Serum level of placental growth hormone is raised in pregnancy rhinitis and may be involved in its pathogeny. Pregnancy rhinitis does not significantly raise weight gain or serum levels of estradiol, progesterone, or insulinlike growth factor I.

The respective contributions of pituitary and placental GH to circulating IGF-I in pregnant women have not been well established. We measured the serum concentrations of placental growth hormone (PGH) and IGF-I in a woman with pit-1 deficiency before, during and after pregnancy, resulting in the birth of a healthy child (not pit-1 deficient). Both PGH and IGF-I concentrations were below the assay detection limit before and after pregnancy. During pregnancy, PGH and IGF-I levels increased steadily; the concentrations of PGH and IGF-I in late pregnancy were comparable with levels previously measured in normal pregnancies. PGH and IGF-I concentrations were strongly correlated throughout pregnancy (r = 0.90; P = 0.002). PGH was undetectable in cord serum, whilst the IGF-I concentration was within the normal range. The findings of this case study corroborate the notion that PGH is the prime regulator of maternal serum IGF-I during pregnancy.

We previously described significant changes in GH-binding protein (GHBP) in pathological human pregnancy. There was a substantial elevation of GHBP in cases of noninsulin-dependent diabetes mellitus and a reduction in insulin-dependent diabetes mellitus. GHBP has the potential to modulate the proportion of free placental GH (PGH) and hence the impact on the maternal GH/insulin-like growth factor I (IGF-I) axis, fetal growth, and maternal glycemic status. The present study was undertaken to investigate the relationship among glycemia, GHBP, and PGH during pregnancy and to assess the impact of GHBP on the concentration of free PGH. We have extended the analysis of specimens to include measurements of GHBP, PGH, IGF-I, IGF-II, IGF-binding protein-1 (IGFBP-1), IGFBP-2, and IGFBP-3 and have related these to maternal characteristics, fetal growth, and glycemia. The simultaneous measurement of GHBP and PGH has for the first time allowed calculation of the free component of PGH and correlation of the free component to indexes of fetal growth and other endocrine markers. PGH, free PGH, IGF-I, and IGF-II were substantially decreased in IUGR at 28 -30 weeks gestation (K28) and 36 -38 weeks gestation (K36). The mean concentration (ϮSEM) of total PGH increased significantly from K28 to K36 (30.0 Ϯ 2.2 to 50.7 Ϯ 6.2 ng/mL; n ϭ 40), as did the concentration of free PGH (23.4 Ϯ 2.3 to 43.7 Ϯ 6.0 ng/mL; n ϭ 38). The mean percentage of free PGH was significantly less in IUGR than in normal subjects (67% vs. 79%; P Ͻ 0.01). Macrosomia was associated with an increase in these parameters that did not reach statistical significance. Multiple regression analysis revealed that PGH/IGF-I and IGFBP-3 account for 40% of the variance in birth weight. IGFBP-3 showed a significant correlation with IGF-I, IGF-II, and free and total PGH at K28 and K36. Noninsulin-dependent diabetes mellitus patients had a lower mean percentage of free PGH (65%; P Ͻ 0.01), and insulin-dependent diabetics had a higher mean percentage of free PGH (87%; P Ͻ 0.01) than normal subjects. Mean postprandial glucose at K28 correlated positively with PGH and free PGH (consistent with the hyperglycemic action of GH). GHBP correlated negatively with both postprandial and fasting glucose. Although GHBP correlated negatively with PGH (r ϭ Ϫ0.52; P Ͻ .001), free PGH and total PGH correlated very closely (r ϭ 0.98). The results are consistent with an inhibitory function for GHBP in vivo and support a critical role for placental GH and IGF-I in driving normal fetal growth. (J Clin Endocrinol

In the present study, we determined circulating serum levels of human placental growth hormone (hPGH) and insulinlike growth factor binding proteins 1 and 3 (IGFBP-1 and IGFBP-3) using two-site radioimmunoassays during the gestational midtrimester of pregnancies affected by chromosomal disorders with the aim of identifying potential marker substances that might have a significant discriminative and predictive value for prenatal diagnosis of fetal chromosomal aberrations and of organ malformations such as neural-tube defect. Our results show that the maternal serum levels of hPGH were significantly elevated in pregnancies affected by chromosomal anomalies or organ malformations as compared with controls. The distribution of IGFBP-1 concentrations for all experimental groups except trisomy 21 were closely similar to the normal population. IGFBP-3 decreased slightly in pregnancies affected by Down syndrome. These findings suggest that hPGH may be useful as an additional marker in prenatal screening for Down syndrome.

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