PMID- 10025474
OWN - NLM
STAT- MEDLINE
DCOM- 19990301
LR  - 20190513
IS  - 0002-9262 (Print)
IS  - 0002-9262 (Linking)
VI  - 149
IP  - 4
DP  - 1999 Feb 15
TI  - Maternal second trimester serum tumor necrosis factor-alpha-soluble receptor p55 
      (sTNFp55) and subsequent risk of preeclampsia.
PG  - 323-9
AB  - Preeclampsia is characterized by diffuse vascular endothelial dysfunction. Tumor 
      necrosis factor-alpha (TNF-alpha), which plays a key role in the cytokine network 
      responsible for immunoregulation, is also known to contribute to endothelial 
      dysfunction and other metabolic disturbances noted in preeclampsia. Results from 
      cross-sectional studies and one longitudinal study indicate that TNF-alpha (or 
      its soluble receptor, sTNFp55) is increased in the peripheral circulation and 
      amniotic fluid of women with preeclampsia as compared with normotensive women. 
      Between December 1993 and August 1994, prediagnostic sTNFp55 concentrations (a 
      marker of excessive TNF-alpha release) were measured in 35 women with 
      preeclampsia and 222 normotensive women to determine whether elevations precede 
      the clinical manifestation of the disorder. Logistic regression procedures were 
      used to calculate maximum likelihood estimates of odds ratios and 95% confidence 
      intervals. Mean second trimester (15-22 weeks' gestation) serum sTNFp55 
      concentrations, measured by enzyme-linked immunosorbent assay, were 14.4% higher 
      in preeclamptic women than in normotensive controls (716.6 pg/ml (standard 
      deviation 193.6) vs. 626.4 pg/ml (standard deviation 158.0); p = 0.003). The 
      relative risk of preeclampsia increased across successively higher quintiles of 
      sTNFp55 (odds ratios were 1.0, 1.3, 2.1, and 3.7, with the lowest quintile used 
      as the referent; p for trend = 0.007). After adjustment for maternal age, 
      adiposity, and parity, the relative risk between extreme quintiles was 3.3 (95% 
      confidence interval 0.8-13.4). These findings indicate that the level of 
      TNF-alpha in maternal circulation is increased prior to the clinical 
      manifestation of the disorder, and they are consistent with the hypothesized role 
      of cytokines in mediating endothelial dysfunction and the pathogenesis of 
      preeclampsia. Further work is needed to identify modifiable risk factors for the 
      excessive synthesis and release of TNF-alpha in pregnancy, and to assess whether 
      lowering of TNF-alpha concentrations in pregnancy alters the incidence and 
      severity of preeclampsia.
FAU - Williams, M A
AU  - Williams MA
AD  - Center for Perinatal Studies, Swedish Medical Center, Seattle, WA, USA.
FAU - Farrand, A
AU  - Farrand A
FAU - Mittendorf, R
AU  - Mittendorf R
FAU - Sorensen, T K
AU  - Sorensen TK
FAU - Zingheim, R W
AU  - Zingheim RW
FAU - O'Reilly, G C
AU  - O'Reilly GC
FAU - King, I B
AU  - King IB
FAU - Zebelman, A M
AU  - Zebelman AM
FAU - Luthy, D A
AU  - Luthy DA
LA  - eng
GR  - CA-15704/CA/NCI NIH HHS/United States
GR  - HD/HL-32562/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Epidemiol
JT  - American journal of epidemiology
JID - 7910653
RN  - 0 (Antigens, CD)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Antigens, CD/*blood
MH  - Cohort Studies
MH  - Cross-Sectional Studies
MH  - Female
MH  - Humans
MH  - Pre-Eclampsia/blood/*diagnosis
MH  - Pregnancy
MH  - Pregnancy Trimester, Second
MH  - Receptors, Tumor Necrosis Factor/*blood
MH  - Receptors, Tumor Necrosis Factor, Type I
MH  - Risk
MH  - Sensitivity and Specificity
MH  - Washington
EDAT- 1999/02/20 00:00
MHDA- 1999/02/20 00:01
CRDT- 1999/02/20 00:00
PHST- 1999/02/20 00:00 [pubmed]
PHST- 1999/02/20 00:01 [medline]
PHST- 1999/02/20 00:00 [entrez]
AID - 10.1093/oxfordjournals.aje.a009816 [doi]
PST - ppublish
SO  - Am J Epidemiol. 1999 Feb 15;149(4):323-9. doi: 
      10.1093/oxfordjournals.aje.a009816.