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Biomedical subjects

Gus Dekker

Publications and source records attributed to Gus Dekker.

9 recordsLinked to original sources
PubMed2006

Endogenous inhibitors of nitric oxide and preeclampsia: a review.

Nitric oxide (NO) is a potent vasodilator. NO is synthesized by NO synthases (NOS) and NOS are inhibited by asymmetrical dimethylarginine (ADMA). ADMA is metabolized by dimethylarginine dimethylaminohydrolase (DDAH) and excreted in the kidneys. Lower ADMA levels in pregnant women compared to non-pregnant controls suggest that ADMA has a role in vascular dilatation and blood pressure changes. Several studies show an increase in ADMA levels in pregnancies complicated with preeclampsia. Elevated ADMA levels in preeclampsia are seen before clinical symptoms have developed; these findings suggest that ADMA has a role in the pathogenesis of preeclampsia.

Amidohydrolases↗
PubMed2005

Transvaginal cervical length measurement; its current application in a regional Australian level II maternity hospital.

OBJECTIVE: To evaluate the impact of cervical length (CL) measurements in pregnant women at risk for preterm delivery on intervention and pregnancy outcome. DESIGN: Retrospective study. SETTING: Regional high-level II maternity unit. METHODS: Hospital databases were reviewed for all women delivering between March 2001 and March 2003. Women at an increased risk for preterm birth with transvaginal (TV) cervical length measurements during pregnancy were included in this audit. Patients (n = 204) were analysed together and in subgroups with different risk profiles. RESULTS: For women with a significant obstetrical history, most of the cervical lengths or= 3 preceding curettages were not found to be a major risk factor for preterm birth.

Adult↗
PubMed2005

Use of uterine Doppler in an Australian level II maternity hospital.

OBJECTIVE: To evaluate the clinical usefulness of uterine Doppler. DESIGN: Retrospective study between March 2001 and March 2003. SETTING: A high-risk population of pregnant women in a busy level II Maternity unit. METHODS: Resistance index (RI) measurements of the right and left uterine artery were obtained by using pulsed wave Colour Doppler. The presence of a unilateral or bilateral early diastolic notch was noted. An abnormal result was defined as a mean RI >or= 0.58 with no, one or two notches or a mean RI < 0.58 in the presence of bilateral notches. RESULTS: Pre-eclampsia was found in 45 (24.7%) women, gestational hypertension (GH) in 22 (12.1%) and intrauterine growth restriction (IUGR) in 42 (23.1%) of women included (total 59.9%). In the overall group, 127 (69.8%) women were found to have abnormal uterine artery Doppler results and 55 (30.2%) of patients had a normal Doppler study. No significant differences were found between the group of women with abnormal uterine artery Doppler and the women with a normal velocity waveform in the prediction of pre-eclampsia, IUGR and GH, this was also true in the various high-risk-subgroups. CONCLUSIONS: Uterine Doppler is not particularly useful to the obstetrician in the management of patients with an a priori very high risk to develop uteroplacental insufficiency.

Adult↗
PubMed2004

Controversies regarding cervical incompetence, short cervix, and the need for cerclage.

Cervical incompetence (CI) is not an all or nothing phenomenon but a continuous variable. CI and preterm labor are not distinct entities but rather part of a spectrum leading to preterm delivery. Cervical length (CL) is an independent variable in the prediction of preterm delivery, to which it is inversely related. Application of a primary transvaginal cervical cerclage appears to be an unnecessary intervention in about 50% of women presenting with a history suggesting cervical incompetence. A better alternative for women with a history of or risk factors for CI is transvaginal ultrasonographic follow-up of CL. To facilitate the comparison of studies of CI, the authors suggest a nomenclature reflecting the different stages of prevention: primary, secondary, and tertiary transvaginal cervical cerclage.

Cerclage, Cervical↗
PubMed2003

The birth interval hypothesis-does it really indicate the end of the primipaternity hypothesis.

Recent Norwegian data suggest the presence of a causal relationship between prolonged birth intervals and the risk for preeclampsia in subsequent pregnancies. It has been proposed that the birth interval data explain the known association between a change in paternity and the risk for preeclampsia. In this review, the authors explore alternative explanations for the Norwegian findings, and as such argue that there is currently no reason to reject the primipaternity hypothesis.

Birth Intervals↗
PubMed2002

Gestational diabetes versus obesity as risk factors for pregnancy-induced hypertensive disorders and fetal macrosomia.

OBJECTIVE: To assess whether obesity and/or gestational diabetes mellitus (GDM) are independent risk factors for fetal macrosomia and/or pregnancy-induced hypertensive disorders. DESIGN: Retrospective computerised database review. SETTING: Lyell McEwin Health Service, South Australia. SAMPLE: All nulliparous women delivering singleton babies in the years 1999 and 2000 MAIN OUTCOME MEASURES: Birth weights, the occurrence of fetal macrosomia, gestational hypertension and preeclampsia were compared between 258 normoglycaemic women (control group), 76 women with only an abnormal glucose challenge test, and 51 women with GDM. RESULTS: Only GDM with fasting hyperglycaemia is a risk factor for macrosomia (risk ratio: 3.3 95% confidence limits 1.229-8.736). Smoking is associated with a decrease in the incidence of pregnancy-induced hypertensive disorders. CONCLUSIONS: Our data strongly suggest that GDM and obesity are not independent risk factors for pregnancy-induced hypertensive disorders.

Adult↗
PubMedDate not supplied

Pre-eclampsia.

Pre-eclampsia is a major cause of maternal mortality (15-20% in developed countries) and morbidities (acute and long-term), perinatal deaths, preterm birth, and intrauterine growth restriction. Key findings support a causal or pathogenetic model of superficial placentation driven by immune maladaptation, with subsequently reduced concentrations of angiogenic growth factors and increased placental debris in the maternal circulation resulting in a (mainly hypertensive) maternal inflammatory response. The final phenotype, maternal pre-eclamptic syndrome, is further modulated by pre-existing maternal cardiovascular or metabolic fitness. Currently, women at risk are identified on the basis of epidemiological and clinical risk factors, but the diagnostic criteria of pre-eclampsia remain unclear, with no known biomarkers. Treatment is still prenatal care, timely diagnosis, proper management, and timely delivery. Many interventions to lengthen pregnancy (eg, treatment for mild hypertension, plasma-volume expansion, and corticosteroid use) have a poor evidence base. We review findings on the diagnosis, risk factors, and pathogenesis of pre-eclampsia and the present status of its prediction, prevention, and management.

Female↗
PubMedDate not supplied

The partner's role in the etiology of preeclampsia.

The etiology of preeclampsia is often considered to be purely maternal, i.e. maternal constitutional factors that impair maternal cardiovascular/endothelial mechanisms normally required to cope with the specific pregnancy demands, being primarily a generalised inflammatory response and a hyperdynamic circulation. Recent data strongly indicate an important role for the male partner in the causation of this common pregnancy disorder. The aim of this review is to discuss the relevant literature and to explain how paternal, relational and sexual factors play an important role in the etiology of preeclampsia.

Biological Evolution↗