To investigate the association between fetal distress (abnormal cardiotocograph tracing and/or a low fetal pH) and the levels of fetal IGFBP-1.
Prospective comparative study.
Twenty-two women in labour with evidence of fetal distress defined by FIGO criteria and 19 women in uncomplicated labour. The gestation range was 37 to 42 weeks and birthweight range was 2500 to 4240 g. IGFBP-1 was determined by radioimmunoassay.
The umbilical levels of IGFBP-1 were significantly higher in the study group compared with the control group (median 282.5 micrograms/l versus 128 micrograms/l, P = 0.0046; Mann-Whitney U test). There was a significant inverse correlation between fetal IGFBP-1 and cord pH (r = 0.58, P < or = 0.0001). There was no difference between the maternal serum levels of IGFBP-1 in the two groups.
Umbilical IGFBP-1 is elevated in association with fetal distress.
[Show abstract][Hide abstract] ABSTRACT: Die vorliegende Arbeit sollte eine mögliche Rolle von Mutationen der Gene IGF-I (Insulin-like Growth Factor-I) und IGF-IR (Insulin-like Growth Factor-I Receptor) in der Pathogenese der intrauterinen Wachstumsretardierung (Intrauterine Growth Retardation/ Restriction, [IUGR]) mit ARED (Absent or Reversed EndDiastolic)-Flow in der Dopplersonographie der A.umbilicalis untersuchen. Die IUGR wird auf Entwicklungsstörungen der Plazenta zurückgeführt. Die Proliferation und Differenzierung des villösen Trophoblasten werden insbesondere von dem Wachstumsfaktor IGF-I und seinem Rezeptor IGF-IR gesteuert. Ausserdem ist das funktionelle IGF-I-System auch in der Angiogenese der Plazentazotten involviert. Die reduzierte Aktivität dieses Systems scheint mit einer eingeschränkten Proliferation des Zytotrophoblasten und einer inadequaten Angiogenese der Plazenta mit der Folge einer postplazentaren Hypoxie einherzugehen. Die geschilderten morphologischen Veränderungen der Plazentazotten sind typisch für Schwangerschaften mit IUGR und ARED-Flow. Bei Schwangerschaften mit IUGR und PED (Preserved EndDiastolic)- Flow bei gleichzeitig pathologischem Dopplerbefund der A.uterina (Notch), zeigt die plazentare Histologie eine Hyperkapillarisierung im Bereich der vermehrt verzweigten Endzotten (uteroplazentare Hypoxie). In der vorliegenden Studie wurden die Gene, die für IGF-I und IGF-IR kodieren, in einem IUGR/ARED-Flow-Kollektiv (19 Mütter und deren 19 Kinder) und einem IUGR/PED-Flow-Kollektiv (14 Mütter und deren 14 Kinder) analysiert. Die DNA wurde aus Frischblut (Mütter und lebende Kinder) und Paraffinblöcken (verstorbene Kinder) isoliert. Das Screening auf genomische Varianten beider Gene erfolgte mittels Einzelstrangkonformationsanalyse (SSCP), Restriktionsanalyse (RFLP) und direkter Sequenzierung. Im IGF-I-Gen konnten bei dem untersuchten Kollektiv keine Mutationen identifiziert werden. Dagegen konnten im IGF-IR-Gen insgesamt fünf Varianten nachgewiesen werden, davon drei bisher noch unbekannte Sequenzveränderungen: eine im 5´- und zwei im 3´-untranslatierten Bereich des Gens, sowie zwei Polymorphismen, die bereits in der Literatur beschrieben worden sind: eine stille Mutation in Exon 16 und eine Deletion in der 3´-untranslatierten Region des Gens. Die neuen Polymorphismen lagen im nicht-kodierenden Bereich des IGF-IR-Gens. Darüber hinaus traten alle genomische Varianten mit etwa gleicher Häufigkeit unter den Patienten und unter den Kontrollen auf. Daraus lässt sich folgern, dass die identifizierten Gen-Polymorphismen keine entscheidende Rolle in der Ätiologie der IUGR mit ARED-Flow spielen. The objective of the present study was to evaluate a possible role of mutations of the genes IGF-I (Insulin-like Growth Factor-I) and IGF-IR (Insulin-like Growth Factor-I Receptor) in the pathogenesis of intrauterine growth retardation/ restriction (IUGR) with ARED (Absent or Reversed EndDiastolic)-flow in the Doppler ultrasonography of the A.umbilicalis. IUGR is caused by abnormal development of the placenta. The proliferation and differentiation of the villous trophoblast are predominantly controlled by growth factor IGF-I and its receptor IGF-IR. The functional IGF-I-system is also involved in the placental angiogenesis. Reduced activity of this system seems to be associated with an impaired proliferation of cytotrophoblastic cells and an inadequate placental angiogenesis, resulting in a postplacental hypoxia. The morphological changes of the placenta, as described above, are characteristic for pregnancies with IUGR and ARED-flow. In pregnancies with IUGR and PED (Preserved EndDiastolic)-flow in the presence of a bilateral abnormal uterine artery Doppler waveform (Notch), the placental histology shows a netlike arrangement of capillaries, forming multiply branched terminal villi (uteroplacental hypoxia). In the present study have been analyzed the genes encoding for IGF-I and IGF-IR in an IUGR/ARED-flow-group (19 mothers and their 19 fetuses) and an IUGR/PED-flow-group (14 mothers and their 14 fetuses). DNA was extracted from blood samples (mothers and alive fetuses) and paraffinblock samples (not-alive fetuses). Both genes were screened for genomic variants by single-strand conformation analysis (SSCP), restriction assays (RFLP) and direct sequencing. In the IGF-I-gene no variants could be identified in the study population. As for the IGF-IR-gene, five variants could be identified, three of them so far unknown: one in the 5´- and two in the 3´-untranslated region of the gene, as well as two polymorphisms that had already been described before in the literature: a silent mutation in exon 16 and a deletion in the 3´-untranslated region of the gene. The new polymorphisms were localized in the non-coding region of the IGF-IR-gene. Furthermore, all genomic variants were detected in similar frequencies in the patient-group and the control-group. Thus we conclude that the identified gene-polymorphisms do not play a relevant role in the aetiology of IUGR with ARED-flow.
[Show abstract][Hide abstract] ABSTRACT: Our purpose was to examine the regulation of fetal serum concentrations of insulin (C-peptide), insulin-like growth factor-I, insulin-like growth factor-II, and insulin-like growth factor binding protein-1, which are growth-regulating factors in the fetus, in monozygotic and dizygotic twin pairs.
Cord serum samples were collected from 110 twin pairs and compared with 178 nonsibling singleton pairs with the same gestational age. Five twin pairs were excluded from the statistical analyses because of severe intrauterine growth restriction and placental abnormalities in one. Zygosity was assigned by histologic examination of the placenta and by a questionnaire sent to the mother when the twins were > or = 6 months old. Analyses included the calculation of correlation coefficients, between-pair variation, and univariate genetic analysis.
Cord serum C-peptide concentrations were highly correlated in monozygotic (r = 0.94) and dizygotic twins (r = 0.79) but not in singleton pairs (r = -0.05); the between-pair variation was also smaller in twins than in singletons. Genetic analysis demonstrated a large contribution of the common environment to the variance in C-peptide concentrations (80%) and a smaller genetic contribution (12%). Insulin-like growth factor-I concentrations were better correlated in monozygotic (r = 0.82) than in dizygotic twins (r = 0.42), with a smaller between-pair variation in the former group (22% +/- 4% vs 51% +/- 5%). Univariate genetic analysis indicated that insulin-like growth factor-I levels were regulated predominantly by genetic mechanisms (93% in boys and 77% in girls). The regulation of insulin-like growth factor-II was more complex, with a gender-specific genetic contribution (50% for both sexes combined, 63% for girls but only 5% for boys). Insulin-like growth factor binding protein-1 was regulated by genetic mechanisms (41%) and the common environment (32%) but also by the specific or unique environment of each fetus (27%). In all five twins with intrauterine growth restriction of one member insulin-like growth factor binding protein-1 concentrations were markedly higher in the growth-restricted fetus.
Insulin secretion in twin fetuses is determined primarily by their common, probably maternal, environment, whereas insulin-like growth factor-I production is predominantly genetically regulated. Insulin-like growth factor-II and insulin-like growth factor binding protein-1 are regulated by both genetic and environmental factors. Of these growth-regulating factors, insulin-like growth factor binding protein-1 appears to be the best marker of intrauterine growth restriction in the individual case.
American Journal of Obstetrics and Gynecology 11/1996; 175(5):1180-8. DOI:10.1016/S0002-9378(96)70025-X · 4.70 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To assess the diagnostic value of three vaginal markers-insulin-like growth factor binding protein 1 (= IGFBP1), diamine-oxidase (= DAO) and pH-for diagnosis of the premature rupture of membranes.
One hundred pregnant women participated in the study. They were divided into three groups: group A (34 cases with intact membranes), group B (35 cases with total rupture of the membranes), group C (31 cases of suspected rupture of the membranes). Each patient underwent three successive tests for each of the three markers. The test order was allocated at random. For pH the reaction is colorimetric, for DAO the reaction is radio-enzymatic and for IGFBP1 the reaction is immuno-chromatographic. All three reactions are qualitative in nature. The parameters studied were conventional statistical parameters (sensitivity = SN, specificity = SP, positive predictive value = PPV and negative predictive value = NPV).
The analysis of the statistics gave the following results in percentages for SN, SP, PPV and NPV respectively; pH: 90.7%, 77.2%, 75%, 91.7%. DAO: 83.7%, 100%, 100%, 89%. IGFBP1: 95.3%, 98.2%, 97.6%, 96.5%.
The determination of variations in pH is not satisfactory. IGFBP1 is at least better than DAO with, additionally, advantages of rapidity and simplicity.
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