Serum activin A, inhibin A, and follistatin concentrations in preeclampsia or small for gestational age pregnancies

• Published in: Obstetrics and gynecology (New York. 1953) Vol. 99; no. 2; pp. 267 - 274
• Main Authors: Keelan, Jeffrey A, Taylor, Rennae, Schellenberg, Jean-Claude, Groome, Nigel P, Mitchell, Murray D, North, Robyn A
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.02.2002; The American College of Obstetricians and Gynecologists; Elsevier Science
• Subjects: Activins - blood; Adult; Biological and medical sciences; Blood Pressure; Case-Control Studies; Cross-Sectional Studies; Diseases of mother, fetus and pregnancy; Female; Fetal Growth Retardation - blood; Follistatin; Gynecology. Andrology. Obstetrics; Humans; Infant, Newborn; Infant, Small for Gestational Age - blood; Inhibin-beta Subunits - blood; Inhibins - blood; Longitudinal Studies; Medical sciences; Pre-Eclampsia - blood; Pregnancy; Pregnancy. Fetus. Placenta; New Zealand; Oceania; Human; Intrauterine growth retardation; Follistatin; Pregnancy disorders; Pathophysiology; Inhibin; Biological marker; Maternal diseases; Pregnancy toxemia; Blood plasma; Fetal diseases; Preeclampsia; Activin; Comparative study
• ISSN: 0029-7844; 1873-233X
• DOI: 10.1016/S0029-7844(01)01674-X

OBJECTIVE: To determine whether maternal serum activin A, inhibin A, and follistatin concentrations in idiopathic small for gestational age (SGA) pregnancies are similar to those in normal pregnancies or elevated as in preeclampsia. METHODS: Maternal serum activin A, inhibin A, and follistatin concentrations were determined in 1) nulliparous women with idiopathic SGA (birth weight <10th percentile; n = 18), preeclampsia (systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg plus proteinuria ≥2+ or >0.3 g/24h; n = 22), and normotensive controls, matched for gestational age at sampling (n = 22), and 2) a longitudinal series of samples collected at five intervals throughout pregnancy from nulliparous women with idiopathic SGA (n = 19), preeclampsia (n = 22), preeclampsia plus SGA (n = 15), or who had uncomplicated pregnancies (n = 20). RESULTS: Serum concentrations of activin A and inhibin A were similar in idiopathic SGA pregnancies to controls. In preeclampsia, activin A and inhibin A levels were markedly increased compared with controls or women with idiopathic SGA (P < .001), particularly in those with early-onset disease. Follistatin concentrations were only modestly (<twofold) elevated in preeclampsia (P < .001). In the longitudinal study, serum activin A or inhibin A concentrations were increased in women who later developed preeclampsia, whereas in women with idiopathic SGA pregnancy, a small overall increase in activin A levels was observed. CONCLUSIONS: In contrast to women with preeclampsia, normotensive women with SGA pregnancies do not have markedly elevated circulating levels of activin A and inhibin A. These data support the hypothesis that increased serum activin A concentrations in preeclampsia may be a manifestation of maternal disease rather than just a marker of abnormal placentation.