Mh. Denninger et al., Cause of portal or hepatic venous thrombosis in adults: The role of multiple concurrent factors, HEPATOLOGY, 31(3), 2000, pp. 587-591
According to a recent hypothesis, venous thrombosis results from the concur
rence of several factors. This hypothesis was assessed in patients with por
tal or hepatic venous thrombosis by simultaneously investigating most of th
e currently identified prothrombotic disorders, local precipitating factors
, and other risk factors such as oral contraceptive use. Patients with a tu
morous obstruction and patients with cirrhosis with portal vein thrombosis
were excluded, The prothrombotic disorders that were investigated included
classical and occult myeloproliferative disorders; antiphospholipid syndrom
e; protein C; protein S and antithrombin deficiency; factor V Leiden; facto
r II; and methylene-tetrahydrofolate-reductase gene mutations. We found 1 o
r several prothrombotic disorders and a local precipitating factor in 26 an
d 10 of the 36 patients with portal vein thrombosis, respectively; and in 2
8 and none of the 32 patients with hepatic vein thrombosis, respectively. W
e found a combination of prothrombotic disorders in 5 and 9 patients with p
ortal and hepatic vein thrombosis, respectively, whereas such a combination
is expected in less than 1% of asymptomatic subjects. Of the 10 patients w
ith a local precipitating factor, 8 had a prothrombotic disorder. Of the 13
patients who use oral contraceptives, 10 had a prothrombotic disorder. We
conclude that portal or hepatic venous thrombosis should be regarded as an
index for 1 or several prothrombotic disorders, whether or not local precip
itating factors or oral contraceptive use are found. Concurrence of prothro
mbotic disorders is more common than expected. Extensive investigation of p
rothrombotic disorders and anticoagulation should be considered in patients
with portal or hepatic venous thrombosis.