mejor opción de tratamiento para estos pacientes. Palabras claveFalla hepática aguda sobre crónica, MARS, síndrome hepatorrenal, encefalopatía hepática, falla orgánica multisistémica, parálisis inmune, puntuación SOFA. AbstractAcute-on-chronic liver failure (ACLF) includes acute deterioration of liver functions in patients with either chronic de novo liver disease or already diagnosed liver disease. ACLF can be triggered by various hepatic or extrahepatic precipitating factors. Among its clinical manifestations are renal dysfunction, hepatic encephalopathy, and multisystem organ failure. If not treated promptly translate the prognosis can be poor. Several scoring systems have been used to assess liver function and patient prognosis. Although multisystem organ failure contraindicates liver transplantation, it remains the treatment of choice for this patients. KeywordsAcute-on-chronic liver failure, MARS, hepatorenal syndrome, hepatic encephalopathy, multisystem organ failure, immune paralysis, SOFA scores. Revisión de tema INTRODUCCIÓNLa falla hepática aguda sobre crónica (ACLF) es una entidad diferente cada vez más reconocida que ha generado controversia debido a la falta de consenso en su definición y a que abarca un deterioro agudo de la función hepática en pacientes con enfermedad hepática crónica conocida o con diagnóstico de novo (1). El concepto clínico de ACLF busca diferenciar esta de los pacientes con cirrosis hepática descompensada, como se muestra en la figura 1. El paciente

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Section: Disfunción Hepáticaunclassified

Falla hepática aguda sobre crónica

Guerra

Cardona

Grajales

et al. 2017

Rev. Colomb. Gastroenterol.

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“…Release of contractile factors from vascular smooth muscle cells, sinusoidal endothelial dysfunction and contraction of activated hepatic stellate cells combine to increase intrahepatic parenchymal resistance. 9 Rises in sinusoidal resistance reduce PV flow and drive formation of extrahepatic collaterals and shunting of splanchnic blood via the portosystemic anastomoses. Reductions of PV flow of as much as 60% can be matched by rises in HA blood flow—the so-called “hepatic arterial buffer response”—but this response is impaired in liver disease, so that reductions in PV flow are met with an inadequate response from the HA and a reduction in total liver blood flow.…”

Section: Liver Imaging—unmet Needsmentioning

confidence: 99%

Vascular assessment of liver disease—towards a new frontier in MRI

Chouhan

Lythgoe

Mookerjee

et al. 2016

BJR

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Complex haemodynamic phenomena underpin the pathophysiology of chronic liver disease. Non-invasive MRI-based assessment of hepatic vascular parameters therefore has the potential to yield meaningful biomarkers for chronic liver disease. In this review, we provide an overview of vascular sequelae of chronic liver disease amenable to imaging evaluation and describe the current supportive evidence, strengths and the limitations of MRI methodologies, including dynamic contrast-enhanced, dynamic hepatocyte-specific contrast-enhanced, phase-contrast, arterial spin labelling and MR elastography in the assessment of hepatic vascular parameters. We review the broader challenges of quantitative hepatic vascular MRI, including the difficulties of motion artefact, complex post-processing, long acquisition times, validation and limitations of pharmacokinetic models, alongside the potential solutions that will shape the future of MRI and deliver this new frontier to the patient bedside.

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“…The early phase involves hepatocyte dysfunction induced by gut-derived norepinephrine, which activates α 2 -adrenoceptors, which stimulate Kupffer cells to enhance TNF-α release and depresses hepatocellular function in the absence of hepatic blood flow alterations . In contrast, the late phase results mainly from a decreased hepatic perfusion, which mechanistically has been linked with increased coagulation, inflammation and derangement of endothelial nitric oxide synthase (eNOS) signalling Mookerjee, 2011). In addition, Kupffer cells can play either a protective or destructive role in the septic response of the liver, in that they are important in the removal and detoxification of LPS, while they can also initiate an exaggerated inflammatory response which can cause further liver damage (Van Amersfoort et al, 2003).…”

Section: Pathophysiologymentioning

confidence: 99%

“…In addition, Kupffer cells can play either a protective or destructive role in the septic response of the liver, in that they are important in the removal and detoxification of LPS, while they can also initiate an exaggerated inflammatory response which can cause further liver damage (Van Amersfoort et al, 2003). Specifically, excessive inflammatory mediators can induce endothelial damage causing barrier breakdown and permeability, and are thought to be the driving force behind increased intra-hepatic resistance Mookerjee, 2011). Furthermore, the development of hyperlipidemia in response to sepsis is believed to result from pathomorphological changes in sinusoidal endothelial cells (Cheluvappa et al, 2010).…”

Section: Pathophysiologymentioning

confidence: 99%