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Despite all the research published in the last three decades on screening and prevention of preeclampsia (PE), this condition remains one of the main causes of maternal and perinatal morbidity and mortality, both in low and high-income countries. It affects 2-8% of all pregnancies, being responsible for one out of five maternal deaths and 15% of all premature deliveries1. An ideal screening test requires identification of women at high-risk of developing severe and early-onset forms of the disease, a high detection rate (DR) with an acceptable false-positive rate (FPR), and the availability of an effective preventive measure2.

Resume Le dosage de l'excretion urinaire d'albumine (EUA) peut se faire sur un echantillon urinaire sur les premieres urines du matin, sur les urines de 24 heures ou sur prelevement urinaire minute. Les valeurs definissant la microalbuminurie sont : urines de 24 heures : 30–300 mg/24 h ; echantillon urinaire : 20–200 mg/ml ou 30–300 mg/g creatinine urinaire ou 2,5–25 mg/mol (chez l'homme), ou 3,5–35 mg/mol (chez la femme) creatinine urinaire ; echantillon urinaire minute : 20–200 μg/min. La place du dosage semi-quantitatif (bandelettes) n'est pas clairement definie. La microalbuminurie est consideree comme un reflet d'une atteinte generalisee de l'endothelium, mais ce n'est pas demontre. Chez le sujet diabetique La microalbuminurie est un marqueur independant de risque cardiovasculaire (CV), renal et de mortalite totale chez les diabetiques de type 1 et 2. L'augmentation de l'EUA au cours du temps est un marqueur de risque CV et renal chez le diabetique de type 1 ; sa regression est associee a une regression de ces risques. Chez le sujet non diabetique La microalbuminurie est un marqueur independant de risque CV, de risque de diabete, d'alteration de la fonction renale et de mortalite totale. Elle est un marqueur de risque de developper une hypertension arterielle chez le sujet normotendu et un marqueur de risque d'evolution defavorable, ou de deces au cours de cancers et de lymphomes. L'elevation ou la persistance d'une EUA elevee au cours du temps est associee a un pronostic pejoratif chez certains hypertendus. La mesure d'EUA peut etre recommandee chez certains hypertendus ayant un ou deux facteurs de risque CV associes dont le risque CV semble mal evalue ou ayant une hypertension arterielle (HTA) refractaire : la microalbuminurie indique ici un risque CV eleve et incite a assurer un controle tensionnel strict. Il y a peu d'etudes chez les sujets non hypertendus et non diabetiques ; elles suggerent globalement que la microalbuminurie est un facteur de comorbidite et de mauvais pronostic comme chez les sujets hypertendus ou diabetiques. En prevention secondaire, la microalbuminurie est un marqueur de risque independant, mais n'a pas de retombees therapeutiques specifiques. Il n'est pas recommande de rechercher systematiquement une microalbuminurie chez le sujet non hypertendu, non diabetique, sans antecedent de maladie renale. Il est recommande d'effectuer une surveillance de la fonction renale annuelle (excretion urinaire d'albumine creatininemie et estimation du debit de filtration glomerulaire) chez les sujets microalbuminuriques. Therapeutique Chez tout patient ayant une microalbuminurie : reduction ponderale et de l'apport sode excessif ( chez le diabetique , prescription d'un inhibiteur de l'enzyme de conversion (diabete de type 1) ou d'un antagoniste des recepteurs de l'angiotensine 2 (diabete de type 2) a dose suffisante en premiere intention. Les diuretiques thiazidiques ont un effet synergique avec les bloqueurs du systeme renine angiotensine sur la reduction de l'EUA ; chez le non diabetique , les cinq grandes classes d'antihypertenseurs (IEC, ARA2, diuretiques, antagonistes calciques, betabloquants) sont utilisables en premiere intention.

La hipertension se detecta en el 6-15% de los embarazos, y en el 2-5% de los casos se asocia a proteinuria (preeclampsia). Se distinguen una preeclampsia «materna» por interaccion entre la placentacion y una enfermedad microvascular materna previa, y una preeclampsia «placentaria» debida a una placenta isquemica e hipoxica en una situacion de estres oxidativo. El primum movens es una alteracion de la invasion trofoblastica endovascular, que normalmente transforma las arterias espiraladas del miometrio para que estas puedan desarrollar un flujo compatible con las futuras necesidades fetoplacentarias. Participan en grados diversos una inadaptacion inmunitaria maternofetal, un defecto de angiogenesis y de proteolisis, y la produccion de un receptor soluble inhibidor de los factores angiogenicos. Tambien actuan los anticuerpos activadores del sistema renina-angiotensina. En una segunda etapa, la placenta isquemica libera hacia la circulacion materna restos celulares, responsables de una reaccion inflamatoria con disfuncion endotelial generalizada, y factores antiangiogenicos. El conjunto es responsable de las manifestaciones clinicas maternas. Las mujeres que han sufrido hipertension durante el embarazo estan mas expuestas que otras a padecer hipertension en el futuro y tienen un riesgo mas alto de mortalidad de causa cardiovascular.

La preeclampsia representa una de las primeras causas de mortalidad materna en los paises desarrollados. Su frecuencia se situa en el 2,5-6,5% de los embarazos de bajo riesgo, y en el 20- 25% de las pacientes de alto riesgo. Su tratamiento final sigue siendo la interrupcion del embarazo y la extraccion de la placenta. No obstante, esta actitud puede provocar complicaciones fetales, sobre todo relacionadas con una posible prematuridad. En todos los casos de preeclampsia, debe realizarse de inmediato una valoracion del estado materno y fetal con la paciente hospitalizada, lo que permite clasificarla en grave o leve, y orientar el tratamiento, teniendo en cuenta la fase del embarazo. En lo que concierne a la preeclampsia grave, la interrupcion de la gestacion y la extraccion de la placenta se imponen a partir de las 34 semanas de amenorrea. En cambio, antes de ese momento, la mortalidad y la morbilidad fetales son muy elevadas e invitan a retrasar la interrupcion del embarazo. Esta actitud permite una ganancia de 7-10 dias de promedio, la realizacion de una corticoterapia preventiva y, por ultimo, una mejora del pronostico perinatal. No obstante, esta actitud conservadora puede originar complicaciones maternas (eclampsia, sindrome HELLP, hematoma retroplacentario), lo que lleva a realizar una vigilancia estrecha y la interrupcion de la fase expectante ante el minimo signo de gravedad materna o fetal. En lo que respecta a la preeclampsia leve, la regla es la actitud expectante. La interrupcion de la gestacion debe plantearse a partir de las 38 semanas de amenorrea, sin precipitarse. La crisis de eclampsia, por sus riesgos de fallecimiento y de secuelas neurologicas, ha sido objeto de estudios recientes sobre la prevencion de su recidiva y de su aparicion. Se ha demostrado con claridad que el sulfato de magnesio es el tratamiento de eleccion en la prevencion de la crisis de eclampsia. Por tanto, este tratamiento debe prescribirse de primera intencion en esta indicacion.

Resume Les meta-analyses les plus recentes et les plus larges temoignent de l’interet de la prescription d’Aspirine a faible dose, lors de certaines grossesses. Schematiquement, il s’agit des patientes a haut risque de presenter une pre-eclampsie ou un retard de croissance intra-uterin. Sont discutes les criteres de choix et les modalites de prescription de ce traitement.

Aspirin is used in pregnant women in order to obviate the imbalance of prostanoids caused by a defective placentation, and also to counteract the widespread thrombotic tendency related to endothelial dysfunction. After a series of controlled trials which showed a very consistent effect of aspirin t prevent preeclampsia and fetal growth retardation, several recent large trials have cast the doubt, and even unbelief. Their results are analyzed in an explicative way. Discrepancies seem largely related to either studying very low-risk populations, or strong differences in aspirin dosage and/or term of introduction. In the last few years, several works have shown the critical importance of an early treatment, and also of a measurable biologic effect, which requires larger dosages than those used in the most recent trials. The doubt largely remains as for the adequate indications of this treatment. New data in the physiology of placentation suggest that it would be logical to give aspirin as early as the first wave of throphoblastic invasion. The effect of so an early treatment need to be evaluated. The search for early markers should be pursued. The combination of aspirin and heparin is under investigation. Finally, other ways of prevention, such as anti-oxidants, are also being studied.

Hypertension and diabetes mellitus are strongly associated conditions from epidemiologic, genetic, and pathophysiologic points of view. The prevalence of hypertension is high in patients with diabetes, and, conversely, many patients with essential hypertension are glucose intolerant. Proteinuria appears in 40-50% of patients with insulin-dependent diabetes mellitus and 20-30% of patients with non-insulin-dependent diabetes mellitus. Progressive renal failure occurs in 30-40 and 3-8% of patients, respectively, hypertension being a leading factor in its rate of progression. In various animal experiments, ACE inhibitors are able to prevent proteinuria and glomerular sclerosis, presumably by lowering transglomerular capillary pressure. In the diabetic human, ACE inhibitors are powerful antihypertensive drugs, devoid of metabolic side effects. Clinical studies indicate that ACE inhibitors reduce proteinuria and possibly slow the rate of decline in renal function. Such an effect is not observed with beta-blockers. Large-scale studies are needed to confirm this very important hypothesis.

The efficacy of low-dose aspirin in preventing fetal growth retardation was tested in a randomised, placebo-controlled, double-blind trial. A secondary aim was to find out whether dipyridamole improves the efficacy of aspirin. 323 women at 15-18 weeks' amenorrhoea were selected at twenty-five participating centres on the basis of fetal growth retardation and/or fetal death or abruptio placentae in at least one previous pregnancy. They were randomly allocated to groups receiving placebo, 150 mg/day aspirin, or 150 mg/day aspirin plus 225 mg/day dipyridamole, for the remainder of the pregnancy. In the first phase of the trial all actively treated patients (n = 156) were compared with the placebo group (n = 73). Mean birthweight was significantly higher in the treated than in the placebo group (2751 [SD 670] vs 2526 [848] g; difference 225 g [95% CI 129-321 g], p = 0.029) and the frequency of fetal growth retardation in the placebo group was twice that in the treated group (19 [26%] vs 20 [13%]; p less than 0.02). The frequencies of stillbirth (4 [5%] vs 2 [1%]) and abruptio placentae (6 [8%] vs 7 [5%]) were also higher in the placebo than in the treated group. The benefits of aspirin treatment were greater in patients with two or more previous poor outcomes than in those with only one. In the second analysis, of aspirin only (n = 127) vs aspirin plus dipyridamole (n = 119), no significant differences were found. There was no excess of maternal or neonatal side-effects in the aspirin-treated patients.

Measurement of urinary albumin excretion (UAE) may be done on a morning urinary sample or on a 24 hour-urine sample. Values defining microalbuminuria are: - 24-hour urine sample: 30-300 mg/24 hours - Morning urine sample: 20-200 mg/mL or 30-300 mg/g creatinine or 2.5-25 mg/mmol creatinine (men) or 3.5-35 mg/mol (women). - Timed urine sample: 20-200 mug/min. The optimal use of semi-quantitative urine test-strip is not clearly defined. It is generally believed that microalbuminuria reflects a generalized impairment of the endothelium; however, no definite proof has been shown in humans. In diabetic subjects, microalbuminuria is a marker of increased risk of cardiovascular (CV) and renal morbidity and mortality in type 1 and type 2 diabetic subjects. The increase in UAE during follow-up is also a marker of CV and renal risk in type 1 and type 2 diabetic subjects; its decrease during follow-up is associated with lower risks. In non-diabetic subjects, microalbuminuria is a marker of increased risk for diabetes mellitus, deterioration of the renal function, CV morbidity and all-cause mortality. It is a marker of increased risk for the development of hypertension in normotensive subjects, and is associated with unfavorable outcome in patients with cancer and lymphoma. Persistence or elevation of UAE overtime is associated with deleterious outcome in some hypertensive subjects. Measurement of UAE may be recommended in hypertensive subjects with 1 or 2 CV risk factors in whom CV risk remains difficult to assess, and in those with refractory hypertension: microalbuminuria indicates a high CV risk and must lead to strict control of arterial pressure. Studies focused on microalbuminuria in non-diabetic, non-hypertensive subjects are limited; most of them suggest that microalbuminuria predicts CV complications and deleterious outcome as it is in diabetic or hypertensive subjects. Subjects with a history of CV or cerebrovascular disease have an even greater CV risk if microalbuminuria is present than if it is not; however, in all cases, therapeutic intervention must be aggressive regardless of whether microalbuminuria is present or not. It is not recommended to measure UAE in non-diabetic non-hypertensive subjects in the absence of history of renal disease. Monitoring of renal function (UAE, serum creatinine and estimation of GFR) is annually recommended in all subjects with microalbuminuria.in patients with microalbuminuria, weight reduction, sodium restriction (6 g/day), smoking cessation, strict glucose control in diabetic subjects, strict arterial pressure control are necessary; in diabetic subjects: use of maximal doses of ACEI or ARB are recommended; ACEI/ARB and thiazides have synergistic actions on arterial pressure and reduction of UAE; in non-diabetic subjects, any of the five classes of anti-hypertensive medications (ACEI, ARB, thiazides, calcium channel blockers or beta-blockers) can be used.

Resume Nous avons etudie, chez 16 patients hypertendus essentiels, les effets sur l'hemodynamique renale d'un traitement d'un mois par une combinaison fixe de captopril (50 mg) et d'hydrochlorothiazide (25 mg). La pression arterielle systolique et diastolique a diminue de maniere significative. Il n'y a pas eu de variation significative du poids corporel, du volume plasmatique, des taux d'hormone antidiuretique et d'aldosterone plasmatique. L'elevation de l'activite renine plasmatique est conforme a ce que l'on pouvait attendre avec ce type de traitement. Sur l'ensemble des patients, les clairances de l'inuline et du PAH ne se sont pratiquement pas modifiees. Nous avons separe les patients en 2 groupes: le groupe 1 comprenait les patients (n = 5) dont la clairance de l'inuline etait initialement elevee > 120 ml/min (133 ± 15 ml/min), le groupe 2 les patients (n = 11) dont la clairance de l'inuline initiale etait normale ou basse

Urinary albumin excretion (UAE) may be assayed on a morning urinary sample or a 24 h-urine sample. Values defining microalbuminuria are: 1) 24-h urine sample: 30-300 mg/24 h; 2) morning urine sample: 20-200 mg/ml or 30-300 mg/g creatinine or 2.5-25 mg/mmol creatinine (men) or 3.5-35 mg/mmol (women); 3) timed urine sample: 20-200 mug/min. The optimal use of semi-quantitative urine test-strip is not clearly defined. It is generally believed that microalbuminuria reflects a generalized impairment of the endothelium; however, no definite proof has been obtained in humans.Microalbuminuria is a marker of increased risk of cardiovascular (CV) and renal morbidity and mortality in type 1 and type 2 diabetic subjects. The increase in UAE during follow-up is associated with greater CV and renal risks in type 1 and type 2 diabetic subjects; its decrease during follow-up is associated with lower risks. IN NON-DIABETIC SUBJECTS: Microalbuminuria is a marker of increased risk for diabetes mellitus, deterioration of renal function, CV morbidity and all-cause mortality. It is a marker of increased risk for the development of hypertension in normotensive subjects, and is associated with unfavorable outcome in patients with cancer and lymphoma. Persistence of elevated UAE during follow-up is associated with poor outcome in some hypertensive subjects. Measurement of UAE may be recommended in hypertensive medium-risk subjects with 1 or 2 CV risk factors in whom CV risk remains difficult to assess, and in those with refractory hypertension: microalbuminuria indicates a high CV risk and must lead to strict control of arterial pressure. Studies focused on microalbuminuria in non-diabetic non-hypertensive subjects are limited; most of them suggest that microalbuminuria predicts CV complications and deleterious outcome. Subjects with a history of CV or cerebrovascular disease have an even greater CV risk if microalbuminuria is present than if it is not; however, in all cases, therapeutic intervention must be aggressive regardless of whether microalbuminuria is present or not. It is not recommended to measure UAE in non-diabetic non-hypertensive subjects in the absence of history of renal disease. Monitoring of renal function (UAE, serum creatinine and estimation of GFR) is recommended annually in all subjects with microalbuminuria.In patients with microalbuminuria, weight reduction, sodium restriction (6 g per day), smoking cessation, strict glucose control in diabetic subjects, strict arterial pressure control are necessary; in diabetic subjects: use of maximal doses of angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARB) are recommended; ACEI/ARB and thiazides have synergistic actions on arterial pressure and reduction of UAE; in non-diabetic subjects, any of the five classes of anti-hypertensive medications (ACEI, ARB, thiazides, calcium channel blockers or beta-blockers) can be used.

The kidney has a key role in blood pressure control, and an abnormal regulation of sodium balance is involved in essential hypertension. It has been suggested that a reduced nephron number at birth could be one possible mechanism. Indeed various strains of hypertensive animals exhibit a reduced nephron number. In human beings, two autopsy studies have clearly shown a lower (about 50%) nephron number in hypertensive subjects. The glomeruli are also enlarged, indicating hyperfiltration. This could be the cause of both high blood pressure and later nephrosclerosis. A low number of nephrons is part of the perinatal programming which occurs together with fetal growth retardation, and this has been reproduced experimentally. There is a negative correlation between birth weight and glomerular number. Such a situation is associated with a largely increased risk of cardiovascular complications in adulthood.

Stroke is a leading cause of death and disability. Patients with suspected stroke are usually managed in emergency departments (ED). Stroke units must be created in our country, but only few French epidemiological data are available to define needs in stroke care.A prospective study was planned to evaluate epidemiology and stroke care for patients with suspected stroke admitted in the 22 ED of our region in the center of France during a two-month period.Patients with suspected stroke seen at the 22 ED were prospectively followed until discharge or one month after admission. Data on demographic characteristics, mode of transport, delay of arrival and imaging, clinical findings at arrival, department of admission, diagnosis, Rankin scale at day 7, in-hospital mortality, and outcome at a month were collected. A global statistical analysis and a comparison between rural and urban ED were performed.Five hundred and ninety-eight patients were included. Mean age was 75 years. Median admission delay was 4 hours and 52 minutes. Predominant mode of transport was a private ambulance. A CT scan was obtained in 91 p.cent of cases with a median delay of 2 hours and 30 minutes. Only a third of the patients were admitted in departments of Neurology. Final diagnosis was: ischemic stroke (61 p.cent), transient ischemic attack (16 p.cent), hemorrhagic stroke (10 p.cent), other vascular disease (3 p.cent), non vascular disease (10 p.cent). In-hospital mortality was 20 p.cent, factors significantly associated with death rate were elevated age and a Glasgow coma scale10 at admission. Mean length of stay was 12 days for stroke patients. At one month, 63 percent of patients were discharged to their home, 28 percent were transferred to an institution or in a rehabilitation unit, and 15 percent were still hospitalized. Significant differences in stroke care were found between rural and urban ED.This prospective study provides epidemiological data for our region. Creation of stroke units and definition of acute stroke networks are necessary to improve stroke care.

Hypertension occurs in 10 to 15 p cent of pregnancies. Among them, 10 to 20% also have proteinuria. This situation defines preeclampsia, and involves a serious threat on fetal and even maternal prognosis. Presence of the hepatic (HELLP) syndrome still severely worsens the prognosis.Pathophysiology of preeclampsia is based on a very early abnormality of placentation, leading to insufficient blood supply to the feto-placental unit. At the maternal level, the main consequence of placental ischemia is generalized endothelial dysfunction, responsible for systemic vasoconstriction and clotting abnormalities. In such a context, lowering blood pressure with drugs is quite inefficient, or even harmful. The prognosis of this disease is mainly related to the pertinence of obstetrical management.An early preventive strategy is the most logical approach of preeclampsia, its modalities remain under discussion.

Hypertension occurs in 10 to 15 p cent of pregnancies. Among them, 10 to 20% also have proteinuria. This situation defines preeclampsia, and involves a serious threat on foetal and even maternal prognosis. Presence of the hepatic (HELLP) syndrome still severely worsens the prognosis. Pathophysiology of preeclampsia is based on a very early abnormality of placentation, leading to insufficient blood supply to the foeto-placental unit. At the maternal level, the main consequence of placental ischemia is diffuse endothelial dysfunction, responsible for systemic vasoconstriction and clotting abnormalities. In such a context, merely lowering blood pressure with drugs is quite inefficient, or even harmful. The prognosis of this disease is mainly related to the pertinence of obstetrical management. An early preventive strategy is the most logical approach of preeclampsia, its modalities remain under discussion. Hypertension has a high recurrence rate on subsequent pregnancies. It is most often linked to a high global vascular risk level, therefore many of those patients will become permanent hypertensives in the near future.

There are three circumstances where hypertension develops specifically in women: oral contraception, pregnancy, and menopause. Oral contraception usually shifts the blood pressure moderately upwards, but hypertension appears in less than 5% of women. Still it may (rarely) be very severe. Hypertension is poorly related to the dosage of the estrogenic compound, but rather to the nature and dosage of the progestive part. This hypertension does not significantly increase the cardiovascular risk of these women. The role of menopause itself in the trigging of hypertension remains uncertain. It seems however that confounding factors such as age, body weight, sodium balance and so on explain the increased incidence of hypertension after menopause. The latter is also associated with an increase of cardiovascular risk, which requires adequate treatment. Hormone replacement therapy is not contra-indicated, even in hypertensive patients.

Aspirin is used in pregnant women in order to obviate the imbalance of prostanoids caused by a defective placentation, and also to counteract the widespread thrombotic tendency related to endothelial dysfunction. After a series of controlled trials which showed a very consistent effect of aspirin t prevent preeclampsia and fetal growth retardation, several recent large trials have cast the doubt, and even unbelief. Their results are analyzed in an explicative way. Discrepancies seem largely related to either studying very low-risk populations, or strong differences in aspirin dosage and/or term of introduction. In the last few years, several works have shown the critical importance of an early treatment, and also of a measurable biologic effect, which requires larger dosages than those used in the most recent trials. The doubt largely remains as for the adequate indications of this treatment. New data in the physiology of placentation suggest that it would be logical to give aspirin as early as the first wave of throphoblastic invasion. The effect of so an early treatment need to be evaluated. The search for early markers should be pursued. The combination of aspirin and heparin is under investigation. Finally, other ways of prevention, such as anti-oxidants, are also being studied.

Pregnancy hypertension remains a frequent disease, sometimes seriously threatening mother and fetus. Its primum movens has been shown to be an abnormal placentation and/or trophoblastic invasion. This abnormality is triggered by various factors which can be immunologic, vascular, or abnormalities of hemostasis. This defective placentation results in a systemic endothelial disease with vasoconstriction and widespread thrombotic tendency. Antihypertensive treatment is of very poor efficiency, and even may worsen the fetal situation through underperfusion. Early prevention is clearly a better way to improve the prognosis. Low-dose aspirin is widely used, although its efficiency has been debated recently, after the publication of negative results. It is likely that proper selection of patients, as well as the timing and dosage of treatment, are key factors for its efficiency.

The aim of the treatment of hypertensive disease is to reduce its associated cardiovascular morbidity and mortality. Simply reducing blood pressure levels is clearly not adequate since its impact on coronary heart disease is particularly unsatisfactory. Moreover, the beneficial effects of antihypertensive treatment seem to plateau for several years, and the incidence of cardiac and renal failure is even increasing. Therefore, recommendations by groups of national or international experts are periodically updated on the basis of current epidemiological data. Two such recommendations appeared in 1997, one from the Agence Nationale d'Accréditation et d'Evaluation en Santé (ANAES) in France and the other from the Joint National Committee (JNC) on Prevention, Detection, Evaluation and Treatment of High Blood Pressure, in the United States. Both advocate the use of lifestyle modifications in all patients. The threshold blood pressure level at which pharmacological therapy is introduced largely depends on associated cardiovascular risk factors and/or involvement of target organs. The JNC recommends a particularly low threshold in patients with diabetes. Pharmacological treatment is usually initiated with a single drug. The choice of any one drug depends on the patient profile and takes into consideration such characteristics as age and associated risk factors or comorbidity. Some represent a contraindication for certain therapeutic classes (for example, asthma for beta-blockers, renovascular hypertension for ACE inhibitors), while others are a specific or even 'compelling' indication (heart failure, angina, renal disease, peripheral vascular disease etc.). This patient profiling is very precisely described in the new recommendations. However, any such single drug therapy provides adequate blood pressure control in no more than about 50 to 60% of patients. When the patient does not respond to the drug used or experiences side effects, substitution of a drug from another pharmacological class is recommended. In contrast, if the patient is a responder but blood pressure remains above the target level, it is preferable to add a second drug from a class offering complementary action. The use of a combination therapy allows blood pressure control in more than 80% of patients. More authors are suggesting that combination therapy as first-line treatment may increase the number of responders and reduce the impact of counter-regulatory effects occurring with single drug therapy (e.g. sodium retention, or sympathetic activation). This alternative strategy is now acknowledged in the recommendations.

The concept of the threshold of therapeutic intervention as a function of the absolute risk is introduced. The definitions of relative risk and absolute risk are then recalled; in the case of absolute risk, only prolonged observation of a cohort combined with multivariate statistical analysis can select the most relevant risk factors and attribute a relative weighting to each factor. Software may be helpful. The roles of the age high-risk productions, their life-style, modalities of therapeutic intervention, and economic implications are discussed.

The pure tetrameric form of Acetylcholinesterase (EC-3.1.1.7) from the electric eel electrophorus electricus has been covalently coupled to oxytocin. This conjugate has been used as tracer in a heterologous competitive immunoassay. Microtiter plates coated with a mouse monoclonal anti-rabbit immunoglobulin antibody were used to separate bound and free moieties of the tracer. Acetylcholinesterase activity bound to the solid phase was measured by a colorimetric assay. The minimum detectable concentration was 0.075 pg/well (ie 1.5 pg/ml) and precision was less than 8% at concentration above 0.15 pg/well. An extraction step improved sensitivity up to 10 times with good recoveries. To assess the validity of this assay, basal levels of oxytocin were measured during the oestrous cycle of a cow.

Our understanding of the pathophysiology underlying the hypertensive diseases of pregnancy has clearly progressed during the past ten years. The key phenomenon is an early defect of placentation occurring at the end of the first trimester and associated with a more widespread endothelial disorder. This results in early activation of the coagulation cascade and imbalance between prostacyclin and thromboxanes. Hypertension and proteinuria only occur after several weeks or months of placental dysfunction. This explains why antihypertensive treatments are ineffective in improving the prognosis of such pregnancies. In contrast, early preventive treatments, such as antiplatelet therapy, seem to be very promising for these patients. In this respect, early prediction of the risk associated with pregnancy has become a key goal.

Pathophysiologic understanding of the hypertensive diseases of pregnancy has largely progressed in the past 10 years. The key phenomenon is an early defect of placentation, occurring at the end of first trimester. It is associated with a more global endothelial disorder. This results in early activation of coagulation, and an imbalance between prostacyclin and thromboxanes. Hypertension and proteinuria only occur after several weeks or months of placental dysfunction. This explains why antihypertensive treatments are ineffective in improving the prognosis of such pregnancies. On the contrary, early preventive treatments, such as antiplatelet therapy, seem very promising for those patients.

This experiment was conducted in 59 Lacaune breed ewes in order to compare milk production and milk distribution between alveolar and cisternal storage after superovulation. After a corpora lutea (CL)-free control period, the ewes were superovulated by different treatments (experimental period) and 5 classes were differentiated according to the number of corpora lutea observed (0, 1, 2, 3 to 6 and6 CL respectively (group A (n = 20), B (n = 7), C (n = 14), D (n = 7), E (n = 11)). Our results showed a positive correlation between the number of corpora lutea and the oxytocin and progesterone levels in plasma, total milk production and cisternal volume, and a negative correlation with alveolar volume. The milk production at the evening milking for groups A and E (388.6 and 384.8 ml respectively during the control period) respectively reached 321.7 ml (-17.2%) and 413.4 ml (+7.4%) during the experimental period; ie, a 24.6% difference between these 2 extreme groups. These results could likely be explained by oxytocin levels reaching those obtained during milking and by the effect of milk transfer from the alveolar to the cisternal lumen. Additionally, progesterone could act directly on milk synthesis at the level of the secretory cells.

This experiment was conducted in 59 Lacaune breed ewes in order to compare milk production and milk distribution between alveolar and cisternal storage after superovulation. After a corpora lutea (CL)-free control period, the ewes were superovulated by different treatments (experimental period) and 5 classes were differentiated according to the number of corpora lutea observed (0, 1, 2, 3 to 6 and > 6 CL respectively (group A (n = 20), B (n = 7), C (n = 14), D (n = 7), E (n = 11)). Our results showed a positive correlation between the number of corpora lutea and the oxytocin and progesterone levels in plasma, total milk production and cisternal volume, and a negative correlation with alveolar volume. The milk production at the evening milking for groups A and E (388.6 and 384.8 ml respectively during the control period) respectively reached 321.7 ml (-17.2%) and 413.4 ml (+7.4%) during the experimental period; ie, a 24.6% difference between these 2 extreme groups. These results could likely be explained by oxytocin levels reaching those obtained during milking and by the effect of milk transfer from the alveolar to the cisternal lumen. Additionally, progesterone could act directly on milk synthesis at the level of the secretory cells.