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Letter
Role of portal venous platelet activation in patients with decompensated cirrhosis and TIPS
  1. Alexander Queck1,
  2. Roberto Carnevale2,3,
  3. Frank Erhard Uschner1,
  4. Robert Schierwagen1,
  5. Sabine Klein1,
  6. Christian Jansen4,
  7. Carsten Meyer5,
  8. Michael Praktiknjo4,
  9. Daniel Thomas5,
  10. Christian Strassburg4,
  11. Stefan Zeuzem1,
  12. Francesco Violi3,6,
  13. Jonel Trebicka1,7
  1. 1Department of Internal Medicine 1, Hospital of the Goethe University Frankfurt, Frankfurt am Main, Germany
  2. 2Department of Medical-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy
  3. 3Mediterranea Cardiocentro, 80122 Napoli, Italy
  4. 4Department of Internal Medicine 1, University Hospital Bonn, Bonn, Germany
  5. 5Department of Radiology, University Hospital Bonn, Bonn, Germany
  6. 6Internal Medicine and Medical Specialties, Universita degli Studi di Roma La Sapienza, Roma, Italy
  7. 7EFCLIF, European Foundation for the Study of Chronic Liver Failure, Barcelona, Spain
  1. Correspondence to Dr Jonel Trebicka, Department of Internal Medicine 1, Hospital of the Goethe University Frankfurt, Frankfurt am Main, Germany; Jonel.Trebicka{at}kgu.de

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We read with interest the recent study by Lv et al,1 who pointed out that transjugular intrahepatic portosystemic shunt (TIPS) placement is feasible for prevention of variceal rebleeding in the majority of cirrhotic patients with portal vein thrombosis and that it is more effective than endoscopic band ligation plus propranolol. Moreover, association with a higher probability of portal vein recanalisation and a lower risk of subsequent rethrombosis was described. However, even after TIPS, in eight out of 24 patients, either portal or superior mesenteric vein thrombosis persisted or reoccurred. While development and progression of splanchnic venous thrombotic events implicate disease progression in cirrhosis,2 their pathogenesis remains unclear. According to Virchow’s triad, pathological coagulation/platelets, decreased flow and impaired vascular wall are the drivers of thrombosis. In TIPS, flow is restored and, to a large extent, also the shear stress (the vascular wall compenent) due to decompression of portal hypertension. However, the prothrombotic milieu (platelet and plasmatic coagulation) has not been investigated to date. One hypothesis for this is the platelet …

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