The conversion of
prothrombin by
ecarin is independent of the presence of gamma carboxyglutamic residues on the N terminal of the molecule.
Ecarin converts therefore also the acarboxylated precursor-
PIVKA II. In a group of 347 patients under
dicoumarol therapy of different intensity and duration
PIVKA was detected in BaSO4 adsorbed PPP only in samples where
prothrombin level (Quick's test) was lower than 50% of normal values. Increase in
PIVKA did not correspond to the decrease of
prothrombin. In some cases where the treatment was longer than two years no
PIVKA was detected even when
prothrombin was under 20%. This is explained by synthesis of partially carboxylated
prothrombin molecules, which can be adsorbed. In
liver diseases the
ecarin test and Quick's time in native, untreated PPP showed about identical decrease of
prothrombin level. This indicates that no
PIVKA is released to plasma. The functional defect of the hepatocyte does not involve gamma carboxylation as long as
vitamin K is provided. In patients with
DIC ecarin test showed significantly higher level of
thrombin activity than those obtained with Quick's test. It is known that during hypercoagulation stage of
DIC prethrombin 1 and 2 are formed by the excess of
thrombin. These split products of
prothrombin are convertible by
ecarin to
meizothrombin 1 and 2. A positive
ecarin test can be also due to acarboxylated precursors which are released during increased proteosynthesis triggered by
consumption coagulopathy.