Abstract
OBJECTIVE: Patients with a history of severe obstetric complications in the
presence of elevated phospholipid antibodies are at high risk for recurrent obstetric
debacle. We report a successful immunologic treatment for prevention of HELLP-Syndrome in
subsequent pregnancy in a patient with elevated Phospholipid antibodies, while under
rheological and hemostaseological monitoring.
METHODS: The patient with prior severe HELLP-Syndrome at term in the presence
of reconfirmed elevated phospholipid antibodies in her first pregnancy received pooled
immunoglobulins (Sandoglobulin 3 g - Novartis) intravenously for immunological treatment
every three weeks in addition to low molecular weight heparin (Clexane 40 mg/d s.c.) and
Aspirin (100 mg/d from 2nd trimester) during her subsequent pregnancy. Before each of 10
treatment cycles blood rheological parameters (Red Blood cell {RBC} aggregation stasis E0,
low shear E1, RBC - deformability low-, moderate-, and high shear force, plasma viscosity
{Pv}), as well as thrombelastometry (ROTEM) and in vitro platelet
function (PFA-100) for hemostaseological evaluation was performed. At the same times
non-invasive, physical thrombosis screening took place using impedance plethysmography
(Filtrass)
RESULTS: During pregnancy a constant increase in PV and E1 (>45
S −1) was accompanied by a delayed but continuous increase in RBC
deformability beginning at the end of the 2nd trimester. Thrombelastometry revealed a
continuous reduction of clot formation time (CFT; extem: 84 to 38 sec) and an increase in
maximal clot firmness (MCF; extem: 64 to 78 sec) after TF-induced coagulation activation
while MCF and CFT after contact activation (intem) was barely unchanged. Platelet
bleeding-time after EPI/Coll stimulation was temporary prolonged by the onset of Aspirin
intake (>300 sec) but normalized soon after 20th gestational week, while ADP/Coll
stimulation revealed a trend towards prolonged bleeding times at the same time. There was
a strong and statistically significant inverse correlation between E1 and TF induced CFT
(r =−0.82; p = 0.002) and a positive correlation
between E1 and TF induced MCF (r = 0.89; p < 0.001),
while the correlation between E1 and contact activated CFT and MCF was weak or absent,
respectively. Until GW 38th routine laboratory- (Platelet-count, Haptoglobin, liver
enzymes) and clinical findings remained normal, without evidence of HELLP-Syndrome
reoccurrence or development of thrombosis.
CONCLUSIONS: During immunotherapy in this high risk patient HELLP-Syndrome
did not reoccur. The aggregability of RBC was closely related with the formation speed and
firmness of clot after TF activated coagulation but not after contact activated
coagulation. At the beginning of 3rd trimester RBC aggregation remained dramatically
higher as compared to the normal value range of pregnant women found in a large recent
trial which may have been an early indicator of imminent HELLP-Syndrome.
