Fulminant hepatic failure can only be treated successfully by liver transplantation, which, however, is not always available. To "bridge" the patient with fulminant hepatic failure until a liver graft is available, various forms of liver support devices had been designed but they were not uniformly successful. To prove the efficacy of a liver support device for fulminant hepatic failure, testing in an animal model is necessary. We attempted to induce a pig model with fulminant hepatic failure by administering galactosamine into pigs and reported the observation. Three pigs were given a dose of 0.5 gm/kg of galactosamine and five pigs were given 1 gm/kg of galactosamine. One pig receiving 0.5 gm/kg galactosamine survived after manifestation of liver failure, while all the other pigs died. The two pigs receiving 0.5 gm/kg galactosamine survived longer than the five pigs receiving 1 gm/kg galactosamine. Before death, a significant elevation of parenchymal liver enzymes, lactate dehydrogenase, bilirubin, bile acid, ammonia, tumour necrosis factor-alpha, activated clotting time, a decrease of platelet concentration, ketone bodies ratio, blood glucose and plasma albumin, and serious impairment of indocyanine green clearance were indicated. At post-mortem, severe liver necrosis was observed. The model may be suitable for testing the efficacy of liver support device for fulminant hepatic failure, preferably 24-48 hours after administration of galactosamine.
Download full-text PDF |
Source |
---|
Best Pract Res Clin Gastroenterol
December 2024
Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. Electronic address:
Acute liver failure (ALF) is a rare but rapidly progressing syndrome, marked by severe liver dysfunction and altered mental status. While definitions of ALF vary across different guidelines, with timelines ranging from 4 to 26 weeks between jaundice onset and encephalopathy, the key defining features remain encephalopathy and coagulopathy. Elevated coagulation markers, particularly prothrombin time and international normalized ratio, have traditionally been associated with bleeding risks.
View Article and Find Full Text PDFExp Clin Transplant
November 2024
From the Department of Hepatobiliary and Pancreatic Surgery, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, PR China.
Objectives: Fulminant hepatic failure is a critical condition with a high mortality rate. Currently, liver transplantation is considered one of the most effective treatment methods, but the shortage of organ resources has presented a major obstacle. The use of marginal donor livers, including those from syphilis-positive donors, offers new opportunities.
View Article and Find Full Text PDFJ Surg Case Rep
November 2024
Department of General and Endoscopic Surgery, Dr. Manuel Gea González General Hospital, Calzada de Tlalpan 4800, Belisario Domínguez Sección XVI, Mexico City 14080, Mexico.
Fulminant amoebic colitis is a rare complication of amoebiasis that carries a high mortality rate. Its diagnosis is challenging and requires a high index of suspicion, and its early recognition is a priority to provide timely medical and surgical treatment. We present the case of a male patient who came to the emergency department with unspecific clinical presentation of abdominal pain, systemic inflammatory response and imaging study showing intestinal perforation of the right colon.
View Article and Find Full Text PDFCardiooncology
November 2024
Breast Cancer Center, Maria Sklodowska-Curie National Research Institute of Oncology, Gliwice, 44-102, Poland.
Background: Budd-Chiari syndrome is a rare and severe vascular liver disease. We presented patient with fulminant liver failure secondary to leiomyosarcoma of the IVC and thrombosis.
Case Presentation: A 44-year-old female presented with fulminant liver failure secondary to inferior vena cava (IVC) thrombosis.
Livers
September 2024
Center for Cell Death, Injury & Regeneration, Medical University of South Carolina, Charleston, SC 29425, USA.
Overdose of acetaminophen (APAP) produces fulminant hepatic necrosis. The underlying mechanism of APAP hepatotoxicity involves mitochondrial dysfunction, including mitochondrial oxidant stress and the onset of mitochondrial permeability transition (MPT). Reactive oxygen species (ROS) play an important role in APAP-induced hepatotoxicity, and iron is a critical catalyst for ROS formation.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!