Mechanisms of enhanced thrombin generating capacity in patients with cirrhosis.

The liver is the site of synthesis of many proteins involved in hemostasis including pro- and anticoagulant proteins, pro- and antifibrinolytic proteins, and thrombopoietin. Consequently, patients with liver disease acquire complex changes within their hemostatic system[1]. Historically, these changes were thought to result in a bleeding diathesis. Although bleeding complications are common in patients with chronic liver disease, the most common bleeding complication, variceal bleeding, is a consequence of portal hypertension, rather than hemostatic failure

The Spectrum of Disease Severity in Cirrhosis and Its Implications for Hemostasis

Bleeding and thrombosis are both common complications that patients with advanced liver disease experience. While hemostatic pathways remain largely intact with cirrhosis, this balance can quickly shift in the direction of bleeding or clotting in an unpredictable manner. A growing body of literature is attempting to shed light on difficult scenarios that clinicians often face, ranging from predicting and mitigating bleeding risk in those who need invasive procedures to determining the best strategies to manage both bleeding and thrombotic complications when they occur. Studies examining hemostasis in those with advanced liver disease, however, often include heterogeneous cohorts with varied methodology. While these studies often select a cohort of all types and degrees of cirrhosis, emerging evidence suggests significant differences in underlying systemic inflammation and hemostatic abnormalities among specific phenotypes of liver disease, ranging from compensated cirrhosis to decompensated cirrhosis and acute-on-chronic liver failure. It is paramount that future studies account for these differing disease severities if we hope to address the many critical knowledge gaps in this field

Effects of restoring portal flow with anticoagulation and partial splenorenal shunt embolization

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/110757/1/hep27241.pd

Haemostatic alterations and management of haemostasis in patients with cirrhosis

Patients with cirrhosis frequently acquire complex changes in their haemostatic system including a decreased platelet count and decreased levels of various haemostatic proteins. Although historically patients with cirrhosis were thought to have a haemostasis-related bleeding tendency, it is now widely accepted that the haemostatic system of patients with cirrhosis remains in balance as a result of simultaneous changes in pro- and anti-haemostatic systems. The concept of rebalanced haemostasis has led to changes in clinical management, although firm evidence from well-designed clinical studies is largely lacking. For example, many invasive procedures in patients with cirrhosis and a prolonged prothrombin time are now performed without prophylaxis with fresh frozen plasma. Conversely, clinicians have become more aware of the need for anti-thrombotic therapy, even in those patients with abnormal routine coagulation tests. This paper will outline recent advances in pathogenesis, prevention and treatment of both bleeding and thrombotic complications in patients with cirrhosis. Among other topics, we will discuss the haemostatic status of acutely ill patients with cirrhosis, the various causes of bleeding in patients with cirrhosis, and how best to prevent or treat bleeding. In addition, we will discuss the hypercoagulable features of patients with cirrhosis, new insights into the pathogenesis of portal vein thrombosis, and how best to prevent or treat thromboses

Vascular Liver Disorders, Portal Vein Thrombosis, and Procedural Bleeding in Patients With Liver Disease:2020 Practice Guidance by the American Association for the Study of Liver Diseases

An overview of the current understanding of bleeding and thrombosis in cirrhosis. An evidence-based justification for bleeding risk assessment in patients with cirrhosis prior to invasive procedures, including current concepts in preprocedural testing and laboratory analysis and their role in predicting bleeding complications. An outline of established and recently identified risk factors for venous thrombosis in the portal and hepatic venous systems in both patients with and without cirrhosis along with thrombophilia testing recommendations

thrombosis of the portal venous system in cirrhotic patients

n/

A summary of the 6th international conference on coagulation in liver disease : discussion, debate, deliberations

Editor’s Preface from Nahum Mendez Sanchez: Below, the Editors of Annals of Hepatology provide a summary report from the 2015 multidisciplinary Coagulation in Liver Disease group meeting. This group which originated in 2005 is dedicated to issues of Coagulation, Hemostasis and Thrombosis in Liver Disease patients and includes members from diverse Specialties including representation from the fields of Hepatology, Hematology, Surgery, Anesthesiology, Pathology, Interventional Radiology, Laboratory Medicine, Transfusion Sciences and Blood Banking with a combined approach of basic and clinical Sciences. The aim of the symposium was to raise points of convergence of interest and research and to provide a forum to facilitate collaboration in order to advance the field. [Introduction]peer-reviewe

Hidden chromosomal abnormalities in pleuropulmonary blastomas identified by multiplex FISH

BACKGROUND: Pleuropulmonary blastoma (PPB) is a rare childhood dysontogenetic intrathoracic neoplasm associated with an unfavourable clinical behaviour. CASES PRESENTATION: We report pathological and cytogenetic findings in two cases of PPB at initial diagnosis and recurrence. Both tumors were classified as type III pneumoblastoma and histological findings were similar at diagnosis and relapse. In both cases, conventional cytogenetic techniques revealed complex numerical and structural chromosomal abnormalities. Molecular cytogenetic analysis (interphase/metaphase FISH and multicolor FISH) identified accurately chromosomal aberrations. In one case, TP53 gene deletion was detected on metaphase FISH. To date, only few cytogenetic data have been published about PPB. CONCLUSION: The PPB genetic profile remains to be established and compared to others embryonal neoplasia. Our cytogenetic data are discussed reviewing cytogenetics PPBs published cases, illustrating the contribution of multicolor FISH in order to identify pathogenetically important recurrent aberrations in PPB