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Biomedical subjects

Katharine D Wenstrom

Publications and source records attributed to Katharine D Wenstrom.

7 recordsLinked to original sources
PubMed2005

Midtrimester amniotic fluid matrix metalloproteinase-8 (MMP-8) levels above the 90th percentile are a marker for subsequent preterm premature rupture of membranes.

OBJECTIVE: We sought to determine whether midtrimester amniotic fluid levels of matrix metalloproteinase-8 were associated with subsequent preterm premature rupture of membranes. STUDY DESIGN: We conducted a case-control study examining 57 asymptomatic women who underwent genetic amniocentesis from 14 to 21 weeks' gestation and subsequently had preterm premature rupture of membranes (<35 wk) and 58 women with subsequent term delivery. Measurement of total matrix metalloproteinase-8 level in amniotic fluid was conducted using a commercially available enzyme-linked immunosorbent assay and association with preterm birth due to preterm premature rupture of membranes was assessed. RESULTS: The overall distribution of matrix metalloproteinase-8 concentrations was similar in women who had preterm premature rupture of membranes and term controls (median 2.39 ng/mL, 25th to 75th percentile 1.1-10.1 vs 2.37 ng/mL, 25th to 75th percentile 1.5-4.7, P = .94). However, 26% of women who had preterm premature rupture of membranes had a matrix metalloproteinase-8 concentration above the 90th percentile (8.7 ng/mL), compared with only 10% of term controls (odds ratio 3.1, 95% CI 1.1-8.7; P = .03). Elevated matrix metalloproteinase-8 remained associated with preterm premature rupture of membranes after adjustment for maternal age, race, parity, gestational age, and year of amniocentesis (odds ratio 3.4, 95% CI 1.2-9.9; P = .03). CONCLUSIONS: The overall distribution of midtrimester amniotic fluid matrix metalloproteinase-8 levels did not differ between women who had preterm premature rupture of membranes and those delivered at term. However, marked elevations of midtrimester amniotic fluid matrix metalloproteinase-8 were highly associated with subsequent preterm premature rupture of membranes, suggesting that the pathophysiologic processes that contribute to preterm premature rupture of membranes may begin in early pregnancy.

Adult↗
PubMed2005

Evaluation of Down syndrome screening strategies.

Women contemplating pregnancy today have many different Down syndrome screening protocols from which to choose. Sensitive and specific first and second trimester screening protocols are now widely available, and strategies that combine first and second trimester markers are moving from investigational use into the clinical arena. Modeling indicates that a high detection rate (85%) associated with a very low screen positive rate (1.3%) can be achieved with contingent screening, in which all women undergo first trimester screening and only a portion (25%) go on to second trimester screening.

Adult↗
PubMed2005

First-trimester Down syndrome screening: component analytes and timing for optimal performance.

The most effective first-trimester Down syndrome screening protocol in current use employs three independent markers: maternal serum levels of PAPP-A and free beta hCG, and measurement of fetal nuchal translucency (NT). Eleven weeks appears to be the optimum gestational age for performing first trimester DS risk assessment. Although the discrimination of free beta hCG improves with increasing gestational age and is greatest at 13 weeks, PAPP-A and NT perform optimally at 10 and 11 weeks, respectively. In addition to accurate pregnancy dating, first trimester screening performance is improved by using a consistent NT measurement technique, NT cut-offs adjusted for gestational age or crown-rump length, and possibly center- or operator-specific NT medians. Whether or not absence or presence of the nasal bone adds to screening accuracy is a matter of some debate. Finally, because enlarged NT has been associated with cardiac defects and other structural anomalies, even in euploid fetuses, its presence should prompt a targeted second trimester ultrasound examination.

Down Syndrome↗
PubMed2004

Fetal open spina bifida: a natural history of disease progression in utero.

OBJECTIVE: To determine the natural history of the prenatal development of ventriculomegaly and talipes in fetuses with open spina bifida. STUDY DESIGN: All fetuses with isolated open spina bifida and managed at our center between January 1996 and March 2000 were retrospectively evaluated. Ultrasonographic images and reports were reviewed from examinations performed every 3 to 4 weeks from the time of diagnosis to delivery for lesion level and type, ventriculomegaly (defined as an atrial width of > or =10 mm), and lower extremity appearance. RESULTS: Of the 53 pregnancies identified, 20 (38%) were electively terminated. In the 33 ongoing gestations, the lesions ranged from lower thoracic to sacral; 79% were characterized as meningomyeloceles and 21% as myeloschises. Fifty-five percent (n = 18) had ventriculomegaly at diagnosis (early onset, mean gestational age at diagnosis 22 +/- 5 weeks), 33% (n = 11) subsequently developed ventriculomegaly (late onset, mean 29 +/- 6 weeks), and 12% (n = 4) had normal ventricle size at the last sonogram before birth (mean 38 +/- 1 weeks). The ventricular size prior to delivery was significantly smaller with late-onset ventriculomegaly than with early-onset: 15 +/- 4 mm versus 28 +/- 10 mm, (p = 0.001). Only 6% (n = 2) had talipes at the initial sonogram, and 18% (n = 6) were subsequently determined to have talipes (mean 30 +/- 6 weeks). CONCLUSION: Most fetuses with open spina bifida develop ventriculomegaly, and the majority do so by 21 weeks' gestation. Fetuses that develop ventriculomegaly later in gestation have less severe ventricular dilation at birth. In contrast, a minority of fetuses have congenital talipes, and because most cases develop after 20 weeks, they are not predicted by early midtrimester sonographic evaluation.

Cerebral Ventricles↗
PubMed2002

Fragile X and other trinucleotide repeat diseases.

Hereditary unstable DNA is composed of strings of trinucleotide repeats, in which three nucleotides are repeated over and over (ie CAGCAGCAGCAG). These repeats are found in several sites within genes; depending on their location, the number of triplet repeats in a string can change as it is passed on to offspring. When the number of repeats increases to a critical size, it can have a variety of affects on gene function. The repeats may cause a loss in gene function (as in Fragile X) or may result in the gain of a new, abnormal protein and thus a new function (as in myotonic dystrophy and Huntington disease). Although a variety of trinucleotide repeat diseases have been reported and merit consideration, this discussion will focus primarily on Fragile X syndrome, myotonic dystrophy, and Huntington disease.

Female↗