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Introduction The paper addresses from the neonatologist clinician's perspective to a category of high risk newborns, affected by pregnancy-induced hypertension, a pathological entity particular only in gestational period. It is different from pre-existing hypertension before pregnancy and disappears after childbirth and delivery of the placenta. Material and method Based on rigorous inclusion and exclusion criteria, were established two equal groups of newborns (n=116): a study group including newborns of mothers with pregnancy-induced hypertension and a study group including newborns whose mothers have not pregnancy-induced hypertension, randomized case-control pattern. There were analyzed for comparison a number of 18 parameters, focused on their postnatal development issues. For their registration it was used the database from Neonatology Clinic "Bega" Timisoara. For statistical data processing we used SPSS 17.0. Results Significant results were considered those who presented major differences in adaptation and neonatal pathology, the group study being affected. For a confidence interval of 95%, we recorded p < 0,05 (significant differences), for next parameters: low birth weight, the degree of immaturity, early neonatal adapting difficulties, the need of neonatal reanimation and mechanical ventilation in the first 24 hours of life and the incidence of neonatal hypoxic pathology. Conclusions By reducing placental blood flow, pregnancy-induced hypertension significantly affect fetal nutrition and oxygenation with whole metabolic consequences. This is more important when the onset is in early pregnancy and the duration of fetal suffering is more prolonged. This category is represented by neonates of mothers who developed pregnancy-induced hypertension. [ABSTRACT FROM AUTHOR]

Introduction. Gestational diabetes mellitus (GDM) is a complication associated with pregnancy defined as any degree of glucose intolerance that occurs- or is first discovered during pregnancy, with normal values signaled before, and usually after pregnancy. Material and Method. This study analyzed the cellular differences that might contribute to the injuries of the feto-placental interface of insulin-controlled GDM patients. An optical microscopic analysis was performed on 26 full term placentas, of which 15 were of gestational diabetes mellitus and 11 control group. The histological observation centered upon the: trophoblast, villous stroma and fetal capillary. The fetal average weight was 3840 g for the studied group vs. 2760 g for the control group. Results. Through optical microscopy were identified varying degrees of lesions consisting of: villous edema, proliferation and villous fibrosis of the capillaries, large number of syncytial knots, important fibrinoid necrosis, moderate fibrin thrombi, hyperplasia of the syncytiotrophoblast, chorangiosis, slightly thickened of the basement membrane of the feto-maternal interface. Conclusion. The increased angiogenesis of feto-placental vessels of the terminal villi - considered to be the cause of the placental abnormalities; and the increased risk of complications for e.g. miscarriage, stillbirth, macrosomia, and congenital anomalies may be prevented by a good control over the glycemic levels. [ABSTRACT FROM AUTHOR]

Objective. To present the main structural modifications of the feto-placental interface, in pregnancy induced hypertension (PIH). Material and Method. We have studied the main microscopical modifications of 68 placentas obtained after delivery for two equal groups: one group (N1=34), representing mothers with PIH and another group (N2 = 34) normotensive mothers. The samples obtained by sections were specificaly prepared for the study of 3 types of histological stains and 2 types of immunohistochemical stains. For the histological examination we used optical microscopy for observing mainly the lumen of spiral arteriole and changes in its tunica intima and media. Results. We registered the following structural modifications in the pregnancies with PIH versus normal ones: changes in endothelium -76,47%, fibrinoid necrosis - 73,52%, the hypertrophy of tunica media - 67,64%, bridging syncytial knots -32,35%, avascular small terminal villi with hyaline fibrosis of the stroma-41,17% and the thrombosis of the spiral arterioles -26,47%. Conclusions. A better understanding of the immunohistological damages demonstrated through our study, concerning the preeclamtic feto-maternal interface, will change in the future, our understanding about the role of this placental unit in PIH. [ABSTRACT FROM AUTHOR]

Background: An accurate monitoring of mucosal inflammation is important for an effective management of children with inflammatory bowel disease (IBD). The aim of the study was to evaluate the efficacy of the fecal calprotectin as indicator of inflammatory activity in children with Crohn's disease (CD) and ulcerative colitis (UC) by correlating it with biological, clinical and endoscopic indices. Methods: A total of 22 children presenting IBD were evaluated (16CD/6UC). Fecal calprotectin, blood tests, Pediatric CD Activity Index (PCDAI), Pediatric UC Activity Index (PUCAI), CD Endoscopic Index of Severity (CDEIS) and Mayo Disease Activity Index (MDAI) were used for children evaluation at diagnosis and after 6 months of treatment. Results: In CD children, calprotectin showed a high correlation (r = 0.775) with the histologic grade of mucosal inflammation, showed by CDEIS and a medium correlation with CRP(r = 0.623). lt didn't correlated with PCDAI (r = 0.325). In UC children, calprotectin correlated moderate (r=0.581) with CRP and it was strongly correlated with PUCAI (r = 0.752) and MDAI (r = 0.796). Calprotectin levels decreased significantly after 6 months of treatment in all IBD patients (p = 0.038). Conclusions: In CD children fecal calprotectin was more accurate in detection of active mucosal inflammation when compared to clinical score and serum marker CRP. The relatively poor correlation between calprotectin levels and PCDAI might not be due to a calprotectin low sensitivity in CD children, but to the fact that PCDAI is mostly a clinical score and is not sensitive enough to detect subclinical activity of the disease. Fecal calprotectin correlated well with endoscopic indices both in CD and UC children. So, it can provide a reliable noninvasive marker for monitoring IBD activity. [ABSTRACT FROM AUTHOR]