Preoperative cystoscopy could determine the severity of placenta accreta spectrum disorders: An observational study.

AIM: In the surgical treatment of placenta accreta spectrum disorders, cystoscopy for prophylactic stent placement is performed to protect the ureters from potential injury. Despite its frequent use, the use of cystoscopy in assessing the severity of these disorders has not been explored. Our objective was to find out if the abnormal findings documented during cystoscopy are associated with disease severity. METHODS: In this retrospective, observational cohort study (n = 56), the bladder wall was evaluated at the time of ureteral stent placement via cystoscopy in prenatally diagnosed placenta accreta spectrum cases. Three abnormal findings were commonly present in these cases: bulging of the posterior bladder wall, neovascularization and arterial pulsatility in the area of neovascularization. These findings were stratified according to severity in histologically confirmed specimens. Continuous variables were compared via two-tailed t-tests and Wilcoxon rank sum tests. Categorical data were evaluated using logistic regression analysis. RESULTS: Neovascularization affected 84%, bulging 71% and pulsatility 54% of the cases. Bulging and neovascularization increased with disease severity. Pulsatility occurred exclusively in percretas. Bulging was associated with a 12-fold (OR = 11.6, 95% CI 2.94-46.33, P = 0.0005) increased likelihood of percreta and neovascularization with a 17-fold (OR = 17.06, 95% CI 2.98-97.79, P = 0.0014) increase. Neovascularization and/or the presence of bulging of the bladder have high positive predictive value for placenta increta and percreta (91.5% and 95.0%, respectively). Cystoscopy can be used to assess the severity of placenta accreta spectrum cases preoperatively, especially when placentation is over the previous uterine scar and is in proximity to the bladder wall.

Prophylactic Hypogastric Artery Ligation during Placenta Percreta Surgery: A Retrospective Cohort Study.

Objective To evaluate if prophylactic hypogastric artery ligation (HAL) decreases surgical blood loss and blood products transfused. Study Design This is a retrospective cohort study comparing patients with placenta percreta undergoing prophylactic HAL at the time of cesarean hysterectomy versus those who did not. Data were presented as means ± standard deviations, proportions, or medians with interquartile ranges. Demographic and clinical data were compared in the groups using Student's t -test for normally distributed data or the Mann-Whitney U test for nonnormally distributed data. Fisher's exact test was used for proportions and categorical variables. Data are reported as significant where p was <0.05. Results There were 26 patients included in the control group with no HAL and 11 patients included in the study group. Estimated blood loss for the study group was 1,000 mL versus 800 mL in the control. Units of PRCBs transfused were 4.5 units in the study group versus 2 units for the control group. None of these measures were found to be statistically significant. Conclusion Our data suggest there was no benefit in the use of prophylactic HAL in decreasing surgical blood loss or amount of blood products transfused in patients who had a cesarean hysterectomy performed for placenta percreta. Précis Prophylactic HAL does not decrease blood loss during surgery for placenta percreta.

Telomere length dynamics in early life: the blood-and-muscle model.

Telomere length (TL) trajectories in somatic tissues during human growth and development are poorly understood. We examined a blood-and-muscle model during early life, focusing on TL trajectories in leukocytes, representing the highly proliferative hematopoietic system, and skeletal muscle, a minimally proliferative tissue. Leukocyte TL (LTL) and skeletal muscle TL (MTL) were measured in 28 fetuses and 73 children. LTL and MTL were highly variable across individuals (sd: fetal LTL = 0.72 kb, MTL = 0.72 kb; children LTL = 0.81 kb, MTL = 0.82 kb) but were highly correlated within individuals (fetuses, r = 0.76, P < 0.0001; children, r = 0.87, P < 0.0001). LTL was shorter than MTL in fetuses (10.63 vs. 11.01 kb; P = 0.0004) and children (8.46 vs. 9.40 kb; <0.0001). The LTL-MTL gap was smaller in fetuses than children. TL in children was inversely correlated with body mass index (BMI) (LTL: -0.047 ± 0.016 kb/BMI, P < 0.005; MTL: -0.037 ± 0.017 kb/BMI, P = 0.03). We conclude that variations in TL across adults and differences in TL between somatic tissues are largely established in early life. Because TL plays a significant role in aging-related diseases, insight into the factors that fashion TL in somatic tissues during early development should contribute to an understanding of the relationship of TL with these disease and longevity in humans.-Sabharwal, S., Verhulst, S., Guirguis, G., Kark, J. D., Labat, C., Roche, N. E., Martimucci, K., Patel, K., Heller, D. S., Kimura, M., Chuang, D., Chuang, A., Benetos, A., Aviv, A. Telomere length dynamics in early life: the blood-and-muscle model.

A founder mutation in the MPL gene causes congenital amegakaryocytic thrombocytopenia (CAMT) in the Ashkenazi Jewish population.

Congenital amegakaryocytic thrombocytopenia (MIM #604498) (CAMT) is a rare inherited disease presenting as severe thrombocytopenia in infancy. Untreated, many CAMT patients develop aplastic anemia within the first decade of life; the only effective treatment of CAMT is bone marrow transplantation. CAMT is the result of the presence of homozygous or compound heterozygous mutations in the thrombopoietin receptor-encoding gene, MPL. We report here the identification and characterization of a founder mutation in MPL in the Ashkenazi Jewish (AJ) population. This mutation, termed c.79+2T>A, is a T to A transversion in the invariant second base of the intron 1 donor splice site. Analysis of a random sample of 2018 individuals of AJ descent revealed a carrier frequency of approximately 1 in 75. Genotyping of six loci adjacent to the MPL gene in the proband and in the 27 individuals identified as carriers of the c.79+2T>A mutation revealed that the presence of this mutation in the AJ population is due to a single founder. The observed carrier frequency predicts an incidence of CAMT in the AJ population of approximately 1 in 22,500 pregnancies. The identification of this mutation will enable population carrier testing and will facilitate the identification and treatment of individuals homozygous for this mutation.