Mistakes in liver function test abnormalities and how to avoid them

Filters:

UEG Mistakes In Articles

Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

Not sure what you can access? Learn more about account types.

Mistakes in liver function test abnormalities and how to avoid them

Eric T.T.L. Tjwa, Joost Drenth, Frans Cuperus

Summary

AI Generated

Liver function tests are routinely used to screen for liver disease, but abnormal results do not always indicate structural liver disease and normal results do not exclude advanced disease.

Elevation of at least one liver function test occurs in more than 20% of the population, making abnormal results frequently encountered in clinical practice.
Many patients with abnormal liver function tests do not have structural liver disease, as these tests can be influenced by factors unrelated to significant liver damage, including pregnancy, cardiac damage, or skeletal muscle damage.
Patients with advanced liver disease such as chronic hepatitis or compensated liver cirrhosis may have normal liver function tests.
When interpreted correctly, liver function test abnormalities may suggest the cause, severity, and prognosis of underlying disease and can be used sequentially to assess treatment efficacy once diagnosis is established.

Download PDF

Was this helpful?

Thanks for your feedback.

This summary was generated by an AI large language model based on the content transcript. It is for informational purposes only and should not be considered a substitute for clinical judgment. Always rely on your professional expertise and the full clinical context when making clinical decisions.

References

Mistakes

References

Mistake 1 Mistake 2 Mistake 3 Mistake 4 Mistake 5 Mistake 6 Mistake 7 Mistake 8 Mistake 9 Mistake 10 Mistake 11 Mistake 12

Donnan PT, McLernon D, Dillon JF, et al. Development of a decision support tool for primary care management of patients with abnormal liver function tests without clinically apparent liver disease: A record-linkage population cohort study and decision analysis (ALFIE). Health Technol Assess (Rockv); 13. Epub ahead of print 2009. DOI: 10.3310/hta13250. [Link]

Haber MM, West AB, Haber AD, et al. Relationship of aminotransferases to liver histological status in chronic hepatitis C. Am J Gastroenterol 1995; 90: 1250–7. [Link]

Bacon BR, Farahvash MJ, Janney CG, et al. Nonalcoholic steatohepatitis: an expanded clinical entity. Gastroenterology 1994; 107: 1103–9. [Link]

Cohen JA, Kaplan MM. The SGOT/SGPT ratio--an indicator of alcoholic liver disease. Dig Dis Sci 1979; 24: 835–8. [Link]

Bunchorntavakul C, Reddy KR. Acetaminophen-related hepatotoxicity. Clin Liver Dis 2013; 17: 587–607, viii. [Link]

Rozen P, Korn RJ, Zimmerman HJ. Computer analysis of liver function tests and their interrelationships in 347 cases of viral hepatitis. Isr J Med Sci 1970; 6: 67–79. [Link]

Dufour DR, Lott JA, Nolte FS, et al. Diagnosis and monitoring of hepatic injury. I. Performance characteristics of laboratory tests. Clin Chem 2000; 46: 2027–49. [Link]

Kazemi-Shirazi L, Veloso MP, Frommlet F, et al. Differentiation of nonalcoholic from alcoholic steatohepatitis: are routine laboratory markers useful? Wien Klin Wochenschr 2008; 120: 25–30. [Link]

Sorbi D, Boynton J, Lindor KD. The ratio of aspartate aminotransferase to alanine aminotransferase: potential value in differentiating nonalcoholic steatohepatitis from alcoholic liver disease. Am J Gastroenterol 1999; 94: 1018–22. [Link]

10.

Whitfield JB. Gamma glutamyl transferase. Crit Rev Clin Lab Sci 2001; 38: 263–355. [Link]

11.

Jacquemin E. Progressive familial intrahepatic cholestasis. Clin Res Hepatol Gastroenterol 2012; 36 Suppl 1: S26-35. [Link]

12.

Allen JP, Litten RZ, Strid N, et al. The role of biomarkers in alcoholism medication trials. Alcohol Clin Exp Res 2001; 25: 1119–25. [Link]

13.

European Association for the Study of the Liver. EASL Clinical Practice Guidelines: management of cholestatic liver diseases. J Hepatol 2009; 51: 237–67. [Link]

14.

Lammers WJ, van Buuren HR, Hirschfield GM, et al. Levels of alkaline phosphatase and bilirubin are surrogate end points of outcomes of patients with primary biliary cirrhosis: an international follow-up study. Gastroenterology 2014; 147: 1338–49.e5; quiz e15. [Link]

15.

Tenhunen R, Marver HS, Schmid R. Microsomal heme oxygenase. Characterization of the enzyme. J Biol Chem 1969; 244: 6388–94. [Link]

16.

SCHMID R, HAMMAKER L, AXELROD J. The enzymatic formation of bilirubin glucuronide. Arch Biochem Biophys 1957; 70: 285–8. [Link]

17.

Cuperus FJC, Hafkamp AM, Havinga R, et al. Effective treatment of unconjugated hyperbilirubinemia with oral bile salts in Gunn rats. Gastroenterology 2009; 136: 673–82.e1. [Link]

18.

Desmet VJ, Gerber M, Hoofnagle JH, et al. Classification of chronic hepatitis: diagnosis, grading and staging. Hepatology 1994; 19: 1513–20. [Link]

19.

Kamath PS, Wiesner RH, Malinchoc M, et al. A model to predict survival in patients with end-stage liver disease. Hepatology 2001; 33: 464–70. [Link]

20.

Bosma PJ, Chowdhury JR, Bakker C, et al. The genetic basis of the reduced expression of bilirubin UDP-glucuronosyltransferase 1 in Gilbert’s syndrome. N Engl J Med 1995; 333: 1171–5. [Link]

21.

Felsher BF, Rickard D, Redeker AG. The reciprocal relation between caloric intake and the degree of hyperbilirubinemia in Gilbert’s syndrome. N Engl J Med 1970; 283: 170–2. [Link]

22.

Vítek L, Jirsa M, Brodanová M, et al. Gilbert syndrome and ischemic heart disease: a protective effect of elevated bilirubin levels. Atherosclerosis 2002; 160: 449–56. [Link]

23.

Kaplan M, Renbaum P, Levy-Lahad E, et al. Gilbert syndrome and glucose-6-phosphate dehydrogenase deficiency: a dose-dependent genetic interaction crucial to neonatal hyperbilirubinemia. Proc Natl Acad Sci U S A 1997; 94: 12128–32. [Link]

24.

Erlinger S, Arias IM, Dhumeaux D. Inherited disorders of bilirubin transport and conjugation: new insights into molecular mechanisms and consequences. Gastroenterology 2014; 146: 1625–38. [Link]

25.

Rothschild MA, Oratz M, Schreiber SS. Serum albumin. Hepatology 1988; 8: 385–401. [Link]

26.

Bernuau J, Goudeau A, Poynard T, et al. Multivariate analysis of prognostic factors in fulminant hepatitis B. Hepatology 1986; 6: 648–51. [Link]

27.

Rej R. Aspartate aminotransferase activity and isoenzyme proportions in human liver tissues. Clin Chem 1978; 24: 1971–9. [Link]

28.

Ruhl CE, Everhart JE. Upper limits of normal for alanine aminotransferase activity in the United States population. Hepatology 2012; 55: 447–54. [Link]

29.

Litin SC, O’Brien JF, Pruett S, et al. Macroenzyme as a cause of unexplained elevation of aspartate aminotransferase. Mayo Clin Proc 1987; 62: 681–7. [Link]

30.

Han J-H, Kwak J-Y, Lee S-S, et al. Markedly Elevated Aspartate Aminotransferase from Non-Hepatic Causes. J Clin Med; 12. Epub ahead of print 30 December 2022. DOI: 10.3390/jcm12010310. [Link]

31.

Rosalki SB, Tarlow D, Rau D. Plasma gamma-glutamyl transpeptidase elevation in patients receiving enzyme-inducing drugs. Lancet 1971; 2: 376–7. [Link]

32.

Kalas MA, Chavez L, Leon M, et al. Abnormal liver enzymes: A review for clinicians. World J Hepatol 2021; 13: 1688–1698. [Link]

33.

Bozkus F, Dikmen N, Sahin H, et al. Serum Gamma-Glutamyl Transferase Activity as a Potential Novel Cardiovascular Biomarker in COPD. Respir Care 2016; 61: 1465–1471. [Link]

34.

Brennan PN, Dillon JF, Tapper EB. Gamma-Glutamyl Transferase (γ-GT) - an old dog with new tricks? Liver Int 2022; 42: 9–15. [Link]

35.

Lowe D STZM et al. Alkaline Phosphatase. StatPearls [Internet]. [Link]

36.

Van Hootegem P, Fevery J, Blanckaert N. Serum bilirubins in hepatobiliary disease: comparison with other liver function tests and changes in the postobstructive period. Hepatology 1985; 5: 112–7. [Link]

37.

Northup PG, Caldwell SH. Coagulation in liver disease: a guide for the clinician. Clin Gastroenterol Hepatol 2013; 11: 1064–74. [Link]

38.

Intagliata NM, Rahimi RS, Higuera-de-la-Tijera F, et al. Procedural-Related Bleeding in Hospitalized Patients With Liver Disease (PROC-BLeeD): An International, Prospective, Multicenter Observational Study. Gastroenterology 2023; 165: 717–732. [Link]

39.

Edoardo G. Giannini, Stephen H. Caldwell. Mistakes in coagulation in liver disease and how to avoid them. UEG Mistakes In Articles. [Link]

40.

Lee WM, Stravitz RT, Larson AM. Introduction to the revised American Association for the Study of Liver Diseases Position Paper on acute liver failure 2011. Hepatology 2012; 55: 965–7. [Link]

41.

Lee WM, Squires RH, Nyberg SL, et al. Acute liver failure: Summary of a workshop. Hepatology 2008; 47: 1401–15. [Link]

42.

O’Grady JG, Alexander GJ, Hayllar KM, et al. Early indicators of prognosis in fulminant hepatic failure. Gastroenterology 1989; 97: 439–45. [Link]

43.

Nguyen-Khac E, Thevenot T, Piquet M-A, et al. Glucocorticoids plus N-acetylcysteine in severe alcoholic hepatitis. N Engl J Med 2011; 365: 1781–9. [Link]

44.

Tenner S, Dubner H, Steinberg W. Predicting gallstone pancreatitis with laboratory parameters: a meta-analysis. Am J Gastroenterol 1994; 89: 1863–6. [Link]

45.

Henry F, Quatresooz P, Valverde-Lopez JC, et al. Blood vessel changes during pregnancy: a review. Am J Clin Dermatol 2006; 7: 65–9. [Link]

46.

Walker I, Chappell LC, Williamson C. Abnormal liver function tests in pregnancy. BMJ 2013; 347: f6055. [Link]

47.

Sarkar M, Brady CW, Fleckenstein J, et al. Reproductive Health and Liver Disease: Practice Guidance by the American Association for the Study of Liver Diseases. Hepatology 2021; 73: 318–365. [Link]

48.

Casey LC, Fontana RJ, Aday A, et al. Acute Liver Failure (ALF) in Pregnancy: How Much Is Pregnancy Related? Hepatology 2020; 72: 1366–1377. [Link]

49.

Magee LA, Brown MA, Hall DR, et al. The 2021 International Society for the Study of Hypertension in Pregnancy classification, diagnosis & management recommendations for international practice. Pregnancy Hypertens 2022; 27: 148–169. [Link]

50.

Westbrook RH, Dusheiko G, Williamson C. Pregnancy and liver disease. J Hepatol 2016; 64: 933–945. [Link]

51.

Williamson C, Nana M, Poon L, et al. EASL Clinical Practice Guidelines on the management of liver diseases in pregnancy. J Hepatol 2023; 79: 768–828. [Link]

52.

Knight M, Nelson-Piercy C, Kurinczuk JJ, et al. A prospective national study of acute fatty liver of pregnancy in the UK. Gut 2008; 57: 951–956. [Link]

53.

Goel A, Ramakrishna B, Zachariah U, et al. How accurate are the Swansea criteria to diagnose acute fatty liver of pregnancy in predicting hepatic microvesicular steatosis? Gut 2011; 60: 138–9; author reply 139-40. [Link]

54.

Brady CW. Liver Disease in Pregnancy: What’s New. Hepatol Commun 2020; 4: 145–156. [Link]

55.

European Association for the Study of the Liver. Electronic address: easloffice@easloffice.eu, Clinical Practice Guideline Panel: Chair:, Panel members, et al. EASL Clinical Practice Guidelines: Drug-induced liver injury. J Hepatol 2019; 70: 1222–1261. [Link]

56.

Haanen J, Obeid M, Spain L, et al. Management of toxicities from immunotherapy: ESMO Clinical Practice Guideline for diagnosis, treatment and follow-up. Ann Oncol 2022; 33: 1217–1238. [Link]

57.

De Martin E, Michot J-M, Papouin B, et al. Characterization of liver injury induced by cancer immunotherapy using immune checkpoint inhibitors. J Hepatol 2018; 68: 1181–1190. [Link]

Abstract

Liver function tests (LFTs) are routinely used to screen for liver disease. A correct interpretation of LFT abnormalities may suggest the cause, severity, and prognosis of an underlying disease. Once the diagnosis has been established, sequential LFT assessment can be used to assess treatment efficacy. Abnormal LFTs are frequently encountered in clinical practice, since elevation of at least one LFT occurs in more than 20% of the population.1 Many patients with abnormal LFTs, however, do not suffer from structural liver disease, since these tests can be influenced by factors unrelated to significant liver damage or liver function loss. During normal pregnancy, for example, serum albumin levels fall due to plasma volume expansion, and alkaline phosphatase (ALP) levels rise due to placental influx. Patients who have elevated transaminase levels may not suffer from liver disease, but rather from cardiac or skeletal muscle damage. Conversely, patients who suffer from advanced liver disease, such as chronic hepatitis or compensated liver cirrhosis, may have normal LFTs.

Topics

Hepatobiliary

Citation

Cuperus FJC, Drenth JPH and Tjwa ET. Mistakes in liver function test abnormalities and how to avoid them. UEG Education 2017: 17; 1–5.

Published

2017

More Like This:

European Society for the Study of Coeliac Disease 2025 Updated Guidelines on the Diagnosis and Management of Coeliac Disease in Adults. Part 1: Diagnostic Approach

Abdulbaqi Al-Toma

Esophageal and Oropharyngeal Dysphagia: Clinical Recommendations From the United European Gastroenterology and European Society for Neurogastroenterology and Motility

Amir Mari

EASL Clinical Practice Guidelines on liver transplantation

Coeliac disease with David Sanders

Pradeep Mundre

Mistakes in hepatitis C and how to avoid them

Gonçalo Alexandrino

EASL–EASD–EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD)

UEG Standards and Guidelines

Clinical Practice Guideline

Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

Not sure what you can access? Learn more about account types.

European Society for the Study of Coeliac Disease 2025 Updated Guidelines on the Diagnosis and Management of Coeliac Disease in Adults. Part 1: Diagnostic Approach

Abdulbaqi Al-Toma

Summary

AI Generated

Summary is not available for this content yet.

Download PDF

Was this helpful?

Thanks for your feedback.

Guideline

ABSTRACT

Introduction

Since the publication of the first European Society for the Study of Coeliac Disease (ESsCD) guidelines in 2019, significant advancements have emerged in the diagnosis of coeliac disease (CeD) in adults. These 2025 guidelines incorporate new evidence to refine diagnostic strategies, aiming for improved accuracy of testing, and enhance overall quality of clinical care.

Methods

A multidisciplinary panel of experts revised the ESsCD guidelines using the AGREE II instrument (Appraisal of Guidelines for Research and Evaluation II) and the GRADE methodology (The Grading of Recommendations Assessment, Development, and Evaluation). Clinical questions were structured using the PICO format, and statements and recommendations were finalised through a Delphi consensus process. Literature quality was assessed using AMSTAR-2 and QUADAS-2 tools.

Results

The updated guidelines are presented in two parts. Part 1 focuses on adult CeD diagnosis, introducing major changes such as a conditional no-biopsy approach for selected adults with high-titre IgA anti-TG2 serology (≥ 10 × ULN). Regarding serology, the use of validated high-performance ELISAs displaying a high diagnostic accuracy is emphasised, while routine use of IgA anti-Endomysium serology is no longer recommended for confirmation. Revised duodenal biopsy protocols now mandate at least four samples from the second part of the duodenum, with bulb biopsies conditionally included. The guidelines provide structured approaches for diagnosing potential CeD, seronegative villous atrophy, and CeD in individuals already on a gluten-free diet. HLA-DQ2/DQ8 typing is recommended for diagnostic clarification in select cases.

Conclusions

The updated 2025 ESsCD guidelines provide a comprehensive framework for the diagnosis of CeD in adults. By integrating evolving diagnostic strategies, minimising over-testing, and patient-centred care approaches, they aim to optimise patient outcomes, quality of life and use of diagnostic resources at the same time.

Guideline

Clinical Practice Guideline

Topics

Small Intestine & Nutrition

Citation

United European Gastroenterology Journal; 2025; 00:1–32

Published

2025

More Like This:

European Society for the Study of Coeliac Disease 2025 Updated Guidelines on the Diagnosis and Management of Coeliac Disease in Adults. Part 1: Diagnostic Approach

Abdulbaqi Al-Toma

Esophageal and Oropharyngeal Dysphagia: Clinical Recommendations From the United European Gastroenterology and European Society for Neurogastroenterology and Motility

Amir Mari

EASL Clinical Practice Guidelines on liver transplantation

Coeliac disease with David Sanders

Pradeep Mundre

Mistakes in hepatitis C and how to avoid them

Gonçalo Alexandrino

EASL–EASD–EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD)

UEG Standards and Guidelines

Consensus

Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

Not sure what you can access? Learn more about account types.

Esophageal and Oropharyngeal Dysphagia: Clinical Recommendations From the United European Gastroenterology and European Society for Neurogastroenterology and Motility

Amir Mari

Summary

AI Generated

Summary is not available for this content yet.

Download PDF

Was this helpful?

Thanks for your feedback.

Guideline

ABSTRACT

Dysphagia is a prevalent symptom of the upper gastrointestinal tract causing health related consequences, impacting quality of life and is associated with global economic burden. Swallowing difficulties are classified into oropharyngeal dysphagia (OD) and esophageal dysphagia. Despite its clinical importance, dysphagia is associated with several uncertainties regarding its optimal diagnostic work-up and management, particularly, considering the progress with diagnostic modalities and technologies. A Delphi consensus was performed with experts from various disciplines who conducted a literature summary and voting process on 41 statements. Quality of evidence was evaluated using the grading of recommendations, assessment, development, and evaluation criteria. Consensus was reached for all the statements. The panel agreed with the definition and prevalence of esophageal and OD types. The role of endoscopy, high-resolution manometry, EndoFLIP, barium swallow and other imaging tests in evaluating esophageal dysphagia has reached overall strong agreement. Videofluoroscopic swallow study, alongside fiber-endoscopic evaluation of swallowing, as the methods of choice for the instrumental assessment of oropharyngeal dysfunction is a strong recommendation. Regarding treatment, a weak recommendation was achieved for the use of PPIs, calcium-channel blockers, nitrates, phosphodiesterase type 5 inhibitors, antidepressants or peppermint oil for the treatment of hypercontractile esophagus. A strong recommendation exists for endoscopic and surgical treatment of achalasia, while a weak recommendation is provided for other esophageal motility disorders. Regarding OD, a weak recommendation was achieved for swallow therapy, to improve swallowing mechanics, reduce symptoms, and enhance quality of life. Swallow therapy could be more effective when using validated assessment tools, consistent treatment parameters, and considering long-term follow-up. A multinational group of European experts summarized the current state of consensus on the definition, diagnosis, and management of dysphagia.

Publisher

European Society of Neurogastroenterology and Motility

Guideline

Consensus

Topics

Neurogastroenterology & Motility Oesophagus

Citation

United European Gastroenterol J, 13: 855-901

Published

2025

More Like This:

European Society for the Study of Coeliac Disease 2025 Updated Guidelines on the Diagnosis and Management of Coeliac Disease in Adults. Part 1: Diagnostic Approach

Abdulbaqi Al-Toma

Esophageal and Oropharyngeal Dysphagia: Clinical Recommendations From the United European Gastroenterology and European Society for Neurogastroenterology and Motility

Amir Mari

EASL Clinical Practice Guidelines on liver transplantation

Coeliac disease with David Sanders

Pradeep Mundre

Mistakes in hepatitis C and how to avoid them

Gonçalo Alexandrino

EASL–EASD–EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD)

UEG Standards and Guidelines

Clinical Practice Guideline

Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

Not sure what you can access? Learn more about account types.

EASL Clinical Practice Guidelines on liver transplantation

Summary

AI Generated

Summary is not available for this content yet.

Download PDF

Was this helpful?

Thanks for your feedback.

Guideline

Summary

Liver transplantation (LT) is an established life-saving procedure. The field of LT has changed in the past 10 years from several perspectives, with the expansion of indications, transplantation of patients with acute-on-chronic liver failure, evolution of transplant oncology, the use of donations after cardiac death, new surgical techniques, and prioritisation of recipients on the waiting list. In addition, the advent of organ perfusion machines, the recognition of new forms of rejection, and the attention paid to the transition from paediatric to adult patients, have all improved the management of LT recipients. The purpose of the EASL guidelines presented here is not to cover all aspects of LT but to focus on developments since the previous EASL guidelines published in 2016.

Keywords

Liver transplantation, recipient, donor, recurrence, transplant oncology, immunosuppression

Publisher

European Association for the Study of the Liver

Guideline

Clinical Practice Guideline

Topics

Hepatobiliary

Citation

Journal of Hepatology, December 2024. vol. 81 | 1040–1086

Published

2024

More Like This:

European Society for the Study of Coeliac Disease 2025 Updated Guidelines on the Diagnosis and Management of Coeliac Disease in Adults. Part 1: Diagnostic Approach

Abdulbaqi Al-Toma

Esophageal and Oropharyngeal Dysphagia: Clinical Recommendations From the United European Gastroenterology and European Society for Neurogastroenterology and Motility

Amir Mari

EASL Clinical Practice Guidelines on liver transplantation

Coeliac disease with David Sanders

Pradeep Mundre

Mistakes in hepatitis C and how to avoid them

Gonçalo Alexandrino

EASL–EASD–EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD)

UEG Podcast Episode

UEG Podcast

Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

Not sure what you can access? Learn more about account types.

Coeliac disease with David Sanders

David S. Sanders, Pradeep Mundre

Summary

AI Generated

Summary is not available for this content yet.

Download PDF

Was this helpful?

Thanks for your feedback.

Abstract

Topics

Small Intestine & Nutrition

Published

2026

More Like This:

European Society for the Study of Coeliac Disease 2025 Updated Guidelines on the Diagnosis and Management of Coeliac Disease in Adults. Part 1: Diagnostic Approach

Abdulbaqi Al-Toma

Esophageal and Oropharyngeal Dysphagia: Clinical Recommendations From the United European Gastroenterology and European Society for Neurogastroenterology and Motility

Amir Mari

EASL Clinical Practice Guidelines on liver transplantation

Coeliac disease with David Sanders

Pradeep Mundre

Mistakes in hepatitis C and how to avoid them

Gonçalo Alexandrino

EASL–EASD–EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD)

UEG Mistakes In Articles

Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

Not sure what you can access? Learn more about account types.

Mistakes in hepatitis C and how to avoid them

Ana Catarina Garcia, Gonçalo Alexandrino

Summary

AI Generated

Summary is not available for this content yet.

Download PDF

Was this helpful?

Thanks for your feedback.

References

Mistakes

References

Mistake 1 Mistake 2 Mistake 3 Mistake 4 Mistake 5 Mistake 6 Mistake 7 Mistake 8 Mistake 9 Mistake 10 Mistake 11 Mistake 12

Haber MM, West AB, Haber AD, et al. Relationship of aminotransferases to liver histological status in chronic hepatitis C. Am J Gastroenterol 1995; 90: 1250–7. [Link]

Bacon BR, Farahvash MJ, Janney CG, et al. Nonalcoholic steatohepatitis: an expanded clinical entity. Gastroenterology 1994; 107: 1103–9. [Link]

Cohen JA, Kaplan MM. The SGOT/SGPT ratio--an indicator of alcoholic liver disease. Dig Dis Sci 1979; 24: 835–8. [Link]

Bunchorntavakul C, Reddy KR. Acetaminophen-related hepatotoxicity. Clin Liver Dis 2013; 17: 587–607, viii. [Link]

Rozen P, Korn RJ, Zimmerman HJ. Computer analysis of liver function tests and their interrelationships in 347 cases of viral hepatitis. Isr J Med Sci 1970; 6: 67–79. [Link]

Dufour DR, Lott JA, Nolte FS, et al. Diagnosis and monitoring of hepatic injury. I. Performance characteristics of laboratory tests. Clin Chem 2000; 46: 2027–49. [Link]

Kazemi-Shirazi L, Veloso MP, Frommlet F, et al. Differentiation of nonalcoholic from alcoholic steatohepatitis: are routine laboratory markers useful? Wien Klin Wochenschr 2008; 120: 25–30. [Link]

10.

Whitfield JB. Gamma glutamyl transferase. Crit Rev Clin Lab Sci 2001; 38: 263–355. [Link]

11.

Jacquemin E. Progressive familial intrahepatic cholestasis. Clin Res Hepatol Gastroenterol 2012; 36 Suppl 1: S26-35. [Link]

12.

Allen JP, Litten RZ, Strid N, et al. The role of biomarkers in alcoholism medication trials. Alcohol Clin Exp Res 2001; 25: 1119–25. [Link]

13.

European Association for the Study of the Liver. EASL Clinical Practice Guidelines: management of cholestatic liver diseases. J Hepatol 2009; 51: 237–67. [Link]

14.

15.

Tenhunen R, Marver HS, Schmid R. Microsomal heme oxygenase. Characterization of the enzyme. J Biol Chem 1969; 244: 6388–94. [Link]

16.

SCHMID R, HAMMAKER L, AXELROD J. The enzymatic formation of bilirubin glucuronide. Arch Biochem Biophys 1957; 70: 285–8. [Link]

17.

Cuperus FJC, Hafkamp AM, Havinga R, et al. Effective treatment of unconjugated hyperbilirubinemia with oral bile salts in Gunn rats. Gastroenterology 2009; 136: 673–82.e1. [Link]

18.

Desmet VJ, Gerber M, Hoofnagle JH, et al. Classification of chronic hepatitis: diagnosis, grading and staging. Hepatology 1994; 19: 1513–20. [Link]

19.

Kamath PS, Wiesner RH, Malinchoc M, et al. A model to predict survival in patients with end-stage liver disease. Hepatology 2001; 33: 464–70. [Link]

20.

Bosma PJ, Chowdhury JR, Bakker C, et al. The genetic basis of the reduced expression of bilirubin UDP-glucuronosyltransferase 1 in Gilbert’s syndrome. N Engl J Med 1995; 333: 1171–5. [Link]

21.

Felsher BF, Rickard D, Redeker AG. The reciprocal relation between caloric intake and the degree of hyperbilirubinemia in Gilbert’s syndrome. N Engl J Med 1970; 283: 170–2. [Link]

22.

Vítek L, Jirsa M, Brodanová M, et al. Gilbert syndrome and ischemic heart disease: a protective effect of elevated bilirubin levels. Atherosclerosis 2002; 160: 449–56. [Link]

23.

24.

Erlinger S, Arias IM, Dhumeaux D. Inherited disorders of bilirubin transport and conjugation: new insights into molecular mechanisms and consequences. Gastroenterology 2014; 146: 1625–38. [Link]

25.

Rothschild MA, Oratz M, Schreiber SS. Serum albumin. Hepatology 1988; 8: 385–401. [Link]

26.

Bernuau J, Goudeau A, Poynard T, et al. Multivariate analysis of prognostic factors in fulminant hepatitis B. Hepatology 1986; 6: 648–51. [Link]

27.

Rej R. Aspartate aminotransferase activity and isoenzyme proportions in human liver tissues. Clin Chem 1978; 24: 1971–9. [Link]

28.

Ruhl CE, Everhart JE. Upper limits of normal for alanine aminotransferase activity in the United States population. Hepatology 2012; 55: 447–54. [Link]

29.

Litin SC, O’Brien JF, Pruett S, et al. Macroenzyme as a cause of unexplained elevation of aspartate aminotransferase. Mayo Clin Proc 1987; 62: 681–7. [Link]

30.

Han J-H, Kwak J-Y, Lee S-S, et al. Markedly Elevated Aspartate Aminotransferase from Non-Hepatic Causes. J Clin Med; 12. Epub ahead of print 30 December 2022. DOI: 10.3390/jcm12010310. [Link]

31.

Rosalki SB, Tarlow D, Rau D. Plasma gamma-glutamyl transpeptidase elevation in patients receiving enzyme-inducing drugs. Lancet 1971; 2: 376–7. [Link]

32.

Kalas MA, Chavez L, Leon M, et al. Abnormal liver enzymes: A review for clinicians. World J Hepatol 2021; 13: 1688–1698. [Link]

33.

Bozkus F, Dikmen N, Sahin H, et al. Serum Gamma-Glutamyl Transferase Activity as a Potential Novel Cardiovascular Biomarker in COPD. Respir Care 2016; 61: 1465–1471. [Link]

34.

Brennan PN, Dillon JF, Tapper EB. Gamma-Glutamyl Transferase (γ-GT) - an old dog with new tricks? Liver Int 2022; 42: 9–15. [Link]

35.

Lowe D STZM et al. Alkaline Phosphatase. StatPearls [Internet]. [Link]

36.

37.

Northup PG, Caldwell SH. Coagulation in liver disease: a guide for the clinician. Clin Gastroenterol Hepatol 2013; 11: 1064–74. [Link]

38.

39.

Edoardo G. Giannini, Stephen H. Caldwell. Mistakes in coagulation in liver disease and how to avoid them. UEG Mistakes In Articles. [Link]

40.

Lee WM, Stravitz RT, Larson AM. Introduction to the revised American Association for the Study of Liver Diseases Position Paper on acute liver failure 2011. Hepatology 2012; 55: 965–7. [Link]

41.

Lee WM, Squires RH, Nyberg SL, et al. Acute liver failure: Summary of a workshop. Hepatology 2008; 47: 1401–15. [Link]

42.

O’Grady JG, Alexander GJ, Hayllar KM, et al. Early indicators of prognosis in fulminant hepatic failure. Gastroenterology 1989; 97: 439–45. [Link]

43.

Nguyen-Khac E, Thevenot T, Piquet M-A, et al. Glucocorticoids plus N-acetylcysteine in severe alcoholic hepatitis. N Engl J Med 2011; 365: 1781–9. [Link]

44.

Tenner S, Dubner H, Steinberg W. Predicting gallstone pancreatitis with laboratory parameters: a meta-analysis. Am J Gastroenterol 1994; 89: 1863–6. [Link]

45.

Henry F, Quatresooz P, Valverde-Lopez JC, et al. Blood vessel changes during pregnancy: a review. Am J Clin Dermatol 2006; 7: 65–9. [Link]

46.

Walker I, Chappell LC, Williamson C. Abnormal liver function tests in pregnancy. BMJ 2013; 347: f6055. [Link]

47.

Sarkar M, Brady CW, Fleckenstein J, et al. Reproductive Health and Liver Disease: Practice Guidance by the American Association for the Study of Liver Diseases. Hepatology 2021; 73: 318–365. [Link]

48.

Casey LC, Fontana RJ, Aday A, et al. Acute Liver Failure (ALF) in Pregnancy: How Much Is Pregnancy Related? Hepatology 2020; 72: 1366–1377. [Link]

49.

50.

Westbrook RH, Dusheiko G, Williamson C. Pregnancy and liver disease. J Hepatol 2016; 64: 933–945. [Link]

51.

Williamson C, Nana M, Poon L, et al. EASL Clinical Practice Guidelines on the management of liver diseases in pregnancy. J Hepatol 2023; 79: 768–828. [Link]

52.

Knight M, Nelson-Piercy C, Kurinczuk JJ, et al. A prospective national study of acute fatty liver of pregnancy in the UK. Gut 2008; 57: 951–956. [Link]

53.

54.

Brady CW. Liver Disease in Pregnancy: What’s New. Hepatol Commun 2020; 4: 145–156. [Link]

55.

56.

Haanen J, Obeid M, Spain L, et al. Management of toxicities from immunotherapy: ESMO Clinical Practice Guideline for diagnosis, treatment and follow-up. Ann Oncol 2022; 33: 1217–1238. [Link]

57.

De Martin E, Michot J-M, Papouin B, et al. Characterization of liver injury induced by cancer immunotherapy using immune checkpoint inhibitors. J Hepatol 2018; 68: 1181–1190. [Link]

Abstract

Hepatitis C virus (HCV) infection remains an important global health concern. It is estimated that there are approximately 50 million people infected with HCV globally, with around 1 million new infections each year and about 242,000 deaths annually attributed to HCV-related complications. Most acute HCV infections (55–85%) become chronic due to the virus’s effective evasion strategies, with spontaneous clearance being rare once chronicity is established. This condition often progresses silently, with many individuals unaware of their infection until advanced liver damage has occurred. If left untreated, HCV can lead to severe complications, including liver cirrhosis and hepatocellular carcinoma (HCC). HCV transmission occurs mainly through percutaneous exposure to infected blood. HCV can also spread from mother to infant (vertical transmission) and, less frequently, via sexual contact.1,2 In recent years, the introduction of oral direct-acting antivirals (DAAs), with remarkable safety and effectiveness profiles, has led to a sustained virological response (SVR) in virtually all (>97%) HCV-infected patients, regardless of HCV genotype or disease stage. However, significant barriers remain, such as issues with diagnosis, access to treatment and awareness of the disease.

Here, we discuss some of the misconceptions in HCV management and provide a practical management approach grounded in evidence and clinical experience.

Topics

Hepatobiliary

Citation

Garcia A.C and Alexandrino G. Mistakes in hepatits C and how to avoid them. UEG Education 2025; 25: 14-17.

Published

2025

More Like This:

European Society for the Study of Coeliac Disease 2025 Updated Guidelines on the Diagnosis and Management of Coeliac Disease in Adults. Part 1: Diagnostic Approach

Abdulbaqi Al-Toma

Esophageal and Oropharyngeal Dysphagia: Clinical Recommendations From the United European Gastroenterology and European Society for Neurogastroenterology and Motility

Amir Mari

EASL Clinical Practice Guidelines on liver transplantation

Coeliac disease with David Sanders

Pradeep Mundre

Mistakes in hepatitis C and how to avoid them

Gonçalo Alexandrino

EASL–EASD–EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD)

UEG Standards and Guidelines

Clinical Practice Guideline

Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

Not sure what you can access? Learn more about account types.

EASL–EASD–EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD)

Summary

AI Generated

Summary is not available for this content yet.

Download PDF

Was this helpful?

Thanks for your feedback.

Guideline

Summary

Metabolic dysfunction-associated steatotic liver disease (MASLD), previously termed non-alcoholic fatty liver disease (NAFLD), is defined as steatotic liver disease (SLD) in the presence of one or more cardiometabolic risk factor(s) and the absence of harmful alcohol intake. The spectrum of MASLD includes steatosis, metabolic dysfunction-associated steatohepatitis (MASH, previously NASH), fibrosis, cirrhosis and MASH-related hepatocellular carcinoma (HCC). This joint EASL-EASD-EASO guideline provides an update on definitions, prevention, screening, diagnosis and treatment for MASLD. Case-finding strategies for MASLD with liver fibrosis, using non-invasive tests, should be applied in individuals with cardiometabolic risk factors, abnormal liver enzymes, and/or radiological signs of hepatic steatosis, particularly in the presence of type 2 diabetes (T2D) or obesity with additional metabolic risk factor(s). A stepwise approach using blood-based scores (such as FIB-4) and, sequentially, imaging techniques (such as transient elastography) is suitable to rule-out/in advanced fibrosis, which is predictive of liver-related outcomes. In adults with MASLD, lifestyle modification – including weight loss, dietary changes, physical exercise and discouraging alcohol consumption – as well as optimal management of comorbidities – including use of incretin-based therapies (e.g. semaglutide, tirzepatide) for T2D or obesity, if indicated – is advised. Bariatric surgery is also an option in individuals with MASLD and obesity. If locally approved and dependent on the label, adults with non-cirrhotic MASH and significant liver fibrosis (stage ≥2) should be considered for a MASH-targeted treatment with resmetirom, which demonstrated histological effectiveness on steatohepatitis and fibrosis with an acceptable safety and tolerability profile. No MASH-targeted pharmacotherapy can currently be recommended for the cirrhotic stage. Management of MASH-related cirrhosis includes adaptations of metabolic drugs, nutritional counselling, surveillance for portal hypertension and HCC, as well as liver transplantation in decompensated cirrhosis.

Source file

https://doi.org/10.1016/j.jhep.2024.04.031

Publisher

European Association for the Study of the Liver

Guideline

Clinical Practice Guideline

Topics

Hepatobiliary

Citation

Journal of Hepatology, Volume 81, Issue 3, 492 - 542

Published

2024

More Like This:

European Society for the Study of Coeliac Disease 2025 Updated Guidelines on the Diagnosis and Management of Coeliac Disease in Adults. Part 1: Diagnostic Approach

Abdulbaqi Al-Toma

Esophageal and Oropharyngeal Dysphagia: Clinical Recommendations From the United European Gastroenterology and European Society for Neurogastroenterology and Motility

Amir Mari

EASL Clinical Practice Guidelines on liver transplantation

Coeliac disease with David Sanders

Pradeep Mundre

Mistakes in hepatitis C and how to avoid them

Gonçalo Alexandrino