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Blood, 1 October 2000, Vol. 96, No. 7, pp. 2364-2368
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Factor V Leiden mutation, prothrombin gene mutation, and
deficiencies in coagulation inhibitors associated with Budd-Chiari
syndrome and portal vein thrombosis: results of a
case-control study
Harry L. A. Janssen,
Johan
R. Meinardi,
Frank P. Vleggaar,
Stan H. M. van
Uum,
Elizabeth B. Haagsma,
Felix J. M. van der
Meer,
Jan van
Hattum,
Robert A. F. M. Chamuleau,
Rob P. Adang,
Jan P. Vandenbroucke,
Bart van Hoek, and
Frits R. Rosendaal
From the Department of Gastroenterology and Hepatology,
Leiden University Medical Center; Department of Hepatogastroenterology,
Erasmus University Hospital, Rotterdam; Division of Haemostasis,
Thrombosis and Rheology, University Hospital, Groningen; Department of
Internal Medicine, University Hospital St. Radboud, Nijmegen;
Department of Gastroenterology and Hepatology, University Hospital,
Groningen; Haemostasis and Thrombosis Research Center Leiden, Leiden
University Medical Center; Department of Gastroenterology, University
Hospital, Utrecht; Department of Internal Medicine, Academic Medical
Center, Amsterdam; Department of Gastroenterology, University Hospital
Maastricht; and Department of Clinical Epidemiology, Leiden University
Medical Center, The Netherlands.
In a collaborative multicenter case-control study, we investigated
the effect of factor V Leiden mutation, prothrombin gene mutation, and
inherited deficiencies of protein C, protein S, and antithrombin on the
risk of Budd-Chiari syndrome (BCS) and portal vein thrombosis (PVT). We
compared 43 BCS patients and 92 PVT patients with 474 population-based
controls. The relative risk of BCS was 11.3 (95% CI 4.8-26.5) for
individuals with factor V Leiden mutation, 2.1(95% CI 0.4-9.6) for
those with prothrombin gene mutation, and 6.8 (95% CI 1.9-24.4) for
those with protein C deficiency. The relative risk of PVT was 2.7 (95%
CI 1.1-6.9) for individuals with factor V Leiden mutation, 1.4 (95% CI
0.4-5.2) for those with prothrombin gene mutation, and 4.6 (95% CI
1.5-14.1) for those with protein C deficiency. The relative risk of BCS or PVT was not increased in the presence of inherited protein S or
antithrombin deficiency. Concurrence of either acquired or inherited
thrombotic risk factors was observed in 26% of the BCS patients and
37% of the PVT patients. We conclude that factor V Leiden mutation and
hereditary protein C deficiency appear to be important risk factors for
BCS and PVT. Although the prevalence of the prothrombin gene mutation
was increased, it was not found to be a significant risk factor for BCS
and PVT. The coexistence of thrombogenic risk factors in many patients
indicates that BCS and PVT can be the result of a combined effect of
different pathogenetic mechanisms.
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