Biomedical subjects
Publications and source records attributed to J N Macri.
Various methods of adjusting maternal serum alpha-fetoprotein levels based on maternal weight have been recommended in order to more appropriately assign risk in maternal serum alpha-fetoprotein screening. These adjustments may, however, result in a larger proportion of pregnancies designated as having increased risk and reduction in detection accuracy.
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An index case of "undetectable" maternal serum alpha-fetoprotein at 16 weeks in the first pregnancy of a 28-year-old woman was associated with birth of an infant with trisomy 18. This fortuitous finding stimulated a retrospective study of prenatally diagnosed chromosomal abnormalities. From among a series of 3,862 genetic amniocenteses, 32 cases of fetal autosomal trisomy were diagnosed for which corresponding maternal serum and amniotic fluid alpha-fetoprotein data could be retrieved. From a second laboratory, nine additional cases were added. The maternal serum alpha-fetoprotein levels expressed as multiples of the median were significantly lower in distribution for these 41 women than those from a group of normal matched control subjects (p less than 0.001). Since maternal age is shown to be a less than adequate predictor of autosomal trisomic birth, we proposed that a low level of maternal serum alpha-fetoprotein obtained through routine screening may prove to be valuable in improving the prenatal detection of these serious anomalies.
Lowered maternal serum alpha-fetoprotein was retrospectively investigated in 20,000 patients who underwent prenatal maternal serum alpha-fetoprotein screening. Two hundred thirty-two patients were initially evaluated as having maternal serum alpha-fetoprotein levels less than 0.25 multiple of the normal median. Correction factors, such as incorrect estimation of gestational age, reduced to 180 the number of patients with low alpha-fetoprotein. In this target group, patients with known pregnancy outcomes sustained a fetal loss in 38% of the cases. It appears that significantly low maternal serum alpha-fetoprotein is associated with a dramatic increase in second-trimester fetal wastage.
Premature rupture of the membranes frequently presents a diagnostic dilemma to the clinician. The presence of alpha-fetoprotein (AFP) in amniotic fluid suggests a possible solution. A rapid, easy-to-use latex agglutination test for AFP was evaluated on 99 amniotic fluid samples of known AFP concentration. Body fluids (maternal serum, urine, vaginal secretions, and seminal fluid) that commonly interfere with other tests were also studied. The sensitivity for amniotic fluids from gestations less than 39 weeks was 93%, and specificity was 94%. The test is most accurate under 35 weeks, when diagnosis is critical. Equivocal results may be resolved by using radioimmunoassay. The results suggest that a rapid assay for AFP may be useful in the diagnosis of ruptured membranes. It has few interfering factors, is safe, and requires no elaborate equipment or training.
Measuring maternal serum alpha-fetoprotein (AFP) levels in the second trimester is an effective screening test for identifying pregnancies at increased risk for neural tube defects. In the absence of a neural tube defect there are many nonpathologic and pathologic causes for elevated AFP including underestimated gestational age, twin gestation, impending fetal death, and rare fetal malformations. In this series, intraplacental sonolucent spaces were detected in a significant percentage of second trimester pregnancies with elevated serum AFP in the absence of any other cause for the elevation. It is postulated that these cystic spaces are a conduit for the transfer of fetal blood into the maternal circulation, thus accounting for the nonpathologic AFP elevation in the maternal serum.
Twenty-two cases of open neural tube defect were found in a population of 17,703 unselected pregnancies (1.2 per 1000) within the Long Island, New York, region. Voluntary screening of maternal serum alpha-fetoprotein levels identified 20 of the 22 cases (91%). Six hundred ninety-two participants demonstrated serial elevations in maternal serum alpha-fetoprotein. Of this group, which was designated at increased risk for open neural tube defect, 24% had underestimated gestational age, 13% had multiple gestations, and 53% were candidates for amniocentesis. In the amniocentesis group, the detection yield of neural tube defect was 20 per 365 (5.5%). Neither false-negative amniotic fluid evaluations nor termination of normal pregnancy due to false-positive amniotic fluid levels occurred. Perinatal outcome data, including pregnancy complications, date, mode of delivery, sex, birth weight, Apgar score, and congenital malformations of the neonate other than neural tube defect, are reported for the first 9300 consecutive participants of the 17,703 population study. These data identify a correlation between rate of perinatal loss and maternal serum alpha-fetoprotein levels.
gamma-Glutamyl transpeptidase (GGTP) activity in normal amniotic fluids and corresponding maternal sera obtained at various gestational periods was measured. The ontogenic pattern of enzyme activity in amniotic fluid is very similar to alpha fetoprotein (AFP). However, the levels of these two proteins behaved differently in corresponding maternal sera. Also, in amniotic fluids obtained from pregnancies with neural tube defects (NTD), only AFP concentration was abnormally high whereas GGTP activity was normal.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
This study presents 3 cases of severe soft-tissue malformations of the fetus. Prenatal diagnosis was established early in the second trimester, and the accuracy of the diagnosis was confirmed by pathological examination in each instance. A clinically oriented work-up plan for early prenatal diagnosis is proposed.
The present investigation documents that, under normal conditions, most fetally produced AFP reaches the maternal circulation via diffusion across the amnion from amniotic fluid. This has been determined by comparing maternal serum AFP levels with amniotic fluid albumin concentrations in paired samples. The proportionally demonstrated between them indicates a proportional, transamniotic exchange of the two proteins, each originating on opposite sides of the amnion. Albumin is known to reach amniotic fluid by transamniotic diffusion from maternal blood. All amnions restrict AFP movement into maternal serum, but some are distinctly more restrictive than others; in such cases, a relatively greater increase in amniotic fluid AFP concentration would likely have to occur from a fetal lesion before being reflected in maternal serum. Inconsistencies found in several paired samples identify that other variables may also influence passage of AFP to the mother.