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1.
Clin Transplant ; 33(7): e13628, 2019 07.
Artículo en Inglés | MEDLINE | ID: mdl-31173413

RESUMEN

BACKGROUND: Postoperative severe cardiopulmonary failure carries a high rate of mortality. Extracorporeal membrane oxygenation (ECMO) can be used as a salvage therapy when conventional therapies fail. METHODS: We retrospectively reviewed our experience with ECMO support in the early postoperative period after liver transplant between September 2011 and May 2016. RESULTS: Out of 537 liver transplants performed at our institution, seven patients required ECMO support with a median age of 52 and a median MELD score of 28. Veno-venous ECMO was used in four patients with severe respiratory failure while the rest required veno-arterial ECMO for circulatory failure. The median time from transplant to cannulation was 3 days with a median duration of ECMO support of 7 days. All patients except one were successfully decannulated. The median hospital length of stay was 58 days with an in-hospital mortality of 28.6%. CONCLUSION: Extracorporeal membrane oxygenation can be considered a viable rescue therapy in the setting of severe postoperative cardiopulmonary failure. Extracorporeal membrane oxygenation therapy was successful in saving patients who were otherwise unsalvageable.


Asunto(s)
Oxigenación por Membrana Extracorpórea/métodos , Rechazo de Injerto/terapia , Paro Cardíaco/terapia , Mortalidad Hospitalaria/tendencias , Trasplante de Hígado/efectos adversos , Complicaciones Posoperatorias/terapia , Insuficiencia Respiratoria/terapia , Adulto , Femenino , Estudios de Seguimiento , Rechazo de Injerto/etiología , Rechazo de Injerto/mortalidad , Supervivencia de Injerto , Paro Cardíaco/etiología , Paro Cardíaco/mortalidad , Humanos , Masculino , Persona de Mediana Edad , Complicaciones Posoperatorias/etiología , Complicaciones Posoperatorias/mortalidad , Insuficiencia Respiratoria/etiología , Insuficiencia Respiratoria/mortalidad , Estudios Retrospectivos , Tasa de Supervivencia , Resultado del Tratamiento
2.
Case Reports Hepatol ; 2019: 4730381, 2019.
Artículo en Inglés | MEDLINE | ID: mdl-31934469

RESUMEN

N-Acetylcysteine (NAC) is reported to have multiple clinical applications in addition to being the specific antidote for acetaminophen toxicity. NAC stimulates glutathione biosynthesis, promotes detoxification, and acts directly as a scavenger of free radicals. It is a powerful antioxidant and a potential treatment option for diseases characterized by the generation of free oxygen radicals. We present a case of postoperative hepatic dysfunction of multifactorial etiology in a patient with therapeutic acetaminophen levels, where hepatic function improved considerably following administration of intravenous NAC. This case suggests that NAC should be considered for treatment of acute liver dysfunction in the postoperative setting, even in the absence of elevated acetaminophen levels.

3.
Nat Commun ; 10(1): 1424, 2019 03 29.
Artículo en Inglés | MEDLINE | ID: mdl-30926808

RESUMEN

The drivers and the specification of CD4+ T cell differentiation in the tumor microenvironment and their contributions to tumor immunity or tolerance are incompletely understood. Using models of pancreatic ductal adenocarcinoma (PDA), we show that a distinct subset of tumor-infiltrating dendritic cells (DC) promotes PDA growth by directing a unique TH-program. Specifically, CD11b+CD103- DC predominate in PDA, express high IL-23 and TGF-ß, and induce FoxP3neg tumor-promoting IL-10+IL-17+IFNγ+ regulatory CD4+ T cells. The balance between this distinctive TH program and canonical FoxP3+ TREGS is unaffected by pattern recognition receptor ligation and is modulated by DC expression of retinoic acid. This TH-signature is mimicked in human PDA where it is associated with immune-tolerance and diminished patient survival. Our data suggest that CD11b+CD103- DC promote CD4+ T cell tolerance in PDA which may underscore its resistance to immunotherapy.


Asunto(s)
Células Dendríticas/inmunología , Interleucina-10/metabolismo , Interleucina-17/metabolismo , Neoplasias Pancreáticas/inmunología , Linfocitos T Reguladores/inmunología , Adenocarcinoma/genética , Adenocarcinoma/inmunología , Adenocarcinoma/patología , Animales , Carcinoma Ductal Pancreático/genética , Carcinoma Ductal Pancreático/inmunología , Carcinoma Ductal Pancreático/patología , Diferenciación Celular , Progresión de la Enfermedad , Factores de Transcripción Forkhead , Regulación Neoplásica de la Expresión Génica , Humanos , Lectinas Tipo C/metabolismo , Ratones Endogámicos C57BL , Neoplasias Pancreáticas/genética , Neoplasias Pancreáticas/patología , Fenotipo , Transducción de Señal , Células Th17/inmunología , Receptor Toll-Like 2/metabolismo , Tretinoina/metabolismo , Neoplasias Pancreáticas
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