Portal vein thrombosis; risk factors, clinical presentation and treatment. BMC Gastroenterol 7:34

Department of Medicine V (Hepatology and Gastroenterology), Aarhus University Hospital, Aarhus C, Denmark.
BMC Gastroenterology (Impact Factor: 2.37). 02/2007; 7(1):34. DOI: 10.1186/1471-230X-7-34
Source: PubMed


Portal vein thrombosis (PVT) is increasingly frequently being diagnosed, but systematic descriptions of the natural history and clinical handling of the condition are sparse. The aim of this retrospective study was to describe risk factors, clinical presentation, complications and treatment of portal vein thrombosis in a single-centre.
Sixty-seven patients were identified in the electronic records from 1992 to 2005. All data were obtained from the patient records.
One or more risk factors (e.g. prothrombotic disorder or abdominal inflammation) were present in 87%. Symptoms were abdominalia, splenomegaly, fever, ascites, haematemesis, and weight loss. Abdominalia and fever occurred more frequently in patients with acute PVT. Frequent complications were splenomegaly, oesophageal- and gastric varices with or without bleeding, portal hypertensive gastropathy and ascites. Varices and bleeding were more frequent in patients with chronic PVT. Patients who received anticoagulant therapy more frequently achieved partial/complete recanalization. Patients with varices who were treated endoscopically in combination with beta-blockade had regression of the varices. The overall mortality was 13% in one year, and was dependent on underlying causes.
Most patients had a combination of local and systemic risk factors for PVT. We observed that partial/complete recanalization was more frequent in patients treated with anticoagulation therapy, and that regression of varices was more pronounced in patients who where treated with active endoscopy combined with pharmacological treatment.

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    • "The formation of a fibrinocruoric thrombus is often multi-factorial. A general prothrombotic cause or a combination of prothrombotic disorders is found in 70% of the cases (malignant blood disease, thrombophilia), a locoregional cause in 30% of the cases (cirrhosis, locoregional inflammation and infection , locoregional surgery) [3] [4]. Sometimes the cause is not identified and the thrombosis is considered to be idiopathic [3]. "
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    ABSTRACT: Purpose To assess the evolution of acute portal vein thrombosis by computed tomography (CT). Patients and methods Retrospective single-centre study (2005–2011) including 23 patients who had an initial CT scan and a CT scan during the first year. The analysis compared the last CT scan available with that of the initial CT scan. Neoplastic thrombosis, extrinsic compressions and cavernomas were excluded. All patients received anticoagulant treatment. Results The causes included: cirrhoses (n = 6), blood disorders (n = 4), locoregional inflammations and infections (n = 8), abdominal surgery (n = 1). The thrombosis was idiopathic in 4 cases. After a mean follow-up of 7.7 months, 7 patients (30%) benefited from a restitutio ad integrum of the portal system, a stable or partially regressive thrombosis was noted in 12 patients (52%) and an aggravation of the thrombosis was noted in 4 patients (18%). In the sub-group of portal vein thrombosis, repermeabilisation was noted in 37.5% of the patients (6/16) and 6 cavernomas developed. Conclusion CT monitoring helps follow the evolution of an acute portal vein thrombosis and demonstrates complete repermeabilisation of the portal vein in 30% of the patients.
    Diagnostic and interventional imaging 06/2014; 95(6). DOI:10.1016/j.diii.2014.02.018
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    • "This phenomenon is strictly time dependent and it is advisable to screen endoscopically all the patients once the diagnosis of PVT is confirmed to rule out the presence of esophageal varices [14]. Other patients can present with thrombosis, abdominal pain, and jaundice or incidental splenomegaly. "
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    ABSTRACT: Portal vein thrombosis (PVT) is characterized by the obstruction of the portal venous system. The venous obstruction can be partial or complete and it is caused by thrombogenic conditions (acquired or hereditary) or nonthrombotic factors. The acquired conditions include abdominal inflammation, infections, surgery, myeloproliferative disorders, obesity, oral contraceptive intake, pregnancy, and postpartum period. Occasionally, it is not possible to recognize any overt cause of PVT. During pregnancy there is an increased venous thromboembolism risk mainly in the systemic venous system and the PVT can occur, but there are no data about its exact prevalence, etiology, and outcome. The portal cavernoma is the cavernomatous transformation of the portal vein. It is a consequence of chronic PVT and occurs when myriads of collateral channels develop to bypass the occlusion. The clinical presentation includes hematemesis due to variceal bleeding, ascites or anaemia, and splenomegaly. The cavernous transformation of the portal vein is easily diagnosed by sonography. We report our case of a 32-year-old, gravida 3 para 2, pregnant woman admitted to our hospital at 13 weeks and 1 day of gestation, clinically asymptomatic. Laboratory test, ultrasound, and endoscopic evaluation were negative. After a detailed counseling, the patient decided on termination of pregnancy at 15 weeks and 1 day of gestation.
    12/2013; 2013:396083. DOI:10.1155/2013/396083
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    • "The most common prothrombotic states seen in children are methylene tetrahydrofolate reductase (MTHFR) deficiency (C677T) and prothrombin gene mutations (G20201A), whereas in adults, primary myeloproliferative disorders (MPD) (with or without janus kinase 2, JAK2 mutation V617F) are the commonest. Overall, a single or more prothrombotic states are seen in 28–62% of cases, but none of the studies has screened for all known prothrombotic states [35] [36] [37] [38] [39] [40] [41] [42] [43] [44] [45] [46] [47] [48] [49] [50] [51] [52] [53] [54] [55] [56] [57] [58] [59] (Table 4). In a recent meta-analysis, the prevalence of MPD and "
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    ABSTRACT: NCPH is a heterogeneous group of liver disorders of vascular origin, leading to PHT with near normal HVPG. NCPF/IPH is a disorder of young adults or middle aged women, whereas EHPVO is a disorder of childhood. Early age acute or recurrent infections in an individual with thrombotic predisposition constitute the likely pathogenesis. Both disorders present with clinically significant PHT with preserved liver functions. Diagnosis is easy and can often be made clinically with support from imaging modalities. Management centers on control and prophylaxis of variceal bleeding. In EHPVO, there are additional concerns of growth faltering, portal biliopathy, MHE and parenchymal dysfunction. Surgical shunts are indicated in patients with failure of endotherapy, bleeding from sites not amenable to endotherapy, symptomatic hypersplenism or symptomatic biliopathy. Persistent growth failure, symptomatic and recurrent hepatic encephalopathy, impaired quality of life or massive splenomegaly that interferes with daily activities are other surgical indications. Rex-shunt or MLPVB is the recommended shunt for EHPVO, but needs proper pre-operative radiological assessment and surgical expertise. Both disorders have otherwise a fairly good prognosis, but need regular and careful surveillance. Hepatic schistosomiasis, CHF and NRH have similar presentation and comparable prognosis.
    Journal of Hepatology 08/2013; 60(2). DOI:10.1016/j.jhep.2013.08.013 · 11.34 Impact Factor
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