scholarly journals Portal Vein Thrombosis and Systemic Amyloidosis in Crohn’s Disease: A Case Report and Review of the Literature

1996 ◽  
Vol 10 (5) ◽  
pp. 297-300 ◽  
Author(s):  
Gad Friedman ◽  
Gary E Wild

Systemic amyloidosis and portal vein thrombosis are relatively rare complications of inflammatory bowel disease. The first case of a patient with Crohn’s disease presenting with both complications is presented. An acquired free protein S deficiency was disclosed in the patient, which may be responsible for the hypercoagulable state observed in Crohn’s disease and the nephrotic syndrome from amyloidosis.

1991 ◽  
Vol 16 (1) ◽  
pp. 245-247 ◽  
Author(s):  
Don E. Brinberg ◽  
Thorarinn B. Stefansson ◽  
Francis A. Greicius ◽  
Sarwan S. Kahlam ◽  
Clifford Molin

2014 ◽  
Vol 1 (11) ◽  
pp. 1383-1386
Author(s):  
Kekathi Vidyasagar ◽  
Saifullah Quraishi S M ◽  
Ravi Theja ◽  
Chandrashekar S

2012 ◽  
Vol 16 (6) ◽  
pp. 1199-1203 ◽  
Author(s):  
Galen G. Leung ◽  
Muthu V. Sivasankaran ◽  
Jacqueline J. Choi ◽  
Celia M. Divino

2020 ◽  
pp. 29-37
Author(s):  
Richmond Ronald Gomes

Venous thromboembolic diseases are a group of heterogeneous diseases with different clinical forms and prognosis. Abdominal venous thrombosis may present either as Budd-Chiari syndrome (BCS) caused by hepatic vein or proximal inferior vena cava (IVC) obstruction or as an extra hepatic portal obstruction (EHPVO) caused by Portal vein thrombosis or mesenteric vein thrombosis. Portal vein thrombosis (PVT) is a rare form of venous thrombosis that affects the hepatic portal vein flow, which can lead to portal hypertension. Treatment of PVT includes anticoagulants, thrombolysis, and insertion of shunts, bypass surgery, and liver transplantation. Single anticoagulation therapy can be associated with a reduction in new thrombotic episodes. Here we experienced a 23 year old young lady with history of recent intrauterine death (IUD) diagnosed as PVT provoked by protein S deficiency with newly diagnosed decompensated cryptogenic chronic liver disease with portal hypertension. PVT was completely recanalized with single oral anticoagulant therapy rivaroxaban as initial low molecular weight heparin, enoxaparin administration caused reversible pancytopenia and there is a concern for bleeding and regular monitoring of INR with warfarin in this patient. Keywords: Portal vein thrombosis; Chronic liver disease; Protein S deficiency; Oral anticoagulant; Portal hypertension; Thrombolysis


1993 ◽  
Vol 18 (2) ◽  
pp. 258 ◽  
Author(s):  
Bertrand Godeau ◽  
Catherine Leroy-Matheron ◽  
Michèle Gouault-Heilmann ◽  
Annette Schaeffer

2018 ◽  
Vol 06 (11) ◽  
pp. E1283-E1288 ◽  
Author(s):  
Haoxiong Zhou ◽  
Jieying Xuan ◽  
Xianyi Lin ◽  
Yunwei Guo

Abstract Background and study aims Esophagogastric variceal bleeding (EGVB) is common in patients with portal vein thrombosis (PVT). Hereditary deficiencies in natural anticoagulant proteins, such as protein S, might contribute to PVT. However, recurrent EGVB caused by PVT in patients with protein S deficiency is seldom reported. Herein, we present the case of a 38-year-old man with protein S deficiency complicated with PVT. The patient suffered recurrent EGVB for 7 years. He underwent splenectomy plus pericardial revascularization and sequential endoscopic therapy, including one gastric variceal obturation (GVO) procedure and two esophageal variceal ligations (EVL) to eradicate the varices. Rivaroxaban was administrated to reduce risk of thrombotic events. The patient is currently well without rebleeding after 1 year of follow-up. To our knowledge there is no consensus on management of recurrent EGVB on the basis of thrombophilia complicated with PVT. According to our practice, sequential endoscopic therapy combined with anticoagulant appears to be effective and safe.


2002 ◽  
Vol 35 (2) ◽  
pp. 184-188 ◽  
Author(s):  
Yoshio Uemura ◽  
Kenji Kobayashi ◽  
Taichi Koyama ◽  
Naofumi Kagara ◽  
Yosuke Seki ◽  
...  

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