High FVIII Level Is Associated with Idiopathic Portal Vein Thrombosis in South India

Koshy, Abraham; Jeyakumari, Mary

doi:10.1016/j.amjmed.2006.02.016

Cited by 17 publications

(15 citation statements)

References 9 publications

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“…36 High factor VIII levels have also been shown to be associated with portal vein thrombosis in Indian patients. 37 Heterozygous MTHFR has been reported in 21% of PVT patients and hyperhomocysteinemia in 7.6% while homozygous MTHFR has not been seen. 11 A strong link of Bacteroides fragillus infection with PVT has also been demonstrated possibly due to transient development of anti-cardiolipin antibodies.…”

Section: Inherited Prothrombotic Disordersmentioning

confidence: 99%

“…Protein C deficiency is seen in 8-9%, protein S deficiency in 3-4%, factor V Leiden mutation in 3-6% and antiphospholipid antibody in 18-23%. 11,[33][34][35] Antithrombin III deficiency and prothrombin gene mutation are however uncommon. However another study from India of 26 PVT patients showed the presence of protein C deficiency in 12, protein S deficiency in 9, antithrombin III deficiency in 8 patients, ACLA in 3 and LA in 4 patients.…”

Section: Inherited Prothrombotic Disordersmentioning

confidence: 99%

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Portal Vein Thrombosis

Chawla

Bodh

2015

Journal of Clinical and Experimental Hepatology

151

147

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Portal vein thrombosis is an important cause of portal hypertension. PVT occurs in association with cirrhosis or as a result of malignant invasion by hepatocellular carcinoma or even in the absence of associated liver disease. With the current research into its genesis, majority now have an underlying prothrombotic state detectable. Endothelial activation and stagnant portal blood flow also contribute to formation of the thrombus. Acute non-cirrhotic PVT, chronic PVT (EHPVO), and portal vein thrombosis in cirrhosis are the three main variants of portal vein thrombosis with varying etiological factors and variability in presentation and management. Procoagulant state should be actively investigated. Anticoagulation is the mainstay of therapy for acute non-cirrhotic PVT, with supporting evidence for its use in cirrhotic population as well. Chronic PVT (EHPVO) on the other hand requires the management of portal hypertension as such and with role for anticoagulation in the setting of underlying prothrombotic state, however data is awaited in those with no underlying prothrombotic states. TIPS and liver transplant may be feasible even in the setting of PVT however proper selection of candidates and type of surgery is warranted. Thrombolysis and thrombectomy have some role. TARE is a new modality for management of HCC with portal vein invasion. ( J CLIN EXP HEPATOL 2015;5:22-40)

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Section: Inherited Prothrombotic Disordersmentioning

confidence: 99%

Section: Inherited Prothrombotic Disordersmentioning

confidence: 99%

Portal Vein Thrombosis

Chawla

Bodh

2015

Journal of Clinical and Experimental Hepatology

151

147

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“…These studies did not assess risk factors in patients with mesenteric venous thrombosis. Other studies have evaluated individual risk factors or multiple risk factors in single venous thrombosis [14][15][16][17] . The aim …”

Section: Introductionmentioning

confidence: 99%

Risk factors of thrombosis in abdominal veins

Dutta¹,

Chacko²,

George³

et al. 2008

WJG

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AIM:To estimate the prevalence of inherited and acquired thrombophilic risk factors in patients with abdominal venous thrombosis and to compare the risk factor profiles between Budd-Chiari syndromes (BCS) and splanchnic vein thrombosis (SVT). METHODS: In this retrospective study, 36 patients with abdominal venous thrombosis were studied. The patients were divided into Budd-Chiari group (hepatic vein, IVC thrombosis) and splanchnic venous thrombosis group (portal, splenic, superior mesenteric veins) based on the veins involved. Hereditary and acquired thrombophilic risk factors were evaluated in all patients. RESULTS: Twenty patients had SVT, 14 had BCS, and 2 had mixed venous thrombosis. Ten patients (28%) had hereditary and 10 patients (28%) acquired thrombophilic risk factors. The acquired risk factors were significantly more common in the SVT group

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“…Bertina reported that Von Leiden factor (FVL) deficiency has been reported in 2% to 30% of patients with portal vein thrombosis [15]. Moreover, the other articles found that FVL deficiency was also highly associated with splenic vein thrombosis [16,17]. As other causes, advanced left renal cancer and myeloproliferative disease are recognized.…”

Section: Pathophysiology/symptoms Of Left-sided Portal Hypertensionmentioning

confidence: 99%

Gastric Varices Secondary to Splenic Vein Occlusion due to Pancreatic Diseases

Kimura¹

2013

Pancreat Disord Ther

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Sato et al., Pancreatic Dis Ther 2013, S3 http://dx.doi.org/10.4172/2165 Gastric Varices Secondary to Splenic Vein Occlusion due to Pancreatic Diseases Takahiro Sato*, Sho Kitagawa, Mutsuumi Kimura, Takumi Ohmura, Yoshiyasu Karino and Jouji Toyota Department of Gastroenterology, Sapporo Kosei General Hospital, Japan occlusion because of the splenic vein, s anatomy. Sutton et al. reported that 35% of their cases of isolated splenic vein occlusion were caused by tumors and only 17% by pancreatitis [9]. On the other hand, Sakorafas et al. found that pancreatitis was the etiology in 87 (60%) of 144 cases, while pancreatic malignancy was detected in only [13] (9%) of the patients [7], and recent reviews have clarified acute or chronic pancreatitis to be the probable cause of splenic vein thrombosis in the majority of cases [18]. There is a possible pathogenetic mechanism implying the increased intra-abdominal pressure leading to compression of the splenic vein in the case of pancreatic pseudocyst [19,20].Due to splenic vein occlusion, splenic venous flow must drain into collateral veins (short gastric vein and left gastroepiploic vein). Then, the increased blood flow dilates the submucosal veins of stomach, resulting in gastric varices (Figure 1). Because blood drainage is diverted by the coronary vein into the patent portal system, the presence of gastric varices without esophageal varices is a very specific sign of splenic vein occlusion [17]. This condition, which is commonly silent clinically, can cause hypersplenism or gastrointestinal hemorrhage.Although splenic vein occlusion is commonly silent clinically, AbstractGastric varices that arise secondary to splenic vein occlusion can result in hypersplenism or gastrointestinal hemorrhaging. This article review gastric varices secondary to splenic vein occlusion due to pancreatic diseases with regard to causes of the condition, as well as diagnostic and therapeutic approaches.Diagnosis of gastric varices is made following esophago-gastro-duodenoscopy, and splenic vein occlusions are diagnosed from enhanced computed tomographic scans in almost all cases. Specific findings of gastric varices secondary to splenic vein occlusion are based on endoscopic ultrasonographic color flow images of gastric variceal flow that clearly depicted round cardiac and fundal regions at the center, with varices expanding to the curvatura ventriculi major of the gastric body.Several treatment options for gastric variceal bleeding secondary to splenic vein occlusion have been proposed. Splenectomy, which decompresses the short gastric vein by cutting off inflow, has generally been considered the best treatment of choice in such condition. Endoscopic injection sclerotherapy using cyanoacrylate, is useful in the treatment of bleeding gastric varices due to splenic vein occlusion. As patients with splenic vein occlusion have normal portal pressure and normal hepatic function, portal systemic shunting is not indicated. Splenic arterial embolization, which reduces blood flow through the sp...

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High FVIII Level Is Associated with Idiopathic Portal Vein Thrombosis in South India

Cited by 17 publications

References 9 publications

Portal Vein Thrombosis

Portal Vein Thrombosis

Risk factors of thrombosis in abdominal veins

Gastric Varices Secondary to Splenic Vein Occlusion due to Pancreatic Diseases

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