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Mistakes in decompensated liver cirrhosis and how to avoid them

Tammo Lambert Tergast, Benjamin Maasoumy

Summary

AI Generated

Early chronic liver disease and compensated cirrhosis can remain asymptomatic for years, but progression to decompensated cirrhosis drastically increases morbidity and mortality.

  • Patients with early chronic liver disease and compensated cirrhosis can present without clinical symptoms, allowing liver disease and damage to remain unidentified for many years.
  • Decompensated cirrhosis is defined by clinically overt signs of portal hypertension or impaired hepatic function, including variceal bleeding, ascites, or overt hepatic encephalopathy.
  • Morbidity and mortality drastically increase once decompensated cirrhosis develops.
  • The first hepatic decompensation event significantly increases the risk of further complications and decompensation episodes.
  • Individuals with advanced liver cirrhosis are four times more susceptible to infection, which is the most frequent trigger of hepatic decompensation.
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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
1.
Jalan R, et al. Bacterial infections in cirrhosis: a position statement based on the EASL Special Conference 2013. J Hepatol 2014; 60: 1310–1324. [Link]
2.
European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol 2018; 69: 406–460. [Link]
3.
Moreau R, et al. Acute-on-chronic liver failure is a distinct syndrome that develops in patients with acute decompensation of cirrhosis. Gastroenterology 2013; 144: 1426–37, 1437.e1–9. [Link]
4.
Arvaniti V, et al. Infections in patients with cirrhosis increase mortality four-fold and should be used in determining prognosis. Gastroenterology 2010; 139: 1246–56, 1256.e1–5. [Link]
5.
Forgacs I and Loganayagam A. Overprescribing proton pump inhibitors. BMJ 2008; 336: 2–3. [Link]
6.
Attwood S, et al. Long‐term safety of proton pump inhibitor therapy assessed under controlled, randomised clinical trial conditions: data from the SOPRAN and LOTUS studies. Aliment Pharmacol Ther 2015; 41: 1162–1174. [Link]
7.
Dam G, et al. Proton pump inhibitors as a risk factor for hepatic encephalopathy and spontaneous bacterial peritonitis in patients with cirrhosis with ascites. Hepatology 2016; 64: 1265–1272. [Link]
8.
Tsai CF, et al. Proton pump inhibitors increase risk for hepatic encephalopathy in patients with cirrhosis in a population study. Gastroenterology 2017; 152: 134–141. [Link]
9.
Tergast TL, et al. Dose dependent impact of proton pump inhibitors on the clinical course of spontaneous bacterial peritonitis. Liver Int 2018; 38: 1602–1613. [Link]
10.
Sturm L, et al. Treatment with proton pump inhibitors increases the risk for development of hepatic encephalopathy after implantation of transjugular intrahepatic portosystemic shunt (TIPS). United European Gastroenterol J 2018; 6: 1380–1390. [Link]
11.
Trikudanathan G, et al. Association between proton pump inhibitors and spontaneous bacterial peritonitis in cirrhotic patients – a systematic review and meta-analysis. Int J Clin Pract 2011; 65: 674–678. [Link]
12.
Hung T, et al. Effect of proton pump inhibitors on mortality in patients with cirrhosis and spontaneous bacterial peritonitis. Annal Hepatol 2018; 17: 933–939. [Link]
13.
Bajaj JS, et al. Systems biology analysis of omeprazole therapy in cirrhosis demonstrates significant shifts in gut microbiota composition and function. Am J Physiol Gastrointest Liver Physiol 2014; 307: G951–G957. [Link]
14.
Mandorfer M and Reiberger T. Beta blockers and cirrhosis, 2016. Dig Liv Dis 2017; 49: 3–10. [Link]
15.
Krag A, et al. The window hypothesis: haemodynamic and non-haemodynamic effects of beta-blockers improve survival of patients with cirrhosis during a window in the disease. Gut 2012; 61: 967–969. [Link]
16.
Senzolo M, et al. Beta-blockers protect against spontaneous bacterial peritonitis in cirrhotic patients: a meta-analysis. Liver Int 2009; 29: 1189–1193. [Link]
17.
Lebrec D, et al. Propranolol for prevention of recurrent gastrointestinal bleeding in patients with cirrhosis: a controlled study. N Engl J Med 1981; 305: 1371–1374. [Link]
18.
Sharma M, et al. Comparison of therapies for primary prevention of esophageal variceal bleeding: a systematic review and network meta‐analysis. Hepatology 2019; 69: 1657–1675. [Link]
19.
Tergast TL, et al. PS-081 Systemic arterial blood pressure determines the therapeutic window of NSBB in patients with decompesanted liver cirrhosis. J Hepatol 2019; 70: e52. [Link]
20.
Villanueva C, et al. β blockers to prevent decompensation of cirrhosis in patients with clinically significant portal hypertension (PREDESCI): a randomised, double-blind, placebo-controlled, multicentre trial. Lancet 2019; 393: 1597–1608. [Link]
21.
Reiberger T and Mandorfer M. Beta adrenergic blockade and decompensated cirrhosis. J Hepatol 2017; 66: 849–859. [Link]
22.
Reiberger T, et al. Carvedilol for primary prophylaxis of variceal bleeding in cirrhotic patients with haemodynamic non-response to propranolol. Gut 2013; 62: 1634–1641. [Link]
23.
Serste T, et al. Deleterious effects of beta-blockers on survival in patients with cirrhosis and refractory ascites. Hepatology 2010; 52: 1017–1022. [Link]
24.
Mandorfer M, et al. Nonselective beta blockers increase risk for hepatorenal syndrome and death in patients with cirrhosis and spontaneous bacterial peritonitis. Gastroenterology 2014; 146: 1680–1690.e1. [Link]
25.
Madsen BS, et al. Keep the sick from harm in spontaneous bacterial peritonitis: dose of beta blockers matters. J Hepatol 2016; 64: 1455–1456. [Link]
26.
Leithead JA, et al. Non-selective beta-blockers are associated with improved survival in patients with ascites listed for liver transplantation. Gut 2015; 64: 1111–1119. [Link]
27.
Mookerjee RP, et al. Treatment with non-selective beta blockers is associated with reduced severity of systemic inflammation and improved survival of patients with acute-on-chronic liver failure. J Hepatol 2016; 64: 574–582. [Link]
28.
Piano S, et al. Epidemiology and effects of bacterial infections in patients with cirrhosis worldwide. Gastroenterology 2019; 156: 1368–1380.e10. [Link]
29.
Fernández J, et al. Multidrug-resistant bacterial infections in patients with decompensated cirrhosis and with acute-on-chronic liver failure in Europe. J Hepatol 2019; 70: 398–411. [Link]
30.
Fernández J, et al. Prevalence and risk factors of infections by multiresistant bacteria in cirrhosis: a prospective study. Hepatology 2012; 55: 1551–1561. [Link]
31.
Lin C, et al. Should bleeding tendency deter abdominal paracentesis? Dig Liv Dis 2005; 37: 946–951. [Link]
32.
Kim JJ, et al. Delayed paracentesis is associated with increased in-hospital mortality in patients with spontaneous bacterial peritonitis. Am J Gastroenterol 2014; 109: 1436–1442. [Link]
33.
Jepsen P. Comorbidity in cirrhosis. World J Gastroenterol 2014; 20: 7223–7230. [Link]
34.
Krag A, et al. Low cardiac output predicts development of hepatorenal syndrome and survival in patients with cirrhosis and ascites. Gut 2010; 59: 105–110. [Link]
35.
Elkrief L, et al. Diabetes mellitus in patients with cirrhosis: clinical implications and management. Liver Int 2016; 36: 936–948. [Link]
36.
Wlazlo N, et al. High prevalence of diabetes mellitus in patients with liver cirrhosis. Diabet Med 2010; 27: 1308–1311. [Link]
37.
Liu TL, et al. Diabetes is associated with clinical decompensation events in patients with cirrhosis. Dig Dis Sci 2016; 61: 3335–3345. [Link]
38.
Jepsen P, et al. Diabetes as a risk factor for hepatic encephalopathy in cirrhosis patients. J Hepatol 2015; 63: 1133–1138. [Link]
39.
Tergast TL, et al. Association between type 2 diabetes mellitus, HbA1c and the risk for spontaneous bacterial peritonitis in patients with decompensated liver cirrhosis and ascites. Clin Transl Gastroenterol 2018; 9: 189. [Link]
40.
Angeli P, et al. Hyponatremia in cirrhosis: results of a patient population survey. Hepatology 2006; 44: 1535–1542. [Link]
41.
John S and Thuluvath PJ. Hyponatremia in cirrhosis: pathophysiology and management. World J Gastroenterol 2015; 21: 3197–3205. [Link]
42.
Leise M and Cárdenas A. Hyponatremia in cirrhosis: implications for liver transplantation. Liver Transpl 2018; 24: 1612–1621. [Link]
43.
Guevara M, et al. Hyponatremia is a risk factor of hepatic encephalopathy in patients with cirrhosis: a prospective study with time-dependent analysis. Am J Gastroenterol 2009; 104: 1382–1389. [Link]
44.
Patel S, et al. Treatment of cirrhosis-associated hyponatremia with midodrine and octreotide. Frontiers Med (Lausanne) 2017; 4: 17. [Link]
45.
McCormick PA, et al. Intravenous albumin infusion is an effective therapy for hyponatraemia in cirrhotic patients with ascites. Gut 1990; 31: 204–207. [Link]
46.
Praktiknjo M, et al. Fat‐free muscle mass in magnetic resonance imaging predicts acute‐on‐chronic liver failure and survival in decompensated cirrhosis. Hepatology 2018; 67: 1014–1026. [Link]
47.
Lattanzi B, D’Ambrosio D and Merli M. Hepatic encephalopathy and sarcopenia: two faces of the same metabolic alteration. J Clin Exp Hepatol 2019; 9: 125–130. [Link]
48.
Kalafateli M, et al. Malnutrition and sarcopenia predict post‐liver transplantation outcomes independently of the Model for End‐stage Liver Disease score. J Cachexia, Sarcopenia Muscle 2017; 8: 113–121. [Link]
49.
van Vugt, et al. A model including sarcopenia surpasses the MELD score in predicting waiting list mortality in cirrhotic liver transplant candidates: a competing risk analysis in a national cohort. J Hepatol 2018; 68: 707–714. [Link]
50.
European Association for the Study of the Liver. EASL Clinical Practice Guidelines on nutrition in chronic liver disease. J Hepatol 2019; 70: 172–193. [Link]
51.
Borhofen SM, et al. The Royal Free Hospital-Nutritional Prioritizing Tool is an independent predictor of deterioration of liver function and survival in cirrhosis. Dig Dis Sci 2016; 61: 1735–1743. [Link]
52.
Mehta G, et al. Inflammation and portal hypertension – the undiscovered country. J Hepatol 2014; 61: 155–163. [Link]
53.
Tripodi A, et al. An imbalance of pro- vs anti-coagulation factors in plasma from patients with cirrhosis. Gastroenterology 2009; 137: 2105–2111. [Link]
54.
Englesbe MJ, et al. Portal vein thrombosis and survival in patients with cirrhosis. Liver Transpl 2010; 16: 83–90. [Link]
55.
Loffredo L, et al. Effects of anticoagulants in patients with cirrhosis and portal vein thrombosis: a systematic review and meta-analysis. Gastroenterology 2017; 153: 480–487.e1. [Link]
56.
Senzolo MM, et al. Prospective evaluation of anticoagulation and transjugular intrahepatic portosystemic shunt for the management of portal vein thrombosis in cirrhosis. Liver Int 2012; 32: 919–927. [Link]
57.
Delgado MG, et al. Efficacy and safety of anticoagulation on patients with cirrhosis and portal vein thrombosis. Clinical Gastroenterol Hepatol 2012; 10: 776–783. [Link]
58.
Intagliata N, et al. Direct oral anticoagulants in cirrhosis patients pose similar risks of bleeding when compared to traditional anticoagulation. Dig Dis Sci 2016; 61: 1721–1727. [Link]
59.
Villa E, et al. Enoxaparin prevents portal vein thrombosis and liver decompensation in patients with advanced cirrhosis. Gastroenterology 2012; 143: 1253–1260.e4. [Link]

Abstract

Patients with early stages of chronic liver disease and even those with compensated cirrhosis can present without any clinical symptoms, which means that liver disease and ongoing liver damage can remain unidentified for many years. However, morbidity and mortality drastically increase once the stage of ‘decompensated cirrhosis’ has been reached.  Decompensated cirrhosis describes the development of clinically overt signs of portal hypertension and/or impairment of hepatic function (e.g. variceal bleeding, ascites or overt hepatic encephalopathy). The first hepatic decompensation event significantly increases the risk that further complications of liver cirrhosis and decompensation episodes will occur.2 Moreover, individuals who have advanced stages of liver cirrhosis are four times more susceptible to infection, which is, in turn, the most frequent trigger of hepatic decompensation.

Topics

Hepatobiliary

Citation

Tergast TL, Beier C and Maasoumy B. Mistakes in decompensated liver cirrhosis and how to avoid them. UEG Education 2019; 19: 25–30. 

Published

2019

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

Log in to continue.

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

Log In Create a free account

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

Mistakes in acute jaundice and how to avoid them

Spyridon Siakavellas, Georgios Papatheodoridis

Summary

AI Generated

Summary is not available for this content yet.

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
1.
Jalan R, et al. Bacterial infections in cirrhosis: a position statement based on the EASL Special Conference 2013. J Hepatol 2014; 60: 1310–1324. [Link]
2.
European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol 2018; 69: 406–460. [Link]
3.
Moreau R, et al. Acute-on-chronic liver failure is a distinct syndrome that develops in patients with acute decompensation of cirrhosis. Gastroenterology 2013; 144: 1426–37, 1437.e1–9. [Link]
4.
Arvaniti V, et al. Infections in patients with cirrhosis increase mortality four-fold and should be used in determining prognosis. Gastroenterology 2010; 139: 1246–56, 1256.e1–5. [Link]
5.
Forgacs I and Loganayagam A. Overprescribing proton pump inhibitors. BMJ 2008; 336: 2–3. [Link]
6.
Attwood S, et al. Long‐term safety of proton pump inhibitor therapy assessed under controlled, randomised clinical trial conditions: data from the SOPRAN and LOTUS studies. Aliment Pharmacol Ther 2015; 41: 1162–1174. [Link]
7.
Dam G, et al. Proton pump inhibitors as a risk factor for hepatic encephalopathy and spontaneous bacterial peritonitis in patients with cirrhosis with ascites. Hepatology 2016; 64: 1265–1272. [Link]
8.
Tsai CF, et al. Proton pump inhibitors increase risk for hepatic encephalopathy in patients with cirrhosis in a population study. Gastroenterology 2017; 152: 134–141. [Link]
9.
Tergast TL, et al. Dose dependent impact of proton pump inhibitors on the clinical course of spontaneous bacterial peritonitis. Liver Int 2018; 38: 1602–1613. [Link]
10.
Sturm L, et al. Treatment with proton pump inhibitors increases the risk for development of hepatic encephalopathy after implantation of transjugular intrahepatic portosystemic shunt (TIPS). United European Gastroenterol J 2018; 6: 1380–1390. [Link]
11.
Trikudanathan G, et al. Association between proton pump inhibitors and spontaneous bacterial peritonitis in cirrhotic patients – a systematic review and meta-analysis. Int J Clin Pract 2011; 65: 674–678. [Link]
12.
Hung T, et al. Effect of proton pump inhibitors on mortality in patients with cirrhosis and spontaneous bacterial peritonitis. Annal Hepatol 2018; 17: 933–939. [Link]
13.
Bajaj JS, et al. Systems biology analysis of omeprazole therapy in cirrhosis demonstrates significant shifts in gut microbiota composition and function. Am J Physiol Gastrointest Liver Physiol 2014; 307: G951–G957. [Link]
14.
Mandorfer M and Reiberger T. Beta blockers and cirrhosis, 2016. Dig Liv Dis 2017; 49: 3–10. [Link]
15.
Krag A, et al. The window hypothesis: haemodynamic and non-haemodynamic effects of beta-blockers improve survival of patients with cirrhosis during a window in the disease. Gut 2012; 61: 967–969. [Link]
16.
Senzolo M, et al. Beta-blockers protect against spontaneous bacterial peritonitis in cirrhotic patients: a meta-analysis. Liver Int 2009; 29: 1189–1193. [Link]
17.
Lebrec D, et al. Propranolol for prevention of recurrent gastrointestinal bleeding in patients with cirrhosis: a controlled study. N Engl J Med 1981; 305: 1371–1374. [Link]
18.
Sharma M, et al. Comparison of therapies for primary prevention of esophageal variceal bleeding: a systematic review and network meta‐analysis. Hepatology 2019; 69: 1657–1675. [Link]
19.
Tergast TL, et al. PS-081 Systemic arterial blood pressure determines the therapeutic window of NSBB in patients with decompesanted liver cirrhosis. J Hepatol 2019; 70: e52. [Link]
20.
Villanueva C, et al. β blockers to prevent decompensation of cirrhosis in patients with clinically significant portal hypertension (PREDESCI): a randomised, double-blind, placebo-controlled, multicentre trial. Lancet 2019; 393: 1597–1608. [Link]
21.
Reiberger T and Mandorfer M. Beta adrenergic blockade and decompensated cirrhosis. J Hepatol 2017; 66: 849–859. [Link]
22.
Reiberger T, et al. Carvedilol for primary prophylaxis of variceal bleeding in cirrhotic patients with haemodynamic non-response to propranolol. Gut 2013; 62: 1634–1641. [Link]
23.
Serste T, et al. Deleterious effects of beta-blockers on survival in patients with cirrhosis and refractory ascites. Hepatology 2010; 52: 1017–1022. [Link]
24.
Mandorfer M, et al. Nonselective beta blockers increase risk for hepatorenal syndrome and death in patients with cirrhosis and spontaneous bacterial peritonitis. Gastroenterology 2014; 146: 1680–1690.e1. [Link]
25.
Madsen BS, et al. Keep the sick from harm in spontaneous bacterial peritonitis: dose of beta blockers matters. J Hepatol 2016; 64: 1455–1456. [Link]
26.
Leithead JA, et al. Non-selective beta-blockers are associated with improved survival in patients with ascites listed for liver transplantation. Gut 2015; 64: 1111–1119. [Link]
27.
Mookerjee RP, et al. Treatment with non-selective beta blockers is associated with reduced severity of systemic inflammation and improved survival of patients with acute-on-chronic liver failure. J Hepatol 2016; 64: 574–582. [Link]
28.
Piano S, et al. Epidemiology and effects of bacterial infections in patients with cirrhosis worldwide. Gastroenterology 2019; 156: 1368–1380.e10. [Link]
29.
Fernández J, et al. Multidrug-resistant bacterial infections in patients with decompensated cirrhosis and with acute-on-chronic liver failure in Europe. J Hepatol 2019; 70: 398–411. [Link]
30.
Fernández J, et al. Prevalence and risk factors of infections by multiresistant bacteria in cirrhosis: a prospective study. Hepatology 2012; 55: 1551–1561. [Link]
31.
Lin C, et al. Should bleeding tendency deter abdominal paracentesis? Dig Liv Dis 2005; 37: 946–951. [Link]
32.
Kim JJ, et al. Delayed paracentesis is associated with increased in-hospital mortality in patients with spontaneous bacterial peritonitis. Am J Gastroenterol 2014; 109: 1436–1442. [Link]
33.
Jepsen P. Comorbidity in cirrhosis. World J Gastroenterol 2014; 20: 7223–7230. [Link]
34.
Krag A, et al. Low cardiac output predicts development of hepatorenal syndrome and survival in patients with cirrhosis and ascites. Gut 2010; 59: 105–110. [Link]
35.
Elkrief L, et al. Diabetes mellitus in patients with cirrhosis: clinical implications and management. Liver Int 2016; 36: 936–948. [Link]
36.
Wlazlo N, et al. High prevalence of diabetes mellitus in patients with liver cirrhosis. Diabet Med 2010; 27: 1308–1311. [Link]
37.
Liu TL, et al. Diabetes is associated with clinical decompensation events in patients with cirrhosis. Dig Dis Sci 2016; 61: 3335–3345. [Link]
38.
Jepsen P, et al. Diabetes as a risk factor for hepatic encephalopathy in cirrhosis patients. J Hepatol 2015; 63: 1133–1138. [Link]
39.
Tergast TL, et al. Association between type 2 diabetes mellitus, HbA1c and the risk for spontaneous bacterial peritonitis in patients with decompensated liver cirrhosis and ascites. Clin Transl Gastroenterol 2018; 9: 189. [Link]
40.
Angeli P, et al. Hyponatremia in cirrhosis: results of a patient population survey. Hepatology 2006; 44: 1535–1542. [Link]
41.
John S and Thuluvath PJ. Hyponatremia in cirrhosis: pathophysiology and management. World J Gastroenterol 2015; 21: 3197–3205. [Link]
42.
Leise M and Cárdenas A. Hyponatremia in cirrhosis: implications for liver transplantation. Liver Transpl 2018; 24: 1612–1621. [Link]
43.
Guevara M, et al. Hyponatremia is a risk factor of hepatic encephalopathy in patients with cirrhosis: a prospective study with time-dependent analysis. Am J Gastroenterol 2009; 104: 1382–1389. [Link]
44.
Patel S, et al. Treatment of cirrhosis-associated hyponatremia with midodrine and octreotide. Frontiers Med (Lausanne) 2017; 4: 17. [Link]
45.
McCormick PA, et al. Intravenous albumin infusion is an effective therapy for hyponatraemia in cirrhotic patients with ascites. Gut 1990; 31: 204–207. [Link]
46.
Praktiknjo M, et al. Fat‐free muscle mass in magnetic resonance imaging predicts acute‐on‐chronic liver failure and survival in decompensated cirrhosis. Hepatology 2018; 67: 1014–1026. [Link]
47.
Lattanzi B, D’Ambrosio D and Merli M. Hepatic encephalopathy and sarcopenia: two faces of the same metabolic alteration. J Clin Exp Hepatol 2019; 9: 125–130. [Link]
48.
Kalafateli M, et al. Malnutrition and sarcopenia predict post‐liver transplantation outcomes independently of the Model for End‐stage Liver Disease score. J Cachexia, Sarcopenia Muscle 2017; 8: 113–121. [Link]
49.
van Vugt, et al. A model including sarcopenia surpasses the MELD score in predicting waiting list mortality in cirrhotic liver transplant candidates: a competing risk analysis in a national cohort. J Hepatol 2018; 68: 707–714. [Link]
50.
European Association for the Study of the Liver. EASL Clinical Practice Guidelines on nutrition in chronic liver disease. J Hepatol 2019; 70: 172–193. [Link]
51.
Borhofen SM, et al. The Royal Free Hospital-Nutritional Prioritizing Tool is an independent predictor of deterioration of liver function and survival in cirrhosis. Dig Dis Sci 2016; 61: 1735–1743. [Link]
52.
Mehta G, et al. Inflammation and portal hypertension – the undiscovered country. J Hepatol 2014; 61: 155–163. [Link]
53.
Tripodi A, et al. An imbalance of pro- vs anti-coagulation factors in plasma from patients with cirrhosis. Gastroenterology 2009; 137: 2105–2111. [Link]
54.
Englesbe MJ, et al. Portal vein thrombosis and survival in patients with cirrhosis. Liver Transpl 2010; 16: 83–90. [Link]
55.
Loffredo L, et al. Effects of anticoagulants in patients with cirrhosis and portal vein thrombosis: a systematic review and meta-analysis. Gastroenterology 2017; 153: 480–487.e1. [Link]
56.
Senzolo MM, et al. Prospective evaluation of anticoagulation and transjugular intrahepatic portosystemic shunt for the management of portal vein thrombosis in cirrhosis. Liver Int 2012; 32: 919–927. [Link]
57.
Delgado MG, et al. Efficacy and safety of anticoagulation on patients with cirrhosis and portal vein thrombosis. Clinical Gastroenterol Hepatol 2012; 10: 776–783. [Link]
58.
Intagliata N, et al. Direct oral anticoagulants in cirrhosis patients pose similar risks of bleeding when compared to traditional anticoagulation. Dig Dis Sci 2016; 61: 1721–1727. [Link]
59.
Villa E, et al. Enoxaparin prevents portal vein thrombosis and liver decompensation in patients with advanced cirrhosis. Gastroenterology 2012; 143: 1253–1260.e4. [Link]

Abstract

Jaundice can be caused by abnormalities in any of the steps comprising the formation, metabolism and excretion of bilirubin. In addition, these processes may be functioning properly, but jaundice can be seen because of an obstruction of the biliary tree at any point, from its intrahepatic origins to its end at the ampulla of Vater. For this reason, it is clear that numerous conditions can result in jaundice. When faced with a patient presenting with jaundice a reasonable and careful diagnostic approach is, therefore, warranted to elucidate the underlying cause of this sign. Conventional wisdom may be that “jaundice by itself never killed anyone,” but it is imperative to find the cause as soon as possible, as prompt intervention saves lives in many cases.

Topics

Hepatobiliary

Citation

Siakavellas S and Papatheodoridis G. Mistakes in acute jaundice and how to avoid them. UEG Education 2018; 18: 24–26.

Published

2025

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UEG Mistakes In Articles
Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

Log in to continue.

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

Log In Create a free account

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.

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
1.
Jalan R, et al. Bacterial infections in cirrhosis: a position statement based on the EASL Special Conference 2013. J Hepatol 2014; 60: 1310–1324. [Link]
2.
European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol 2018; 69: 406–460. [Link]
3.
Moreau R, et al. Acute-on-chronic liver failure is a distinct syndrome that develops in patients with acute decompensation of cirrhosis. Gastroenterology 2013; 144: 1426–37, 1437.e1–9. [Link]
4.
Arvaniti V, et al. Infections in patients with cirrhosis increase mortality four-fold and should be used in determining prognosis. Gastroenterology 2010; 139: 1246–56, 1256.e1–5. [Link]
5.
Forgacs I and Loganayagam A. Overprescribing proton pump inhibitors. BMJ 2008; 336: 2–3. [Link]
6.
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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

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Episode 6: UEG Journal October Spotlight

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Abstract

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Endoscopy Hepatobiliary IBD Pancreas

Published

2025

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ECCO Guidelines on Therapeutics in Crohn's Disease: Surgical Treatment

Michel Adamina

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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.

Guideline

Abstract

This article is the second in a series of two publications on the European Crohn’s and Colitis Organisation [ECCO] evidence-based consensus on the management of Crohn’s disease. The first article covers medical management; the present article addresses surgical management, including preoperative aspects and drug management before surgery. It also provides technical advice for a variety of common clinical situations. Both articles together represent the evidence-based recommendations of the ECCO for Crohn’s disease and an update of prior ECCO Guidelines.

Publisher

European Crohn’s and Colitis Organisation logo
European Crohn’s and Colitis Organisation

Guideline

Clinical Practice Guideline

Topics

IBD Surgery

Citation

Journal of Crohn's and Colitis, Volume 18, Issue 10, October 2024, Pages 1556–1582

Published

2024

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

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EASL Clinical Practice Guidelines on the management of hepatitis B virus infection

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AI Generated

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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.

Guideline

Summary

The updated EASL Clinical Practice Guidelines on the management of hepatitis B virus (HBV) infection provide comprehensive, evidence-based recommendations for its management. Spanning ten thematic sections, the guidelines address diagnostics, treatment goals, treatment indications, therapeutic options, hepatocellular carcinoma surveillance, management of special populations, HBV reactivation prophylaxis, post-transplant care, HBV prevention strategies, and finally address open questions and future research directions. Chronic HBV remains a global health challenge, with over 250 million individuals affected and significant mortality due to cirrhosis and hepatocellular carcinoma. These guidelines emphasise the importance of early diagnosis, risk stratification based on viral and host factors, and tailored antiviral therapy. Attention is given to simplified algorithms, vaccination, and screening to support global HBV elimination targets. The guidelines also discuss emerging biomarkers and evolving definitions of functional and partial cure. Developed through literature review, expert consensus, and a Delphi process, the guidelines aim to equip healthcare providers across disciplines with practical tools to optimise HBV care and outcomes worldwide.

Publisher

European Association for the Study of the Liver logo
European Association for the Study of the Liver

Guideline

Clinical Practice Guideline

Topics

Hepatobiliary

Citation

Journal of Hepatology, Volume 83, Issue 2, 502 - 583

Published

2025

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

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EASL Clinical Practice Guidelines on the management of extrahepatic cholangiocarcinoma

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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.

Guideline

Summary

Recent years have witnessed significant advances in the imaging, molecular profiling, and systemic treatment of cholangiocarcinoma (CCA). Despite this progress, the early detection, precise classification, and effective management of CCA remain challenging. Owing to recent developments and the significant differences in CCA subtypes, EASL commissioned a panel of experts to draft evidence-based recommendations on the management of extrahepatic CCA, comprising distal and perihilar CCA. Particular attention is given to the need for accurate classification systems, the integration of emerging molecular insights, and practical strategies for diagnosis and treatment that reflect real-world clinical scenarios.

Publisher

European Association for the Study of the Liver logo
European Association for the Study of the Liver

Guideline

Clinical Practice Guideline

Topics

Digestive Oncology Hepatobiliary

Citation

Journal of Hepatology, Volume 83, Issue 1, 211 - 238

Published

2025

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