Counselling Patients for Trial of Labour after Cesarean (TOLAC) and Invasive Placentation: Are We Missing the Mark? The Importance of Local Data and Informed Choice.

OBJECTIVE: Rates of cesarean delivery are increasing, and these procedures carry potential complications, like the risk of invasive placentation, which increases with each cesarean. A trial of labour after cesarean (TOLAC) is a viable option for patients; however, it has been associated with uterine rupture, a complication with maternal and fetal risks. To better counsel patients considering TOLAC, we aimed to determine local uterine rupture rates and maternal and neonatal outcomes with TOLAC and compare these with outcomes related to invasive placentation. METHODS: A 4-year retrospective chart review was conducted at our tertiary centre of all patients with a history of a previous cesarean delivery. We assessed rates of TOLAC, vaginal delivery after cesarean (VBAC), and uterine rupture, as well as maternal and neonatal outcomes associated with invasive placentation. Cases of uterine rupture from 1988 to the present were also reviewed, and their outcomes were compared with those of invasive placentation. RESULTS: Our uterine rupture rate was 0.44% and VBAC rate was 73.8%. We identified 8 cases of uterine rupture since 1988 and 67 invasive placentas during the 4-year chart review. Invasive placentation was associated with a significantly increased risk of neonatal respiratory morbidity, hysterectomy, maternal complications, and longer length of maternal hospital stay when compared with uterine rupture. CONCLUSION: While uterine rupture remains a potential complication of TOLAC, it is rare with overall excellent maternal and neonatal outcomes. Invasive placentation, the risk of which increases with cesarean delivery, carries potentially higher complication rates than uterine rupture. Local complication data is important for individual sites offering TOLAC. The implications of invasive placentation cannot be overlooked when counselling patients considering TOLAC.

Ruptured Degenerating Fibroid Causing Preterm Labour and Systemic Inflammatory Response Syndrome.

BACKGROUND: Fibroids are present in at least 10% of pregnancies and are recognized to cause a variety of complications. A few case reports have described fibroids as an etiological factor in uterine rupture, sometimes with life-threatening hemorrhage. CASE: A 28-year-old G1, P0 woman at 20 weeks gestation developed systemic inflammatory response syndrome with acute renal failure and massive ascites secondary to a ruptured degenerated fibroid. This resulted in preterm delivery and neonatal death. At 6 weeks postpartum, she successfully underwent an abdominal myomectomy. CONCLUSION: This is a rare case of uterine fibroid rupture causing preterm labour and systemic inflammatory response syndrome. This report discusses the diagnosis of uterine rupture related to the fibroid with imaging and subsequent management, which included fertility-preserving surgery.

Barriers to the uptake of postexposure prophylaxis among Nairobi-based female sex workers.

INTRODUCTION: Female sex workers (FSWs) in sub-Saharan Africa are at a particularly high risk for HIV infection. Postexposure prophylaxis (PEP) is available as part of an HIV care and prevention program through dedicated FSW clinics in Nairobi, Kenya, but is underutilized. We evaluated PEP knowledge, access, and adherence among clinic attendees. METHODS: An anonymous questionnaire was administered to unselected HIV-uninfected FSWs. Participants were dichotomized into high and low HIV risk categories based on self-reported sexual practices. Prior PEP use, knowledge, and adherence were then evaluated. RESULTS: One hundred and thirty-four HIV-uninfected FSWs participated, with 64 (48%) categorized as being at high risk for HIV acquisition. High-risk FSWs were less likely to have heard of or accessed PEP than lower risk FSWs (37.5 vs. 58.6%, P = 0.014; and 21.9 vs. 40.6%, P = 0.019, respectively). Among higher risk FSWs, those who had accessed PEP were more likely to report treatment for a genital infection (71.4 vs. 42.0%, P = 0.049) or sex with an HIV-infected man (62.5 vs. 37.5%, P = 0.042) during the last 6 months. However, only 35.7% of high-risk women accessing PEP completed a full course of treatment, and noncompleters were more likely to report prior unprotected sex with an HIV-infected man (P = 0.023). CONCLUSION: Despite freely available PEP for Nairobi-based FSWs, women at highest risk were less likely to have heard of PEP, access PEP, or complete the full course of therapy once initiated. Program delivery needs to be improved to ensure that FSW most at risk are able to benefit from this resource.

Kaposi's sarcoma-associated herpesvirus G-protein-coupled receptor prevents AU-rich-element-mediated mRNA decay.

During lytic Kaposi's sarcoma-associated herpesvirus (KSHV) infection, host gene expression is severely restricted by a process of global mRNA degradation known as host shutoff, which rededicates translational machinery to the expression of viral proteins. A subset of host mRNAs is spared from shutoff, and a number of these contain cis-acting AU-rich elements (AREs) in their 3' untranslated regions. AREs are found in labile mRNAs encoding cytokines, growth factors, and proto-oncogenes. Activation of the p38/MK2 signal transduction pathway reverses constitutive decay of ARE-mRNAs, resulting in increased protein production. The viral G-protein-coupled receptor (vGPCR) is thought to play an important role in promoting the secretion of angiogenic molecules from KSHV-infected cells during lytic replication, but to date it has not been clear how vGPCR circumvents host shutoff. Here, we demonstrate that vGPCR activates the p38/MK2 pathway and stabilizes ARE-mRNAs, augmenting the levels of their protein products. Using MK2-deficient cells, we demonstrate that MK2 is essential for maximal vGPCR-mediated ARE-mRNA stabilization. ARE-mRNAs are normally delivered to cytoplasmic ribonucleoprotein granules known as processing bodies (PBs) for translational silencing and decay. We demonstrate that PB formation is prevented during KSHV lytic replication or in response to vGPCR-mediated activation of RhoA subfamily GTPases. Together, these data show for the first time that vGPCR impacts gene expression at the posttranscriptional level, coordinating an attack on the host mRNA degradation machinery. By suppressing ARE-mRNA turnover, vGPCR may facilitate escape of certain target mRNAs from host shutoff and allow secretion of angiogenic factors from lytically infected cells.