Early-pregnancy soluble Fas levels in idiopathic small-for-gestational-age pregnancies.

OBJECTIVE: We sought to determine first- and second-trimester serum soluble Fas (sFas) and placental growth factor (PlGF) levels in idiopathic small-for-gestational-age (SGA) pregnancies. STUDY DESIGN: We measured sFas and PlGF levels in women who delivered SGA infants uncomplicated by preeclampsia and in control subjects. For sFas there were 34 cases and 318 control subjects in the first trimester and 9 cases and 11 control subjects in the second trimester. For PlGF there were 31 cases and 281 control subjects in the first trimester and 8 cases and 11 control subjects in the second trimester. RESULTS: SGA pregnancies had lower sFas levels than control subjects in the second trimester (3703 + or - 209 pg/mL vs 4562 + or - 241 pg/mL; P = .015), but not in the first trimester (4892 + or - 191 pg/mL vs 4971 + or - 177 pg/mL; P = .68). There was no difference in PlGF levels between SGA and normal pregnancies in both trimesters. CONCLUSION: Serum sFas levels were lower in idiopathic SGA pregnancies in the second trimester, but not in the first. There was no difference in serum PlGF levels in either trimester.

Angiogenic factor abnormalities and fetal demise in a twin pregnancy.

BACKGROUND: An otherwise healthy 31-year-old gravida 2 para 1 woman with a spontaneous dichorionic, diamniotic twin pregnancy presented with hypertension, nephrotic syndrome and renal insufficiency at 19 weeks' gestation. Fetal ultrasound revealed severe intrauterine growth restriction of one fetus and measurement of serum anti-angiogenic and angiogenic factors were consistent with a profound anti-angiogenic state. After one fetus died and the placenta became increasingly echogenic, the patient improved clinically, and weekly ultrasound assessments of the intact co-twin from 22 weeks onwards demonstrated symmetrical fetal growth along the 10th centile. Repeat serum angiogenic factors at 24 weeks' gestation revealed considerable improvement of the anti-angiogenic state and paralleled resolution of the clinical syndrome. INVESTIGATIONS: Physical examination, laboratory evaluations including full blood count, liver function tests, electrolytes, renal function tests, screening for glomerular-based disease, 24-h urine collection for total protein, analysis of serum anti-angiogenic and angiogenic factors, fetal ultrasonography and placental Doppler examination. DIAGNOSIS: Spontaneous resolution of early-onset pre-eclampsia after single fetal demise in a twin pregnancy. MANAGEMENT: Labetalol was given to treat hypertension and furosemide was given as needed for edema. The patient was closely followed up throughout pregnancy in a combined nephrology/obstetrics outpatient clinic.

Angiogenic factors and preeclampsia.

Preeclampsia/eclampsia is a major cause of maternal and fetal morbidity worldwide. Although the etiology of preeclampsia is still unclear, the clinical phenotypes of preeclampsia have been demonstrated to be related to high circulating levels of anti-angiogenic proteins secreted by the placenta such as soluble Fms-like tyrosine kinase 1 (sFlt1) and soluble endoglin. Because, alterations in circulating sFlt1 and soluble endoglin precede the onset of clinical disease, these factors may be useful to screen or identify patients at risk for preeclampsia. Investigations are currently underway of various pharmacologic agents to counteract the effects of sFlt1 and/or sEng as a potential treatment for preeclampsia. Recently several isoforms of sFlt1 have been described, such as sFlt1-14 which is expressed only in primates, and is thought to be the primary isoform produced by the placenta in preeclamptic subjects. Although several novel pathways have been proposed to play key roles in inducing sFlt1 production, the exact role of these pathways in human preeclampsia is still not known. Women with a history of preeclampsia have an increased risk of hypertension, and cardiovascular and renal disease. Whether these long-term observations are due to persistent and subtle endothelial damage as result of preeclampsia, or simply reflect the consequences of the vascular risk factors which are more common in these women remains unknown.