Myeloproliferative neoplasms in Budd-Chiari syndrome and portal vein thrombosis: a meta-analysis

Smalberg, Jasper H.; Arends, Lidia R.; Valla, Dominique; Kiladjian, Jean‐Jacques; Janssen, Harry L.A.; Leebeek, Frank W.G.

doi:10.1182/blood-2011-09-376517

Cited by 321 publications

(291 citation statements)

References 73 publications

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“…JAK2 mutation in splanchnic venous thrombosis without MPD features was able to identify MPD in 15.4% of PVT patients. 24 In Asians, the prevalence of JAK2 mutation is [24][25][26].6% in non-cirrhotic non-malignant PVT versus 1.4% in cirrhosis with PVT. 25,26 An Indian study reported 14% prevalence of JAK2 mutation in portal vein thrombosis out of 58 patients of intraabdominal venous thrombosis (which included portal vein thrombosis and Budd-Chiari syndrome).…”

Section: Acute Non-cirrhotic Portal Vein Thrombosis Procoagulant Statementioning

confidence: 99%

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: Acute Non-cirrhotic Portal Vein Thrombosis Procoagulant Statementioning

confidence: 99%

Portal Vein Thrombosis

Chawla

Bodh

2015

Journal of Clinical and Experimental Hepatology

151

147

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“…The etiology of these diseases encompasses both inherited and acquired risk factors, of which MPN are the most common with a prevalence ranging between 20%-50%. [1][2][3] Detecting presence of MPN in patients with BCS and PVT is important, given the prognostic and potential therapeutic implications regarding anticoagulant therapy.…”

mentioning

confidence: 99%

Somatic calreticulin mutations in patients with Budd-Chiari syndrome and portal vein thrombosis

et al. 2015

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“…A meta-analysis of MPD in patients with PVT reported a mean prevalence of 31.5%. 23 One study showed the figure to be 30.7%, with 16.7% being occult MPD and 13.8% being classical MPD. 24 Another recent study, looking at 44 patients, reported PVT to be the first manifestation of MPD in 31 patients (70%).…”

Section: Jak2 Mutation and Pvtmentioning

confidence: 99%