Liver transplantation: An overview

Maddrey, Willis C.; Thiel, David H. Van

doi:10.1002/hep.1840080440

Cited by 141 publications

(31 citation statements)

References 93 publications

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“…[1][2][3][4] Kupffer cells (KC) have been reported as playing an important role in its pathogenesis. [5][6][7][8][9] It is suggested that blood hypercoagulation exists in patients following OLT, as thrombin and antithrombin III complex concentrations were markedly increased in the plasma.…”

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confidence: 99%

Selective bowel decontamination of recipients for prevention against liver injury following orthotopic liver transplantation: Evaluation with rat models†

et al. 1998

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Gut-derived substances can activate Kupffer cells to provoke hepatic necrosis after partial hepatectomy in rats.A similar situation may occur during orthotopic liver transplantation (OLT), as congestion in the intestinal wall, caused by portal vein occlusion, is inevitable during the operation. The contribution of such substances to liver injury following OLT was investigated in rats. Oral administration of polymyxin B sulfate for 7 days significantly altered intestinal bacterial flora in rats; Enterobacteriaceae diminished and anaerobes such as Bifidobacterium , Lactobacillus, Bacteroides, and Eubacterium increased in number, compared with the control rats. Also, this treatment significantly reduced endotoxin concentration in the portal blood 30 minutes after blood reflow following portal vein occlusion. When OLT was performed in rats using the liver preserved in cold University of Wisconsin solution for 18 hours, tissue factor activity in Kupffer cells (KC) isolated from the transplanted liver 1 hour after the operation was significantly higher than in that of normal rats. This increase was significantly reduced by pretreatment of the recipients with polymyxin B sulfate. In these recipients, serum alanine aminotransferase activity, tumor necrosis factor ␣ (TNF␣) concentration, and histological extent of liver necrosis were significantly attenuated at 24 hours after the operation compared with those of control rats. We conclude that the substances derived from bacilli sensitive to polymyxin B sulfate in the gut may be a contributing factor to liver injury following OLT in rats; we feel that this probably occurs by entering of the substances into the portal blood during the ahepatic phase of the operation to activate KC. Selective bowel decontamination of recipients with polymyxin B sulfate would be a candidate for protection against early graft failure following OLT. (HEPATOLOGY 1998;27:123-127.)

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Selective bowel decontamination of recipients for prevention against liver injury following orthotopic liver transplantation: Evaluation with rat models†

et al. 1998

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“…One-year survival rates after OLTx exceed 70% at most centers 0-3). Despite improvements in organ procurement, surgical technique, postoperative care and immuosuppression, primary failure of a hepatic allograft remains an important clinical problem (1)(2)(3), and primary graft failure often determines the success or failure of a given transplant procedure. This unpredictable complication leads to early retransplantation in 10% to 20% of the patients undergoing OLTx (1)(2)(3)(4)(5)(6)(7)(8).…”

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“…Despite improvements in organ procurement, surgical technique, postoperative care and immuosuppression, primary failure of a hepatic allograft remains an important clinical problem (1)(2)(3), and primary graft failure often determines the success or failure of a given transplant procedure. This unpredictable complication leads to early retransplantation in 10% to 20% of the patients undergoing OLTx (1)(2)(3)(4)(5)(6)(7)(8). Available data from several institutions indicate that graft rejection, technical problems and ischemic injury of the allograft account for most of these early graft failures (1,3,(5)(6)(7).…”

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Cause and timing of first allograft failure in orthotopic liver transplantation: A study of 177 consecutive patients

et al. 1991

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The cause and timing of first liver allograft failure was evaluated in 177 patients who underwent a second liver transplant between January 1984 and December 1988. The population studied consisted of 94 men and 83 women with a mean age 41.3 ± 1.0 yr (mean ± S.E.M.). Mean first-graft survival was 130.6 ± 22.9 days (range = 0 to 2.073 days). Sixty·eight percent of the grafts failed in the first postoperative month. 26% failed between the second and twelfth month and only 6% failed beyond the twelfth month from the date of the initial transplant. Six principal causes of graft failure were identified. Early allograft losses occurred as a result of four major problems: primary graft nonfunction (30.0% of all grafts; mean graft survival = 3.4 ± 0.3 days); ischemic injury of the graft without overt vascular injury (9.6%; mean graft survival = 17.5 ± 1.9 days); acute rejection (10.7%; mean graft survival = 30.4 ± 6.4 days); and overt vascular complications (26.6%; mean graft survival = 59.6 ± 24.1 days). Late graft failures were the result of either chronic rejection (11.3%: mean graft survival = 496.3 ± 138.0 days) or recurrence of the primary liver disease (6.8%: mean graft survival = 550.5 ± 172.1 days). Graft failure occurred as a result of a variety of miscellaneous causes in 5% of the cases (mean graft survival in this group = 300.0 ± 110.6 days). Overall 6-mo patient survival after a second liver transplant was 46.3%. Patients who had a retransplant because of chronic rejection and ischemic injury had the greatest (65%) and least (23%) 6-mo survival rates respectively after second grafting (p < 0.05). Those who survived the second transplant procedure for 6 mo or more tended to be younger (p < 0.01) and had a reduced first transplant requirement for red blood cells (p < 0.05), platelets (p < 0.01) and fresh frozen plasma (p < 0.01) than did those who died during the 6 mo after their second transplant procedure.

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“…16 Liver transplantation remains the final therapeutic option in cases with end-stage disease. 17 Hepatic stellate cells (HSC), also referred to as Ito cells, fatstoring cells and lipocytes, were observed for the first time in 1876 by von Kupffer, being scarcely studied for almost 100 years. In 1982, Knook related the metabolic functions of these cells isolated in culture.…”

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confidence: 99%

Liver cirrhosis and hepatic stellate cells

Brandão¹,

Ramalho²,

Ramalho³

et al. 2006

Acta Cir. Bras.

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The cirrhosis represents the final stage of several chronic hepatic diseases and it is characterized by the presence of fibrosis and morphologic conversion from the normal hepatic architecture into structurally abnormal nodules. In the evolution of the disease there is loss of the normal vascular relationship and portal hypertension. There are also regenerative hepatocelular alterations that become more prominent with the progression of the disease. The liver transplantation continues to be the only therapeutic option in cases of disease in terminal phase. The hepatic stellate cells (HSC) are perisinusoidal cells that store vitamin A and produce growth factors, citocins, prostaglandins and other bioactive substances. They can suffer an activation process that convert them to cells with a phenotype similar to myofibroblasts. When activated, they present increased capacity of proliferation, mobility, contractility and synthesis of collagen and other components of extracelular matrix. They possess cytoplasmic processes adhered to sinusoids and can affect the sinusoidal blood flow. HSC are important in pathogenesis of fibrosis and portal hypertension. Key words: Liver. Stellate Cells. Hepatic Fibrosis. Hepatic Cirrhosis. Perisinusoidal Cells. Portal Hypertension. RESUMOA cirrose representa o estágio final de diversas doenças hepáticas crônicas e é caracterizada pela presença de fibrose e conversão da arquitetura hepática normal em nódulos estruturalmente anormais. Na evolução da doença ocorre perda da relação vascular normal e hipertensão portal. Há também alterações regenerativas hepatocelulares que se tornam mais proeminentes com a progressão da doença. O transplante hepático permanece como a única opção terapêutica nos casos de doença em fase terminal. As células estreladas hepáticas (CEH) são células perisinusoidais que armazenam vitamina A e produzem fatores de crescimento, citocinas, prostaglandinas e outras substâncias bioativas. Podem sofrer um processo de ativação para um fenótipo semelhante a miofibroblastos. Quando ativadas apresentam maior capacidade de proliferação, motilidade, contractilidade, síntese de colágeno e componentes da matriz extracelular. Possuem processos citoplasmáticos aderidos aos sinusóides e podem afetar o fluxo sangüíneo sinusoidal. As CEH são importantes na patogênese da fibrose e hipertensão portal. Descritores: Fígado. Células Estreladas. Fibrose Hepática. Cirrose Hepática. Células Peri-sinusoidais. Hipertensão Portal.

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Liver transplantation: An overview

Cited by 141 publications

References 93 publications

Selective bowel decontamination of recipients for prevention against liver injury following orthotopic liver transplantation: Evaluation with rat models†

Selective bowel decontamination of recipients for prevention against liver injury following orthotopic liver transplantation: Evaluation with rat models†

Cause and timing of first allograft failure in orthotopic liver transplantation: A study of 177 consecutive patients

Liver cirrhosis and hepatic stellate cells

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