Successful Management of the Recurrent Uterine Rupture After the Uterine Septum Resection

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Uterine Rupture with Massive Late Postpartum Hemorrhage due to Placenta Percreta Left Partially In Situ

Placental adhesive disorders involve the growth of placental tissue into or through the uterine wall. Among these disorders, placenta percreta is the rarest one. However, it may cause significant complications. This report aimed to report a neglected patient with placenta percreta who developed uterine rupture with life-threatening late postpartum intra-abdominal hemorrhage. On admission, the patient had acute abdomen with moderate abdominal distention and was subjected to emergency laparotomy. A full-thickness defect of the anterior uterine wall involving the hysterotomy site was seen. Placental tissues occupied both sides of the incision and posterior bladder wall was also invaded by placenta. Total abdominal hysterectomy with partial resection of the posterior bladder wall was performed

Free Protein S Reference Ranges In Gravidas Without Hereditary And Acquired Thrombophilia

We carried out a retrospective cohort study to construct reference ranges for free protein S (FPS) levels during pregnancy and identify any conditions or factors that may affect FPS levels. Patients that were ordered thrombophilia screening tests during gestational period were identified. Patients demonstrated to have hereditary or acquired thrombophilia were excluded. Reference ranges were constructed using regression analysis. Outcome of the index pregnancy and pregnancy complications was used to identify any confounding factors. A total of 455 pregnant women were included. The quadratic equation for FPS according to gestational age (GA) was [75.497 + (-1.516*GA) + 0.018*GA*GA]. FPS level and GA were negatively correlated (Spearmans rho statistic [r(s)] = -0.436, p = 0.001). FPS level and fetal growth restriction (FGR) were negatively correlated ([r(s)] = -0.093, p = 0.049). FPS level and placental abruption were positively correlated ([r(s)] = 0.098, p = 0.039). Stepwise linear regression model constructed to predict FPS level with gestational age, placental abruption and FGR as the predictor variables. Gestational age was the only variable retaining statistically significant relation with FPS level (chi(2) = 0.216, df = 3, p = 0.001). FPS levels decrease significantly throughout gestation in gravidas without hereditary and/or acquired thrombophilias. In patients without thrombophilia FPS levels are not associated with pregnancy complications. The obtained reference intervals may be useful for the clinicians ordering FPS during pregnancy

Disruption of ALX1 Causes Extreme Microphthalmia and Severe Facial Clefting: Expanding the Spectrum of Autosomal-Recessive ALX-Related Frontonasal Dysplasia

We present an autosomal-recessive frontonasal dysplasia (FND) characterized by bilateral extreme microphthalmia, bilateral oblique facial cleft, complete cleft palate, hypertelorism, wide nasal bridge with hypoplasia of the ala nasi, and low-set, posteriorly rotated ears in two distinct families. Using Affymetrix 250K SNP array genotyping and homozygosity mapping, we mapped this clinical entity to chromosome 12q21. In one of the families, three siblings were affected, and CNV analysis of the critical region showed a homozygous 3.7 Mb deletion containing the ALX1 (CART1) gene, which encodes the aristaless-like homeobox 1 transcription factor. In the second family we identified a homozygous donor-splice-site mutation (c.531+1G > A) in the ALX1 gene, providing evidence that complete loss of function of ALX1 protein causes severe disruption of early craniofacial development. Unlike loss of its murine ortholog, loss of human ALX1 does not result in neural-tube defects; however, it does severely affect the orchestrated fusion between frontonasal, nasomedial, nasolateral, and maxillary processes during early-stage embryogenesis. This study further expands the spectrum of the recently recognized autosomal-recessive ALX-related FND phenotype in humans