Placental growth hormone is increased in the maternal and fetal serum of patients with preeclampsia

Abstract

Objectives: Placental growth hormone (PGH) is a pregnancy-specific protein produced by syncytiotrophoblast and extravillous cytotrophoblast. No other cells have been reported to synthesize PGH Maternal. PGH Serum concentration increases with advancing gestational age, while quickly decreasing after delivery of the placenta. The biological properties of PGH include somatogenic, lactogenic, and lipolytic functions. The purpose of this study was to determine whether the maternal serum concentrations of PGH change in women with preeclampsia (PE), women with PE who deliver a small for gestational age neonate (PE + SGA), and those with SGA alone.

Study design: This cross-sectional study included maternal serum from normal pregnant women (n = 61), patients with severe PE (n = 48), PE + SGA (n = 30), and SGA alone (n = 41). Fetal cord blood from uncomplicated pregnancies (n = 16) and PE (n = 16) was also analyzed. PGH concentrations were measured by ELISA. Non-parametric statistics were used for analysis.

Results: (1) Women with severe PE had a median serum concentration of PGH higher than normal pregnant women (PE: median 23,076 pg/mL (3473-94 256) vs. normal pregnancy: median 12 157 pg/mL (2617-34 016); p < 0.05), pregnant women who delivered an SGA neonate (SGA: median 10 206 pg/mL (1816-34 705); p < 0.05), as well as pregnant patients with PE and SGA (PE + SGA: median 11 027 pg/mL (1232-61 702); p < 0.05). (2) No significant differences were observed in the median maternal serum concentration of PGH among pregnant women with PE and SGA, SGA alone, and normal pregnancy (p > 0.05). (3) Compared to those of the control group, the median umbilical serum concentration of PGH was significantly higher in newborns of preeclamptic women (PE: median 356.1 pg/mL (72.6-20 946), normal pregnancy: median 128.5 pg/mL (21.6-255.9); p < 0.01). (4) PGH was detected in all samples of cord blood.

Conclusions: (1) PE is associated with higher median concentrations of PGH in both the maternal and fetal circulation compared to normal pregnancy. (2) Patients with PE + SGA had lower maternal serum concentrations of PGH than preeclamptic patients without SGA. (3) Contrary to previous findings, PGH was detectable in the fetal circulation. The observations reported herein are novel and suggest that PGH may play a role in the mechanisms of disease in preeclampsia and fetal growth restriction.

Figure 1

Maternal serum placental growth hormone (PGH) concentrations among the study groups. Patients with severe preeclampsia had a significantly higher median maternal serum PGH concentration than women with normal pregnancies (severe preeclampsia: median 23076 pg/mL; range 3473-94,256 vs. normal pregnancy: median12157 pg/mL; range: 2617-34016; p<0.05), women with preeclampsia +small for gestional age (median: 11,027.3 pg/mL; range 1232-61,702; p<0.05), as well as women with pregnancies complicated by SGA alone (median 10,206 pg/mL; range: 1816-34,705; p<0.05). Multiple comparisons among normal pregnancy, preeclampsia +SGA, and SGA showed no significant differences in median maternal serum PGH concentration among these groups.

Figure 2

Umbilical cord blood median placental growth hormone (PGH) concentrations from normal pregnant women and women with severe preeclampsia. The median umbilical cord serum concentration of PGH was significantly higher in pregnancies complicated by severe preeclampsia when compared to normal pregnancies (preeclampsia: median 356.1 pg/mL; range 72.6-20,946 vs. normal pregnancy, median: 128.5 pg/mL; range 21.6-255.9; p<0.01).