RESUMO
Renal dysfunction is a common finding in cirrhotic patients and has a great physiologic, and therefore, prognostic relevance. The combination of liver disease and renal dysfunction can occur as a result of systemic conditions that affect both the liver and the kidney, although primary disorders of the liver complicated by renal dysfunction are much more common. As most of the renal dysfunction scenarios in cirrhotic patients correspond to either prerenal azotemia or hepatorenal syndrome (HRS), physicians tend to conceive renal dysfunction in cirrhotic patients as mainly HRS. However, there are many systemic conditions that may cause both a "baseline" chronic kidney damage and a superimposed kidney dysfunction when this systemic condition worsens. The main aim of this article is to review some of the most important non prerenal non-HRS considerations regarding acute on chronic kidney dysfunction in cirrhotic patients, including renal manifestation of related to non-alcoholic steatohepatitis (NASH) viral hepatitis, the effect of cardiorenal syndrome in cirrhotics and corticosteroid-deficiency associated renal dysfunction.
Assuntos
Injúria Renal Aguda/metabolismo , Síndrome Cardiorrenal/metabolismo , Hepatite Viral Humana/metabolismo , Cirrose Hepática/metabolismo , Hepatopatia Gordurosa não Alcoólica/metabolismo , Insuficiência Renal Crônica/metabolismo , Injúria Renal Aguda/etiologia , Injúria Renal Aguda/fisiopatologia , Corticosteroides/deficiência , Síndrome Cardiorrenal/complicações , Síndrome Cardiorrenal/fisiopatologia , Hepatite Viral Humana/complicações , Hepatite Viral Humana/fisiopatologia , Humanos , Cirrose Hepática/complicações , Cirrose Hepática/fisiopatologia , Hepatopatia Gordurosa não Alcoólica/complicações , Hepatopatia Gordurosa não Alcoólica/fisiopatologia , Insuficiência Renal Crônica/etiologia , Insuficiência Renal Crônica/fisiopatologiaRESUMO
Prohibitin (PHB) 1 is involved in multiple regulatory pathways in liver disease to protect hepatocytes, and its function is associated with subcellular localization. PHB1 located in the nucleus, cytoplasm and the mitochondrial inner membrane has anti-oxidative stress and anti-inflammatory effects in hepatitis and cirrhosis, which can protect liver cells from damage caused by inflammatory factors and reactive oxygen species (ROS) stimulation. The low expression of PHB1 located in the nucleus of liver cancer cells inhibits the proliferation and metastasis of liver cancer; thus, PHB1 exhibits the function of a tumor suppressor gene. Understanding the mechanisms of PHB1 in liver diseases may be useful for further research on the disease and may provide new ideas for the development of targeted therapeutic drugs in the future. Therefore, this review puts forward an overview of the role of PHB1 and its protective mechanism in liver diseases.
Assuntos
Carcinoma Hepatocelular/metabolismo , Hepatite Viral Humana/metabolismo , Cirrose Hepática/metabolismo , Neoplasias Hepáticas/metabolismo , Proteínas Repressoras/metabolismo , Núcleo Celular/metabolismo , Proliferação de Células , Citoplasma/metabolismo , Hepatócitos/metabolismo , Humanos , Inflamação/metabolismo , Hepatopatias/metabolismo , Membranas Mitocondriais/metabolismo , Metástase Neoplásica , Estresse Oxidativo , Proibitinas , Espécies Reativas de Oxigênio/metabolismo , Proteínas Repressoras/fisiologiaRESUMO
Intrahepatic hypoxia may occur during the inflammatory and fibrotic processes that characterize several chronic liver diseases of viral and autoimmune origin. As a consequence, new vascular structures are formed to provide oxygen and nutrients. Angiogenesis involves a tightly regulated network of cellular and molecular mechanisms that result in the formation of functional vessels. Of particular importance are growth factors and molecules involved in matrix remodeling and cell migration, as weel as vessel maturation-related factors. In recent years a number of studies have investigated the expression and function of many pro- and antiangiogenic molecules in chronic liver diseases and liver regeneration. This review examines the potential pathogenic role of angiogenesis in the context of viral hepatitis, autoinmmune hepatitis, primary biliary cirrhosis and hepatocellular carcinoma.
Assuntos
Hepatite Autoimune/patologia , Hepatite Viral Humana/patologia , Cirrose Hepática Biliar/patologia , Neoplasias Hepáticas/irrigação sanguínea , Neovascularização Patológica , Proteínas Angiogênicas/sangue , Proteínas Angiogênicas/metabolismo , Vasos Sanguíneos/metabolismo , Vasos Sanguíneos/patologia , Carcinoma Hepatocelular/irrigação sanguínea , Carcinoma Hepatocelular/metabolismo , Carcinoma Hepatocelular/patologia , Colangite Esclerosante/metabolismo , Colangite Esclerosante/patologia , Doença Crônica , Hepatite Autoimune/metabolismo , Hepatite Viral Humana/metabolismo , Humanos , Cirrose Hepática Biliar/metabolismo , Neoplasias Hepáticas/metabolismo , Neoplasias Hepáticas/patologiaRESUMO
The mechanism by which the virus associated with dengue fever can cause a fatal hepatitis is not well understood. The purpose of this study was to examine 9 cases of fatal dengue hemorrhagic fever-associated hepatitis, and to correlate the histologic findings with viral detection and cytokine response. The histologic changes were nonspecific and included massive hepatic necrosis and a pauci-cellular acute hepatitis. Viral cDNA detection by reverse transcriptase in situ polymerase chain reaction demonstrated that the fatal hepatitis was due to infection on average of >90% of hepatocytes and many Kupffer cells. Similar results were obtained using immunohistochemistry for viral protein using an automated highly sensitive system. Immunohistochemical analysis for tumor necrosis factor alpha, and interleukin-2, showed rare positive Kupffer cells. In comparison, fatal cases of hepatitis C associated liver failure demonstrated far fewer infected hepatocytes and a concomitant strong up-regulation of many cytokines, notably tumor necrosis factor alpha and interleukin-2. It is concluded that fatal dengue hemorrhagic fever is associated with acute, severe liver damage due primarily to massive direct infection of hepatocytes and Kupffer cells with minimal cytokine response. The infection can be readily detected in a few hours using an automated system that has a sensitivity equivalent to reverse transcriptase in situ polymerase chain reaction.
Assuntos
Vírus da Dengue/isolamento & purificação , Hepatite Viral Humana/patologia , Imuno-Histoquímica , Fígado/patologia , Dengue Grave/patologia , Vírus da Dengue/genética , Hepatite Viral Humana/etiologia , Hepatite Viral Humana/metabolismo , Hepatite Viral Humana/virologia , Humanos , Interleucina-2/análise , Fígado/química , Fígado/virologia , Necrose , RNA Viral/análise , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Dengue Grave/complicações , Dengue Grave/metabolismo , Dengue Grave/virologia , Fator de Necrose Tumoral alfa/análise , Proteínas Virais/análiseRESUMO
Os autores analisam as medidas terapeuticas modernamente intriduzidas no tratamento das hepatites virais fulminantes. Sao discutidos procedimentos de suporte de vida, novas drogas(N-acetyl-L-cisteina, interferon, prostaglandinas) procedimentos hemodialiticos e transplante hepatico. Destacam a importancia da reducao do edema cerebral, controles metabolicos e antiinfecciosos.
Assuntos
Humanos , Hepatite Viral Humana/metabolismo , Hepatite Viral Humana/terapiaRESUMO
Se investigan diferentes variables lipídicas en 67 niños, menores de 15 años, los cuales se dividen en 2 grupos: el grupo A, integrado por pacientes con la tansaminasa glutámico pivúrica (TGP) y el timol incrementado; y grupo B, donde se presenta la TGP normal y el timol con cifras elevadas. Las variables en estudio fueron, el colesterol total, HDL colesterol, colesterol de beta y pre-beta, beta y pre-beta lipoproteínas, triglíceridos y electroforesis de lipoproteínas. Se demuestra en el análisis comparativo del grupo A, que algunas de las variables en estudio se incrementan de forma significativas, excepto las variables HDL colesterol, las VLDL y HDL. Este grupo también demostró una ausencia de pré-beta (VLDL) en el 36% de los casos y un predominio del tipo II b, así como el 84% de casos con hiperlipoproteinemia (HLP). En el grupo B, el colesterol total, las LDL y VLDL, diminuyen sus valores, al igual que la HDL colesterol (aunque ésta disminuye de forma significativa), el resto de las variables se mantiene aumentado signfificativamente con respecto al control, pero en concentraciones inferiores al grupo A. También se produjo el 40% de niños con HLP, aunque inferior al grupo A (84%) y 8 pacientes con tipo IV. Se estudian además 5 pacientes diagnosticados con hepatitis viral aguda, cuyas variantes lipídicas incrementan significativamente sus valores de forma considerable