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Severe Liver Damage (severe + liver_damage)
Selected AbstractsRole of V, 14 NKT cells in the development of impaired liver regeneration in vivoHEPATOLOGY, Issue 5 2003Hiroyasu Ito Although we have previously demonstrated that IL-12 stimulation increases the number of hepatic natural killer (NK) T (NKT) cells and enhances liver injury during the early phase of liver regeneration, the role of NKT cells has remained unknown. We therefore evaluated the influence of NKT cells activated by IL-12 or by ,-galactosylceramide (,-GalCer) on murine liver regeneration using V, 14 NKT knockout (J, 281,/,) mice. Levels of serum alanine aminotransferase (sALT) 24 hours after partial hepatectomy were enhanced in J, 281+/+ but not in J, 281,/, mice by both procedures. Hepatic NKT cells expressed considerably more interferon (IFN) , and tumor necrosis factor , (TNF-,) messenger RNA (mRNA) after stimulation with both factors in J, 281+/+ mice. Either anti-IFN-, or TNF-, antibody inhibited the enhancement of liver injury. Furthermore, recombinant TNF-, injection similarly caused injury in hepatectomized livers of both J, 281+/+ and J, 281,/, mice; indeed, adoptively transferred TNF-,+/+ NKT cells enhanced liver injury after hepatectomy in TNF-, knockout mice. TNF receptor expressions on hepatocytes increased and peaked 24 hours after partial hepatectomy. In conclusion, simultaneous TNF-, synthesis and high levels of TNF receptor expression on hepatocytes cause severe liver damage by activated NKT cells during liver regeneration. [source] Acute liver failure and living donor liver transplantationHEPATOLOGY RESEARCH, Issue 2008Nobuhisa Akamatsu Acute liver failure (ALF) is defined by the presence of hepatic encephalopathy due to severe liver damage in patients without pre-existing liver disease. Although the mortality of ALF without liver transplantation is over 80%, the survival rates of ALF patients have improved considerably with the advent of liver transplantation, up to 60,80% in the last decade. Living donor liver transplantation (LDLT), which has mainly evolved in Asian countries where organ availability from deceased donors is extremely scarce, has also improved the survival rate of ALF patients. According to recent reports, the overall survival rate of adult ALF patients who underwent LDLT is 60% to 90%. Although there is still controversy regarding the graft type, the optimal graft volume, and ethical issues of defining the indications for LDLT in ALF patients with respect to donor risk, LDLT has become an established treatment option for ALF in areas where the use of deceased donors organs is severely restricted. [source] Acute liver damage and subsequent hypophosphatemia in malnourished patients: Case reports and review of literatureINTERNATIONAL JOURNAL OF EATING DISORDERS, Issue 2 2008Takatoshi Saito MD Abstract Objective: The relationship between liver damage and subsequent hypophosphatemia in malnourished patients will be discussed. Method: The authors report two malnourished females who developed severe liver damage and subsequent hypophosphatemia. Liver damage commenced suddenly after over a week of hospitalization and deteriorated rapidly. Although the precise pathology of the liver damage could not be determined and the specific cause was not identified, steatohepatitis associated with fatty liver might be considered. Results: Hypophosphatemia following liver damage was considered to be the result of hepatocyte regeneration and replacement of phosphorus was an effective treatment. Conclusion: Hypophosphatemia in these cases suggested improvement from liver damage; however, it is commonly known that hypophosphatemia has a central role in refeeding syndrome in malnourished patients. Therefore, it was concluded that attention should be paid to hypophosphatemia after liver damage. © 2007 by Wiley Periodicals, Inc. Int J Eat Disord 2008 [source] Acute liver damage in anorexia nervosaINTERNATIONAL JOURNAL OF EATING DISORDERS, Issue 1 2004Lorenza Di Pascoli Abstract We report a case of a 26-year-old White woman with a history of anorexia nervosa who developed severe liver damage and multiorgan dysfunction. At admission to our medical unit, her body mass index (BMI) was 10.8. Biochemical evaluation showed a marked increase in serum levels of aspartate aminotransferases (AST = 9,980 IU/L), alanine aminotransferase (ALT = 3,930 IU/L), amylase (1,002 IU/L), lipase (1,437 IU/L), creatine phosphokinase (CPK; 783 IU/L), and lactate dehydrogenase (LDH = 6,830 IU/L). Glomerular filtration rate was reduced (35 ml/min), reflecting dehydration and prerenal azotemia. No other cause of acute liver damage except malnutrition was evidenced. Hydration and nutritional support were the unique medical treatment. A rapid recovery occurred in few days and all laboratory data were normal at discharge after a 37-day hospitalization. © 2004 by Wiley Periodicals, Inc. Int J Eat Disord 36: 114,117, 2004. [source] Conformational anti-cytochrome P4502E1 (CYP2E1) auto-antibodies contribute to necro-inflammatory injury in chronic hepatitis CJOURNAL OF VIRAL HEPATITIS, Issue 10 2010S. Sutti Summary., Circulating auto-antibodies against cytochrome P4502E1 (CYP2E1) have been observed in a significant fraction of patients with chronic hepatitis C (CHC). This study investigated the clinical significance of these auto-antibodies in relation to their antigen specificity. The presence of anti-CYP2E1 IgG was investigated in 137 consecutive patients with biopsy-proven CHC. Anti-CYP2E1 IgG above control threshold levels was detected in 52 (38%) subjects. By combined immunoprecipitation and western blotting, we observed that among anti-CYP2E1 IgG-positive sera, 23 (44%) were unreactive towards denaturated CYP2E1, indicating a prevalent recognition of conformational CYP2E1 antigens. Conformational anti-CYP2E1 auto-antibodies were unrelated to circulating gamma-globulins, alcohol intake or infection by specific HCV genotypes. The presence of anti-CYP2E1 auto-antibodies was associated with an 11-fold (OR 10.9 95%CI 1.4,86.6 P = 0.008) increased prevalence of necro-inflammatory grading ,4 (Ishack's criteria) and 4-fold (OR 4.0; 95%CI 1.3-11-7: P = 0.014) increased prevalence of fibrosis staging ,2, respectively. Multivariate analysis confirmed conformational anti-CYP2E1 IgG (P = 0.005) and age (P = 0.033) as independent predictors of necro-inflammatory grading ,4. The development of anti-CYP2E1 auto-antibodies targeting conformational CYP2E1 epitopes is associated with more severe liver damage in CHC. [source] Continuous infusion of prostaglandin E1 via the superior mesenteric artery can prevent hepatic injury in hepatic artery interruption through passive portal oxygenationLIVER INTERNATIONAL, Issue 2 2000Tsutomu Sato Abstract:Aims/Background: Hepatic artery interruption (HAI) causes severe ischemic liver damage, especially following hepatopancreatobiliary surgery. In order to inhibit a decrease in oxygen delivery after HAI, continuous infusion of PGE1 via the superior mesenteric artery (SMA) was administered in pigs and changes in hepatic blood flow and oxygen delivery were investigated. Furthermore, its effectiveness in the prevention of liver injury was evaluated by histology and serum enzyme levels. Methods: Animals were subjected to HAI without PGE1 infusion (control group n=6) and to continuous infusion of PGE1 (0.02 ,g/kg/min) into the SMA (PGE1 group n=6). Results and Conclusion: PGE1 infusion via the SMA not only increased the portal blood flow but also elevated the oxygen content of the portal blood. The reduction in oxygen delivery to the liver was 50% in the control group, and only 13% in the PGE1 group. Serum aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) levels 24 h after HAI in the control group were 3415±1283 IU/L and 9839±2959 respectively while in the PGE1 group they were 939±426 IU/L and 5510±1545 IU/L respectively. Histological examination showed massive necrosis in the control group at 72 h but only focal liver cell necrosis in the PGE1 group. Based on this finding and the fact that this treatment can be performed easily and safely, continuous infusion of PGE1 via the SMA may be a useful intervention to prevent severe liver damage after hepatic artery interruption. [source] | ||||||||||