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1
Rajaram, Priyanka, and Ram Subramanian. "Acute Liver Failure." Seminars in Respiratory and Critical Care Medicine 39, no. 05 (October 2018): 513–22. http://dx.doi.org/10.1055/s-0038-1673372.
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AbstractAcute liver failure (ALF) is a condition that can rapidly progress to multiorgan failure. This article focuses on the diagnosis and management of ALF. We provide a detailed review of the common etiologies of ALF, including acetaminophen overdose, viral hepatitis, drug-induced liver injury, Wilson's disease, and autoimmune hepatitis. The article then addresses how to recognize ALF and reviews the role of common laboratory and imaging tests in establishing this diagnosis. The remainder of the article details the management of hepatic and extrahepatic organ dysfunctions in ALF. The article concludes with a discussion regarding the prognostication of patients with ALF and the criteria for considering liver transplantation.
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Kanda, Tatsuo, Reina Sasaki-Tanaka, Tomotaka Ishii, Hayato Abe, Masahiro Ogawa, and Hirayuki Enomoto. "Acute Liver Failure and Acute-on-Chronic Liver Failure in COVID-19 Era." Journal of Clinical Medicine 11, no. 14 (July 21, 2022): 4249. http://dx.doi.org/10.3390/jcm11144249.
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Punzalan, Carmi S., and Curtis T. Barry. "Acute Liver Failure." Journal of Intensive Care Medicine 31, no. 10 (July 9, 2016): 642–53. http://dx.doi.org/10.1177/0885066615609271.
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Acute liver failure is life threatening liver injury with coagulopathy and hepatic encephalopathy within 26 weeks and generally, in the absence of preexisting liver disease. Fulminant liver failure occurs when hepatic encephalopathy occurs within 8 weeks of jaundice. The majority of patients with ALF are women with the median age of 38 years. In the United States, drug induced liver injury including acetaminophen causes the majority of ALF cases. The etiology of ALF should be determined, if possible, because many causes have a specific treatment. The mainstay for ALF is supportive care and liver transplantation, if necessary. There are multiple prognostic criteria available. Prognosis can be poor and patients should be referred to a liver transplantation center as soon as possible.
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Bunchorntavakul, Chalermrat. "Acute liver failure." Thai Journal of Hepatology 1, no. 1 (April 24, 2018): 1–13. http://dx.doi.org/10.30856/th.jhep2018vol1iss1_63.
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Acute liver failure (ALF) is a life threatening condition defined by the evidence of hepatic injury, jaundice, coagulopathy, and encephalopathy in a patient without preexisting cirrhosis and with an illness duration of <26 weeks. The etiologies of ALF are heterogeneous: viral hepatitis being the most common in the East, whereas drug-induced, particularly acetaminophen, being the most common in the West. Over the past decades, the outcomes of ALF have been improving with early recognition and prompt initiation of etiology-specific therapy (especially N-acetylcysteine), complex intensive care protocols and urgent liver transplantation (LT). The most commonly used prognostic scoring systems include King’s College Criteria (more specific) and MELD (more sensitive). Cerebral edema and intracranial hypertension are reasons for high morbidity and mortality in the early phase; hypertonic saline is suggested for patients with high-risk for developing intracranial hypertension (ICH) and when ICH develops, mannitol is recommended as first-line therapy. Bacterial and fungal infections are very common necessitating strict preventive measures, careful surveillance and prompt aggressive antimicrobial therapy. Acute kidney injury develops in 50-70% of patients; mostly reversible in survivors and temporary dialysis is required in about 30% of cases. Overall 1-year survival after LT has been reported to be lower in patients with ALF as compared to those with cirrhosis; however following the first year this trend has been to be reversed and ALF patients have a better long-term survival. Extracorporeal liver support system, such as albumin dialysis and plasmapheresis, may serve as a bridge to LT and may increase LT-free survival in select cases.
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Bunchorntavaku, Chalermrat l. "Acute liver failure." Thai Journal of Hepatology 1, no. 1 (April 27, 2018): 1–13. http://dx.doi.org/10.30856/th.jhep2018vol1iss1_001.
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Acute liver failure (ALF) is a life threatening condition defined by the evidence of hepatic injury, jaundice, coagulopathy, and encephalopathy in a patient without preexisting cirrhosis and with an illness duration of <26 weeks. The etiologies of ALF are heterogeneous: viral hepatitis being the most common in the East, whereas drug-induced, particularly acetaminophen, being the most common in the West. Over the past decades, the outcomes of ALF have been improving with early recognition and prompt initiation of etiology-specific therapy (especially N-acetylcysteine), complex intensive care protocols and urgent liver transplantation (LT). The most commonly used prognostic scoring systems include King’s College Criteria (more specific) and MELD (more sensitive). Cerebral edema and intracranial hypertension are reasons for high morbidity and mortality in the early phase; hypertonic saline is suggested for patients with high-risk for developing intracranial hypertension (ICH) and when ICH develops, mannitol is recommended as first-line therapy. Bacterial and fungal infections are very common necessitating strict preventive measures, careful surveillance and prompt aggressive antimicrobial therapy. Acute kidney injury develops in 50-70% of patients; mostly reversible in survivors and temporary dialysis is required in about 30% of cases. Overall 1-year survival after LT has been reported to be lower in patients with ALF as compared to those with cirrhosis; however following the first year this trend has been to be reversed and ALF patients have a better long-term survival. Extracorporeal liver support system, such as albumin dialysis and plasmapheresis, may serve as a bridge to LT and may increase LT-free survival in select cases.
Figure 1 CT brain ของผู้ป่วยเพศหญิง อายุ 22 ปี มีภาวะ ตับวายเฉียบพลันจากยา แรกรับมี encephalopathy grade III CT brain พบ mild cerebral edema with loss of sulci and gyri, blurring of grey - white junctions and mild narrowing of ventricles (A) 3 วันหลังเข้ารับการรักษา ในโรงพยาบาล ผู้ป่วยมีอาการแย่ลง encephalopathy grade IV, sluggish pupillary response to light both eyes: CT brain พบ progression of cerebral edema, loss of grey-white junctions and brain herniation (B)
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Bunchorntavakul, Chalermrat. "Acute liver failure." Thai Journal of Hepatology 1, no. 1 (April 24, 2018): 1–13. http://dx.doi.org/10.30856/th.jhep2018vol1iss1_01.
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Acute liver failure (ALF) is a life threatening condition defined by the evidence of hepatic injury, jaundice, coagulopathy, and encephalopathy in a patient without preexisting cirrhosis and with an illness duration of <26 weeks. The etiologies of ALF are heterogeneous: viral hepatitis being the most common in the East, whereas drug-induced, particularly acetaminophen, being the most common in the West. Over the past decades, the outcomes of ALF have been improving with early recognition and prompt initiation of etiology-specific therapy (especially N-acetylcysteine), complex intensive care protocols and urgent liver transplantation (LT). The most commonly used prognostic scoring systems include King’s College Criteria (more specific) and MELD (more sensitive). Cerebral edema and intracranial hypertension are reasons for high morbidity and mortality in the early phase; hypertonic saline is suggested for patients with high-risk for developing intracranial hypertension (ICH) and when ICH develops, mannitol is recommended as first-line therapy. Bacterial and fungal infections are very common necessitating strict preventive measures, careful surveillance and prompt aggressive antimicrobial therapy. Acute kidney injury develops in 50-70% of patients; mostly reversible in survivors and temporary dialysis is required in about 30% of cases. Overall 1-year survival after LT has been reported to be lower in patients with ALF as compared to those with cirrhosis; however following the first year this trend has been to be reversed and ALF patients have a better long-term survival. Extracorporeal liver support system, such as albumin dialysis and plasmapheresis, may serve as a bridge to LT and may increase LT-free survival in select cases.
Figure 1 CT brain ของผู้ป่วยเพศหญิง อายุ 22 ปี มีภาวะตับวายเฉียบพลันจากยา แรกรับมี encephalopathy grade III CT brain พบ mild cerebral edema with loss of sulciand gyri, blurring of grey - white junctions and mild narrowing of entricles (A) 3 วันหลังเข้ารับการรักษาในโรงพยาบาล ผู้ป่วยมีอาการแย่ลง encephalopathy grade IV, sluggish pupillary response to light botheyes: CT brain พบ progression of cerebral edema, loss of grey-white junctions and brain herniation (B)
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Mazumder, Md Wahiduzzaman, Fahmida Begum, and ASM Bazlul Karim. "Acute Liver Failure : Management Update." Bangladesh Journal of Child Health 41, no. 1 (August 20, 2017): 53–59. http://dx.doi.org/10.3329/bjch.v41i1.33636.
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Acute liver failure (ALF) is a rare but challenging clinical syndrome with multiple causes; about 50% of pediatric cases a specific etiology cannot be identified. The course of ALF is variable and the mortality rate is high. Liver transplantation is the only therapy of proven benefit, but the rapidity of progression and the variable course of ALF limit its use. Management requires a multidisciplinary approach and is directed at establishing the etiology where possible and monitoring, anticipating, and managing the multisystem complications that occur in children with ALF. Excellent intensive care is critical in management of patients with ALF. Nonspecific therapies are of unproven benefit. Future possible therapeutic approaches include N-acetylcysteine, hypothermia, liver assist devices, and hepatocyte transplantation. Advances in stem cell research may allow provision of cells for bioartificial liver support. ALF presents many challenging opportunities in both clinical and basic research.Bangladesh J Child Health 2017; VOL 41 (1) :53-59
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Adukauskienė, Dalia, Ilona Dockienė, Rima Naginienė, Egidijus Kėvelaitis, Juozas Pundzius, and Limas Kupčinskas. "Acute liver failure in Lithuania." Medicina 44, no. 7 (July 9, 2008): 536. http://dx.doi.org/10.3390/medicina44070069.
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Objectives. Acute liver failure (ALF) is a life-threatening condition that can rapidly progress into coma and death due to the cerebral edema and multi-organ dysfunction. The ALF etiology and risk factors have been investigated inWest Europe, North America, and Asia; however, there are still no published data about the causes and prognosis of ALF in Central and East European countries. The aim of our study was to analyze the causes, outcomes, and prognostic factors of ALF in patients referred to tertiary care center in Lithuania. Material and methods. A total of 28 consecutive patients admitted to the tertiary care center (one of two university-level medical centers in Lithuania) over the period of January 1996 and December 2004 and who fulfilled the entry criteria of ALF (presence of hepatic encephalopathy (HE) and prothrombin international normalized ratio (INR) >1.5) were included into a prospective study. Results. In our study the most frequent causes of ALF were acute viral hepatitis B (21.4 %), drug-induced hepatitis (21.4%), and indeterminate hepatitis (17.9%); other etiologies included Budd-Chiari syndrome (10.7%), ischemic hepatitis (10.7%), Wilson’s disease (7.1%), Amanita phalloides-induced liver damage (3.6%), acute fatty liver of pregnancy (3.6%), and malignant infiltration of the liver (3.6%). Among patients with drug-induced liver injury, only one case of acetaminophen poisoning was diagnosed. Clinical status of 9 persons in all patients with ALF corresponded to criteria for liver transplantation (LT) (one liver transplantation was performed), 6 of them had contraindications, and 13 patients did not fulfill requirements for urgent LT. The patients’ survival rate in these groups was 11.1%, 16.7% and 69.2%, respectively. In 27 nontransplanted patients univariate analysis revealed the grade of HE on the day of enrolment, total serumbilirubin, pH, and prothrombin INR as risk factors for death fromALF.Multivariate logistic regressive analysis determined only prothrombin INR >3.24 and serum pH £7.29 as independent predictors of lethal outcome in ALF. Conclusions. Acute viral hepatitis B, drug-induced liver injury, and indeterminate hepatitis are the main ALF causes in Lithuania. In non-transplanted patients, the main predictors of lethal outcome were severe coagulopathy and metabolic acidosis. Improvement of liver donation system for urgent liver transplantation is essential requirement for amelioration of ALF patient’s survival.
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MacDonald, Andrew, and Constantine Karvellas. "Emerging Role of Extracorporeal Support in Acute and Acute-on-Chronic Liver Failure: Recent Developments." Seminars in Respiratory and Critical Care Medicine 39, no. 05 (October 2018): 625–34. http://dx.doi.org/10.1055/s-0038-1675334.
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AbstractAcute liver failure (ALF) and acute-on-chronic liver failure (ACLF) are life-threatening illnesses requiring intensive care admission and potentially liver transplantation. Artificial extracorporeal liver support (ECLS) systems remove water-soluble and albumin-bound toxins to maintain normal serum chemistry, prevent further hepatic/organ system damage, and create an environment for potential hepatic regeneration/recovery (ALF) or bridge to liver transplantation (ALF and ACLF). Use of artificial ECLS has been studied in both ALF and ACLF. Artificial ECLS systems have been found to be safe and have demonstrated the following benefits: improvement of biochemistries, hemodynamic status, and hepatic encephalopathy. Despite this, only one prospective randomized controlled trial examining the use of high-volume plasma exchange has demonstrated improvement in transplant-free survival. Bioartificial (cell-based) ECLS systems build on the technology of artificial systems, incorporating living hepatocytes in a bioactive platform to further mimic endogenous hepatic detoxification and synthetic functions. Currently, no bioartificial system has been found to confer a mortality benefit; however, these platforms offer the greatest potential for future development.
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Abenavoli, Ludovico, Valentina Maurizi, Luigi Boccuto, Arianna Di Berardino, Nena Giostra, Pierangelo Santori, Maria Laura Scarcella, Anna Caterina Procopio, Carlo Rasetti, and Emidio Scarpellini. "Nutritional Support in Acute Liver Failure." Diseases 10, no. 4 (November 18, 2022): 108. http://dx.doi.org/10.3390/diseases10040108.
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Acute liver failure (ALF) presents with an acute abnormality of liver blood tests in an individual without underlying chronic liver disease. The clinical course leads to the development of coagulopathy and hepatic encephalopathy. The role of nutrition in its prevention and treatment remains uncertain. We aimed to review literature data on the concept of ALF and the role of nutrition in its treatment and prevention, considering the impact of gut microbiota dysbiosis and eubiosis. We conducted a review of the literature on the main medical databases using the following keywords and acronyms and their associations: liver failure, nutrition, branched-chain amino acids, gut microbiota, dysbiosis, and probiotics. Upon their arrival at the emergency department, an early, accurate nutritional assessment is crucial for individuals with ALF. Branched-chain amino acids (BCAAs), stable euglycemia maintenance, and moderate caloric support are crucial for this subset of patients. An excessive protein load must be avoided because it worsens hepatic encephalopathy. Preclinical evidence supports future probiotics use for ALF treatment/prevention. Nutritional support and treatment for ALF are crucial steps against patient morbidity and mortality. BCAAs and euglycemia remain the mainstay of nutritional treatment of ALF. Gut dysbiosis re-modulation has an emerging and natural-history changing impact on ALF.
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Hyun, Jeongeun, Seh-Hoon Oh, Richard T. Premont, Cynthia D. Guy, Carl L. Berg, and Anna Mae Diehl. "Dysregulated activation of fetal liver programme in acute liver failure." Gut 68, no. 6 (January 22, 2019): 1076–87. http://dx.doi.org/10.1136/gutjnl-2018-317603.
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ObjectiveUncertainty about acute liver failure (ALF) pathogenesis limits therapy. We postulate that ALF results from excessive reactivation of a fetal liver programme that is induced in hepatocytes when acutely injured livers regenerate. To evaluate this hypothesis, we focused on two molecules with known oncofetal properties in the liver, Yes-associated protein-1 (YAP1) and Insulin-like growth factor-2 RNA-binding protein-3 (IGF2BP3).DesignWe compared normal liver with explanted livers of patients with ALF to determine if YAP1 and IGF2BP3 were induced; assessed whether these factors are upregulated when murine livers regenerate; determined if YAP1 and IGF2BP3 cooperate to activate the fetal programme in adult hepatocytes; and identified upstream signals that control these factors and thereby hepatocyte maturity during recovery from liver injury.ResultsLivers of patients with ALF were massively enriched with hepatocytes expressing IGF2BP3, YAP1 and other fetal markers. Less extensive, transient accumulation of similar fetal-like cells that were proliferative and capable of anchorage-independent growth occurred in mouse livers that were regenerating after acute injury. Fetal reprogramming of hepatocytes was YAP1-dependent and involved YAP1-driven reciprocal modulation of let7 microRNAs and IGF2BP3, factors that negatively regulate each other to control fate decisions in fetal cells. Directly manipulating IGF2BP3 expression controlled the fetal-like phenotype regardless of YAP1 activity, proving that IGF2BP3 is the proximal mediator of this YAP1-directed fate.ConclusionAfter acute liver injury, hepatocytes are reprogrammed to fetal-like cells by a YAP1-dependent mechanism that differentially regulates let7 and IGF2BP3, identifying novel therapeutic targets for ALF.
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Lin, Jiacheng, Qihua Ling, Liang Yan, Bowu Chen, Fang Wang, Yihan Qian, Yueqiu Gao, et al. "Ancient Herbal Formula Mahuang Lianqiao Chixiaodou Decoction Protects Acute and Acute-on-Chronic Liver Failure via Inhibiting von Willebrand Factor Signaling." Cells 11, no. 21 (October 25, 2022): 3368. http://dx.doi.org/10.3390/cells11213368.
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Background: Acute liver failure (ALF) and acute-on-chronic liver failure (ACLF) are characterized by systemic inflammation and high mortality, but there is no effective clinical treatment. As a classic traditional Chinese medicine (TCM) formula, MaHuang-LianQiao-ChiXiaoDou decoction (MHLQD) has been used clinically for centuries to treat liver diseases. Methods: The LPS/D−GalN-induced ALF mice model and the CCl4+LPS/D−GalN-induced ACLF mice model were used to observe the therapeutic effects of MHLQD on mice mortality, hepatocytes death, liver injury, and immune responses. Results: MHLQD treatment significantly improved mice mortality. Liver injury and systemic and hepatic immune responses were also ameliorated after MHLQD treatment. Mechanistically, proteomic changes in MHLQD-treated liver tissues were analyzed and the result showed that the thrombogenic von Willebrand factor (VWF) was significantly inhibited in MHLQD-treated ALF and ACLF models. Histological staining and western blotting confirmed that VWF/RAP1B/ITGB3 signaling was suppressed in MHLQD-treated ALF and ACLF models. Furthermore, mice treated with the VWF inhibitor ADAMTS13 showed a reduced therapeutic effect from MHLQD treatment. Conclusions: Our study indicated that MHLQD is an effective herbal formula for the treatment of ALF and ACLF, which might be attributed to the protection of hepatocytes from death via VWF/RAP1B/ITGB3 signaling.
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Edhi, Ahmed I., Siefeldin Hakim, Christienne Shams, Mitual Amin, and Mitchell S. Cappell. "Clarithromycin-Induced Acute Liver Failure (ALF)." American Journal of Gastroenterology 113, Supplement (October 2018): S1297. http://dx.doi.org/10.14309/00000434-201810001-02303.
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Shalimar. "Antibiotics in Acute Liver Failure (ALF)." Journal of Clinical and Experimental Hepatology 5, no. 1 (March 2015): 95–97. http://dx.doi.org/10.1016/j.jceh.2015.01.004.
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Lee, Maunoo, Joshua McCarron, Aaron Balinski, and Richard Bower. "Intravenous acetaminophen associated with acute liver failure." BMJ Case Reports 15, no. 11 (November 2022): e251305. http://dx.doi.org/10.1136/bcr-2022-251305.
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A woman in her mid-60s, without known liver disease, was admitted to the hospital with a partial malignant colonic obstruction. Over a 6-day course, she received a total of 13 g of intravenous acetaminophen not exceeding 4 g over a 24-hour period. She developed encephalopathy and an international normalised ratio of 6.1 meeting criteria for acute liver failure (ALF). She was treated with intravenous N-acetyl cysteine and other causes of liver failure were excluded. The patient was discharged with subsequent resolution of encephalopathy and improvement of her liver chemistries. Though ALF is rare, in countries where acetaminophen is readily available, almost 50% of ALF cases are acetaminophen-induced hepatotoxicity and most have been documented as oral ingestion of acetaminophen. We present a rare case of intravenous acetaminophen-induced ALF.
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Warrillow, Stephen, Caleb Fisher, Heath Tibballs, Michael Bailey, Colin McArthur, Pia Lawson-Smith, Bheemasenachar Prasad, et al. "Continuous renal replacement therapy and its impact on hyperammonaemia in acute liver failure." Critical Care and Resuscitation 22, no. 2 (June 1, 2020): 158–65. http://dx.doi.org/10.51893/2020.2.oa6.
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Objective: Hyperammonaemia contributes to complications in acute liver failure (ALF) and may be treated with continuous renal replacement therapy (CRRT), but current practice is poorly understood. Design: We retrospectively analysed data for baseline characteristics, ammonia concentration, CRRT use, and outcomes in a cohort of Australian and New Zealand patients with ALF. Setting: All liver transplant ICUs across Australia and New Zealand. Participants: Sixty-two patients with ALF. Main outcome measures: Impact of CRRT on hyperammonaemia and patient outcomes. Results: We studied 62 patients with ALF. The median initial (first 24 h) peak ammonia was 132 mol/L (interquartile range [IQR], 91–172), median creatinine was 165 mol/L (IQR, 92–263) and median urea was 6.9 mmol/L (IQR, 3.1–12.0). Most patients (43/62, 69%) received CRRT within a median of 6 hours (IQR, 2–12) of ICU admission. At CRRT commencement, three-quarters of such patients did not have Stage 3 acute kidney injury (AKI): ten patients (23%) had no KDIGO creatinine criteria for AKI, 12 (28%) only had Stage 1, and ten patients (23%) had Stage 2 AKI. Compared with non-CRRT patients, those treated with CRRT had higher ammonia concentrations (median, 141 mol/L [IQR, 102–198] v 91 mol/L [IQR, 54–115]; P = 0.02), but a nadir Day 1 pH of only 7.25 (standard deviation, 0.16). Prevention of extreme hyperammonaemia (> 140 mol/L) after Day 1 was achieved in 36 of CRRT-treated patients (84%) and was associated with transplant-free survival (55% v 13%; P = 0.05). Conclusion: In Australian and New Zealand patients with ALF, CRRT is typically started early, before Stage 3 AKI or severe acidaemia, and in the presence hyperammonaemia. In these more severely ill patients, CRRT use was associated with prevention of extreme hyperammonaemia, which in turn, was associated with increased transplant-free survival.
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Toptas, Tayfur, Birkan Ilhan, Huseyin Bilgin, Elif Dincses, Osman Ozdogan, Isik Kaygusuz-Atagunduz, Zekaver Odabasi, Volkan Korten, and Tulin Firatli-Tuglular. "Miliary Tuberculosis Induced Acute Liver Failure." Case Reports in Infectious Diseases 2015 (2015): 1–3. http://dx.doi.org/10.1155/2015/759341.
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Hepatobiliary tuberculosis is uncommon even in endemic countries. It is associated with a high mortality and is even diagnosed early in the disease course. Acute liver failure (ALF) caused by tuberculosis bacilli has been reported in only a few reports. All previous cases have been diagnosed by postmortem examination. Time to antituberculosis treatment is very critical. In case of suggestive findings on clinical and radiologic examination, antituberculosis treatment should be initiated immediately. Drug use can be a challenge in patients with ALF. However, as long as the other possible causes of ALF can be excluded and hepatotoxic drugs were avoided during the early course of treatment, such a highly fatal presentation of tuberculosis can be treated safely. Here, we report a case of acute liver failure as a presentation of miliary tuberculosis. He was treated successfully with antituberculosis treatment.
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Santi, Luca, Caterina Maggioli, Marianna Mastroroberto, Manuel Tufoni, Lucia Napoli, and Paolo Caraceni. "Acute Liver Failure Caused byAmanita phalloidesPoisoning." International Journal of Hepatology 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/487480.
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Mushroom poisoning is a relatively rare cause of acute liver failure (ALF). The present paper analyzes the pathogenesis, clinical features, prognostic indicators, and therapeutic strategies of ALF secondary to ingestion ofAmanita phalloides, which represents the most common and deadly cause of mushroom poisoning. Liver damage fromAmanita phalloidesis related to the amanitins, powerful toxins that inhibit RNA polymerase II resulting in a deficient protein synthesis and cell necrosis. After an asymptomatic lag phase, the clinical picture is characterized by gastrointestinal symptoms, followed by the liver and kidney involvement. Amatoxin poisoning may progress into ALF and eventually death if liver transplantation is not performed. The mortality rate afterAmanita phalloidespoisoning ranges from 10 to 20%. The management of amatoxin poisoning consists of preliminary medical care, supportive measures, detoxification therapies, and orthotopic liver transplantation. The clinical efficacy of any modality of treatment is difficult to demonstrate since randomized, controlled clinical trials have not been reported. The use of extracorporeal liver assist devices as well as auxiliary liver transplantation may represent additional therapeutic options.
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Yang, Runkuan, Xiaoping Zou, Jyrki Tenhunen, and Tor Inge Tønnessen. "HMGB1 and Extracellular Histones Significantly Contribute to Systemic Inflammation and Multiple Organ Failure in Acute Liver Failure." Mediators of Inflammation 2017 (2017): 1–6. http://dx.doi.org/10.1155/2017/5928078.
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Acute liver failure (ALF) is the culmination of severe liver cell injury from a variety of causes. ALF occurs when the extent of hepatocyte death exceeds the hepatic regenerative capacity. ALF has a high mortality that is associated with multiple organ failure (MOF) and sepsis; however, the underlying mechanisms are still not clear. Emerging evidence shows that ALF patients/animals have high concentrations of circulating HMGB1, which can contribute to multiple organ injuries and mediate gut bacterial translocation (BT). BT triggers/induces systemic inflammatory responses syndrome (SIRS), which can lead to MOF in ALF. Blockade of HMGB1 significantly decreases BT and improves hepatocyte regeneration in experimental acute fatal liver injury. Therefore, HMGB1 seems to be an important factor that links BT and systemic inflammation in ALF. ALF patients/animals also have high levels of circulating histones, which might be the major mediators of systemic inflammation in patients with ALF. Extracellular histones kill endothelial cells and elicit immunostimulatory effect to induce multiple organ injuries. Neutralization of histones can attenuate acute liver, lung, and brain injuries. In conclusion, HMGB1 and histones play a significant role in inducing systemic inflammation and MOF in ALF.
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Xie, Chencheng, Jonathan M. Fenkel, Dina L. Halegoua-DeMarzio, Jesse M. Civan, Danielle M. Tholey, Steven K. Herrine, Manish Thapar, et al. "Acute Liver Failure Requiring Liver Transplantation due to Acute Hepatitis A Virus Infection." Case Reports in Transplantation 2021 (December 27, 2021): 1–4. http://dx.doi.org/10.1155/2021/5159934.
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Introduction. Hepatitis A infection (HAV) is generally characterized by an acute icteric illness or may have a subclinical self-limited course, although rarely, can result in fulminant hepatitis and death. In 2019, the City of Philadelphia declared a public health emergency due to an HAV outbreak. We are reporting a series of four cases of acute liver failure (ALF) requiring liver transplantation (LT) due to acute HAV. Methods. Chart review and case descriptions of four patients with acute HAV-related ALF who were expeditiously evaluated, listed as Status 1A, and who underwent LT between August 2019 and October 2019 at Thomas Jefferson University Hospital. Results. All four patients presented with acute hepatocellular jaundice and had a positive HAV IgM, and all other causes of ALF were excluded. All four cases met the American Association for the Study of Liver Diseases (AASLD) criteria for ALF. Three of the four cases met King’s College Criteria of poor prognosis for nonacetaminophen-induced ALF. All four patients underwent successful LT and were discharged six to twelve days postoperatively. One patient died of disseminated Aspergillus infection five months after LT, while the others have had excellent clinical outcomes shown by one-year follow-ups. All four explants had remarkably similar histological changes, revealing acute hepatitis with massive necrosis accompanied by a prominent lymphoplasmacytic inflammatory infiltrate and bile ductular proliferation. Conclusion. Although rare, patients presenting with acute HAV need close monitoring as they may rapidly progress to ALF. Early referral to a transplant center afforded timely access to LT and yielded overall good one-year survival. Widespread HAV vaccination for high-risk individuals is an essential strategy for preventing disease and curbing such future outbreaks.
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Nabi, Tauseef, and Nadeema Rafiq. "N-acetylcysteine treatment in viral-induced acute liver failure." International Journal of Clinical Trials 6, no. 3 (July 24, 2019): 106. http://dx.doi.org/10.18203/2349-3259.ijct20193213.
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<p class="abstract"><strong>Background:</strong> Acute liver failure (ALF) is characterized by acute derangement of liver function and carries high mortality. Viral hepatitis is still one of the main causes of ALF in the India as well in world. A prospective case control study was carried with the aim to determine the effect of N-acetylcysteine (NAC) on survival of viral-ALF patients.</p><p class="abstract"><strong>Methods:</strong> 37 patients with a diagnosis of viral-ALF were included in the study. 18 patients received NAC infusion for 72 hrs whereas 19 patients in control group received placebo. The variables evaluated were demographic, biochemical, outcome and length of hospital stay.</p><p class="abstract"><strong>Results:</strong> Out of 37 viral-ALF patients, acute HEV-induced ALF (48.6%) was most common followed by HBV (24.3%) and HAV (21.6%). The two groups were comparable for the various baseline characteristics (age, INR, bilirubin, ALT, creatinine, albumin, grade of encephalopathy, mean grade of coma etc.). Use of NAC was associated with a shorter length of hospital stay of survived patients (p=0.024). A total of 20 of 37 (54.1%) patients died with ALF complications; 7 (38.9%) patients belonged to NAC group and 13 (68.4%) patients to control group (p=0.079). HEV induced ALF showed significant improved in survival than Non HEV induced ALF with NAC administration (p=0.022).</p><p><strong>Conclusions: </strong>HEV was the most frequently cause of viral-ALF. Overall survival was not improved by NAC. HEV induced ALF showed significant improved in survival than Non HEV induced ALF with NAC administration. NAC reduced duration of hospital stay.</p>
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Shammout, Reem, Turki Alhassoun, and Fadi Rayya. "Acute Liver Failure due to Hepatitis A Virus." Case Reports in Gastroenterology 15, no. 3 (November 2, 2021): 927–32. http://dx.doi.org/10.1159/000514393.
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Acute liver failure (ALF) is a syndrome, rather than a specific disease, with several possible causes, and viral hepatitis is a major cause. The relationship between self-limited and ALF hepatitis A is still poorly understood. A 45-year-old woman presented to our hospital with ALF diagnosis (from another hospital). She suffered from hospital-acquired pneumonia. The patient recovered within 4 weeks and returned to her normal life after 6 months of follow-up.
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Gorospe, Emmanuel C., and Jemilat Badamas. "Acute Liver Failure Secondary to Metastatic Medullary Thyroid Cancer." Case Reports in Hepatology 2011 (2011): 1–4. http://dx.doi.org/10.1155/2011/603757.
Full textAbstract:
Acute liver failure (ALF) is a rare presentation of liver metastases. Although cases of ALF from metastatic disease have been reported, etiologies have been largely confined to lymphoma, metastatic breast, lung, and gastric cancers. ALF from medullary thyroid cancer (MTC) has never been reported. We present a 59-year-old male with newly diagnosed MTC, who was admitted with ALF. He presented with jaundice, hepatic encephalopathy, and synthetic dysfunction. His clinical course was marked by rapid decompensation within 6 days from initial presentation of jaundice to development of hepatic coma. Although liver metastases from medullary thyroid cancer have been reported, to our knowledge, this is the first described case of MTC resulting in acute liver failure.
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Sowa, Jan-Peter, Guido Gerken, and Ali Canbay. "Acute Liver Failure - It's Just a Matter of Cell Death." Digestive Diseases 34, no. 4 (2016): 423–28. http://dx.doi.org/10.1159/000444557.
Full textAbstract:
Background: Acute liver failure (ALF) is characterized by a sudden loss of hepatic function due to hepatocyte cell death and dysfunction in previously healthy individuals. The clinical presentation of ALF is associated with coagulopathy (international normalized ratio ≥1.5) and hepatic encephalopathy, although the latter may be less pronounced. Without appropriate and timely intensive care or liver transplantation (LTx), ALF will result in multi-organ failure and death. Various causes may induce ALF, with acetaminophen (APAP) intoxication and acute hepatitis B infection as most common causes in industrialized countries. While conventional terminology discerns acute, acute-on-chronic and acute-on cirrhosis liver failure, some chronic liver diseases (i.e. autoimmune hepatitis (AIH), Wilson's disease) can remain undiagnosed until an initial presentation as ALF. Key Messages: Upon definite diagnosis of ALF, the underlying cause must be identified, since etiology affects prognosis and clinical management. Individual prognosis should be evaluated with one of various available scoring systems. Most widely used are Model for End-Stage Liver Disease, the King's College Criteria and the Clichy criteria. Other markers, that is, cell death markers, lactate or thyroid status, may improve diagnostic accuracy of classic scores, though routine use of these is not yet established. Etiology-specific treatment under intensive care should be performed, if possible (APAP and amanita intoxication, acute viral hepatitides and AIH). LTx is the only curative option for other causes, unknown reasons of ALF or when etiology-specific therapy fails. In ambiguous cases, that is, suspected drug induced ALF or AIH, co-infection with hepatitis E virus should be tested, as this might be more common than it is currently supposed to be. Conclusions: Despite major improvements in clinical management of ALF patients, a significant proportion of ALF cases remains without clear identification of the underlying cause or unrecognized multiple causes. In depth analyzes of ambiguous ALF cases is warranted to further improve clinical management.
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HIMMA, KENNETH EINAR. "A Critique of UNOS Liver Allocation Policy." Cambridge Quarterly of Healthcare Ethics 8, no. 3 (July 1999): 311–20. http://dx.doi.org/10.1017/s0963180199803065.
Full textAbstract:
The United Network for Organ Sharing (UNOS) recently changed the policy by which donor livers are allocated to liver failure patients in the United States. Formerly, all liver failure patients were characterized as status 1 and placed at the top of the transplant list. Under the new policy, only patients with liver failure due to acute illness (“ALF patients”) are eligible for status 1; patients with liver failure due to chronic liver disease (“CLF patients”) are characterized as status 2. Since donor organs are allocated first to status 1 patients and then to status 2 patients, the new policy moves all CLF patients down on the waiting list relative to all ALF patients. This means that some livers that would have gone to CLF patients under the old policy will now go to ALF patients. Accordingly, while the new policy will likely increase the number of ALF patients saved, it will also increase the number of deaths among CLF patients waiting for a transplant.
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Tavabie, Oliver D., and William Bernal. "How to manage: acute liver failure." Frontline Gastroenterology 11, no. 1 (April 29, 2019): 70–74. http://dx.doi.org/10.1136/flgastro-2018-101105.
Full textAbstract:
Acute liver failure (ALF) is a rare but life-threatening clinical syndrome with a broad range of causes. Significant improvements in outcome have occurred over the last 50 years, resulting not only from incremental improvements in specialist critical care and a step-change following the introduction of transplantation for this indication, but also better and more effective treatment started early at the site of first presentation.1 2 Emergency liver transplantation (LTx) remains an important intervention and the decision regarding the need for LTx remains key to management, though non-transplant therapies now appear effective for many causes of the condition. In this short review, we will outline issues in the recognition and management of ALF and ongoing challenges in its treatment.
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Alves, Arthur DR, Juliana G. Melgaço, Rita de Cássia NC Garcia, Jessica V. Raposo, Vanessa S. de Paula, Cristina CV Araújo, Marcelo A. Pinto, and Luciane A. Amado. "Persistence of Parvovirus B19 in liver from transplanted patients with acute liver failure." Future Microbiology 15, no. 5 (March 2020): 307–17. http://dx.doi.org/10.2217/fmb-2019-0224.
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Aim: In this study, we investigated the presence of B19V in liver tissues from patients with acute liver failure (ALF) and evaluated the viral activity in infected liver. Methods: Serum and liver samples from 30 patients who underwent liver transplantation for ALF were investigated for B19V infection by real-time PCR, serological tests and examination of B19V mRNA (transcript) expression in the liver. Results: The serum and liver samples from seven patients were B19V DNA positive (103–105 copies/ml). Most of them presented detectable anti-B19V IgG, indicating persistent infection. B19V mRNA was detected in all patients, demonstrating intra-hepatic replication. Conclusion: B19V infection of the liver during the course of non-A-E ALF suggested a role of B19V, which produced the worst outcome in co-infected patients and in patients with cryptogenic ALF, in liver damage.
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Fábrega, Emilio, Miguel Ángel Mieses, Alvaro Terán, Irene Moraleja, Fernando Casafont, Javier Crespo, and Fernando Pons-Romero. "Etiologies and Outcomes of Acute Liver Failure in a Spanish Community." International Journal of Hepatology 2013 (2013): 1–5. http://dx.doi.org/10.1155/2013/928960.
Full textAbstract:
Previous retrospective study (1992 to 2000) performed in Spain showed that drug toxicity, viral hepatitis, and indeterminate etiology were the most prevalent causes of acute liver failure (ALF). In the last decade, there is no information about ALF in our country. For these reasons we analyze retrospectively, in a ten-year period (2000 to 2010), the presumed causes, clinical characteristics, course, and outcome of ALF in a Spanish community. Causes of ALF were indeterminate in 4 patients (24%), acute hepatitis B infection in 4 patients (24%), drug or toxic reactions in 4 patients (24%), including one case of acetaminophen overdose, followed by miscellaneous causes. The overall short-term survival (6 weeks after admission) was 65%. Liver transplantation was performed in 11 patients with a survival of 82%. Despite fulfilling criteria, 2 patients were not transplanted because of contraindications; they both died. In summary, acute hepatitis B and indeterminate cause are still being the most frequent causes of ALF in our region, and patients with ALF have an excellent chance of survival after emergency liver transplantation. Acetaminophen overdose still represents a very rare cause of ALF in our community.
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Kamal, Tom, and Nadim Haboubi. "Epstein-Barr virus and acute liver failure: an exceedingly rare amalgamation." Journal of the Royal College of Physicians of Edinburgh 51, no. 1 (March 2021): 46–48. http://dx.doi.org/10.4997/jrcpe.2021.111.
Full textAbstract:
Epstein-Barr virus (EBV) associated acute liver failure (ALF) is an exceedingly uncommon event. Despite this, EBV-associated ALF has a very high fatality rate. When looking at the number of reported cases of EBV-associated ALF requiring an emergency liver transplant, we see even fewer numbers. This presents challenges to clinicians in the diagnosis, awareness and appropriate case management. There is limited information in the medical literature about the hepatic demonstration and complications of EBV. We therefore report a case of EBV-associated ALF in a 17-year-old immunocompetent female who was treated successfully with an orthotopic liver transplantation.
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Gottlieb, Aline, Maren Kottmann, Paul Manka, Sotiria Bedreli, Johannes Hadem, Lars Bechmann, Jan-Peter Sowa, Guido Gerken, and Ali Canbay. "How to Define Acute Liver Failure Patients with Pre-Existing Liver Disease without Signs of Cirrhosis." Digestive Diseases 37, no. 2 (September 18, 2018): 147–54. http://dx.doi.org/10.1159/000492869.
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Background: The definition of acute liver failure (ALF) usually implies no previous liver injury. Though, some patients admitted to liver transplantation centers with the diagnosis of ALF are obese or have diabetes. Elevated liver enzymes were not recorded previously, and no signs of cirrhosis or prior decompensation of the liver function were ever present. Still, these patients differ from the “typical” ALF-patient. Goals: In this study, we aimed to confirm acute-on-chronic-liver failure (AOCLF) in patients diagnosed with ALF and to identify possible differences between ALF and AOCLF. Study: Patients were retrospectively recruited from all patients admitted to the University Hospital Essen with diagnosis of ALF between 2008 and 2015. Data of 163 patients were evaluated, resulting in a reclassification of 32 patients as AOCLF (remaining ALF: 131). Demographic and clinical data as well as serum parameters, including cell death markers, were correlated with clinical outcome. Results: Patients with AOCLF were significantly older, had a higher body mass index (BMI), and were more often male. The cause for liver failure in these patients differed significantly from patients who had an actual ALF. Significant differences were also found for serum liver enzymes. Outcome of patients did not differ between AOCLF and ALF. Though, lower BMI and MELD and higher AST and GLDH were predictors for a beneficial outcome. Conclusion: AOCLF is still commonly misdiagnosed as ALF. While clinical outcome does not significantly differ between ALF and AOCLF, risk factors for adverse outcome may significantly differ between these entities.
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Pravita, Aravinda, Kresna Adhiatma, and Juferdy Kurniawan. "Liver Support System and Transplant-Free Survival Patients with Liver Failure: An Evidence-Based Case Report." Indonesian Journal of Gastroenterology, Hepatology, and Digestive Endoscopy 23, no. 2 (September 6, 2022): 261–65. http://dx.doi.org/10.24871/2322022261-265.
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Background: The mortality rate in patients with acute liver failure (ALF) and acute on chronic liver failure (ACLF) is still very high. Currently, liver support systems are an alternative therapy in bridging liver transplantation. However, its effectiveness in reducing mortality is still controversial when compared to standard medical therapy (SMT). Our study aims to review the efficacy of liver support system compared to standard medical therapy (SMT) among acute liver failure patients without liver transplantation.Method: We conducted systematic literature searching using PubMed/MEDLINE, EBSCO-CINAHL, ProQuest, and Cochrane databases. Selected articles were examined for duplicates and were screened by abstract and title. Then, we appraised the articles based on the critical appraisal tools from Centre for Evidence-Based Medicine (CEBM) University of OxfordResults: One systematic review and meta-analysis of randomized control trials study was extracted after thorough research. Alhamshi et al showed that extracorporeal liver support has significantly reduced mortality in both ALF and ACLF patients as the primary outcome. Other main findings about adverse events including hepatic encephalopathy, thrombocytopenia, bleeding, and infection were still unclear.Conclusion: The use of liver support system demonstrated better outcome in reducing mortality to standard medical therapy in transplant free patients with liver failure, but best modality recommendation was inconclusive.
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Ni, Shunlan, Shanshan Li, Naibin Yang, Xinyue Tang, Shengguo Zhang, Danping Hu, and Mingqin Lu. "Deregulation of Regulatory T Cells in Acute-on-Chronic Liver Failure: A Rat Model." Mediators of Inflammation 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/1390458.
Full textAbstract:
Aims. Acute-on-chronic liver failure (ACLF) and acute liver failure (ALF) are similar in many respects during their acute exacerbation; however, ACLF generally has a poorer prognosis. We aimed to investigate the role and dynamic changes of regulatory T cell (Treg) and T helper 17 (Th17) cell proportions during ACLF progress. Methods. All rats were classified into two groups randomly: ACLF group and ALF group (control group). The rat model of ACLF was preestablished by intraperitoneal injection of carbon tetrachloride for 2 months. Then acute liver injury was induced by combined D-galactosamine and lipopolysaccharide. Six time points were examined before or after acute induction. Liver samples were performed with hematoxylin-eosin and Masson staining; circulatory Treg and Th17 cell frequencies were determined using flow cytometry assays; serum levels of alanine aminotransferase, aspartate aminotransferase, interleukin-10 (IL-10), and interferon-γ (IFN-γ) were examined. Results. In group ACLF, both Th17 cell proportion and IFN-γ level presented upgrade firstly and then descend latter tendency; the trends of Treg cell proportion and IL-10 level were observed to gradually decrease and became stable. Conclusion. The Treg cells played an important role in the immunologic mechanism during the process of ACLF. And the function of Treg cells in ACLF was defective.
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Costa, Ana Rita Gonçalves, Inês Freitas, Joana Raposo, Gustavo Barbosa, Helena P. Miranda, and Filipe Nery. "Budd-Chiari Syndrome and Acute Liver Failure: An Uncommon Presentation of Acute Myeloid Leukaemia." GE - Portuguese Journal of Gastroenterology 28, no. 1 (May 27, 2020): 62–66. http://dx.doi.org/10.1159/000507335.
Full textAbstract:
Acute liver failure (ALF) is a rare entity, particularly in the context of Budd-Chiari syndrome (BCS). BCS is an uncommon disorder with multiple risk factors, most commonly myeloproliferative disorders. In BCS, active search and exclusion of underlying malignancy is mandatory, particularly in the context of ALF, as it may contraindicate liver transplantation (LT). We present the case of a healthy 29-year-old male, without known risk factors for liver disease, who presented to the emergency department with abdominal pain, ascites, and jaundice. BCS with consequent severe acute liver injury with rapid progression to ALF was diagnosed. The patient was listed for LT. The study of peripheral blood finally revealed myeloid blasts, and flow cytometry showed a population of blast cells with abnormal immunophenotypic profile (CD33+ and myeloperoxidase, MPO+). The bone marrow biopsy showed morphological and immunophenotypic aspects of acute myeloid leukaemia (AML) FAB M1. This diagnosis was considered a formal contraindication to LT, so the patient was delisted. ALF contraindicated rescue chemotherapy and AML contraindicated LT. The patient died 48 h after ICU admission. The search for underlying neoplasia is mandatory in the context of BCS, moreover with associated ALF, as it may limit lifesaving treatments and interventions to supportive and palliative care.
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Rabadán, Alejandra T., Natalia Spaho, Diego Hernández, Adrián Gadano, and Eduardo de Santibañes. "Intraparenchymal intracranial pressure monitoring in patients with acute liver failure." Arquivos de Neuro-Psiquiatria 66, no. 2b (June 2008): 374–77. http://dx.doi.org/10.1590/s0004-282x2008000300018.
Full textAbstract:
BACKGROUND: Elevated intracranial pressure (ICP) is a common cause of death in acute liver failure (ALF) and is determinant for decision-making regarding the timing of liver transplantation. The recommended type ICP monitoring device is controversial in ALF patients. Epidural devices had less risk of hemorrhagic complications, but they are less reliable than intraparenchymal ones. METHOD: Twenty-three patients with ALF were treated, and 19 of them received a liver transplant. Seventeen patients had ICP monitoring because of grade III-IV encephalopathy. All patients received fresh plasma (2-3 units) before and during placing the intraparenchymal device. RESULTS: Eleven cases (64.7%) had elevated ICP, and 6 patients (35.2%) had normal values. One patient (5.9%) had an asymptomatic small intraparenchymal haemorrhage <1cm³ in CTscan, which did not prevent the liver transplantation. CONCLUSION: In our experience, intraparenchymal ICP monitoring in patients with ALF seems to be an accurate method with a low risk of complications.
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Cai, Lei, Jun Weng, Lei Feng, Guolin He, Jiasheng Qin, Zhi Zhang, Yang Li, et al. "Establishment of a Novel Simplified Surgical Model of Acute Liver Failure in the Cynomolgus Monkey." BioMed Research International 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/3518989.
Full textAbstract:
Models using large animals that are suitable for studying artificial liver support system (ALSS) are urgently needed. Presently available acute liver failure (ALF) models mainly involve pigs or dogs. Establishment of current surgical ALF models (hepatectomy/devascularization) requires either very good surgical skills or multistep processes—even multiple stages of surgery. Therefore, it is necessary to develop a simplified surgical method. Here we report a novel simplified surgical ALF model using cynomolgus monkeys. Six monkeys underwent portal-right renal venous shunt combined with common bile duct ligation and transection (PRRS + CBDLT). Postoperatively, the monkeys had progressively increased listlessness, loss of appetite, and obvious jaundice. Blood biochemistry levels (Amm, ALT, AST, TBiL, DBiL, ALP, LDH, CK, and Cr) and prothrombin time (PT) were significantly increased (all P<0.01) and albumin (ALB) was markedly reduced (P<0.01) compared with baseline values. Histological examination of liver specimens on postoperative day 10 revealed cholestasis and inflammation. PRRS + CBDLT produced ALF that closely correlated with clinical situations. Compared with other surgical or drug ALF models, ours was simplified and animals were hemodynamically stable. This model could provide a good platform for further research on ALSS, especially regarding their detoxification functions.
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Zhao, Jinqiu, Zhengyu Shi, Shu Liu, Jiajun Li, and Wenxiang Huang. "Ginsenosides Rg1 fromPanax ginseng: A Potential Therapy for Acute Liver Failure Patients?" Evidence-Based Complementary and Alternative Medicine 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/538059.
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Acute liver failure (ALF) is a rapidly progressing critical illness with a high mortality rate. Circulating inflammatory cytokines, such as tumor necrosis factor-α(TNF-α), play a significant role in the pathophysiology of ALF through promoting hepatocellular apoptosis. Ginsenoside Rg1, the primary active ingredient inPanax ginseng(also termed Asian or Korean ginseng), has been reported to inhibit TNF-αproduction and has been shown to significantly attenuate liver fibrosis development. Here, we assessed ginsenoside Rg1’s potential as a therapy for ALF by investigating the effect of ginsenoside Rg1 treatment on circulating inflammatory markers, hepatocellular apoptosis, and relevant apoptotic signaling pathways in a well-established murine ALF model. We found that ginsenoside Rg1 significantly reduces liver damage in a murine ALF model through inhibiting TNF-α-induced, caspase-dependent hepatocellular apoptosis. These results support the further investigation of ginsenoside Rg1 as a therapeutic candidate for ALF.
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Putra, Agung, Arini Dewi Antari, Azizah Retno Kustiyah, Yulice Soraya Nur Intan, Nur Anna C. Sadyah, Nugraha Wirawan, Samara Astarina, Nasrul Zubir, and Delfitri Munir. "Mesenchymal stem cells accelerate liver regeneration in acute liver failure animal model." Biomedical Research and Therapy 5, no. 11 (November 14, 2018): 2802–10. http://dx.doi.org/10.15419/bmrat.v5i11.498.
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Introduction: The massive hepatic necrosis of acute liver failure (ALF) results in a sudden loss of hepatic cells. Although most hepatocyte cells of ALF are completely lost, stem cell-derived circulating cells and endogenous progenitor cells rapidly regenerate them. Mesenchymal stem cells (MSCs) have a critical role in the regeneration of liver injury through regulating platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) levels. However, their fluctuating levels in the healing process and correlation to the decrease of liver function markers remain unclear. The aim of this study was to analyze the effects of MSCs in accelerating liver regeneration of ALF by measuring VEGF and PDGF levels on day 2 and 7, as well as SGPT and SGOT levels, and assessing histopathology appearance.
Methods: Using an ALF rat model, 12 animals were randomly assigned into two groups: umbilical cord (UC)-MSC injection (T1) and vehicle control (Veh). ELISA assay was employed to measure PDGF and VEGF levels, an automatic analyzer was used to assess serum glutamic pyruvic transaminase (SGPT) and serum glutamic oxaloacetic transaminase (SGOT), and hematoxylin and eosin (H&E) staining was used to evaluate morphological appearance.
Results: The study showed an significant (P<0.001) increase of PDGF and VEGF levels on the 2nd day, followed by a decrease on the 7th day, along with a decrease of SGPT and SGOT levels as well as the normality of histology appearance.
Conclusion: In conclusion, administration of MSCs may accelerate liver regeneration of ALF through PDGF and VEGF regulation.
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Chen, Zhaochun, Giacomo Diaz, Teresa Pollicino, Huaying Zhao, Ronald E. Engle, Peter Schuck, Chen-Hsiang Shen, et al. "Role of humoral immunity against hepatitis B virus core antigen in the pathogenesis of acute liver failure." Proceedings of the National Academy of Sciences 115, no. 48 (November 12, 2018): E11369—E11378. http://dx.doi.org/10.1073/pnas.1809028115.
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Hepatitis B virus (HBV)-associated acute liver failure (ALF) is a dramatic clinical syndrome leading to death or liver transplantation in 80% of cases. Due to the extremely rapid clinical course, the difficulties in obtaining liver specimens, and the lack of an animal model, the pathogenesis of ALF remains largely unknown. Here, we performed a comprehensive genetic and functional characterization of the virus and the host in liver tissue from HBV-associated ALF and compared the results with those of classic acute hepatitis B in chimpanzees. In contrast with acute hepatitis B, HBV strains detected in ALF livers displayed highly mutated HBV core antigen (HBcAg), associated with increased HBcAg expression ex vivo, which was independent of viral replication levels. Combined gene and miRNA expression profiling revealed a dominant B cell disease signature, with extensive intrahepatic production of IgM and IgG in germline configuration exclusively targeting HBcAg with subnanomolar affinities, and complement deposition. Thus, HBV ALF appears to be an anomalous T cell-independent, HBV core-driven B cell disease, which results from the rare and unfortunate encounter between a host with an unusual B cell response and an infecting virus with a highly mutated core antigen.
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Cardoso, Liana Monteiro da Fonseca, Lucio Filgueiras Pacheco Moreira, Marcelo Alves Pinto, Andrea Henriques-Pons, and Luiz Anastácio Alves. "Domino Hepatocyte Transplantation: A Therapeutic Alternative for the Treatment of Acute Liver Failure." Canadian Journal of Gastroenterology and Hepatology 2018 (July 2, 2018): 1–9. http://dx.doi.org/10.1155/2018/2593745.
Full textAbstract:
Background and Aims. Acute liver failure (ALF) is a severe syndrome with an elevated mortality rate, ranging from 40 to 80 %. Currently, liver transplantation is the only definitive treatment for these patients and new therapies aiming to treat ALF include artificial organs implant and stem cells therapy, for example. However, a major limitation of liver donors exists. Living donor liver transplantation (LDLT), split liver transplantation (SLT), and domino liver transplantation (DLT) are some of the available alternatives to treat ALF patients, but these do not reduce the number of patients on waiting lists. Herein, we discuss domino hepatocyte transplantation (DHT) using livers that would not meet transplantation criteria. Methods. We conducted a literature search on PubMed/Medline using acute liver failure, liver transplantation, hepatocyte transplantation, and domino liver transplantation as key words. Results. New sources of biochemically functional hepatocytes and therapeutic treatments, in parallel to organ transplantation, may improve liver injury recovery and decrease mortality rates. Moreover, the literature reports hepatocyte transplantation as a therapeutic alternative for organ shortage. However, a major challenge remains for a wide clinical application of hepatocytes therapy, i.e., the availability of sufficient amounts of cells for transplantation. Ideally, hepatocytes isolated from livers rejected for transplantation may be a promising alternative for this problem. Conclusion. Our review suggests that DHT may be an excellent strategy to increase cell supplies for hepatocyte transplantation.
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Tujios, Shannan, R. Todd Stravitz, and William M. Lee. "Management of Acute Liver Failure: Update 2022." Seminars in Liver Disease 42, no. 03 (August 2022): 362–78. http://dx.doi.org/10.1055/s-0042-1755274.
Full textAbstract:
Abbreviated pathogenesis and clinical course of the acute liver failure syndrome. The pathogenesis and clinical course of the syndrome of acute liver failure (ALF) differs depending upon the etiology of the primary liver injury. In turn, the severity of the liver injury and resulting synthetic failure is often the primary determinant of whether a patient is referred for emergency liver transplantation. Injuries by viral etiologies trigger the innate immune system via pathogen-associated molecular patterns (PAMPs), while toxin-induced (and presumably ischemia-induced) injuries do so via damage-associated molecular patterns (DAMPs). The course of the clinical syndrome further depends upon the relative intensity and composition of cytokine release, resulting in an early proinflammatory phenotype (SIRS) and later compensatory anti-inflammatory response phenotype (CARS). The outcomes of overwhelming immune activation are the systemic (extrahepatic) features of ALF (cardiovascular collapse, cerebral edema, acute kidney injury, respiratory failure, sepsis) which ultimately determine the likelihood of death.Acute liver failure (ALF) continues to carry a high risk of mortality or the need for transplantation despite recent improvements in overall outcomes over the past two decades. Optimal management begins with identifying that liver failure is indeed present and its etiology, since outcomes and the need for transplantation vary widely across the different etiologies. Most causes of ALF can be divided into hyperacute (ischemia and acetaminophen) and subacute types (other etiologies), based on time of evolution of signs and symptoms of liver failure; the former evolve in 3 to 4 days and the latter typically in 2 to 4 weeks. Both involve intense release of cytokines and hepatocellular contents into the circulation with multiorgan effects/consequences.Management involves optimizing fluid balance and cardiovascular support, including the use of continuous renal replacement therapy, vasopressors, and pulmonary ventilation. Early evaluation for liver transplantation is advised particularly for acetaminophen toxicity, which evolves so rapidly that delay is likely to lead to death.Vasopressor support, high-grade hepatic encephalopathy, and unfavorable (subacute) etiologies heighten the need for urgent listing for liver transplantation. Prognostic scores such as Kings Criteria, Model for End-Stage Liver Disease, and the Acute Liver Failure Group prognostic index take these features into account and provide reasonable but imperfect predictive accuracy. Future treatments may include liver support devices and/or agents that improve hepatocyte regeneration.
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Wu, Jian, Yurong Guo, Xuan Lu, Fen Huang, Feifei Lv, Daqiao Wei, Anquan Shang, et al. "Th1/Th2 Cells and Associated Cytokines in Acute Hepatitis E and Related Acute Liver Failure." Journal of Immunology Research 2020 (November 17, 2020): 1–8. http://dx.doi.org/10.1155/2020/6027361.
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Background and Aims. The involvement of cellular immunity in the development of hepatitis E virus (HEV) infection is rare. We aimed to study the roles of viral load and Th cell responses in acute hepatitis E (AHE) and HEV-related acute liver failure (HEV-ALF). Methods. We evaluated viral load and Th1/Th2 cytokine levels in 34 patients with HEV infection, including 17 each with AHE or HEV-ALF. Seventeen healthy controls (HCs) were also included who were negative for anti-HEV IgM and IgG. Results. There was no significant difference in viral load and HEV RNA in the AHE and HEV-ALF groups (both P > 0.05 ). The Th lymphocyte levels (CD3+, CD4+) in the AHE and HEV-ALF groups were significantly higher than those in the HC group (both P < 0.05 ), but there was no significant difference between the AHE and HEV-ALF groups ( P > 0.05 ). Both IFN-γ and IL-10 showed gradual upward trend from the HC group to the AHE (both P < 0.01 ), but IFN-γ showed a sharp downward trend from the AHE group to the HEV-ALF group ( P < 0.01 ) and IL-4 showed gradual upward trend from the AHE group to the HEV-ALF group ( P < 0.01 ).There was no significant difference in Th1 and Th2 cytokines between the HEV RNA(+) group and HEV RNA(-) group (all P > 0.05 ). Th2 bias was observed from the AHE ( ratio = 58.65 ) to HEV-ALF ( ratio = 1.20 ) groups. The level of IFN-γ was associated with the outcome of HEV-ALF patients. Conclusions. HEV viral load was not associated with aggravation of AHE, and the HEV-ALF patients showed significant Th2 bias, which may be involved in the aggravation of AHE.
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Tost, J. R. "Characteristics of acute liver failure (ALF) in spain." Journal of Hepatology 32 (2000): 57. http://dx.doi.org/10.1016/s0168-8278(00)80550-4.
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Patel, Pranav D., Dipen Khanapara, Nader Emami, Kamran Zahid, and Hilary Hertan. "Pseudocirrhosis: A Cause of Acute Liver Failure (ALF)." American Journal of Gastroenterology 112 (October 2017): S1258—S1259. http://dx.doi.org/10.14309/00000434-201710001-02298.
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Ye, Bingjue, Shiwei Chen, Huiting Guo, Weiyang Zheng, Guohua Lou, Xue Liang, Yanning Liu, Cheng Zhou, and Min Zheng. "The Inhibition of Bruton Tyrosine Kinase Alleviates Acute Liver Failure via Downregulation of NLRP3 Inflammasome." Journal of Immunology 209, no. 6 (September 15, 2022): 1156–64. http://dx.doi.org/10.4049/jimmunol.2001323.
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Abstract There is no effective treatment for acute liver failure (ALF) except for an artificial liver support system (ALSS) and liver transplant. Bruton tyrosine kinase (Btk) plays important immunoregulatory roles in the inflammatory diseases, but its possible function in ALF remains to be characterized. In this study, we detected the phosphorylation level of Btk in ALF mouse liver and analyzed the protective effects of Btk inhibitor on survival rate and liver damage in ALF mouse models. We measured the expression levels of various inflammatory cytokines in the ALF mouse liver and primary human monocytes. In addition, we examined the expression of the NLRP3 inflammasome in mouse models with or without Btk inhibition. Clinically, we observed the dynamic changes of Btk expression in PBMCs of ALSS-treated patients. Our results showed that Btk was upregulated significantly in the experimental ALF mouse models and that Btk inhibition alleviated liver injury and reduced the mortality in these models. The protective effect of Btk inhibitors on ALF mice partially depended on the suppression of NLRP3 inflammasome signaling. Clinical investigations revealed that the dynamic changes of Btk expression in PBMCs could predict the effect of ALSS treatment. Our work shows that Btk inhibition is an effective therapeutic strategy for ALF. Moreover, Btk is a useful indicator to predict the therapeutic effect of ALSS on liver failure, which might have great value in clinical practice.
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Himma, Kenneth Einar. "Reply to Burdick: Constraining Physician Discretion." Cambridge Quarterly of Healthcare Ethics 9, no. 2 (April 2000): 280–83. http://dx.doi.org/10.1017/s0963180100222135.
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In “A Critique of UNOS Liver Allocation Policy,” I argued that the UNOS policy of placing acute liver failure patients (ALF patients) above chronic liver failure patients (CLF patients) on the transplant list fails to satisfy the principles of utility and justice that ostensibly guide UNOS allocation policy. Further, I argued that physician discretion in evaluating ALF and CLF patients should be expanded—not constrained. In response, Dr. Burdick attempts to justify the policy constraints on physician discretion on the strength of objective differences between ALF and CLF; as he puts it, “the distinction between acute liver failure and progression of chronic liver disease … is clear in the way brain death is.”
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Tian, Zhen, Yi Chen, Naijuan Yao, Chunhua Hu, Yuchao Wu, Dandan Guo, Jinfeng Liu, et al. "Role of mitophagy regulation by ROS in hepatic stellate cells during acute liver failure." American Journal of Physiology-Gastrointestinal and Liver Physiology 315, no. 3 (September 1, 2018): G374—G384. http://dx.doi.org/10.1152/ajpgi.00032.2018.
Full textAbstract:
Liver sinusoids serve as the first line of defense against extrahepatic stimuli from the intestinal tract. Hepatic stellate cells (HSCs) are pericytes residing in the perisinusoidal space that integrate cytokine-mediated inflammatory responses in the sinusoids and relay these signals to the liver parenchyma. Oxidative stress has been shown to promote inflammation during acute liver failure (ALF). Whether and how oxidative stress is involved in HSC inflammation during ALF remains unclear. Level of systemic oxidative stress is reflected by superoxide dismutase (SOD). Thus, ALF patients were recruited to investigate the correlation between plasma SOD levels and clinical features. Liver tissues were collected from chronic hepatitis patients by biopsy and from ALF patients who had undergone liver transplantation. SOD2 expression and HSCs activation were investigated by immunohistochemistry. Inflammation, mitophagy, and apoptosis were investigated by immunoblot analysis and flow cytometry in HSCs treated with lipopolysaccharide (LPS) and reactive oxygen species (ROS) donors. The plasma SOD level was significantly increased in patients with ALF compared with those with cirrhosis (444.4 ± 23.58 vs. 170.07 ± 3.52 U/ml, P < 0.01) and was positively correlated with the Model for End-Stage Liver Disease-Na score ( R2 = 0.4720, P < 0.01). In vivo observations revealed that SOD2 immunostaining was increased in ALF patients and mice models, and in vitro experiments demonstrated that LPS/ROS promoted inflammation via inhibiting mitophagy. Moreover, the regulation of inflammation was apoptosis independent in HSCs. LPS-induced increases in oxidative stress promote inflammation through inhibiting mitophagy in HSCs during the process of ALF, providing a novel strategy for the treatment of patients with ALF. NEW & NOTEWORTHY Here we demonstrate that the serum superoxide dismutase (SOD) level is significantly increased in patients with acute liver failure (ALF), and, correlated with the Model for End-Stage Liver Disease-Na score, SOD level dropped in the remission stage of ALF. We identify that, in liver tissue from ALF patients and mice models, manganese-dependent SOD was overexpressed, and show lipopolysaccharide/H2O2 inhibits mitophagy via reactive oxygen species in hepatic stellate cells (HSCs). We show that inhibited mitophagy promotes inflammation in HSCs, whereas mitophagy inducer rescues HSCs from lipopolysaccharide-induced inflammation.
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Prueksapraopong, Chattip, Varisa Piriyakitpaiboon, and Dissajee Lumbiganon. "Twin-to-twin transfusion syndrome as a cause of neonatal acute liver failure." Asian Biomedicine 13, no. 4 (March 31, 2020): 163–70. http://dx.doi.org/10.1515/abm-2019-0055.
Full textAbstract:
AbstractBackgroundAcute liver failure (ALF) is a rare condition during neonatal period.ObjectiveTo report a case of recipient twin with fulminant ALF secondary to hydrops fetalis caused by twin-to-twin transfusion syndrome (TTTS).MethodThe patient was admitted to the neonatal intensive care unit (NICU) for respiratory failure requiring mechanical ventilation and fulminant ALF with prolonged international normalized ratio (INR) and elevated liver enzymes with highest aspartate aminotransferase of 4,580 U/L.ResultsLaboratory investigation for secondary causes of liver failure was not revealing. Her liver enzymes and coagulation levels were dramatically normalized as the clinical symptoms of hypervolemia improved within 1 week.ConclusionTTTS can be a possible cause of neonatal ALF. Early detection with proper management of TTTS is important to avoid adverse outcomes. However, pathogenesis of hepatic dysfunction in TTTS is rarely described, and further studies are needed to help understanding the correlation between liver diseases and TTTS.
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Rockstrom, Matthew, Jonathan Rice, Tomio Tran, and Anna Neumeier. "High Volume Plasma Exchange in Acute Liver Failure: A Brief Review." Southwest Journal of Pulmonary and Critical Care 22, no. 5 (May 4, 2021): 102–5. http://dx.doi.org/10.13175/swjpcc009-21.
Full textAbstract:
Acute liver failure (ALF) is characterized by acute liver injury, coagulopathy, and altered mental status. Acetaminophen overdose contributes to almost half the cases of ALF in the United States. In the era of liver transplantation, mortality associated with this condition has improved dramatically. However, many patients are not transplant candidates including many who present with overt suicide attempt from acetaminophen overdose. High volume plasma exchange (HVP) is a novel application of plasma exchange. Prior research has shown that HVP can correct the pathophysiologic derangements underlying ALF. A randomized control trial demonstrated improved transplant-free survival when HVP was added to standard medical therapy. In this case, we examine a patient who presented to the intensive care unit with ALF caused by intentional acetaminophen overdose. She was denied transplant due to overt suicide attempt, was treated with HVP, and made a rapid recovery, eventually discharged to inpatient psychiatry and then home.
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Cauli, Omar, Regina Rodrigo, Jordi Boix, Blanca Piedrafita, Ana Agusti, and Vicente Felipo. "Acute liver failure-induced death of rats is delayed or prevented by blocking NMDA receptors in brain." American Journal of Physiology-Gastrointestinal and Liver Physiology 295, no. 3 (September 2008): G503—G511. http://dx.doi.org/10.1152/ajpgi.00076.2008.
Full textAbstract:
Developing procedures to delay the mechanisms of acute liver failure-induced death would increase patients' survival by allowing time for liver regeneration or to receive a liver for transplantation. Hyperammonemia is a main contributor to brain herniation and mortality in acute liver failure (ALF). Acute ammonia intoxication in rats leads to N-methyl-d-aspartate (NMDA) receptor activation in brain. Blocking these receptors prevents ammonia-induced death. Ammonia-induced activation of NMDA receptors could contribute to ALF-induced death. If this were the case, blocking NMDA receptors could prevent or delay ALF-induced death. The aim of this work was to assess 1) whether ALF leads to NMDA receptors activation in brain in vivo and 2) whether blocking NMDA receptors prevents or delays ALF-induced death of rats. It is shown, by in vivo brain microdialysis, that galactosamine-induced ALF leads to NMDA receptors activation in brain. Blocking NMDA receptors by continuous administration of MK-801 or memantine through miniosmotic pumps affords significant protection against ALF-induced death, increasing the survival time approximately twofold. Also, when liver injury is not 100% lethal (1.5 g/kg galactosamine), blocking NMDA receptors increases the survival rate from 23 to 62%. This supports that blocking NMDA receptors could have therapeutic utility to improve survival of patients with ALF.
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Tetova, Vera B., O. A. Burgasova, V. M. Volkova, and N. M. Belyaeva. "INTERDISCIPLINARY APPROACH TO THE SYNDROME OF ACUTE HEPCENARY FAILURE." Epidemiology and Infectious Diseases 22, no. 3 (June 15, 2017): 144–52. http://dx.doi.org/10.17816/eid40977.
Full textAbstract:
In the review the data concerning an etiopathogenesis and clinical manifestations of the acute liver failure (ALF) and also potential options of alternative treatment are considered: Orthotopic transplantation of liver and modern approaches to patient maintenance. The ALF syndrome, despite the progress in the intensive therapy modes, represents a clinical syndrome with the high mortality rate. In healthy adults, especially in cases aged of up to 30 years ALF syndrome represents a significant intredisciplinary problem in terms of diagnostics and maintenance tactics. The clinical picture is most often presented by the hepatic dysfunction, development of a coagulopathy and change of biochemical indices of the liver function, with the development of encephalopathy and polyorganic insufficiency. The lethality rate in this syndrome reaches 50%. The high mortality rate, severity of the course, etiologic heterogeneity causes the need of the development of standards for the supporting therapy. Thanks to achievements in the field of the intensive therapy and the use of the emergency transplantation of a liver allograft survival indices have considerably been improved in recent years.