Background: Transjugular intrahepatic portosystemic shunt (TIPS) is the standard procedure in the treatment of refractory ascites and variceal bleeding in the setting of portal hypertension. Secondary obstruction of the shunt is a classic but potentially lethal complication.
Methods: We present here the case of a cirrhotic patient that underwent a TIPS for refractory ascites, with early complete thrombosis without lethal complication.
Results: Obstruction of the TIPS led to thrombosis of both the right hepatic and the right portal veins with progressive total atrophy of the right liver and marked hypertrophy of the left liver. Despite initial poor liver function, biological hepatic markers improved slowly until complete recovery.
Conclusion: Hence, we suggest the concept of combined right portal and hepatic vein embolization as a new procedure to induce partial liver hypertrophy before major liver resection, even in cirrhotic patients.
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http://dx.doi.org/10.1007/s11605-016-3133-z | DOI Listing |
Rev Esp Anestesiol Reanim (Engl Ed)
January 2025
Hospital Universitario Gregorio Marañón, Madrid, Spain.
Liver transplantation (LT) has an incidence of intraoperative cardiopulmonary arrest (CPA) of around 5%. Patients who experience CPA during this procedure have a reduced survival rate of approximately 50%. Most CPAs occur during the neohepatic phase due to reperfusion syndrome, but this is not always the underlying cause, and a broad differential diagnosis must be performed.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
The Roger Williams Institute of Liver Studies, School of Immunology and Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London & Foundation for Liver Research, London SE5 9NT, UK.
Bacterial translocation-induced inflammation and immune dysfunction are recognised factors contributing to the pathogenesis of primary biliary cholangitis (PBC). However, the specific involvement of interferons (IFNs) and soluble checkpoints (sol-CRs) in shaping the immune landscape in PBC patients remains unexplored. Furthermore, the influence of ursodeoxycholic acid (UDC) on these immune mediators is unknown.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Gastroenterology-Liver-Endoscopy Unit, 2nd Department of Internal Medicine, General Hospital of Athens "Hippocration", National and Kapodistrian University of Athens, 115 27 Athens, Greece.
The microbiome of the human intestine is a regulator of health that modulates immune response and plays an important role in metabolism. The diversity, and abundance of microbiota communities in the gut have been shown to change in cirrhosis and its complications. We aimed to review the current knowledge regarding microbiota alterations in cirrhosis, its potential differences according to etiology, and its role in the development of cirrhosis complications.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Division of Endocrinology, Department of Internal Medicine, University Medical Center Groningen, University of Groningen, P.O. Box 30001, 9700 RB Groningen, The Netherlands.
Low-grade chronic inflammation may impact liver disease. We investigated the extent to which circulating GlycA, a glycoprotein biomarker of low-grade inflammation, and high-sensitivity C-reactive protein (hs-CRP) are altered in patients with cirrhosis and liver transplant recipients (LTRs) and examined their associations with all-cause mortality. Plasma GlycA (nuclear magnetic resonance spectroscopy) and hs-CRP (nephelometry) were assessed in 129 patients with cirrhosis on the waiting list for liver transplantation and 367 LTRs (TransplantLines cohort study; NCT03272841) and compared with 4837 participants from the population-based PREVEND cohort.
View Article and Find Full Text PDFMedicina (Kaunas)
December 2024
Clinic for Gastroenterology and Hepatology, University Clinical Centre of Serbia, 11 000 Belgrade, Serbia.
Cirrhotic cardiomyopathy (CCM) is a diagnostic entity defined as cardiac dysfunction (diastolic and/or systolic) in patients with liver cirrhosis, in the absence of overt cardiac disorder. Pathogenically, CCM stems from a combination of systemic and local hepatic factors that, through hemodynamic and neurohormonal changes, affect the balance of cardiac function and lead to its remodeling. Vascular changes in cirrhosis, mostly driven by portal hypertension, splanchnic vasodilatation, and increased cardiac output alongside maladaptively upregulated feedback systems, lead to fluid accumulation, venostasis, and cardiac dysfunction.
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