Cited by 19Drug-Induced Hepatotoxicity and ProtectionPharmacovigilance and Adverse Drug ReactionsLiver physiology and pathology

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index; none of the 126 sources its claims cite is checked for support yet.

Drug-induced liver injury. Part I: Classification, diagnosis and treatment

Open access
Kozielewicz, Dorota M., Stalke, Piotr, Skrzypek, Julita·2025·Clinical and Experimental Hepatology

Abstract

Drug-induced liver injury (DILI) is a growing clinical problem. Antibiotics remain the most common cause of DILI in Europe. Their clinical spectrum is very broad, from asymptomatic to acute liver failure. Currently, DILI is categorized as hepatocellular (R ≥ 5), cholestatic (R ≤ 2) or mixed (R = 2-5) injury based on the serum alanine aminotransferase (ALT)/alkaline phosphatase (ALP) ratio. DILI is a diagnosis of exclusion and requires a wide differential diagnosis. The most important step in management is discontinuation of the drug suspected of causing liver damage. The list of specific antidotes that eliminate the effects of hepatotoxins is unfortunately very short. In symptomatic treatment, glucocorticosteroids and ursodeoxycholic acid have been used in selected cases. Liver transplantation is an optional treatment in patients with acute liver failure.

Overview

AI snapshot

Written from the paper’s full text.

TL;DR

This review summarizes drug-induced liver injury (DILI) classification, diagnosis, and treatment, emphasizing that DILI is a diagnosis of exclusion and that prompt discontinuation of the suspected drug is the key management step. It outlines biochemical R-ratio categorization, causality assessment tools, histologic patterns, and the limited specific antidotes available.

Key findings

DILI is categorized by the serum ALT/ALP R ratio as hepatocellular (R ≥ 5), cholestatic (R ≤ 2), or mixed (R = 2–5); severity is classified by the International DILI Expert Working Group from mild (ALT ≥ 5 or ALP ≥ 2 and TBL < 2× ULN) to fatal/liver transplantation. Antibiotics remain the most common cause of DILI in Europe, with amoxicillin-clavulanate first, followed by antituberculosis drugs, NSAIDs, immunosuppressants, and other antibiotics; more than 1,100 substances with potential hepatotoxic effects are known, and idiosyncratic DILI occurs in 1 in 1,000 to 1 in 1,000,000 exposed individuals. Management centers on prompt drug discontinuation; specific antidotes are few, including N-acetylcysteine for acetaminophen poisoning (total 300 mg/kg over 24 hours), cholestyramine 4 g every 6–8 hours for 2 weeks for persistent cholestasis, L-carnitine 100 mg/kg IV then 15 mg/kg every 8 hours for valproate-induced hyperammonemia, defibrotide 6.25 mg/kg every 6 hours for severe sinusoidal obstruction syndrome, and ursodeoxycholic acid 10–15 mg/kg. Genetic risk factors include PTPN22 rs2476601 (OR 1.4 overall; amoxicillin-clavulanate in Europeans OR 1.62, 95% CI 1.32–1.98, allele frequency 13.3%) and specific HLA alleles such as HLA-B*57:01 for flucloxacillin, HLA-B*35:02 for minocycline, and HLA-A*33:01 for terbinafine.

Methods

Review article synthesizing prior literature, clinical guidelines, and registry data on DILI classification, diagnosis, and treatment. No primary study design, sample, or statistical analysis is reported. The text describes diagnostic and management approaches, including biochemical R-ratio categorization, causality assessment tools (RUCAM, CDS, DDW-J, RECAM), liver imaging, elastography, biopsy, genetic testing, and antidotal/supportive therapies.

Limitations

The paper states that despite ongoing research, there are still no diagnostic or prognostic biomarkers for DILI; it also notes that RECAM has been tested only in the United States and Spain and has not been used in patients with liver damage caused by herbs and dietary supplements, and that it appears too early to recommend elastography for monitoring drug hepatotoxicity. Evident from the text: as a review, it reports no primary data, sample size, or systematic search strategy, inclusion criteria, or quality appraisal, so conclusions rely on cited literature and guidelines. The article does not include a formal limitations section.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.5114/ceh.2025.148329

Cites

1 of 1 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Verification

Claims the paper makes

0 of 126 cited sources checked · 0 supported · 0 flagged

  • Premisecitation

    Some cases of DILI are due to direct reaction, which is predictable, dose-dependent and occurs in nearly all exposed individuals if a threshold dose or duration is exceeded.

    “Some cases of DILI are due to direct reaction, which is predictable, dose-dependent and occurs in nearly all exposed individuals if a threshold dose or duration is exceeded.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [7] Björnsson HK, Björnsson ES. Drug-induced liver injury: Pathogenesis, epidemiology, clinical features, and practical management. Eur J Intern Med 2022; 97: 26- 31. 34772600 source
    • cites [8] Fontana RJ, Liou I, Reuben A, et al. AASLD practice guidance on drug, herbal, and dietary supplement – induced liver injury. Hepatology 2023; 77: 1036- 1065. 35899384 PMC9936988 source
  • Premisecitation

    Proper dose selection can prevent direct hepatotoxicity.

    “Proper dose selection can prevent their development [7, 8].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [7] Björnsson HK, Björnsson ES. Drug-induced liver injury: Pathogenesis, epidemiology, clinical features, and practical management. Eur J Intern Med 2022; 97: 26- 31. 34772600 source
    • cites [8] Fontana RJ, Liou I, Reuben A, et al. AASLD practice guidance on drug, herbal, and dietary supplement – induced liver injury. Hepatology 2023; 77: 1036- 1065. 35899384 PMC9936988 source
  • Premisecitation

    Most DILIs are idiosyncratic.

    “Most DILIs are idiosyncratic.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [7] Björnsson HK, Björnsson ES. Drug-induced liver injury: Pathogenesis, epidemiology, clinical features, and practical management. Eur J Intern Med 2022; 97: 26- 31. 34772600 source
    • cites [8] Fontana RJ, Liou I, Reuben A, et al. AASLD practice guidance on drug, herbal, and dietary supplement – induced liver injury. Hepatology 2023; 77: 1036- 1065. 35899384 PMC9936988 source
  • Premisecitation

    Conventional drugs remain the most common cause of DILI in Europe and North America.

    “Conventional drugs remain the most common cause of DILI in Europe and North America.”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [3] Chalasani N, Bonkovsky HL, Fontana R, et al. Features and outcomes of 899 patients with drug-induced liver injury: The DILIN prospective study. Gastroenterology 2015; 148: 1340- 1352.e7. 25754159 PMC4446235 source
    • cites [4] Björnsson ES, Bergmann OM, Björnsson HK, et al. Incidence, presentation, and outcomes in patients with drug-induced liver injury in the general population of Iceland. Gastroenterology 2013; 144: 1419- 1425, 1425.e1-3; quiz e19-20. 23419359 source
    • cites [5] Hayashi PH, Rockey DC, Fontana RJ, et al. Death and liver transplantation within 2 years of onset of drug-induced liver injury. Hepatology 2017; 66: 1275- 1285. 28543844 PMC5605419 source
  • Premisecitation

    In Spain and Germany, antibiotics or NSAIDs appear to be more common causes of ALF than acetaminophen.

    “In Spain and Germany, other drugs, such as antibiotics or non-steroidal anti-inflammatory drugs, appear to be more common causes of ALF [6].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [6] Devarbhavi H, Asrani SK, Arab JP, et al. Global burden of liver disease: 2023 update. J Hepatol 2023; 79: 516- 537. 36990226 source
  • Probably not a substantial claim. 11
  • It may state two separate claims as one. 25
  • Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.

    Premisecitation

    DILI is one of the most common drug side effects and a significant cause of acute hepatitis and acute liver failure worldwide.

    “Worldwide, drug-induced liver injury (DILI) is one of the most common drug side effects and significant causes of acute hepatitis and acute liver failure (ALF) [1].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [1] Hu PH, Xie WF. Corticosteroid therapy in drug-induced liver injury: Pros and cons. J Dig Dis 2019; 20: 122- 126. 30582289
  • Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.

    Premisecitation

    The drugs following amoxicillin-clavulanate as common causes of DILI include antituberculosis drugs (isoniazid, pyrazinamide, rifampicin), NSAIDs (diclofenac, ibuprofen), immunosuppressants (azathioprine, infliximab), and other antibiotics (nitrofurantoin, minocycline, azithromycin, levofloxacin).

    “It is followed by antituberculosis drugs (isoniazid, pyrazinamide, rifampicin), nonsteroidal antiinflammatory drugs (diclofenac, ibuprofen), immunosuppressants (azathioprine, infliximab) and other antibiotics (nitrofurantoin, minocycline, azithromycin, levofloxacin) [3-5].”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [3] Chalasani N, Bonkovsky HL, Fontana R, et al. Features and outcomes of 899 patients with drug-induced liver injury: The DILIN prospective study. Gastroenterology 2015; 148: 1340- 1352.e7. 25754159 PMC4446235 source
    • cites [4] Björnsson ES, Bergmann OM, Björnsson HK, et al. Incidence, presentation, and outcomes in patients with drug-induced liver injury in the general population of Iceland. Gastroenterology 2013; 144: 1419- 1425, 1425.e1-3; quiz e19-20. 23419359 source
    • cites [5] Hayashi PH, Rockey DC, Fontana RJ, et al. Death and liver transplantation within 2 years of onset of drug-induced liver injury. Hepatology 2017; 66: 1275- 1285. 28543844 PMC5605419 source
  • It may state two separate claims as one.

    Premisecitation

    Direct hepatotoxicity symptoms appear quickly, within hours or days after exposure, and their severity depends on the drug dose taken.

    “Symptoms appear quickly, within hours or days after exposure, and their severity depends on the drug dose taken.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [7] Björnsson HK, Björnsson ES. Drug-induced liver injury: Pathogenesis, epidemiology, clinical features, and practical management. Eur J Intern Med 2022; 97: 26- 31. 34772600 source
    • cites [8] Fontana RJ, Liou I, Reuben A, et al. AASLD practice guidance on drug, herbal, and dietary supplement – induced liver injury. Hepatology 2023; 77: 1036- 1065. 35899384 PMC9936988 source
  • Probably not a substantial claim. It may state two separate claims as one.

    Premisecitation

    The biochemical pattern of DILI is based on increased activity of aminotransferases and ALP, and can be categorized as primarily hepatocellular (serum ALT, AST activity at least 5× ULN or R ratio above 5), cholestatic (ALP activity at least twice the ULN or R ratio less than 2), or mixed (R ratio between 2 and 5).

    “The biochemical pattern of DILI is based on increased activity of aminotransferases and ALP, and in general it can be categorized as primarily hepatocellular (serum ALT, AST activity at least 5× ULN or R ratio above 5), cholestatic (ALP activity at least twice the ULN or R ratio less than 2), or mixed (R ratio between 2 and 5).”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [10] Danan G, Benichou C. Causality assessment of adverse reactions to drugs. Part 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. 8229110 source
    • cites [11] Aithal GP, Watkins PB, Andrade RJ, et al. Case definition and phenotype standardization in drug-induced liver injury. Clin Pharmacol Ther 2011; 89: 806- 815. 21544079 source
  • It may state two separate claims as one.

    Premisecitation

    Indirect DILI reactions are generally independent of the dose of drug administered and have a latency of weeks to months with varying clinical manifestations.

    “Like idiosyncratic DILI, indirect reactions are generally independent of the dose of drug administered and have a latency of weeks to months with varying clinical manifestations [7-9].”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [7] Björnsson HK, Björnsson ES. Drug-induced liver injury: Pathogenesis, epidemiology, clinical features, and practical management. Eur J Intern Med 2022; 97: 26- 31. 34772600 source
    • cites [8] Fontana RJ, Liou I, Reuben A, et al. AASLD practice guidance on drug, herbal, and dietary supplement – induced liver injury. Hepatology 2023; 77: 1036- 1065. 35899384 PMC9936988 source
    • cites [9] Hoofnagle JH, Björnsson ES. Drug-induced liver injury – types and phenotypes. N Engl J Med 2019; 381: 264- 273. 31314970 source
  • It may state two separate claims as one.

    Premisecitation

    Idiosyncratic DILI is unpredictable, largely dose-independent, and symptoms may appear after a long latency period.

    “They are unpredictable, largely dose-independent, and symptoms may appear after a long latency period [7, 8].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [7] Björnsson HK, Björnsson ES. Drug-induced liver injury: Pathogenesis, epidemiology, clinical features, and practical management. Eur J Intern Med 2022; 97: 26- 31. 34772600 source
    • cites [8] Fontana RJ, Liou I, Reuben A, et al. AASLD practice guidance on drug, herbal, and dietary supplement – induced liver injury. Hepatology 2023; 77: 1036- 1065. 35899384 PMC9936988 source
  • Probably not a substantial claim.

    Interpretationreasoning

    The biochemical characterization of DILI may be helpful in managing patients' therapy, including the decision about hospitalization.

    “The biochemical characterization of DILI may be helpful in managing patients’ therapy, including the decision about hospitalization.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Premisecitation

    The third, recently described, mechanism of DILI is indirect; it arises when the biological action of a drug affects the host immune system, leading to a secondary form of liver injury.

    “The third, recently described, mechanism of DILI has been defined as indirect. It arises when the biological action of a drug affects the host immune system, leading to a secondary form of liver injury.”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [7] Björnsson HK, Björnsson ES. Drug-induced liver injury: Pathogenesis, epidemiology, clinical features, and practical management. Eur J Intern Med 2022; 97: 26- 31. 34772600 source
    • cites [8] Fontana RJ, Liou I, Reuben A, et al. AASLD practice guidance on drug, herbal, and dietary supplement – induced liver injury. Hepatology 2023; 77: 1036- 1065. 35899384 PMC9936988 source
    • cites [9] Hoofnagle JH, Björnsson ES. Drug-induced liver injury – types and phenotypes. N Engl J Med 2019; 381: 264- 273. 31314970 source
  • It may state two separate claims as one.

    Premisecitation

    A higher degree of necrosis, fibrosis, microvesicular steatosis, and bile duct loss is associated with a worse prognosis, whereas eosinophils and granulomas are more often found in those with a milder degree of DILI.

    “A higher degree of necrosis, fibrosis, microvesicular steatosis, and bile duct loss is associated with a worse prognosis, whereas eosinophils and granulomas are more often found in those with a milder degree of DILI [24].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [24] European Association for the Study of the Liver. EASL Clinical Practice Guideline: Drug-induced liver injury. J Hepatol 2019; 70: 1222- 1261. 30926241
  • It may state two separate claims as one.

    Interpretationreasoning

    Identified HLA alleles have low positive predictive value because of the low incidence of DILI in the general population, but high negative predictive value.

    “In general, the identified HLA alleles have low positive predictive value, because of the low incidence of DILI in the general population, but a high negative predictive value.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Premisecitation

    The total dose of NAC is 300 mg/kg over 24 hours.

    “The total dose of NAC is 300 mg/kg over 24 hours.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [8] Fontana RJ, Liou I, Reuben A, et al. AASLD practice guidance on drug, herbal, and dietary supplement – induced liver injury. Hepatology 2023; 77: 1036- 1065. 35899384 PMC9936988 source
  • It may state two separate claims as one.

    Premisecitation

    The Roussel Uclaf Causality Assessment Method (RUCAM) is the oldest available tool for DILI causality assessment, introduced in 1993 and modified in 2016.

    “The oldest available tool is the Roussel Uclaf Causality Assessment Method (RUCAM), also known as the Council for International Organizations of Medical Sciences scale, introduced in 1993 and modified in 2016.”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [10] Danan G, Benichou C. Causality assessment of adverse reactions to drugs. Part 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. 8229110 source
    • cites [33] Benichou C, Danan G, Flahault A. Causality assessment of adverse reactions to drugs. Part II: an original model for validation of drug causality assessment methods: case reports with positive rechallenge. J Clin Epidemiol 1993; 46: 1331- 1336. 8229111 source
    • cites [34] Danan G, Teschke R. RUCAM in drug and herb induced liver injury: the update. Int J Mol Sci 2015; 17: 14- 30. 26712744 PMC4730261 source
  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Premisecitation

    The Revised Electronic Causality Assessment Method (RECAM) is currently available online.

    “The latest Revised Electronic Causality Assessment Method (RECAM) is currently available online.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [39] Hayashi PH, Lucena MI, Fontana RJ, et al. A revised electronic version of RUCAM for the diagnosis of drug induced liver injury. Hepatology 2022; 76: 18- 31. 35014066 PMC9233102
  • Probably not a substantial claim. The paper may give no reason why it holds.

    Interpretationnone given

    Idiosyncratic DILI is a rare but life-threatening side effect of drugs.

    “Idiosyncratic DILI is a rare but life-threatening side effect of drugs.”
    Quote in the paperNot a substantial claim
  • It may state two separate claims as one.

    Premisecitation

    Interface hepatitis, emperipolesis, and hepatocyte rosette formation are also found in 89%, 34% and 40% of DIAIH cases, respectively.

    “are also found in 89%, 34% and 40% of DIAIH cases, respectively [25, 26].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [25] Lohse AW, Sebode M, Bhathal PS, et al. Consensus recommendations for histological criteria of autoimmune hepatitis from the International AIH Pathology Group: Results of a workshop on AIH histology hosted by the European Reference Network on Hepatological Diseases and the European Society of Pathology. Liver Int 2022; 42: 1058- 1069. 35230735
    • cites [26] Suzuki A, Brunt EM, Kleiner DE, et al. The use of liver biopsy evaluation in discrimination of idiopathic autoimmune hepatitis versus drug-induced liver injury. Hepatology 2011; 54: 931- 939. 21674554 PMC3192933 source
  • Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.

    Premisecitation

    The RUCAM score ranges from -9 to +14 points, with five likelihood categories.

    “The score ranges from –9 to +14 points, with the same five likelihood categories [10, 33, 34].”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [10] Danan G, Benichou C. Causality assessment of adverse reactions to drugs. Part 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. 8229110 source
    • cites [33] Benichou C, Danan G, Flahault A. Causality assessment of adverse reactions to drugs. Part II: an original model for validation of drug causality assessment methods: case reports with positive rechallenge. J Clin Epidemiol 1993; 46: 1331- 1336. 8229111 source
    • cites [34] Danan G, Teschke R. RUCAM in drug and herb induced liver injury: the update. Int J Mol Sci 2015; 17: 14- 30. 26712744 PMC4730261 source
  • It may state two separate claims as one.

    Premisecitation

    An analysis within DILIN covering over 2,000 patients showed that liver biopsy was performed statistically significantly more often when the time between taking a potentially hepatotoxic drug and the onset of liver injury symptoms was longer, on average 2 months, or when more severe liver damage was observed.

    “An analysis conducted within the Drug-Induced Liver Injury Network (DILIN), a nationwide registry of DILI in the United States, covering over 2,000 patients, showed that liver biopsy was performed statistically significantly more often when the time between taking a potentially hepatotoxic drug and the onset of liver injury symptoms was longer, on average 2 months, or when more severe liver damage”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [23] Ahmad J, Barnhart HX, Bonacini M, et al. Value of liver biopsy in the diagnosis of drug-induced liver injury. J Hepatol 2022; 76: 1070- 1078. 35074471 PMC9018618 source
  • It may state two separate claims as one.

    Premisecitation

    The CDS is not used widely in clinical practice because it was shown to be inferior to RUCAM.

    “The CDS is not used widely in clinical practice because it was shown to be inferior to the RUCAM [35, 36].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [35] Maria VA, Victorino RM. Development and validation of a clinical scale for the diagnosis of drug-induced hepatitis. Hepatology 1997; 26: 664- 669. 9303497 source
    • cites [36] Lucena M, Camargo R, Andrade RJ, et al. Comparison of two clinical scales for causality assessment in hepatotoxicity. Hepatology 2001; 33: 123- 130. 11124828 source
  • It may state two separate claims as one.

    Premisecitation

    Transient and self-limited aminotransferase elevations are encountered with drugs such as isoniazid and statins and can resolve with continued dosing, presumably because of metabolic and/or immunological adaptation.

    “Transient and self-limited aminotransferase elevations are encountered with drugs such as isoniazid and statins that can resolve with continued dosing, presumably because of metabolic and/or immunological adaptation [7].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [7] Björnsson HK, Björnsson ES. Drug-induced liver injury: Pathogenesis, epidemiology, clinical features, and practical management. Eur J Intern Med 2022; 97: 26- 31. 34772600 source
  • It may state two separate claims as one.

    Premisecitation

    The Maria-Victorino Clinical Diagnostic Scale (CDS) uses similar variables to RUCAM but excludes concomitant medications and includes points for extrahepatic manifestations.

    “The Maria-Victorino Clinical Diagnostic Scale (CDS) uses similar variables to the RUCAM but excludes concomitant medications and includes points for extrahepatic manifestations.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [35] Maria VA, Victorino RM. Development and validation of a clinical scale for the diagnosis of drug-induced hepatitis. Hepatology 1997; 26: 664- 669. 9303497 source
    • cites [36] Lucena M, Camargo R, Andrade RJ, et al. Comparison of two clinical scales for causality assessment in hepatotoxicity. Hepatology 2001; 33: 123- 130. 11124828 source
  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Premisecitation

    The DDW-J score ranges from −5 to +17 points.

    “Scores range from −5 to +17 points.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [37] Takikawa H, Takamori Y, Kumagi T, et al. Assessment of 287 Japanese cases of drug induced liver injury by the diagnostic scale of the international consensus meeting. Hepatol Res 2003; 27: 192- 195. 14585395 source
    • cites [38] Hanatani T, Sai K, Tohkin M, et al. A detection algorithm for drug-induced liver injury in medical information databases using the Japanese diagnostic scale and its comparison with the Council for International Organizations of medical sciences/the Roussel Uclaf causality assessment method scale. Pharmacoepidemiol Drug Saf 2014; 23: 984- 988. 24596340 source
  • It may state two separate claims as one.

    Premisecitation

    In one of the 5 evaluated patients, stiffness did not return to normal and the patient showed biochemical features of liver damage.

    “In one of the 5 evaluated patients, stiffness did not return to normal and the patient showed biochemical features of liver damage [21].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [21] Oki E, Kakeji Y, Taketomi A, et al. Transient elastography for the prediction of oxaliplatin-associated liver injury in colon cancer patients: a preliminary analysis. J Gastrointest Cancer 2008; 39: 82- 85. 19377909 source
  • It may state two separate claims as one.

    Premisecitation

    A clear change in liver stiffness after FOLFOX chemotherapy was observed within 48 hours, and stiffness normalized in most cases after 2 weeks.

    “They observed a clear change in stiffness of the liver after chemotherapy within 48 hours, and the stiffness was normalized in most cases after 2 weeks.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [21] Oki E, Kakeji Y, Taketomi A, et al. Transient elastography for the prediction of oxaliplatin-associated liver injury in colon cancer patients: a preliminary analysis. J Gastrointest Cancer 2008; 39: 82- 85. 19377909 source
  • It may state two separate claims as one.

    Premisecitation

    Oxaliplatin rarely causes a transient increase in serum aminotransferase activity, but it is often associated with sinusoidal obstruction syndrome (SOS) and nodular regenerative hyperplasia (NRH) with portal hypertension that does not cause cirrhosis.

    “Oxaliplatin rarely causes a transient increase in serum aminotransferase activity, but it is often associated with sinusoidal obstruction syndrome (SOS) and nodular regenerative hyperplasia (NRH) with portal hypertension that does not cause cirrhosis [22].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [22] Liver Tox: Clinical and Research Information on Drug-Induced Liver Injury. https://www.ncbi.nlm.nih.gov/books/NBK548456/

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • It may state two separate claims as one.

    Premisecitation

    RECAM is at least as effective as RUCAM in diagnosing DILI, but better than the prototype in extreme diagnostic cases.

    “This scale is at least as effective as RUCAM in diagnosing DILI, but better than the prototype in extreme diagnostic cases.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [39] Hayashi PH, Lucena MI, Fontana RJ, et al. A revised electronic version of RUCAM for the diagnosis of drug induced liver injury. Hepatology 2022; 76: 18- 31. 35014066 PMC9233102
  • It may state two separate claims as one.

    Premisecitation

    Ursodeoxycholic acid (UDCA) may improve symptoms of pruritus and hasten DILI recovery.

    “Ursodeoxycholic acid (UDCA) may improve symptoms of pruritus and hasten DILI recovery, but large, randomized controlled trials are needed to determine the optimal dose and duration.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [8] Fontana RJ, Liou I, Reuben A, et al. AASLD practice guidance on drug, herbal, and dietary supplement – induced liver injury. Hepatology 2023; 77: 1036- 1065. 35899384 PMC9936988 source
    • cites [48] Lang SM, Ortmann J, Rostig S, et al. Ursodeoxycholic acid attenuates hepatotoxicity of multidrug treatment of mycobacterial infections: a prospective pilot study. Int J Mycobacterol 2019; 8: 89- 92. 30860185
  • It may state two separate claims as one.

    Interpretationreasoning

    Pretreatment HLA testing will likely not prove useful in most circumstances to prevent DILI, but HLA testing may be helpful in DILI diagnosis and causality assessment.

    “Therefore, pretreatment HLA testing will likely not prove useful in most circumstances to prevent DILI, but HLA testing may be helpful in DILI diagnosis and causality assessment [29-32].”
    Quote in the paperSubstantial claim0 of 4 sources checked
    • cites [29] Daly AK, Donaldson PT, Bhatnagar P, et al. HLA-B*5701 genotype is a major determinant of drug-induced liver injury due to flucloxacillin. Nat Genet 2009; 41: 816- 819. 19483685
    • cites [30] Lucena MI, Molokhia M, Shen Y, et al. Susceptibility to amoxicillin-clavulanate-induced liver injury is influenced by multiple HLA class I and II alleles. Gastroenterology 2011; 141: 338- 347. 21570397 PMC3129430 source
    • cites [31] Nicoletti P, Aithal GP, Bjornsson ES, et al. Association of liver injury from specific drugs, or groups of drugs, with polymorphisms in HLA and other genes in a genome-wide association study. Gastroenterology 2017; 152: 1078- 1089. 28043905 PMC5367948 source
    • cites [32] Urban TJ, Nicoletti P, Chalasani N, et al. Minocycline hepatotoxicity: Clinical characterization and identification of HLA-B *35:02 as a risk factor. J Hepatol 2017; 67: 137- 144. 28323125 PMC5634615 source
  • It may state two separate claims as one.

    Premisecitation

    Substantial liver fibrosis on SWE was observed in about 5% of MTX-treated patients with RA and was associated with only a high body mass index.

    “Substantial liver fibrosis on SWE was observed in about 5% of MTX-treated patients with RA and was associated with only a high body mass index, suggesting that other comorbidities might have a more important role in liver fibrosis [20].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [20] Frankowski M, Świerkot J, Gomułkiewicz M, et al. Usefulness of nonivasive diagnostic procedures for assessment of methotrexate hepatotoxicity in patients with rheumatoid arthritis. Rheumatol Int 2022; 42: 631- 638. 34870735 PMC8940880
  • It may state two separate claims as one.

    Premisecitation

    A short course of corticosteroids (1-3 months) with rapid tapering may be of benefit in patients with autoimmune features (DIAIH) on biopsy and in patients with DILI caused by immune checkpoint inhibitors or tyrosine kinase inhibitors.

    “In some instances, a short course of corticosteroids (i.e., 1-3 months) with rapid tapering may be of benefit in patients with autoimmune features (DIAIH) on biopsy as well as for patients with DILI caused by immune checkpoint inhibitors or tyrosine kinase inhibitors [47].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [47] Hu PF, Wang PQ, Chen H, et al. Beneficial effect of corticosteroids for patients with severe drug-induced liver injury. J Dig Dis 2016; 17: 618- 627. 27426618
  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Premisecitation

    Cholestyramine is used at a dose of 4 g every 6-8 hours for 2 weeks.

    “Cholestyramine is used at a dose of 4 g every 6-8 hours for 2 weeks [40].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [40] Stine JG, Lewis JH. Current and future directions in the treatment and prevention of drug induced liver injury: a systematic review. Expert Rev Gastroenterol Hepatol 2016; 10: 517- 536. 26633044 PMC5074808
  • It may state two separate claims as one.

    Premiseown data

    Histology review changed the causality score in 34 cases (68%), with an increase in DILI likelihood in 24 (48%) and a decrease in 10 (20%).

    “Histology review changed the causality score in 34 cases (68%), with an increase in DILI likelihood in 24 (48%) and a decrease in 10 (20%).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [23] Ahmad J, Barnhart HX, Bonacini M, et al. Value of liver biopsy in the diagnosis of drug-induced liver injury. J Hepatol 2022; 76: 1070- 1078. 35074471 PMC9018618 source
  • It may state two separate claims as one.

    Premisecitation

    RECAM has been tested only in the United States and Spain and has not been used in patients with liver damage caused by herbs and dietary supplements.

    “It has been tested only in the United States and Spain and has not been used in patients with liver damage caused by herbs and dietary supplements [39].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [39] Hayashi PH, Lucena MI, Fontana RJ, et al. A revised electronic version of RUCAM for the diagnosis of drug induced liver injury. Hepatology 2022; 76: 18- 31. 35014066 PMC9233102
32 of 32
  • The paper relies on this without support.

    DILI is largely a clinical diagnosis of exclusion requiring detailed medical history, physical examination, the pattern and course of liver biochemistry before and after drug discontinuation, and exclusion of other causes of liver disease.

    “DILI is largely a clinical diagnosis of exclusion, relying on a detailed medical history including medication exposure (start and stop date of the suspected drug, dose changes – if any and when, previous use of the medication, whether the drug was re-dosed), physical examination, the pattern and course of liver biochemistry tests before and after drug discontinuation, and exclusion of other causes”
  • The paper relies on this without support.

    Most cases of DILI occur in the first 6 months of taking a new medication, although the latency period can vary from days to months and even years.

    “Most cases of DILI occur in the first 6 months of taking a new medication, although the latency period from start of intake to onset of liver injury can vary from days to months and even years.”
  • The paper relies on this without support.

    Liver enzyme activity decreases rapidly after termination of the suspected drug therapy.

    “The activity of liver enzymes should decrease rapidly after termination of the suspected drug therapy.”
  • The paper relies on this without support.

    Biochemical improvement occurs faster in hepatocellular than in cholestatic type of liver damage.

    “Biochemical improvement occurs faster in hepatocellular than in cholestatic type of liver damage.”
  • The paper relies on this without support.

    The time to decrease of liver enzymes activity may be longer in drugs with a long half-life.

    “The time to decrease of liver enzymes activity may be longer in drugs with a long half-life.”
  • The paper relies on this without support.

    Certain drugs have their own specific pattern of liver injury: hepatocellular with isoniazid, nitrofurantoin, and disulfiram; cholestatic with anabolics; and mixed with amoxicillin-clavulanate and amiodarone.

    “Certain drugs have their own specific pattern of liver injury, such as hepatocellular with isoniazid, nitrofurantoin, and disulfiram; cholestatic with anabolics; and a mixed pattern with amoxicillin-clavulanate and amiodarone.”
  • The paper relies on this without support.

    The results of liver imaging in DILI are usually normal.

    “The results of liver imaging in DILI are usually normal; nevertheless, all patients with suspected DILI should undergo some type of liver imaging.”
  • The paper relies on this without support.

    Methotrexate causes liver fibrosis and cirrhosis through a direct reaction mechanism.

    “This drug causes liver fibrosis and cirrhosis through a direct reaction mechanism.”
  • The paper relies on this without support.

    A liver biopsy is not a routine tool in every case of suspected DILI but can be helpful in excluding other causes of liver disease.

    “A liver biopsy is not a routine tool use in every case of suspected DILI but it can be helpful in excluding other causes of liver disease.”
  • The paper relies on this without support.

    Certain medications are associated with specific histological patterns of liver injury that can be confirmed by biopsy (e.g., autoimmune-like hepatitis, vanishing bile duct syndrome, or SOS).

    “Certain medications are associated with specific histological patterns of liver injury that can be confirmed by biopsy (e.g., autoimmune-like hepatitis, vanishing bile duct syndrome – VBDS, or SOS).”
  • The paper relies on this without support.

    Histological features may be inconclusive, especially when a single drug causes several different changes.

    “On the other hand, histological features may be inconclusive, especially when a single drug causes several different changes.”
  • The paper relies on this without support.

    The spectrum of histological features observed in idiosyncratic DILI is very wide.

    “The spectrum of histological features observed in idiosyncratic DILI is very wide.”
  • The paper relies on this without support.

    Liver biopsy may assess the severity of the disease and prognosis.

    “Liver biopsy may assess the severity of the disease and prognosis.”
  • The paper relies on this without support.

    Elastography is an effective and simple tool for monitoring liver injury in patients with psoriasis treated with methotrexate.

    “It is an effective and simple tool for monitoring liver injury in patients with psoriasis treated with methotrexate (MTX).”
  • The paper relies on this without support.

    In DIAIH, the presence of portal neutrophil infiltrates and cholestasis is more frequently demonstrated.

    “In DIAIH, the presence of portal neutrophil infiltrates and cholestasis is more frequently demonstrated.”
  • The paper relies on this without support.

    Patients with pre-existing liver disease, especially cirrhosis, are at increased risk of a severe course of liver disease.

    “There is evidence showing that patients with pre-existing liver disease, especially cirrhosis, are at increased risk of a severe course of liver disease.”
16 of 16

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • N-acetylcysteine infusion schedule does not last 24 hours

    Minor

    The stated infusion stages last 15-60 minutes, 4 hours, and 16 hours: a total of 20 hours 15 minutes to 21 hours, not 24 hours. The stated doses do add to 300 mg/kg, but their scheduled duration does not match the reported duration.

  • R-ratio categories overlap and use inconsistent boundaries

    Minor

    The abstract places R = 2 in both the cholestatic and mixed categories, and R = 5 in both the mixed and hepatocellular categories. The diagnosis section instead uses strict cutoffs of less than 2 and above 5 for the first two categories.

2 of 2

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 44

  1. [1]Hu PH, Xie WF. Corticosteroid therapy in drug-induced liver injury: Pros and cons. J Dig Dis 2019; 20: 122- 126. 30582289
  2. [3]Chalasani N, Bonkovsky HL, Fontana R, et al. Features and outcomes of 899 patients with drug-induced liver injury: The DILIN prospective study. Gastroenterology 2015; 148: 1340- 1352.e7. 25754159 PMC4446235
  3. [4]Björnsson ES, Bergmann OM, Björnsson HK, et al. Incidence, presentation, and outcomes in patients with drug-induced liver injury in the general population of Iceland. Gastroenterology 2013; 144: 1419- 1425, 1425.e1-3; quiz e19-20. 23419359
  4. [5]Hayashi PH, Rockey DC, Fontana RJ, et al. Death and liver transplantation within 2 years of onset of drug-induced liver injury. Hepatology 2017; 66: 1275- 1285. 28543844 PMC5605419
  5. [6]Devarbhavi H, Asrani SK, Arab JP, et al. Global burden of liver disease: 2023 update. J Hepatol 2023; 79: 516- 537. 36990226
  6. [7]Björnsson HK, Björnsson ES. Drug-induced liver injury: Pathogenesis, epidemiology, clinical features, and practical management. Eur J Intern Med 2022; 97: 26- 31. 34772600
  7. [8]Fontana RJ, Liou I, Reuben A, et al. AASLD practice guidance on drug, herbal, and dietary supplement – induced liver injury. Hepatology 2023; 77: 1036- 1065. 35899384 PMC9936988
  8. [9]Hoofnagle JH, Björnsson ES. Drug-induced liver injury – types and phenotypes. N Engl J Med 2019; 381: 264- 273. 31314970
  9. [10]Danan G, Benichou C. Causality assessment of adverse reactions to drugs. Part 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. 8229110
  10. [11]Aithal GP, Watkins PB, Andrade RJ, et al. Case definition and phenotype standardization in drug-induced liver injury. Clin Pharmacol Ther 2011; 89: 806- 815. 21544079
  11. [12]Phongkitkarun S, Kobayashi S, Varavithya V, et al. Bile duct complications of hepatic arterial infusion chemotherapy evaluated by helical CT. Clin Radiol 2005; 60: 700- 709. 16038698
  12. [14]Schwab GP, Wetscher GJ, Vogl W, et al. Methimazole-induced cholestatic liver injury, mimicking sclerosing cholangitis. Langenbecks Arch Chir 1996; 381: 225- 227. 8817448
  13. [15]Horsley-Silva JL, Dow EN, Menias CO, et al. Docetaxel induced sclerosing cholangitis. Dig Dis Sci 2015; 60: 3814- 3816. 26501143
  14. [16]Gisondi P, Targher G, Zoppini G, et al. Non-alcoholic fatty liver disease in patients with chronic plaque psoriasis. J Hepatol 2009; 51: 758- 764. 19560226
  15. [17]Van der Voort EA, Koehler EM, Dowlatshahi EA, et al. Psoriasis is independently associated with nonalcoholic fatty liver disease in patients 55 years old or older: results from a population-based study. J Am Acad Dermatol 2014; 70: 517- 524. 24373781
  16. [18]Roberts KK, Cochet AE, Lamb PB, et al. The prevalence of NAFLD and NASH among patients with psoriasis in a tertiary care dermatology and rheumatology clinic. Aliment Pharmacol Ther 2015; 41: 293- 300. 25521607
  17. [19]Narayanasamy K, Sanmarkan AD, Rajendran K, et al. Relationship between psoriasis and non-alcoholic fatty liver disease. Prz Gastroenterol 2016; 11: 263- 269. 28053681 PMC5209456
  18. [20]Frankowski M, Świerkot J, Gomułkiewicz M, et al. Usefulness of nonivasive diagnostic procedures for assessment of methotrexate hepatotoxicity in patients with rheumatoid arthritis. Rheumatol Int 2022; 42: 631- 638. 34870735 PMC8940880
  19. [21]Oki E, Kakeji Y, Taketomi A, et al. Transient elastography for the prediction of oxaliplatin-associated liver injury in colon cancer patients: a preliminary analysis. J Gastrointest Cancer 2008; 39: 82- 85. 19377909
  20. [22]Liver Tox: Clinical and Research Information on Drug-Induced Liver Injury. https://www.ncbi.nlm.nih.gov/books/NBK548456/
  21. [23]Ahmad J, Barnhart HX, Bonacini M, et al. Value of liver biopsy in the diagnosis of drug-induced liver injury. J Hepatol 2022; 76: 1070- 1078. 35074471 PMC9018618
  22. [24]European Association for the Study of the Liver. EASL Clinical Practice Guideline: Drug-induced liver injury. J Hepatol 2019; 70: 1222- 1261. 30926241
  23. [25]Lohse AW, Sebode M, Bhathal PS, et al. Consensus recommendations for histological criteria of autoimmune hepatitis from the International AIH Pathology Group: Results of a workshop on AIH histology hosted by the European Reference Network on Hepatological Diseases and the European Society of Pathology. Liver Int 2022; 42: 1058- 1069. 35230735
  24. [26]Suzuki A, Brunt EM, Kleiner DE, et al. The use of liver biopsy evaluation in discrimination of idiopathic autoimmune hepatitis versus drug-induced liver injury. Hepatology 2011; 54: 931- 939. 21674554 PMC3192933
  25. [27]Febres-Aldana CA, Alghamdi S, Krishnamurthy K, et al. Liver fibrosis helps to distinguish autoimmune hepatitis from DILI with autoimmune features: a review of twenty cases. J Clin Transl Hepatol 2019; 7: 21- 26. 30944815 PMC6441645
  26. [28]Cirulli ET, Nicoletti P, Abramson K, et al. A missense variant in PTPN22 is a risk factor for drug-induced liver injury. Gastroenterology 2019; 156: 1707- 1716.e2. 30664875 PMC6511989
  27. [29]Daly AK, Donaldson PT, Bhatnagar P, et al. HLA-B*5701 genotype is a major determinant of drug-induced liver injury due to flucloxacillin. Nat Genet 2009; 41: 816- 819. 19483685
  28. [30]Lucena MI, Molokhia M, Shen Y, et al. Susceptibility to amoxicillin-clavulanate-induced liver injury is influenced by multiple HLA class I and II alleles. Gastroenterology 2011; 141: 338- 347. 21570397 PMC3129430
  29. [31]Nicoletti P, Aithal GP, Bjornsson ES, et al. Association of liver injury from specific drugs, or groups of drugs, with polymorphisms in HLA and other genes in a genome-wide association study. Gastroenterology 2017; 152: 1078- 1089. 28043905 PMC5367948
  30. [32]Urban TJ, Nicoletti P, Chalasani N, et al. Minocycline hepatotoxicity: Clinical characterization and identification of HLA-B *35:02 as a risk factor. J Hepatol 2017; 67: 137- 144. 28323125 PMC5634615
  31. [33]Benichou C, Danan G, Flahault A. Causality assessment of adverse reactions to drugs. Part II: an original model for validation of drug causality assessment methods: case reports with positive rechallenge. J Clin Epidemiol 1993; 46: 1331- 1336. 8229111
  32. [34]Danan G, Teschke R. RUCAM in drug and herb induced liver injury: the update. Int J Mol Sci 2015; 17: 14- 30. 26712744 PMC4730261
  33. [35]Maria VA, Victorino RM. Development and validation of a clinical scale for the diagnosis of drug-induced hepatitis. Hepatology 1997; 26: 664- 669. 9303497
  34. [36]Lucena M, Camargo R, Andrade RJ, et al. Comparison of two clinical scales for causality assessment in hepatotoxicity. Hepatology 2001; 33: 123- 130. 11124828
  35. [37]Takikawa H, Takamori Y, Kumagi T, et al. Assessment of 287 Japanese cases of drug induced liver injury by the diagnostic scale of the international consensus meeting. Hepatol Res 2003; 27: 192- 195. 14585395
  36. [38]Hanatani T, Sai K, Tohkin M, et al. A detection algorithm for drug-induced liver injury in medical information databases using the Japanese diagnostic scale and its comparison with the Council for International Organizations of medical sciences/the Roussel Uclaf causality assessment method scale. Pharmacoepidemiol Drug Saf 2014; 23: 984- 988. 24596340
  37. [39]Hayashi PH, Lucena MI, Fontana RJ, et al. A revised electronic version of RUCAM for the diagnosis of drug induced liver injury. Hepatology 2022; 76: 18- 31. 35014066 PMC9233102
  38. [40]Stine JG, Lewis JH. Current and future directions in the treatment and prevention of drug induced liver injury: a systematic review. Expert Rev Gastroenterol Hepatol 2016; 10: 517- 536. 26633044 PMC5074808
  39. [41]Perrott J, Murphy NG, Zed PJ. L-carnitine for acute valproic acid overdose: a systematic review of published cases. Ann Pharmacother 2010; 44: 1287- 1293. 20587742
  40. [44]Lee WM, Hynan LS, Rossaro L, et al. Intravenous N-acetylcysteine improves transplant-free survival in early stage non-acetaminophen acute liver failure. Gastroenterology 2009; 137: 856- 864. 19524577 PMC3189485
  41. [45]Squires RH, Dhawan A, Alonso E, et al. Intravenous N-acetylcysteine in pediatric patients with nonacetaminophen acute liver failure: a placebo-controlled clinical trial. Hepatology 2015; 57: 1542- 1549. PMC3509266 22886633
  42. [46]Avancini J, Maragno L, Santi CG, et al. Drug reaction with eosinophilia and systemic symptoms/drug-induced hypersensitivity syndrome: clinical features of 27 patients. Clin Exp Dermatol 2015; 40: 851- 859. 26271788
  43. [47]Hu PF, Wang PQ, Chen H, et al. Beneficial effect of corticosteroids for patients with severe drug-induced liver injury. J Dig Dis 2016; 17: 618- 627. 27426618
  44. [48]Lang SM, Ortmann J, Rostig S, et al. Ursodeoxycholic acid attenuates hepatotoxicity of multidrug treatment of mycobacterial infections: a prospective pilot study. Int J Mycobacterol 2019; 8: 89- 92. 30860185

Cited by

Sorted by citations

Metadata

Authors
Kozielewicz, D. M., Stalke, P., & Skrzypek, J.
Affiliations
  • Nicolaus Copernicus University (PL)
  • Gdańsk Medical University (PL)
  • Wojewódzki Szpital Obserwacyjno-Zakaźny im. Tadeusza Browicza w Bydgoszczy (PL)
Corresponding author
Kozielewicz, Dorota M.
Venue
Clinical and Experimental Hepatology
Published
2025
Volume
11
Issue
1
Pages
25-33
ISSN
2392-1099 (ISSN-L)
OpenAlex
W4409035403
Cited by
19
References
1
Citations by year
2026: 15 · 2025: 4
FWCI
2.48
Type
journal article
Language
en
Open access
Licence
cc-by-nc-sa
Locations
  • Clinical and Experimental Hepatology (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Pharmacovigilance and Adverse Drug Reactions
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords
drug-induced liver injury, antibiotics, hepatotoxicity, cholestatic liver injury, acute liver failure, differential diagnosis, drug discontinuation, antidotes, glucocorticoids, ursodeoxycholic acid, liver transplantation

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

A language model drew the claims from the paper on 2026-11-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).

A second model labelled each claim on 2026-11-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review