Emergency TIPS in a Child-Pugh B patient: When does the window of opportunity open and close?

Trebicka, Jonel

doi:10.1016/j.jhep.2016.10.025

Cited by 74 publications

(70 citation statements)

References 82 publications

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“…Especially, when PHT is present (increased pressure in the portal vein and the mesenteric veins collecting blood from the splanchnic organs to the liver), complications arise [42]. A TIPS is the most effective treatment of PHT and yet, even after this procedure, many patients develop complications of liver disease [43,44], especially due to the spillover of inflammation with resulting development of ACLF as shown by recent data [5,45,46]. Additionally, it was found that the presence of ascites, as a sign of decompensation, determines the composition of the circulating microbiome in the portal vein compared to the hepatic vein, right atrium, and peripheral venous blood, and that specific circulating microbiome members correlate with inflammatory markers [47].…”

Section: Bacterial Translocation and Systemic Inflammationmentioning

confidence: 99%

Gut-Liver Axis Links Portal Hypertension to Acute-on-Chronic Liver Failure

2018

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Acute-on-chronic liver failure (ACLF) is considered a distinct syndrome in patients with liver disease, with systemic inflammation playing a central role. Portal hypertension (PHT) is also aggravated by inflammation and may subsequently impact the course of ACLF. PHT is more than just an increase in portal pressure in the portal venous system; it aggravates the course of liver disease and, thus, also facilitates the development of acute decompensation and ACLF. A critical mechanistic link between PHT and ACLF might be the gut-liver axis, which is discussed in this review.

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Section: Bacterial Translocation and Systemic Inflammationmentioning

confidence: 99%

Gut-Liver Axis Links Portal Hypertension to Acute-on-Chronic Liver Failure

2018

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“…As outlined above, severe liver fibrosis with portal hypertension induces acute decompensation (AD), such as variceal bleeding, refractory ascites, or hepatorenal syndrome, which can be treated with transjugular intrahepatic portosystemic shunt implantation (TIPS) 14. In selected patients, TIPS decompresses the portal venous system, successfully treats ascites and variceal bleeding, and improves survival 14, 15, 16, 17.…”

Section: Introductionmentioning

confidence: 99%

“…In selected patients, TIPS decompresses the portal venous system, successfully treats ascites and variceal bleeding, and improves survival 14, 15, 16, 17. However, AD of liver cirrhosis can progress and develop into acute‐on‐chronic liver failure (ACLF) with poor survival 18.…”

Section: Introductionmentioning

confidence: 99%

Acute decompensation boosts hepatic collagen type III deposition and deteriorates experimental and human cirrhosis

Praktiknjo

Lehmann

Nielsen

et al. 2018

Hepatology Communications

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Patients with end‐stage liver disease develop acute decompensation (AD) episodes, which become more frequent and might develop into acute‐on‐chronic liver failure (ACLF). However, it remains unknown how AD induces acceleration of liver disease. We hypothesized that remodeling of collagen type III plays a role in the acceleration of liver cirrhosis after AD and analyzed its formation (Pro‐C3) and degradation (matrix metalloproteinase‐degraded type III collagen [C3M]) markers in animal models and human disease. Bile duct ligation induced different stages of liver fibrosis in rats. Fibrosis development (hydroxyprolin content, sirius red staining, α‐smooth muscle actin immunohistochemistry, messenger RNA of profibrotic cytokines), necroinflammation (aminotransferases levels), fibrolysis (matrix metalloproteinase 2 expression and activity, C1M, C4M), and Pro‐C3 and C3M were analyzed 2, 3, 4, 5, and 6 weeks after bile duct ligation (n = 5 each group). In 110 patients with decompensated liver cirrhosis who underwent a transjugular intrahepatic portosystemic shunt procedure for AD, clinical and laboratory parameters as well as Pro‐C3 and C3M were measured in blood samples from portal and hepatic veins and were collected just before the transjugular intrahepatic portosystemic shunt placement and 1‐3 weeks later. Animal studies showed increased markers of collagen type III deposition with fibrosis, necroinflammation, and decompensation of liver cirrhosis, defined as ascites development. Higher Pro‐C3 levels were associated with injury, disease severity scores (Model for End‐Stage Liver Disease, Child‐Pugh, chronic liver failure‐C AD), ACLF development, and mortality. C3M decreased with AD and the chronic liver failure‐C AD score. Collagen type III deposition ratio increased with the risk of ACLF development and mortality. Conclusion: We show for the first time that AD boosts collagen type III deposition in experimental and human cirrhosis, possibly contributing to the worsened outcome in patients with decompensated cirrhosis. (Hepatology Communications 2018;2:211–222)

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“…TIPS leads to immediate decompression in the portal venous system and subsequent increase of effective blood volume. It stops variceal rebleeding and improves renal function . The clinical stratification of patients receiving TIPS has been investigated in several studies, selecting either high‐risk patients receiving TIPS for variceal bleeding or patients with a lower risk receiving TIPS for refractory ascites and hepatorenal syndrome .…”

mentioning

confidence: 99%

“…It stops variceal rebleeding and improves renal function . The clinical stratification of patients receiving TIPS has been investigated in several studies, selecting either high‐risk patients receiving TIPS for variceal bleeding or patients with a lower risk receiving TIPS for refractory ascites and hepatorenal syndrome . However, while the indication for TIPS might be one of the above, many patients present with other complications of portal hypertension and acute decompensation (AD) of liver cirrhosis .…”

mentioning

confidence: 99%