Diagnostic value of combined transhepatic venography and inferior vena cavography in chronic Budd-Chiari syndrome

Datta, D. V.; Vashishta, S.; Samanta, Animesh; Chhuttani, P. N.

doi:10.1007/bf01263104

Cited by 37 publications

(13 citation statements)

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“…Membranous obstruction of the IVC has been reported in the past to be a frequent finding in patients with chronic BCS in Asia, [21][22][23][24] India, [25][26][27] and South Africa. 28 The origin and nature of this membrane are disputed.…”

Section: Discussionmentioning

confidence: 99%

Hereditary thrombophilia as a cause of Budd-Chiari syndrome: A study from Western India

et al. 2001

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The inherited deficiencies of protein C, protein S, antithrombin III, factor V Leiden mutation, prothrombin gene polymorphism, and antiphospholipids were studied in 53 Budd-Chiari syndrome (BCS) and 33 portal vein thrombosis (PVT) cases and compared with 223 age-and sex-matched controls. Protein C deficiency was detected in 7 (13.2%), protein S in 3 (5.7%), and antithrombin III in 2 (3.8%) of the BCS cases. Factor V Leiden was the most common risk factor, i.e., 14 of 53 (26.4%) in BCS cases followed by protein C, as compared with PVT cases, i.e., 2 of 33 (6.06%) and controls, i.e., 5 of 223 (2.3%). In PVT cases, protein C deficiency was present in 3 (9.09%), protein S deficiency in 1 (3.03%), and factor V Leiden mutation in 2 (6.06%) of the cases. The prothrombin gene polymorphism was not found in either the controls or the patients. The antiphospholipids were seen in 11 (20.75%) of the BCS cases and 6 (18.18%) of the PVT cases. Other acquired risk factors like pregnancy, surgery, and oral contraceptives were present in 8 (15.09%) of BCS and 3 (9.09%) of PVT cases. Thus overall, 59% of the BCS and 30% of the PVT cases could be explained by at least one of the etiologic factors studied. (HEPATOLOGY 2001;34: 666-670.)Budd-Chiari syndrome (BCS) is a rare disorder, the cause of which remains undetermined in the majority of cases. It is caused by the occlusion of hepatic outflow either at the level of hepatic veins or inferior vena cava. The disease, however, has been associated with a variety of conditions like malignancy, 1,2 polycythemia rubra vera, 3 paroxysmal nocturnal hemoglobinuria, 4 trauma, 5 pregnancy, 6 oral contraceptives, 7 and infection. 8 The clinical manifestations include hepatomegaly, portal hypertension, and liver function failure. Portal vein thrombosis (PVT) manifests itself as portal hypertension with decreased portal flow. Hypercoagulability has been implicated in both BCS and PVT.Except for a single report 9 published recently, there have not been many reports on the prevalence of the common factors for hypercoaguability, i.e., protein C, protein S, antithrombin III, factor V Leiden, and prothrombin gene polymorphism, studied in a large group of patients. There have only been isolated case reports in the literature describing BCS cases and the association of single prothrombotic factors 10-13 ; however, a systematic prospective study investigating all the prothrombotic factors simultaneously in BCS and PVT cases is lacking. MATERIALS AND METHODSPatients. The patients were referred from the Department of Gastroenterology, KEM Hospital, Mumbai, India, between 1995 and 2000. The diagnostic criteria for BCS was partial or complete obstruction of hepatic outflow or inferior vena cava, and for PVT, partial or complete obstruction of portal vein. The confirmation was done by Doppler sonography, magnetic resonance imaging, computed tomography scanning, and venography. The clinical details were recorded in a well-defined clinical proforma, which included details like number of thrombotic events, famil...

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Section: Discussionmentioning

confidence: 99%

Hereditary thrombophilia as a cause of Budd-Chiari syndrome: A study from Western India

et al. 2001

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“…The diagnosis of HVD was based on clinical features and ultrasound (US) examination [23,24]. It was confirmed by inferior vena cavography [10] in 31, hepatography or transhepatic venography [25] in 5, and liver biopsy in 34 patients. Patients were assessed for other risk factors for cirrhosis and HCC such as alcohol (alcohol consumption of C40 g of ethanol per day for C5 years was considered significant), hepatitis B (HBsAg, anti-HBc, and HBV DNA) and hepatitis C virus (HCV) infections (anti-HCV, HCV RNA) by methods described earlier [20].…”

Section: Methodsmentioning

confidence: 99%

Liver cirrhosis and hepatocellular carcinoma in hepatic vena cava disease, a liver disease caused by obstruction of inferior vena cava

Shrestha¹

2009

Hepatol Int

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Purpose Hepatic vena cava disease (HVD), a form of Budd-Chiari syndrome, is caused by the obstruction of hepatic portion of the inferior vena cava. It is a chronic disease characterized by the development of liver cirrhosis (LC) and hepatocellular carcinoma (HCC). As HVD occurred in areas with high incidence of hepatitis B virus (HBV) infection and some patients tested HBsAg positive, it was thought to be the cause of LC and HCC. To assess the pathogenesis of LC or HCC in HVD, a long-term follow-up study was done. Method Fifty-six patients with HVD diagnosed by ultrasound (US) and confirmed by cavography in 31 and liver biopsy in 34 were followed up for an average of 14.8 ± 9 years. The occurrence of LC was diagnosed by US and/or liver biopsy and that of HCC by US, elevated level of a-fetoprotein, and liver biopsy or fine-needle aspiration cytology, or computed tomographic scan. Other risk factors for LC/HCC such as alcohol use and HBV and hepatitis C virus (HCV) infections were assayed. Results Forty-four (78.5%) and 6 (10.7%) patients developed cirrhosis and HCC, respectively. LC/HCC occurred more frequently among those who had severe or frequent acute exacerbations (P = 0.017), but it was not related to alcohol use or HBV and HCV infections. Conclusion HVD is independent risk factors for LC and HCC. Severe and/or recurrent loss of hepatocytes caused by hepatic venous outflow obstruction and/or thrombotic obstruction of small radicals of hepatic and portal veins that occurred during acute exacerbations was considered important in the pathogenesis of LC and HCC in HVD.

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“…An approxi mation of the relative prevalence of these conditions is given. This estimation is de rived from several series published during the last 25 years [5,7,[9][10][11][12][13][14][15][16][17][18][19][20], Most of those series were reported from western countries, and their findings may not be relevant to the etiology of hepatic vein occlusion in other parts of the world.…”

Section: Primary Lesions O F the Major Hepatic Veinsmentioning

confidence: 99%

Obstruction of the Hepatic Veins

Valla

1990

Dig Dis

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Diagnostic value of combined transhepatic venography and inferior vena cavography in chronic Budd-Chiari syndrome

Cited by 37 publications

References 14 publications

Hereditary thrombophilia as a cause of Budd-Chiari syndrome: A study from Western India

Hereditary thrombophilia as a cause of Budd-Chiari syndrome: A study from Western India

Liver cirrhosis and hepatocellular carcinoma in hepatic vena cava disease, a liver disease caused by obstruction of inferior vena cava

Obstruction of the Hepatic Veins

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