Elevation of maternal serum human chorionic gonadotropin (hcg) is not a marker of increased trophoblast mitogenic activity

OBJECTIVE: Second trimester elevation of maternal serum (MS) hCG has been associated with untoward pregnancy outcome, yet its pathogenesis is unknown. We have hypothesized that elevated hCG is due to increased trophoblast proliferation. To test this hypothesis we have measured amniotic fluid (AF) levels of hepatocyte growth factor (HGF), a potent mitogenic and angiogenic factor released by and active on second trimester syncytiotrophoblast. STUDY DESIGN: AF levels of HGF {Quantikine, R&D Systems) in women with elevated MS hCG at the triple screening who underwent second trimester amniocentesis (n=20) were compared with those of women who had normal MS hCG levels at triple screening and underwent amniocentesis for standard genetic indications (n = 40). Included were singleton gestations with no evidence of fetal structural or chromosomal anomalies. Statistical analysis included x2. one-way ANOVA, multivariate analysis and correlation after log-transformation. RESULTS: Mean ±standard deviation maternal age {29±8 vs 36±7 years, p<0.05) and gestational age at sampling f 19±4 weeks vs 17±2 weeks, p<0.05) were different between women with high MS hCG vs those of women with normal or unknown hCG levels. AF HGF levels were not significantly different between the two groups (95,165± 68,825 vs 71,507±56,414, respectively, p=0.62). The lack of significance persisted after correcting for maternal age, gestational age at sampling, and year of sampling. CONCLUSIONS: Elevation of MS hCG is not associated with increased production and release of the mitogen HGF into the AF.