OBJECTIVE: Systemic inflammation might contribute to the pathogenesis of pr
eeclampsia. In addition, the association between obesity and inflammation i
n preeclampsia. has not been examined in detail. We determined whether firs
t-trimester elevation of serum C-reactive protein, an index of systemic inf
lammation, was associated with preeclampsia.
METHODS: We conducted a prospective, nested case-control study among women
enrolled in the Massachusetts General Hospital Obstetrical Maternal Study c
ohort. High-resolution C-reactive protein assays were performed on first-tr
imester (11 +/- 2 weeks' gestation) serum samples in 40 women in whom preec
lampsia developed (blood pressure [BP] greater than 140/90 mmHg, and protei
nuria, either 2+ or more by dipstick or greater than 300 mg per 24 hours),
and in 80 matched controls. This sample size had greater than 80% power to
detect a difference in C-reactive protein levels between cases and controls
. We used nonparametric tests to compare C-reactive protein levels and cond
itional logistic regression to control for confounding variables.
RESULTS: First-trimester C-reactive protein levels were significantly highe
r among women in whom preeclampsia subsequently developed compared with con
trols (4.6 compared with 2.3 mg/L, P = .04). When women were subdivided int
o C-reactive protein quartiles, the odds ratio (OR) of being in the highest
quartile of C-reactive protein was 3.2 (95% confidence interval [CI] 1.1,
9.3, P = .02) among cases of preeclampsia compared with controls. When body
mass index (BMI) was added to the multivariable model, the highest quartil
e of C-reactive protein was no longer associated with increased risk of pre
eclampsia (OR 1.1, 95% CI .3, 4.3, P = .94). In the same model without BMI,
the highest quartile of C-reactive protein was associated with increased r
isk of preeclampsia (OR 3.5, 95% CI 1.3,9.5, P = .01).
CONCLUSION. In women with preeclampsia, there was evidence of increased sys
temic inflammation in the first trimester. Inflammation might be part of a
causal pathway through which obesity predisposes to preeclampsia. (Obstet G
ynecol 2001;98:757-62. (C) 2001 by the American College of Obstetricians an
d Gynecologists).