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Clinicopathologic study on pathogenesis and hepatic carcinogenesis in Budd-Chiari syndrome endemic in Nepal

Research Project

Project/Area Number 13576004
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section海外学術
Research Field Human pathology
Research InstitutionKURUME UNIVERSITY

Principal Investigator

KAGE Masayoshi  Kurume University, School of Medicine, Professor, 医学部, 教授 (80148840)

Co-Investigator(Kenkyū-buntansha) TOYONAGA Atsushi  Kurume University, School of Medicine, Professor, 医学部, 教授 (00098881)
KOJIRO Masamichi  Kurume University, School of Medicine, Professor, 医学部, 教授 (90080580)
Project Period (FY) 2001 – 2002
Project Status Completed (Fiscal Year 2002)
Budget Amount *help
¥7,500,000 (Direct Cost: ¥7,500,000)
Fiscal Year 2002: ¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2001: ¥4,200,000 (Direct Cost: ¥4,200,000)
Keywordsobstruction of inferior vena cava / Budd-Chiari syndrome / collateral / alcoholic / infection / ascites / thrombosis / pathology / うっ血肝 / 門脈圧亢進 / 肝部下静脈閉塞 / 細菌感染 / 血栓 / 肝部下大静脈 / 肝静脈
Research Abstract

We examined 81 patients with Budd-Chiari syndrome who were seen at the Liver Unit, Bir Hospital, Kathmandu, and were biopiedClinically, our patient group could be divided into acute (n = 21), subacute (n = 29) and chronic (n = 31) cases. The important clinical features are hepatomegaly and/or ascites and, in chronic cases, prominent dilated superficial veins over the body trunk with cephalad flow. Ultrasound is the most helpful diagnostic procedure, especially in subacute and chronic cases, as it frequently demonstrates caval obstruction, thrombosis, dilated hepatic veins and intrahepatic collaterals. Diagnosis is confirmed by cavography, which shows a caval obstruction of varying lengths at the cavo-atrial junction or a marked narrowing of the hepatic portion of the vena cava. In subacute and chronic cases cavography also demonstrates collateral veins. Chronic cases had periods of exacerbation often associated with bacterial infection.
Histologically, the acute cases frequently showed alcoholic liver injury. Histological features of passive congestion were less frequently observed. The subacute cases showed mixed passive congestion, non-specific reactive hepatitis, reflecting sepsis and alcoholic liver injury. The chronic cases revealed more advanced fibrosis and cirrhosis due to passive congestion. A few cases of alcolic liver injury were found in the chronic cases.
The aetiology of inferior vena cava obstruction at its hepatic portion is not known, but there seems to be a frequent association of bacterial infection with the disease.

Report

(3 results)
  • 2002 Annual Research Report   Final Research Report Summary
  • 2001 Annual Research Report

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Published: 2001-04-01   Modified: 2016-04-21  

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