Browsing by Subject "Liver Failure, Acute"
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Item Acetaminophen and the liver: poison or panacea?(2016-05-20) Lee, William M.Item Acetaminophen Dose Does Not Predict Outcome in Acetaminophen-Induced Acute Liver Failure(2010-04-09) Gregory, Blake Elizabeth; Lee, William M.Acetaminophen is a dose-dependent toxin. Prognosis in severe acute liver injury is related presumably in part to the dose ingested. We sought to assess the value of acetaminophen dosing information in patients with acute liver failure due to acetaminophen toxicity to determine the role of dose as a prognostic indicator. Methods: Prospective data from 113 acute liver failure patients having single time point ingestions of acetaminophen were analyzed. Multivariate and chi-square tests were used to determine the relationship of dose to clinical outcome. We also used the Mann-Whitney U test to compare prognosis and survival in ALF with acetaminophen dose ingested. Results: Multivariate and chi-square analysis failed to show any relationship between acetaminophen dose and spontaneous survival. A separate analysis showed no correlation between acetaminophen dose and clinical prognostic indicators. Conclusions: Dose of acetaminophen ingested did not seem to play a role in prognosis. The most important prognostic factor was coma grade on admission to study. Acetaminophen dosing information is not always obtainable. When it is, it adds little to the clinical assessment. Severity of encephalopathy is a more reliable indicator of prognosis in these critically ill patients.Item Acute liver failure 2006(2006-10-13) Lee, William M.Item Acute liver failure: devastating disease or orphan syndrome?(1998-06-11) Lee, William M.Item Cerebral edema in patients with acute liver and renal failure(2017-07-21) Hamdi, TamimItem Histological and Immunohistochemical Findings in Two Subtypes of Hepatitis B Related Acute Liver Failure(2017-01-17) Choo, Vincent; Peng, Lan; Dao, Doan Y.; Hameed, Bilal; Lee, William M.; Acute Liver Failure Study Group (ALFSG)BACKGROUND: Acute liver failure (ALF) occurs when rapid-onset, severe liver cell damage results in coagulopathy and encephalopathy. Multiple etiologies yield a remarkably similar syndrome including acetaminophen overdose, drug-induced liver injury, and Hepatitis B Virus (HBV) infection. ALF in the setting of HBV occurs in 1% of primary acute HBV infections (AHBV-ALF), but can also evolve during chronic HBV infection (CHBV-ALF), particularly in reactivation, when patients receive immunosuppressive or cancer chemotherapy. OBJECTIVE: To determine whether differences between the two varieties of HBV-ALF, primary acute HBV infection and reactivation of HBV, are reflected in differences in HBV immunohistochemical bio-markers in liver: HBV core antigen (HBcAg) & HBV surface antigen (HBsAg). METHODS: A total of 21 patients from the Acute Liver Failure Study Group (ALFSG) were identified as having sufficient liver tissue for the staining panel required. Samples were immunostained using dye-labeled antibodies for HBV core antigen (HBcAg) and HBV surface antigen (HBsAg). We performed routine hematoxylin & eosin (H&E) staining for overall morphology (degree of necrosis, presence of plasma cells) and reviewed clinical history to stratify each case as either AHBV-ALF (primary infection, N=11) or CHBV-ALF (reactivation, N=10). For H&E, we assessed number of plasma cells, percent tissue necrosis, and degree of collapse. Eleven biopsies had <25% viable hepatocytes, making further analysis of staining patterns unsuccessful. The remaining acute HBV cases had very little, if any, HBsAg staining and variable levels of nuclear HBcAg staining. In contrast, one CHBV-ALF case had intense staining for both HBsAg and HBcAg, probably related to the presence of immunosuppression. SUMMARY/CONCLUSION: Immunohistochemical staining of liver biopsies/explants revealed scant viable hepatocytes in more than half, limiting assessment of location of viral products within cells. In general, when assessment was possible, AHBV-ALF demonstrated little to no HBsAg and variable amounts of HBcAg staining. Immunosuppression leads to much higher levels of HBV proteins within hepatocytes, and perhaps suggests that the virus is directly cytotoxic in this setting. By the time of liver transplantation, virtually all HBsAg had disappeared from hepatocytes in AHBV-ALF, but high quantities of HBsAg and HBcAg were found in immunosuppressed patients with reactivation. These two forms of acute liver failure due to hepatitis B have remarkably different pathogenetic phenotypes.Item [Southwestern News](2002-12-17) Morrison, SusanItem [UT Southwestern Medical Center News](2009-10-08) Ladson, LaKisha