TY - JOUR
T1 - Evaluation of maternal serum immunoreactive inhibin as a first trimester marker of Down's syndrome
AU - Wallace, E. M.
AU - Harkness, L. M.
AU - Burns, S.
AU - Liston, W. A.
PY - 1994/1/1
Y1 - 1994/1/1
N2 - Background and Objective - Maternal serum immunoreactive inhibin has been shown to be significantly elevated in Down's affected pregnancies in the second trimester, suggesting that it may be useful in prenatal diagnosis. We have investigated whether it is similarly elevated in the first trimester. Design - Stored maternal sera from women with Down's affected pregnancies and chromosomally normal control pregnancies were retrieved for analysis. These sera had been collected prospectively at either 11 or 12 weeks gestation as a routine antenatal booking procedure. Subjects - From records, 11 women were identified as having had a Down's pregnancy. For each of these, 4 controls matched for gestation and duration-of-storage were also identified. Measurements - Two different inhibin immunoassays were evaluated, one using an antibody raised against 31 kDa bovine inhibin and the other, a commercial two-site assay, using two antibodies directed against two distinct α-subunit epitopes. Results - Neither assay detected a significant effect of gestation on serum inhibin levels. After combining the data from both gestations, no significant difference between the Down's samples and controls for either assay was detected. However, analysis of the data for each gestation separately revealed that one assay detected a significant difference in inhibin levels between Down's affected and unaffected pregnancies at 11 weeks gestation (mean ± SEM 3186 ± 195 vs 2020 ± 172 ng/l, P < 0.01) but not at 12 weeks. The other, commercial, assay did not detect a significant difference at either gestation. In addition, there was poor association between the results of the two assays. Conclusions - These data suggest that immunoreactive inhibin, as detected by these assays, will not be useful as a late first trimester marker for Down's syndrome and also that these two assays detect different inhibin species in pregnancy serum.
AB - Background and Objective - Maternal serum immunoreactive inhibin has been shown to be significantly elevated in Down's affected pregnancies in the second trimester, suggesting that it may be useful in prenatal diagnosis. We have investigated whether it is similarly elevated in the first trimester. Design - Stored maternal sera from women with Down's affected pregnancies and chromosomally normal control pregnancies were retrieved for analysis. These sera had been collected prospectively at either 11 or 12 weeks gestation as a routine antenatal booking procedure. Subjects - From records, 11 women were identified as having had a Down's pregnancy. For each of these, 4 controls matched for gestation and duration-of-storage were also identified. Measurements - Two different inhibin immunoassays were evaluated, one using an antibody raised against 31 kDa bovine inhibin and the other, a commercial two-site assay, using two antibodies directed against two distinct α-subunit epitopes. Results - Neither assay detected a significant effect of gestation on serum inhibin levels. After combining the data from both gestations, no significant difference between the Down's samples and controls for either assay was detected. However, analysis of the data for each gestation separately revealed that one assay detected a significant difference in inhibin levels between Down's affected and unaffected pregnancies at 11 weeks gestation (mean ± SEM 3186 ± 195 vs 2020 ± 172 ng/l, P < 0.01) but not at 12 weeks. The other, commercial, assay did not detect a significant difference at either gestation. In addition, there was poor association between the results of the two assays. Conclusions - These data suggest that immunoreactive inhibin, as detected by these assays, will not be useful as a late first trimester marker for Down's syndrome and also that these two assays detect different inhibin species in pregnancy serum.
UR - http://www.scopus.com/inward/record.url?scp=0028047981&partnerID=8YFLogxK
U2 - 10.1111/j.1365-2265.1994.tb02579.x
DO - 10.1111/j.1365-2265.1994.tb02579.x
M3 - Article
C2 - 7955459
AN - SCOPUS:0028047981
SN - 0300-0664
VL - 41
SP - 483
EP - 486
JO - Clinical Endocrinology
JF - Clinical Endocrinology
IS - 4
ER -