Radioimmunoassay of SP1 (pregnancy-specific beta1-glycoprotein) in maternal blood and in amniotic fluid normal and pathologic pregnancies.

Sp1, the pregnancy-specific beta 1-glycoprotein, was studied in normal and pathologic pregnancies. We developed a highly specific and sensitive double-antibody-radioimmunoassay by radioiodination of purified placental SP1. This RIA allowed the estimation of SP1 concentrations as low as 2 ng/ml. In a collective of 227 women with normal pregnancies we established the normal distribution curve in maternal plasma from the fifth week of gestation to term. The median value rose steadily from 3 microgram/ml in the 8th week to 140 microgram/ml in the 36th week when a plateau was formed. In more than 400 patients with pregnancies complicated by a variety of pathologic disorders the SP1 levels were controlled by either single assays or serial estimations throughout pregnancy and were compared with the normal distribution range. SP1 was also determined in about 200 samples of amniotic fluid gained by amniocentesis and during parturition of normal pregnant women from the 13th gestational week until term. The normal range was established up to the 20th w.o.p. The concentrations rose from below 0.2 microgram/ml in early pregnancy to 3 microgram/ml and generally amounted to approximately 1% of the respective serum value. Pathologic cases with diverse chromosomal anomalies, Rh-incompatibility, anencephaly, hydramnios and other abnormal conditions were examined. From these only twin-pregnancies with slightly elevated levels and cases with fetal trisomies with reduced SP1 concentrations showed aberrations from the normal distribution. The estimation of serum concentrations in mothers with diabetes or Rh-incompatibility were not significantly different from the normal collective. In diabetes a characteristic course of the follow-up curves was observed. Abortion in early pregnancy was frequently but not always indicated by reduced SP1 values. Threatened abortion with subsequent continuation of pregnancy exhibited SP1 values scattered within the normal range. Since the radioimmunological determination of SP1 is possible in the early stage of gestation (from week 8) it may serve as a useful tool for prediction at times when the determination of placental lactogen is not yet possible. In pregnancies with "small-for-date babies" the correlation between SP1 in maternal plasma and fetal growth retardation was reflected in a pronounced tendency to low SP1 levels. Serial determinations of SP1 in the serum of women with EPH-gestosis were compared with the corresponding HPL determinations and showed the equality of SP1 concerning the assessment of the placental function.