Acute Liver Failure Due to Assumed Drug Induced Liver Injury but Lack of Any Validated Causality Algorithm: Evidence by 36 Cohort Reports with 21,709 Cases
-
Department of Internal Medicine II, Division of Gastroenterology and Hepatology, Klinikum Hanau, D-63450 Hanau, Academic Teaching Hospital of the Medical Faculty, Goethe University Frankfurt/Main, Frankfurt/Main, Germany
* Correspondence: Rolf Teschke
Academic Editor: Chirag S. Desai
Special Issue: Diagnostic Requirements Including Algorithms and Biomarkers in Liver Transplantation
Received: January 08, 2025 | Accepted: February 10, 2025 | Published: February 14, 2025
OBM Transplantation 2025, Volume 9, Issue 1, doi:10.21926/obm.transplant.2501234
Recommended citation: Teschke R, Eickhoff A. Acute Liver Failure Due to Assumed Drug Induced Liver Injury but Lack of Any Validated Causality Algorithm: Evidence by 36 Cohort Reports with 21,709 Cases. OBM Transplantation 2025; 9(1): 234; doi:10.21926/obm.transplant.2501234.
© 2025 by the authors. This is an open access article distributed under the conditions of the Creative Commons by Attribution License, which permits unrestricted use, distribution, and reproduction in any medium or format, provided the original work is correctly cited.
Abstract
Liver transplantation (LT) can be the only option for patients with acute liver failure (ALF) where medical approaches are ineffective. Causes of ALF are multiple and commonly easily detectable, but uncertainty remained on the role of drug-induced liver injury (DILI) within the published ALF cohorts. Therefore, an analysis was undertaken to clarify which drugs may have caused the DILI and how the diagnosis of the liver injury was established. Using the PubMed database and Google Science, the search term of acute liver failure combined with drugs provided 36 publications of ALF cohorts, which included 21,709 DILI cases. Whereas non-drug causes were detectable by specific diagnostic biomarkers, the diagnosis of DILI among the ALF cohorts was neglected, as evidenced by the lacking use of a validated diagnostic algorithm like the Roussel Uclaf Causality Assessment Method (RUCAM), best qualified to verify causality for individual drugs or combined drugs. This lack of firm diagnosis leads to a long list of drugs with highly questionable causality of suspected DILI, prevents calculation of incidence or prevalence data of DILI among ALF cohorts, and cannot help find an appropriate therapy for selected cases of drug-induced autoimmune hepatitis (DIAIH) or overdosed N-acetyl-para-aminophenol (APAP) also known as paracetamol, aiming to prevent LT. Under discussion is also the high rate of indeterminate cases of up to 78% among the published cohorts, which confounds any quantitative approach in this setting. In conclusion, there is much room for improvement in future ALF cohorts, requiring the application of validated tools.
Keywords
Liver transplantation; acute liver failure; drug-induced liver injury; RUCAM; Roussel Uclaf Causality Assessment Method; indeterminate causes
1. Introduction
Liver transplantation (LT) is often the ultimate chance for patients with acute liver failure (ALF) where drug cessation and medical therapy have failed. Yet in 2024, reports on ALF were continuously published in Europe [1] and worldwide in countries including China [2], Germany [3], Greece [4], India [5,6], Iran [7], Mexico [8], Pakistan [9], Spain [10], and the US [11,12]. Information on LT and ALF focused on the clinical practice guidelines of the European Association for the Study of the Liver (EASL) [1] and mechanisms leading to ALF, the role of pyroptosis as a form of lytic programmed cell death, and the involvement of damage-associated molecular patterns (DAMPs) [2]. Other details were provided for the epidemiology and etiology [3], the artificial intelligence (AI) used for better outcomes [4], and prognostic models with a focus on management [5]. Promoted were consensus recommendations of the Indian Society of Pediatric Gastroenterology, Hepatology, and Nutrition (ISPGHAN) regarding the diagnosis and management of pediatric acute liver failure [6], the role of circulating lncRNAs HOTTIP and HOTAIR as potential biomarkers in ALF of Crigler-Najjar syndrome [7], and the management update and prognosis [8]. Discussions were expanded on the causes and clinical parameters in acute-on-chronic liver failure [9], a practical update on ALF [10], highlights from the American College of Gastroenterology (ACG) guidelines for acute liver failure [11], and the future of LT [12]. Limited interest was attributed to idiosyncratic drug-induced liver injury (iDILI), its incidence or prevalence, and how the diagnosis was established. For several decades, shortcomings were known for ALF as an outcome of patients with iDILI requiring a liver transplant, with major diagnostic issues of indeterminate causes and lacking validated causality assessment.
This review aims to analyze published reports on ALF cohorts due to DILI regarding causative drugs and the use of a robust, validated causality assessment that may help provide a firm characterization of clinical features and proposals for medical treatment to prevent LT.
2. Search Method and Terms
Using the PubMed database and Google Science, the search term of acute liver failure combined with drugs provided 36 publications of ALF cohorts, which included 21,709 DILI cases. They were analyzed through the use of a validated causality assessment.
3. DILI Types
By convention, two types of DILI are described: the idiosyncratic and the intrinsic one. Both forms traditionally lack overt immune features [13,14,15]. In addition to the non-immune idiosyncratic DILI (iDILI) form, four subtypes of iDILI were identified with auto-immune or immune characteristics found in four cohorts. Accordingly, the first two types refer to the idiosyncratic drug-induced autoimmune hepatitis (DIAIH) [16,17,18,19,20,21] to be differentiated from the classic drug-unrelated idiosyncratic autoimmune hepatitis (AIH) [22] and the human leucocyte antigen (HLA) based idiosyncratic drug-induced autoimmune hepatitis [23,24,25,26]. The third and fourth types consider the anti-cytochrome P450 (CYP) based idiosyncratic drug-induced autoimmune hepatitis [16,18,27,28,29] and the immune-based idiosyncratic drug-induced liver injury associated with Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) [1,30,31,32]. Listed iDILI reports were all assessed for causality using the Roussel Uclaf Causality Assessment Method (RUCAM).
4. RUCAM
RUCAM was published in 1993 as a novel diagnostic algorithm method to assess causality in iDILI, resulting from international consensus meetings with participants known for their expertise in iDILI issues [33]. Among these experts were J. P. Benhamou (France), J. Bircher (Germany), G. Danan (France), W. C. Maddrey (USA), J. Neuberger (UK), F. Orlandi (Italy), N. Tygstrup (Denmark), and H. J. Zimmerman (USA) [33,34]. Using iDILI cases with positive reexposure test results serving as a gold standard, RUCAM was well validated in the course of the internal validation process [34]. In 2016, the updated RUCAM was published, and it is now the preferred algorithm to assess iDILI [13]. International support of RUCAM came from external validation [35,36,37,38,39], including interrater reliability [35,36,37]. RUCAM represents a structured diagnostic algorithm for objective, standardized, and quantitative causality assessment in iDILI cases [13,33] and is a means of assigning points for clinical, biochemical, reexposure, and serologic features and searching for non-drug causes. Summing up the individual scores derived from each key element provides final RUCAM causality gradings: score ≤0, excluded causality; 1–2, unlikely; 3–5, possible; 6–8, probable; and ≥9, highly probable, which reflects the likelihood that the hepatic injury is due to a specific medication [13,33]. RUCAM is applied up to now throughout the world in almost 100,000 iDILI cases [40] and outperforms any other method [13,16] concerning both method quality and case numbers [16]. Its high appreciation may be traced back to being user-friendly and cost-effective, with results available in time and without the need for expert rounds that commonly provide subjective and arbitrary opinions [13,16]. RUCAM helps clarify epidemiology aspects related to iDILI [41,42] and is, with its inventors and users, well, esteemed as outlined by a scientometric investigation [43].
5. Published Reports of Acute Liver Failure by Suspected DILI
There is little valid information on the percentage contribution of DILI cases among study cohorts that included instances of transplantation performed for ALF due to various causatives. Using the PubMed database and Google Science for the search terms of acute liver failure combined with drugs, abundant reports were provided. In addition to verified causatives of the ALF, in many case series, offending agents often remained unknown, making it difficult to give a firm percentage contribution of iDILI. Even worse, inhomogeneity among the study cohorts prevailed due to lumping together iDILI with intrinsic DILI and conventional drugs with non-drugs such as herbal medicines, including traditional Chinese medicine (TCM). Drugs causing assumed DILI with ALF are listed (Table 1) [44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78].
Table 1 Compounds inducing suspected DILI among ALF cohorts.
The current analysis of the 36 published ALF reports and DILI caused by 21,709 drugs and drug combinations as potential causes provides shortcomings (Table 1) [44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79]: (1) with respect to DILI used as term, the inhomogeneity of ALF study cohorts due to lumping iDILI together with intrinsic DILI cases, and if N-acetyl-para-aminophenol (APAP) syn paracetamol as an agent of intrinsic DILI is mentioned, it is often unclear whether DILI is caused by overdose (often) or as iDILI due to recommended dose; (2) it is questionable when a report entitled “Acute liver failure induced by idiosyncratic reaction to drugs” attributes ALF etiology to APAP that causes intrinsic DILI in 46% of the study cohort versus iDILI with a contribution of only 11% [72]; (3) included are also unspecified toxins [49,56] that have nothing to do with DILI; (4) not listed in the Table 1 but in various reports were herbal products including herbal traditional Chinese Medicines (TCM) or herbal dietary supplements [7,49,58,59], all of which can cause herb induced liver injury (HILI) rather than DILI; (5) the percentage contribution of ALF cases due to DILI among the ALF cohort remains clouded because high rates of unknown causes were found in all reports with values of up to 70% [74] or 78% [60]; even worse (6) the diagnosis of iDILI cases was not verified by using the RUCAM for individual or combined drugs implicated in DILI, ignoring the fact that many cases of suspected DILI were not due to drugs but must be attributed to alternative non-drug causes [80,81]; (7) as the 36 reports considered ALF cases with respect on all potential causes, there are no specific data on how many patients with ALF due to DILI finally received a liver transplant or and/or died; (8) there was no stratification regarding non-immune iDILI, which corresponds only partially to steroid treatment, and DIAIH, which as autoimmune triggered disorder fully respond to steroid treatments preventing LT in most cases; and finally (9) due to the above mentioned shortcomings of case analysis there are no appropriate data available to define exact epidemiology figures of DILI among the ALF cohort focusing on incidence, which reflects the number of new cases of a given medical condition in a population within a specified period of time, while prevalence considers the proportion of a particular population found to be affected by a medical condition at a specific time.
6. Future Perspectives
Future cohort studies on patients with ALF requiring LT should include detailed information on iDILI to be different from intrinsic DILI due to overdosing APAP as opposed to iDILI due to APAP intake at regular doses. Essential is the mandatory use of RUCAM, now the updated RUCAM of 2016, to rule out any alternative causes of the liver injury that may confound the diagnosis of iDILI; Appreciated are reports that include data on natural course with complete remission, need of a LT, or death.
7. Conclusion
ALF cohorts commonly provide good data on causatives like hepatitis viruses through specific serum antibody and RNA measurements or genetic liver diseases such as Wilson disease or hemochromatosis through particular tests. Still, such careful analyses are largely missing when the question comes up whether the injury is caused by a drug. In these cases, the use of RUCAM helps establish the diagnosis of DILI and excludes alternative, non-drug causes commonly viewed as confounders in DILI cohorts. Established therapeutic approaches are available for patients with DIAIH where steroids are effectively applied for the immunology disruption and for patients with APAP overdose where N-acetylcysteine (NAC) is effectively applied. As a result, only an exact diagnosis of DILI can provide appropriate medical therapy in selected cases with the chance of preventing the need for a LT or death.
Author Contributions
RT and AE developed the outline of this invited article; AE provided the literature and the draft of Table 1; RT wrote the first draft, which was edited by AE. All authors agreed to the final version to be submitted.
Competing Interests
None of the authors have a conflict of interest regarding this article.
References
- European Association for the Study of the Liver. EASL clinical practice guidelines on liver transplantation. J Hepatol. 2024; 81: 1040-1086. [CrossRef]
- An R, Wang JL. Acute liver failure: A clinically severe syndrome characterized by intricate mechanisms. World J Hepatol. 2024; 16: 1067-1069. [CrossRef]
- Altinbas A, Pospiech J, Canbay A. Acute liver failure. Hepatology. 2024. In press.
- Avramidou E, Todorov D, Katsanos G, Antoniadis N, Kofinas A, Vasileiadou S, et al. AI innovations in liver transplantation: From big data to better outcome. Livers. 2025. In press.
- Maiwall R, Kulkarni AV, Arab JP, Piano S. Acute liver failure. Lancet. 2024; 404: 789-802. [CrossRef]
- Lal BB, Khanna R, Sood V, Alam S, Nagral A, Ravindranath A, et al. Diagnosis and management of pediatric acute liver failure: Consensus recommendations of the Indian society of pediatric gastroenterology, hepatology, and nutrition (ISPGHAN). Hepatol Int. 2024; 18: 1343-1381. [CrossRef]
- Motazedian N, Mokhtari M, Azarpira N, Falamarzi K, Mohammadi M, Dehghani SM, et al. Circulating lncRNAs HOTTIP and HOTAIR as potential biomarkers in Crigler-Najjar syndrome: A preliminary report from shiraz liver transplant research center. OBM Transplant. 2024; 8: 217. [CrossRef]
- Martínez-Martínez LM, Rosales-Sotomayor G, Jasso-Baltazar EA, Torres-Díaz JA, Aguirre-Villarreal D, de León IH, et al. Acute liver failure: Management update and prognosis. Rev Gastroenterol Mex. 2024; 89: 404-417. [CrossRef]
- Hafsa F, Chaudary ZI, Tariq O, Riaz Z, Shehzad A, Jamil MI, et al. Acute-on-chronic liver failure: Causes, clinical parameters, and predictors of mortality. Cureus. 2024; 16: e52690. [CrossRef]
- Fernandez J, Bassegoda O, Toapanta D, Bernal W. Acute liver failure: A practical update. JHEP Rep. 2024; 6: 101131. [CrossRef]
- Shingina A. Highlights from the ACG guidelines for acute liver failure. Gastroenterol Hepatol. 2024; 20: 61-63.
- Feng S, Roll GR, Rouhani FJ, Fueyo AS. The future of liver transplantation. Hepatology. 2024; 80: 674-697. [CrossRef]
- Danan G, Teschke R. RUCAM in drug and herb induced liver injury: The update. Int J Mol Sci. 2015; 17: 14. [CrossRef]
- Hosack T, Damry D, Biswas S. Drug-induced liver injury: A comprehensive review. Therap Adv Gastroenterol. 2023; 16. doi: 10.1177/17562848231163410. [CrossRef]
- Clinton JW, Kiparizoska S, Aggarwal S, Woo S, Davis W, Lewis JH. Drug-induced liver injury: Highlights and controversies in the recent literature. Drug Saf. 2021; 44: 1125-1149. [CrossRef]
- Teschke R, Danan G. Advances in idiosyncratic drug-induced liver injury issues: New clinical and mechanistic analysis due to Roussel Uclaf causality assessment method use. Int J Mol Sci. 2023; 24: 10855. [CrossRef]
- Teschke R, Danan G. Idiosyncratic DILI and RUCAM under one hat: The global view. Livers. 2023; 3: 397-433. [CrossRef]
- Teschke R. Molecular idiosyncratic toxicology of drugs in the human liver compared with animals: Basic considerations. Int J Mol Sci. 2023; 24: 6663. [CrossRef]
- Chung Y, Morrison M, Zen Y, Heneghan MA. Defining characteristics and long‐term prognosis of drug‐induced autoimmune‐like hepatitis: A retrospective cohort study. U Eur Gastroenterol J. 2024; 12: 66-75. [CrossRef]
- Licata A, Maida M, Cabibi D, Butera G, Macaluso FS, Alessi N, et al. Clinical features and outcomes of patients with drug-induced autoimmune hepatitis: A retrospective cohort study. Dig Liver Dis. 2014; 46: 1116-1120. [CrossRef]
- Martínez‐Casas OY, Díaz‐Ramírez GS, Marín‐Zuluaga JI, Muñoz‐Maya O, Santos O, Donado‐Gómez JH, et al. Differential characteristics in drug‐induced autoimmune hepatitis. JGH Open. 2018; 2: 97-104. [CrossRef]
- Hennes EM, Zeniya M, Czaja AJ, Parés A, Dalekos GN, Krawitt EL, et al. Simplified criteria for the diagnosis of autoimmune hepatitis. Hepatology. 2008; 48: 169-176. [CrossRef]
- Teschke R, Danan G. Human leucocyte antigen genetics in idiosyncratic drug-induced liver injury with evidence based on the Roussel Uclaf causality assessment method. Medicines. 2024; 11: 9. [CrossRef]
- Teschke R. Idiosyncratic hepatocellular drug-induced liver injury by flucloxacillin with evidence based on Roussel Uclaf causality assessment method and HLA B* 57: 01 genotype: From metabolic CYP 3A4/3A7 to immune mechanisms. Biomedicines. 2024; 12: 2208. [CrossRef]
- Daly AK, Donaldson PT, Bhatnagar P, Shen Y, Pe'er I, Floratos A, et al. HLA-B* 5701 genotype is a major determinant of drug-induced liver injury due to flucloxacillin. Nat Genet. 2009; 41: 816-819. [CrossRef]
- Nicoletti P, Aithal GP, Chamberlain TC, Coulthard S, Alshabeeb M, Grove JI, et al. Drug‐induced liver injury due to flucloxacillin: Relevance of multiple human leukocyte antigen alleles. Clin Pharmacol Ther. 2019; 106: 245-253. [CrossRef]
- Spracklin DK, Hankins DC, Fisher JM, Thummel KE, Kharasch ED. Cytochrome P450 2E1 is the principal catalyst of human oxidative halothane metabolism in vitro. J Pharmacol Exp Ther. 1997; 281: 400-411. [CrossRef]
- Nicoll A, Moore D, Njoku D, Hockey B. Repeated exposure to modern volatile anaesthetics may cause chronic hepatitis as well as acute liver injury. Case Rep. 2012; 2012. doi: 10.1136/bcr-2012-006543. [CrossRef]
- Bourdi M, Chen W, Peter RM, Martin JL, Buters JT, Nelson SD, et al. Human cytochrome P450 2E1 is a major autoantigen associated with halothane hepatitis. Chem Res Toxicol. 1996; 9: 1159-1166. [CrossRef]
- Teschke R. Liver injury in immune Stevens-Johnson syndrome and toxic epidermal necrolysis: Five new classification types. J Clin Trans Hepatol. 2025. In press. [CrossRef]
- Devarbhavi H, Sridhar A, Kurien SS, Gowda V, Kothari K, Patil M, et al. Clinical and liver biochemistry phenotypes, and outcome in 133 patients with anti-seizure drug-induced liver injury. Dig Dis Sci. 2023; 68: 2099-2106. [CrossRef]
- Zhang Z, Li S, Zhang Z, Yu K, Duan X, Long L, et al. Clinical features, risk factors, and prognostic markers of drug-induced liver injury in patients with Stevens-Johnson syndrome/toxic epidermal necrolysis. Indian J Dermatol. 2020; 65: 274-278. [CrossRef]
- Danan G, Benichou C. Causality assessment of adverse reactions to drugs-I. A novel method based on the conclusions of international consensus meetings: Application to drug-induced liver injuries. J Clin Epidemiol. 1993; 46: 1323-1330. [CrossRef]
- Benichou C, Danan G, Flahault A. Causality assessment of adverse reactions to drugs-II. An original model for validation of drug causality assessment methods: Case reports with positive rechallenge. J Clin Epidemiol. 1993; 46: 1331-1336. [CrossRef]
- Björnsson E, Olsson R. Outcome and prognostic markers in severe drug‐induced liver disease. Hepatology. 2005; 42: 481-489. [CrossRef]
- Naseralallah LM, Aboujabal BA, Geryo NM, Al Boinin A, Al Hattab F, Akbar R, et al. The determination of causality of drug induced liver injury in patients with COVID-19 clinical syndrome. PLoS One. 2022; 17: e0268705. [CrossRef]
- Bishop B, Hannah N, Doyle A, Amico F, Hockey B, Moore D, et al. A prospective study of the incidence of drug‐induced liver injury by the modern volatile anaesthetics sevoflurane and desflurane. Aliment Pharmacol Ther. 2019; 49: 940-951. [CrossRef]
- Lunardelli MJ, Becker MW, Blatt CR. Tradução e validação de algoritmo para identificação de lesão hepática induzida por medicamentos. Rev Cont Saúde. 2020; 20: 226-235. [CrossRef]
- Lunardelli MM, Becker MW, Ortiz GX, Blatt CR. Drug-induced liver injury causality assessment data from a crosssectional study in Brazil: A call for the use of updated RUCAM in hospital pharmacy. Rev Bras Farm Hosp Serv Saud. 2022; 13: 0791. [CrossRef]
- Teschke R, Danan G. Worldwide use of RUCAM for causality assessment in 81,856 idiosyncratic DILI and 14,029 HILI cases published 1993-mid 2020: A comprehensive analysis. Medicines. 2020; 7: 62. [CrossRef]
- Kobayashi T, Iwaki M, Nogami A, Yoneda M. Epidemiology and management of drug-induced liver injury: Importance of the updated RUCAM. J Clin Transl Hepatol. 2023; 11: 1239-1245. [CrossRef]
- Chen Y, Wang C, Yang H, Huang P, Shi J, Tong Y, et al. Epidemiology of drug‐and herb‐induced liver injury assessed for causality using the updated RUCAM in two hospitals from China. Biomed Res Int. 2021; 2021: 8894498. [CrossRef]
- Ke L, Lu C, Shen R, Lu T, Ma B, Hua Y. Knowledge mapping of drug-induced liver injury: A scientometric investigation (2010-2019). Front Pharmacol. 2020; 11: 842. [CrossRef]
- O'Grady JG, Alexander GJ, Hayllar KM, Williams R. Early indicators of prognosis in fulminant hepatic failure. Gastroenterology. 1989; 97: 439-445. [CrossRef]
- Daas M, Plevak DJ, Wijdicks EF, Rakela J, Wiesner RH, Piepgras DG, et al. Acute liver failure: Results of a 5-year clinical protocol. Liver Transplant. 1995; 1: 210-219. [CrossRef]
- Shakil AO, Kramer D, Mazariegos GV, Fung JJ, Rakela J. Acute liver failure: Clinical features, outcomeanalysis, and applicability of prognostic criteria. Liver Transplant. 2000; 6: 163-169. [CrossRef]
- Kato Y, Nakata K, Omagari K, Kusumoto Y, Mori I, Furukawa R, et al. Clinical features of fulminant hepatitis in Nagasaki Prefecture, Japan. Intern Med. 2001; 40: 5-8. [CrossRef]
- Ostapowicz G, Fontana RJ, Schiødt FV, Larson A, Davern TJ, Han SH, et al. Results of a prospective study of acute liver failure at 17 tertiary care centers in the United States. Ann Intern Med. 2002; 137: 947-954. [CrossRef]
- Tessier G, Villeneuve E, Villeneuve JP. Etiology and outcome of acute liver failure: Experience from a liver transplantation centre in Montreal. Can J Gastroenterol. 2002; 16: 672-676. [CrossRef]
- Gow PJ, Jones RM, Dobson JL, Angus PW. Etiology and outcome of fulminant hepatic failure managed at an Australian liver transplant unit. J Gastroenterol Hepatol. 2004; 19: 154-159. [CrossRef]
- Wigg AJ, Gunson BK, Mutimer DJ. Outcomes following liver transplantation for seronegative acute liver failure: Experience during a 12‐year period with more than 100 patients. Liver Transplant. 2005; 11: 27-34. [CrossRef]
- Escorsell À, Mas A, de la Mata M, Spanish Group for the Study of Acute Liver Failure. Acute liver failure in Spain: Analysis of 267 cases. Liver Transplant. 2007; 13: 1389-1395. [CrossRef]
- Mudawi HM, Yousif BA. Fulminant hepatic failure in an African setting: Etiology, clinical course, and predictors of mortality. Dig Dis Sci. 2007; 52: 3266-3269. [CrossRef]
- Wei G, Bergquist A, Broomé U, Lindgren S, Wallerstedt S, Almer S, et al. Acute liver failure in Sweden: Etiology and outcome. J Intern Med. 2007; 262: 393-401. [CrossRef]
- Adukauskienė D, Dockienė I, Naginienė R, Kėvelaitis E, Pundzius J, Kupčinskas L. Acute liver failure in Lithuania. Medicina. 2008; 44: 536-540. [CrossRef]
- Bhatia V, Singhal A, Panda SK, Acharya SK. A 20‐year single‐center experience with acute liver failure during pregnancy: Is the prognosis really worse? Hepatology. 2008; 48: 1577-1585. [CrossRef]
- Hadem J, Stiefel P, Bahr MJ, Tillmann HL, Rifai K, Klempnauer J, et al. Prognostic implications of lactate, bilirubin, and etiology in German patients with acute liver failure. Clin Gastroenterol Hepatol. 2008; 6: 339-345. [CrossRef]
- Lee WM, Squires Jr RH, Nyberg SL, Doo E, Hoofnagle JH. Acute liver failure: Summary of a workshop. Hepatology. 2008; 47: 1401-1415. [CrossRef]
- Marudanayagam R, Shanmugam V, Gunson B, Mirza DF, Mayer D, Buckels J, et al. Aetiology and outcome of acute liver failure. HPB. 2009; 11: 429-434. [CrossRef]
- Oketani M, Ido A, Tsubouchi H. Changing etiologies and outcomes of acute liver failure: A perspective from Japan. J Gastroenterol Hepatol. 2011; 26: 65-71. [CrossRef]
- Bariş Z, Saltik Temızel IN, Uslu N, Usta Y, Demır H, Gürakan F, et al. Acute liver failure in children: 20-year experience. Turk J Gastroenterol. 2012; 23: 127-134. [CrossRef]
- Germani G, Theocharidou E, Adam R, Karam V, Wendon J, O’Grady J, et al. Liver transplantation for acute liver failure in Europe: Outcomes over 20 years from the ELTR database. J Hepatol. 2012; 57: 288-296. [CrossRef]
- Lee WM. Acute liver failure. Semin Respir Crit Care Med. 2012; 33: 36-45. [CrossRef]
- Mendizabal M, Marciano S, Videla MG, Anders M, Zerega A, Balderramo DC, et al. Changing etiologies and outcomes of acute liver failure: Perspectives from 6 transplant centers in Argentina. Liver Transplant. 2014; 20: 483-489. [CrossRef]
- Bernal W, Lee WM, Wendon J, Larsen FS, Williams R. Acute liver failure: A curable disease by 2024? J Hepatol. 2015; 62: S112-S120. [CrossRef]
- Kathemann S, Bechmann LP, Sowa JP, Manka P, Dechêne A, Gerner P, Let al. Etiology, outcome and prognostic factors of childhood acute liver failure in a German single center. Ann Hepatol. 2015; 14: 722-728. [CrossRef]
- Donnelly MC, Davidson JS, Martin K, Baird A, Hayes PC, Simpson KJ. Acute liver failure in Scotland: Changes in aetiology and outcomes over time (the Scottish Look-Back study). Aliment Pharmacol Ther. 2017; 45: 833-843. [CrossRef]
- Moini M, Pahlevan-Sabagh MR, Dehghani SM. Acute liver failure, etiology, and outcome: An experience in a referral liver transplant venter. Hepat Mon. 2017; 17: e14086. [CrossRef]
- Somasekar S, Lee D, Rule J, Naccache SN, Stone M, Busch MP, et al. Viral surveillance in serum samples from patients with acute liver failure by metagenomic next-generation sequencing. Clin Infect Dis. 2017; 65: 1477-1485. [CrossRef]
- Ganger DR, Rule J, Rakela J, Bass N, Reuben A, Stravitz RT, et al. Acute liver failure of indeterminate etiology: A comprehensive systematic approach by an expert committee to establish causality. Off J Am Coll Gastroenterol. 2018; 113: 1319. [CrossRef]
- Tujios SR, Lee WM. Acute liver failure induced by idiosyncratic reaction to drugs: Challenges in diagnosis and therapy. Liver Int. 2018; 38: 6-14. [CrossRef]
- Hey P, Hanrahan TP, Sinclair M, Testro AG, Angus PW, Peterson A, et al. Epidemiology and outcomes of acute liver failure in Australia. World J Hepatol. 2019; 11: 586-595. [CrossRef]
- Nabi T, Rafiq N, Arifa QA. Etiological profile and clinical characteristics in fulminant hepatic failure in North India. Int J Community Med Public Health. 2019; 6: 1639-1644. [CrossRef]
- Thanapirom K, Treeprasertsuk S, Soonthornworasiri N, Poovorawan K, Chaiteerakij R, Komolmit P, et al. The incidence, etiologies, outcomes, and predictors of mortality of acute liver failure in Thailand: A population-base study. BMC Gastroenterol. 2019; 19: 18. [CrossRef]
- Amoroso P, Buonocore S, Lettieri G, Pesce G, Pierri P, De Sena R, et al. Changing epidemiology of acute liver failure in Italy: A single-center experience over 25 years. Minerva Med. 2020; 111: 330-336. [CrossRef]
- Chiou FK, Logarajah V, Ho CW, Goh LS, Karthik SV, Aw MM, et al. Demographics, aetiology and outcome of paediatric acute liver failure in Singapore. Singapore Med J. 2022; 63: 659-666. [CrossRef]
- Patel PV, Livingston S, Rakela JL, Stravitz RT, Reuben A, Bass NM, et al. Indeterminate etiology of acute liver failure in North America: Less common, still grave prognosis. Clin Transplant. 2023; 37: e15128. [CrossRef]
- Stravitz RT, Fontana RJ, Karvellas C, Durkalski V, McGuire B, Rule JA, et al. Future directions in acute liver failure. Hepatology. 2023; 78: 1266-1289. [CrossRef]
- Amaris NR, Marenco-Flores A, Barba R, Rubio-Cruz D, Medina-Morales E, Goyes D, et al. Acute liver failure etiology determines long-term outcomes in patients undergoing liver transplantation: An analysis of the UNOS database. J Clin Med. 2024; 13: 6642. [CrossRef]
- Teschke R, Frenzel C, Wolff A, Eickhoff A, Schulze J. Drug induced liver injury: Accuracy of diagnosis in published reports. Ann Hepatol. 2014; 13: 248-255. [CrossRef]
- Teschke R, Danan G. Drug induced liver injury with analysis of alternative causes as confounding variables. Br J Clin Pharmacol. 2018; 84: 1467-1477. [CrossRef]