Absence of enhanced systemic inflammatory response at 18 weeks of gestation in women with subsequent pre-eclampsia.
OBJECTIVE
To compare indicators of systemic inflammatory response in the second trimester in women who developed pre-eclampsia with normal pregnancies.


METHODS
Prospective nested case control study derived from a cohort of 2190 pregnant women. Blood samples were obtained at 18 weeks of gestation. The following inflammatory parameters were measured: tumour necrosis factor-alpha (TNF-alpha), plasminogen activator inhibitor-1 (PAI-1), interleukin-1beta (IL-1beta), IL-6, IL-10, microCRP and tissue factor (TF).


METHODS
Institute of Medical Genetics, University of Oslo, and Department of Medical Genetics, Ullevål University Hospital and Departments of Obstetrics and Gynecology, Aker University Hospital, Oslo, Norway.


METHODS
The cases were 71 women who subsequently developed pre-eclampsia. The controls were 71 healthy, pregnant women matched for age, parity and first trimester body mass index (BMI).


METHODS
Venous blood was drawn from fasting subjects into 5 mL test tubes containing EDTA. Samples were analysed for inflammatory parameters: IL-1-beta, IL-6, IL-10, TNF-alpha, PAI-1, TF (ELISA-technique) and CRP (latex-enhanced immunonephelometric assay), strictly according to the manufacturer's recommendation.


METHODS
The matched case and control subjects were compared by the paired two-tailed Wilcoxon signed rank test. All P values were two-tailed and P < 0.05 was deemed statistically significant.


RESULTS
We found no differences in plasma concentrations of PAI-1, IL-1beta, IL-6,IL-10, microCRP, TNF-alpha or TF at 18 weeks of gestation between women who subsequently developed pre-eclampsia and matched control women.


CONCLUSIONS
In contrast to findings from women with overt pre-eclampsia, the present study indicates that there are no indications of intensified systemic inflammatory response at 18 weeks of gestation in women who later develop pre-eclampsia.
Institute of Medical Genetics, University of Oslo, Norway.
Srdjan
S
Djurovic
Torun
T
Clausen
Ragnhild
R
Wergeland
Frank
F
Brosstad
Kåre
K
Berg
Tore
T
Henriksen
D002097:C-Reactive Protein / Q000032:analysis; D016022:Case-Control Studies; D015331:Cohort Studies; D005260:Female; D006801:Humans; D007378:Interleukins / Q000097:blood; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D011225:Pre-Eclampsia / Q000097:blood / Q000175:diagnosis* / Q000209:etiology; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000097:blood / Q000175:diagnosis*; D011446:Prospective Studies; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood / Q000175:diagnosis*; D013925:Thromboplastin / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D007378:Interleukins; D017395:Plasminogen Activator Inhibitor 1; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D013925:Thromboplastin