C Cirrhosis (c + cirrhosis)

Distribution by Scientific Domains
Medical Sciences100%

Kinds of C Cirrhosis

  • hepatitis c cirrhosis
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    Selected Abstracts

    Evaluation of hernia repair operation in Child,Turcotte,Pugh class C cirrhosis and refractory ascites

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 3 2007
    Joo Kyung Park
    Abstract Background and Aim:, Abdominal wall hernia is a common feature of decompensated liver cirrhosis and frequently causes life-threatening complications or severe pain. However, there have been no data reported on postoperative mortality, hepatic functional deterioration and recurrence rate according to Child,Turcotte,Pugh (CTP) class and to the presence of refractory ascites. Methods:, The study population comprised 53 liver cirrhosis patients who underwent hernia repair operation. Comparisons were made of 30-day mortality among the different CTP classes, and between those with or without refractory ascites. Liver function was also analyzed just before the operation, in the immediate postoperative period, and in the remote postoperative period. Results:, Seventeen patients were in CTP class A, 27 patients in class B, and 9 patients in class C. The median follow-up duration was 24 months. There was single 30-day postoperative mortality in class C, and no CTP class deterioration after 30 days of operation. There was no mortality or recurrences in 17 patients with medically refractory ascites. The difference in 30-day mortality according to CTP class and the presence of refractory ascites did not show statistical significance (P = 0.17 and 0.97, respectively). Conclusion:, Hernia operation could be done safely in CTP class A and B with low rate of recurrences, and there was no definitive increase in the operative risk in class C. In addition, refractory ascites did not increase operative risk and recurrence rate. Therefore, surgical repair might be recommended even in patients with refractory ascites and poor hepatic function to prevent life-threatening complications or severe pain. [source]

    Models of influence in chronic liver disease

    LIVER INTERNATIONAL, Issue 5 2010
    Amnon Sonnenberg
    Abstract Background & Aims: Liver disease is often characterized by an intricate network of multiple, simultaneously interacting factors with organ-specific, as well as systemic effects. The aim of the present study is to introduce a new mathematical model on how to weigh a variety of factors contributing to chronic liver disease by the relevance of their influence on the overall disease processes. Methods: Liver disease is modelled as the interaction of multiple internal and external factors. Each factor can potentially interact with any of the other factors in the model. The strength of interactions is expressed as per cent. The sum of all interactions contributing to each individual factor adds up to 100%. This model corresponds mathematically to a transposed Markov matrix. The analysis uses the two examples of hepatitis C virus (HCV) and autoimmune hepatitis (AIH). Results: Impaired liver function is the most influential factor and increases in relevance as the degree of hepatic fibrosis increases. The relative importance of treating the primary disease process (HCV or AIH) diminishes as fibrosis develops. Similarly, psychosocial factors become less important with disease progression. Liver transplant is most important for Child's C cirrhosis. It is relatively influential for the early phase of AIH but not HCV, reflecting the fact that some cases of non-cirrhotic AIH can progress rapidly to acute liver failure. Conclusion: In a disease process characterized by a large array of multiple interacting factors, the decision tool of a transposed Markov chain helps to sort the contributing factors by the magnitude of their influence. [source]

    Up-regulation of proproliferative genes and the ligand/receptor pair placental growth factor and vascular endothelial growth factor receptor 1 in hepatitis C cirrhosis

    LIVER INTERNATIONAL, Issue 7 2007
    Xiao X. Huang
    Abstract Background/Aims: Cirrhosis can lead to hepatocellular carcinoma (HCC). Non-diseased liver and hepatitis C virus (HCV)-associated cirrhosis with or without HCC were compared. Method: Proliferation pathway genes, immune response genes and oncogenes were analysed by a quantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and immunostaining. Results: Real-time RT-PCR showed up-regulation of genes in HCV cirrhosis including the proliferation-associated genes bone morphogenetic protein 3 (BMP3), placental growth factor 3 (PGF3), vascular endothelial growth factor receptor 1 (VEGFR1) and soluble VEGFR1, the oncogene FYN, and the immune response-associated genes toll-like receptor 9 (TLR9) and natural killer cell transcript 4 (NK4). Expressions of TLR2 and the oncogenes B-cell CLL/lymphoma 9 (BCL9) and PIM2 were decreased in HCV cirrhosis. In addition, PIM2 and TLR2 were increased in HCV cirrhosis with HCC compared with HCV cirrhosis. The ligand/receptor pair PGF and VEGFR1 was intensely expressed by the portal tract vascular endothelium. VEGFR1 was expressed in reactive biliary epithelial structures in fibrotic septum and in some stellate cells and macrophages. Conclusion: PGF and VEGFR1 may have an important role in the pathogenesis of the neovascular response in cirrhosis. [source]

    Improvement in hepatopulmonary syndrome after methadone withdrawal: A case report with implications for disease mechanism

    LIVER TRANSPLANTATION, Issue 7 2010
    Edmund M. T. Lau
    Spontaneous resolution of hepatopulmonary syndrome (HPS) without liver transplantation or improvement in the underlying liver disease has rarely been reported in the literature. Increased endogenous production of nitric oxide has been implicated in the pathogenesis of HPS. We report the case of a 50-year-old man with hepatitis C cirrhosis who demonstrated dramatic improvement in HPS after withdrawal from chronic methadone therapy. We speculate on the potential role of opiate receptors in the pulmonary vasculature and their effect on nitric oxide signaling as a potential mechanism accounting for the patient's clinical improvement. Liver Transpl 16:870,873, 2010. © 2010 AASLD. [source]

    The natural history of hepatitis C cirrhosis after liver transplantation

    LIVER TRANSPLANTATION, Issue 9 2009
    Roberto J. Firpi
    Hepatitis C after liver transplantation leads to graft cirrhosis in up to 30% of patients within 5 years, but limited data exist regarding the clinical course of cirrhosis after transplantation. The aims of this study were to report the natural history of hepatitis C cirrhosis after liver transplantation and to identify risk factors for decompensation and survival. Hepatitis C patients underwent protocol liver biopsies yearly after liver transplantation. After cirrhosis was identified by biopsy, the outcomes of interest were the development of decompensation, death, or retransplantation for hepatitis C. Kaplan-Meier and Cox regression analysis was used to determine survival and risk factors for decompensation and mortality. Out of 502 liver transplants performed for hepatitis C, 88 patients (18%) had cirrhosis within 3.7 years. Seventy-one patients were compensated at diagnosis. The cumulative probability of decompensation 1 year after cirrhosis was 30%. A Model for End-Stage Liver disease score , 16 was predictive of decompensation and poor survival, whereas successful interferon treatment was found to reduce this risk (relative risk = 0.05). Once decompensation occurred, 1-year survival was 46%. In conclusion, the results confirm an accelerated natural history of hepatitis C cirrhosis after liver transplantation and demonstrate poor survival after decompensation. The Model for End-Stage Liver Disease can stratify risk for decompensation and survival, whereas successful antiviral therapy may be protective. Liver Transpl 15:1063,1071, 2009. © 2009 AASLD. [source]

    Amelioration of hypertrophic cardiomyopathy using nonsurgical septal ablation in a cirrhotic patient prior to liver transplantation

    LIVER TRANSPLANTATION, Issue 2 2005
    Anil S. Paramesh
    A 53-year-old male with hepatitis C cirrhosis, who had been refused liver transplantation because of hypertrophic cardiomyopathy (HC), underwent nonsurgical septal ablation using alcohol with resolution of his ventricular outflow obstruction. This patient was able to subsequently undergo a successful deceased donor liver transplantation. This is the first reported case of alcohol induced septal ablation being performed in a cirrhotic patient with HC. Such nonsurgical procedures may be attractive in cirrhotic patients who are refused access to liver transplantation because of high surgical risk. (LiverTranspl 2005;11:236,238.) [source]

    Clinical improvement in patients with decompensated liver disease caused by hepatitis B after treatment with lamivudine

    LIVER TRANSPLANTATION, Issue 6 2000
    Craig A. Sponseller
    Lamivudine is effective in inhibiting hepatitis B virus (HBV) replication, and its clinical use in patients with chronic hepatitis B is associated with improvements in serum aminotransferase levels and liver histopathologic characteristics. Few data are available on its use in patients with advanced liver disease. We report on the outcomes of 5 patients with hepatic decompensation caused by chronic hepatitis B treated long term with lamivudine. All patients were adult white men seropositive for hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) before therapy. All 5 patients had biopsy-proven cirrhosis with clinical and biochemical evidence of hepatic decompensation. Two patients had Child's class C cirrhosis; 2 patients, class B; and 1 patient, class A (although this patient had persistent portasystemic encephalopathy and developed variceal bleeding). HBV DNA became undetectable in all patients and remained so throughout the study. Both patients with Child's class C and 1 patient with class B cirrhosis had significant clinical improvement. Child-Pugh scores improved from 12 to 7 and 11 to 7 in the 2 patients with Child's class C cirrhosis, and the patient with class B cirrhosis had complete resolution of troublesome encephalopathy. Serum aminotransferase, albumin, and total bilirubin levels improved significantly in 3 of 5 patients. One patient with Child's class B cirrhosis underwent orthotopic liver transplantation at week 13 after dramatic increases in liver tests and clinical worsening. The patient subsequently cleared HBeAg and HBsAg from serum posttransplantation. In conclusion, prolonged therapy with lamivudine resulted in improved serum biochemical values and loss of HBV DNA in patients with decompensated cirrhosis. Clinical improvements, reflected in Child-Pugh classification and functional status, may also occur, particularly among those with Child's class C disease initially. [source]