Search

Nous rapportons 2 complications graves dues aux antagonistes de l’angiotensine II (agtII : sartans). Le 1 er cas est une enfant née à 33SA pour RCIU et anamnios avec vessie non visualisée. L’adaptation à la vie extra utérine est médiocre avec détresse respiratoire sévère, HTAP, anurie et hypotension. L’interrogatoire retrouve une prise d’olmesartan arrêté à 29 SA. L’évolution, de part l’arrêt précoce, sera favorable avec cependant une insuffisance rénale chronique modérée. Le 2ème cas est une enfant estimée à 36 SA, RCIU, née en anamnios post déni de grossesse, avec traitement pendant toute celle-ci par valsartan. Elle présente une séquence de Potter avec anurie et hypoxie par hypoplasies rénale et pulmonaire avec décès à J1. La prise aux 2 et 3ème trimestres de sartan entraîne fœtopathies sévères avec insuffisance rénale par dysgénésie tubulaire, défaut d’ossification du crâne et hypoplasie pulmonaire (létalité supérieure à 50%). Il s’agit d’un antagoniste spécifique de l’agtll (système rénine-angiotensine-aldostérone) actif sur le récepteur AT1 (protection contre inflammation, fibrose, apoptose), inhibant son effet vasoconstricteur, hypertenseur et natriurétique. Ce traitement contre-indiqué pendant la grossesse reste trop souvent prescrit chez des femmes en âge de procréer. [ABSTRACT FROM AUTHOR]

The objective of this study was to analyse the effects of maternal hyperglycemia during the periconception period on fetal and postnatal development using a rabbit model. Diabetes was induced in adult New Zealand female does by a single intravenous alloxan injection (group D). Glycemia was maintained between 3 and 5gL-1with 2 daily subcutaneous insulin injections. Does from group D and contemporary controls (group C) were naturally mated 1wk after induction of diabetes in group D animals, without superovulation, and embryos collected after sacrifice on Day 4 post-coitum. In Expt. 1, embryos from D (n=11) and C (n=13) groups were transferred respectively to the right and left horns of 3 female recipients, which were killed on Day 28. In Expt. 2, 17 D and 16 C females were mated naturally. 68 D and 98 C embryos were collected and transferred to 26 non-diabetic recipients (6–7 embryos per doe). 17 females were pregnant with no difference between C and D recipients. Fetal development was monitored by ultrasound. At birth, litters were equilibrated in number. 15 D and 7 C pups (from 4 D and 2 C litters) were killed at weaning (1 month of age). The remaining 13 D and 26 C pups (4 D and 7 C litters) were allocated to 1 of 2 feeding groups: control or obesogenic diet. The obesogenic diet was based on the control diet supplemented with animal fat (suet, 200%) and glucose (200%). Bodyweight, adiposity, and glucose metabolism were monitored until sacrifice at 5 months of age. Data were analysed by ANOVA using litter (fetuses), litter and sex (weaning), and litter and diet (5 months) as co-factors. Sex effects at 5 months were not analysed due to small numbers of animals. Fetal development was not different between D and C groups. Fetal, placental, and fetal organ weights did not differ at Day 28, except for brain weight, which was significantly lower in D fetuses (0.86±0.1 v.1.05±0.08g; P<0.05). There was no difference in litter size at birth (3.3±0.3 v.3.6±0.5 pups for D and C groups, respectively; P=0.5), but birthweight was significantly increased in D offspring (211±6 v.194±6g; P<0.05). There was no difference in weight after 14 days. At 1 month of age, adiposity, plasma insulin and leptin concentrations were not different between groups. In contrast, in male D offspring, fasting glycemia was significantly lower (1.7±0.2 v.2.1±0.02gL-1; P<0.01), plasma insulin-like growth factor 1 was significantly increased (P<0.05) and kidney/bodyweight ratio was significantly reduced (0.41±0.03 v.0.45±0.04; P<0.01). From 12wk of age, bodyweight became significantly different between D and C groups and according to diet (P<0.005), with D individuals being lighter than C individuals for each dietary group. Finally, fasting glycemia was significantly higher in the animals fed the obesogenic diet (1.35±0.05 v.1.19±0.05gL-1; P<0.04), regardless of group. These data suggest that maternal hyperglycemia during the periconceptional period affects glucose metabolism and organ development in offspring with sexual dimorphism. [ABSTRACT FROM AUTHOR]

Background: Single-dose human fibrinogen concentrate (FCH) might have haemostatic benefits in complex cardiovascular surgery.Methods: Patients undergoing elective aortic surgery requiring cardiopulmonary bypass were randomly assigned to receive FCH or placebo. Study medication was administered to patients with a 5 min bleeding mass of 60-250 g after separation from bypass and surgical haemostasis. A standardized algorithm for allogeneic blood product transfusion was followed if bleeding continued after study medication.Results: 519 patients from 34 centres were randomized, of whom 152 (29%) met inclusion criteria for study medication. Median (IQR) pretreatment 5 min bleeding mass was 107 (76-138) and 91 (71-112) g in the FCH and placebo groups, respectively (P=0.13). More allogeneic blood product units were administered during the first 24 h after FCH, 5.0 (2.0-11.0), when compared with placebo, 3.0 (0.0-7.0), P=0.026. Fewer patients avoided transfusion in the FCH group (15.4%) compared with placebo (28.4%), P=0.047. The FCH immediately increased plasma fibrinogen concentration and fibrin-based clot strength. Adverse event rates were comparable in each group.Conclusions: Human fibrinogen concentrate was associated with increased allogeneic blood product transfusion, an unexpected finding contrary to previous studies. Human fibrinogen concentrate may not be effective in this setting when administered according to 5-minute bleeding mass. Low bleeding rates and normal-range plasma fibrinogen concentrations before study medication, and variability in adherence to the complex transfusion algorithm, may have contributed to these results.Clinical Trial Registration: ClinicalTrials.gov identifier no. NCT01475669; EudraCT trial no. 2011-002685-20. [ABSTRACT FROM AUTHOR]

Nous rapportons le cas d’un enfant né à 29SA présentant à J29 un choc septique avec méningite purulente à streptocoque du groupe B (SGB) sérotype III avec clone hypervirulent Séquence Type 17 compliquée d’un état de mal convulsif. Apparaissent rapidement des lésions cérébrales avec ventriculite puis une hydrocéphalie symptomatique : pose d’une dérivation ventriculo-péritonéale avec occlusion nécessitant une reprise chirurgicale. Le retour à domicile aura lieu à J91. Le SGB est une des 2 causes majeures de sepsis néonatal dont 30–40% de méningites notamment par le ST17 (75% des infections tardives et 81% des méningites en France et le sérotype I (13%), et le IV aux USA. L’antibioprophylaxie per partum a permis de diminuer le taux d’infection précoce, à l’instar de l’ E.coli , mais celui des infections tardives est constant (1,4‰ des naissances prématurées, 0,24‰ à terme) avec des formes moins sévères. Les voies de contamination sont l’infection par le lait de mère surtout en présence d’une mastite (culture négative pour notre cas) avec récurrences possibles et la transmission horizontale par porteurs sains (famille, soignants). Les mesures préventives des récidives (arrêt allaitement, pasteurisation) sont discutées devant le taux de morbi-mortalité élevé (62% et 14%). [ABSTRACT FROM AUTHOR]