Aetiology and physiopathology of preeclampsia and related forms.

Preeclampsia, a pregnancy-specific syndrome characterized by hypertension, proteinuria and oedema, resolves on placental delivery. Its pathogenesis is thought to be associated to a hypoxic placenta. Placental hypoxia is responsible for the maternal vascular dysfunction via the increased placental release of anti-angiogenic factors such as soluble flt1 and endoglin. These soluble receptors bind VEGF, PLGF and TGFbeta1 and 3 in the maternal circulation, causing endothelial dysfunction in many maternal tissues. Despite these recent and important new molecular findings, it is important to consider that normal pregnancy is also characterized by systemic inflammation, oxidative stress and alterations in levels of angiogenic factors and vascular reactivity. Both the placenta and maternal vasculatures are major sources of reactive oxygen and nitrogen species which can produce powerful pro-oxidants that covalently modify proteins and alter vascular function in preeclampsia. Finally, the recent demonstration of activating auto-antibodies to the Angiotensin 1 receptor that experimentally play a major pathogenic role in preeclampsia further indicates the pleiotropism of aetiologies of this condition.

Dysregulation of anti-angiogenic agents (sFlt-1, PLGF, and sEndoglin) in preeclampsia--a step forward but not the definitive answer.

Preeclampsia (PE) is a pregnancy-specific syndrome characterized by hypertension, proteinuria and edema, which resolves on placental delivery. It is thought to be the consequence of impaired placentation due to inadequate trophoblastic invasion of the maternal spiral arteries. In PE the maternal plasma concentration of free vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) is decreased whereas the concentration of soluble fms-like tyrosine kinase-1 (sFlt-1) and of soluble endoglin (sEng) is increased. These soluble receptors may bind VEGF, PLGF and TGFbeta1 and TGFbeta3 in the maternal circulation, causing endothelial dysfunction in many maternal tissues. Hence there is a view that the pathogenesis is more or less clarified. According to the vascular theory, poor placentation leads to poor uteroplacental perfusion and hypoxia, which stimulates sFlt-1 and sEng production causing the maternal syndrome. This assumption has been recently challenged. The role of hypoxia as the main stimulus for release of sFlt-1 has been questioned and the role of inflammatory mechanisms has been emphasized. According to this inflammatory theory, poor placentation may predispose more to placental oxidative stress than hypoxia and endothelial dysfunction may be part of a broader disorder of systemic inflammation. Finally, the recent demonstration of activating auto-antibodies to the angiotensin 1 receptor that experimentally play a major pathogenic role in PE further suggests a pleiotropism of aetiologies for this condition. The purpose of this review is to critically evaluate the recent hypotheses and their possible insights on early diagnosis, prevention and treatment.

[A bilateral dysgerminoma: a rare presentation of the Swyer syndrome]. / Le cas clinique du mois: un dysgerminome bilatéral: une présentation rare du syndrome de Swyer.

Swyer syndrome is a pure gonad dysgenesis associating 46 XY karyotype, primary amenorrhea, presence of female internal genital tract and bilateral streak gonads in a phenotypic female. The diagnosis is usually made at adolescence when the primary amenorrhea is investigated. We report the case of a 25-year-old XY woman who developed a bilateral dysgerminoma from undifferentiated gonads.

[Group B streptococcus in the antenatal clinic and in the delivery room: a matter of systematic attitude]. / Le streptocoque du groupe B en clinique anténatale et en salle de travail: un problème d'attitude systématique.

OBJECTIVES: We wanted to evaluate the compliance to the local recommendations, similar to the CDC (Centers for Disease Control and prevention) recommendations launched in 1996, for the prevention of perinatal group B streptococcal (GBS) disease in the clinical practice of a academic maternity and to identify the causes of missed screening and antibiotic prophylaxis. MATERIALS AND METHODS: Retrospective study of 1249 consecutive pregnancies between 1st January and 31th August 2002. The screening methods for GBS colonisation were the culture of rectovaginal swabs collected between 35 and 37 weeks and/or a rapid antigenic screening performed on a vaginal swab collected at the patient's admission for labor. RESULTS: Rate of global screening was very high (97.8%): 28.8% of antenatal screening versus 90.3% during labor. An appropriate antibiotic prophylaxis was administered to only one-third of positive women when the screening was performed at admission to the labor room, whereas two-thirds of GBS-positive women screened between 35 and 37 weeks received their antibiotic prophylaxis. 2.4%o of the newborns were infected and 2.9% were colonized. Among the different risk factors, intrapartum fever was more often associated with maternal GBS colonisation. The observed sensitivity of the rapide antigenic test was 20.4%. CONCLUSION: Compliance to guidelines is sometimes difficult in the clinical practice of an academic maternity. In our hands the rapid test for GBS screening had low sensitivity. The analysis of these data led to introducing a computerized algorithm in our maternity to improve the prevention of perinatal group B streptococcal disease.