Pregnancy outcomes in women with gestational diabetes mellitus by models of care: a retrospective cohort study.

OBJECTIVE: To compare birth outcomes of women with gestational diabetes mellitus (GDM) with background obstetric population, stratified by models of care. DESIGN: Retrospective cohort study. SETTING: A tertiary referral centre in Sydney, Australia. PARTICIPANTS: All births 1 January 2018 to 30 November 2020. Births <24 weeks, multiple gestations and women with pre-existing diabetes were excluded. METHODS: Data were obtained from electronic medical records. Women were classified according to GDM status and last clinic attended prior to delivery. Model of care included attendance at dedicated GDM obstetric clinics, and routine antenatal care. MAIN OUTCOME MEASURES: Hypertensive disorders of pregnancy (HDP), pre-term birth (PTB), induction of labour (IOL), operative delivery, small for gestational age (SGA), large for gestational age, postpartum haemorrhage, obstetric anal sphincter injury (OASIS), neonatal hypoglycaemia, neonatal hypothermia, neonatal respiratory distress, neonatal intensive care unit (NICU) admission. RESULTS: The GDM rate was 16.3%, with 34.0% of women managed in dedicated GDM clinics. Women with GDM had higher rates of several adverse outcomes. Only women with GDM attending non-dedicated clinics had increased odds of HDP (adjusted OR (adj OR) 1.6, 95% CI 1.2 to 2.0), PTB (adj OR 1.7, 95% CI 1.4 to 2.0), OASIS (adj OR 1.4, 95% CI 1.0 to 2.0), similar odds of induction (adj OR 1.0, 95% CI 0.9 to 1.1) compared with non-GDM women. There were increased odds of NICU admission (adj OR 1.5, 95% CI 1.3 to 1.8) similar to women attending high-risk GDM clinics. CONCLUSIONS: Women with GDM receiving care in lower risk clinics had similar or higher rates of adverse outcomes. Pathways of care need to be similar in all women with GDM.

Aspirin and pre-eclampsia prevention in women with pre-existing diabetes: a retrospective study.

BACKGROUND: Aspirin is routinely prescribed in high-risk pregnancies to prevent pre-eclampsia; however, there is a paucity of data in women with pre-existing diabetes. AIMS: To assess the efficacy and safety of aspirin in women with pre-existing diabetes in preventing pre-eclampsia. METHODS: A retrospective review of women with pre-existing diabetes who attended antenatal clinics in a tertiary referral hospital between 2013 and 2019 was conducted. Cases were those receiving aspirin prior to 16 weeks, with pre-eclampsia as the primary outcome. The relationship between early pregnancy glycaemic control and pre-eclampsia was also assessed. RESULTS: Of the 164 women included in the study, 45 received aspirin. There were no differences in pre-eclampsia (odds ratio (OR) 0.9 (0.3-3.0), P = 0.924) or any other measure of placental insufficiency (OR 1.7 (0.7-4.3), P = 0.243) between the aspirin and control groups after adjusting for baseline differences. Aspirin therapy was associated with an increased risk of postpartum haemorrhage (PPH) (OR 3.1 (1.1-9.1), P = 0.041). The incidence of pre-eclampsia increased stepwise according to early pregnancy HbA1c subgroups of ≤6.0% (n = 47), 6.1-7.5% (n = 57) and > 7.5% (n = 39), with rates of 0, 12.3 and 20.5% (P = 0.007) respectively. CONCLUSIONS: The aspirin group had a higher baseline risk of pre-eclampsia and placental insufficiency, therefore the absence of difference between the groups favoured the efficacy of aspirin. PPH was highlighted as a potential complication of therapy, and early pregnancy HbA1c as a novel risk stratification tool for pre-eclampsia in women with pre-existing diabetes.

The management of severe pre-eclampsia and HELLP syndrome in a twin pregnancy with a known morbidly adherent placenta: A case report.

INTRODUCTION: Morbidly adherent placenta (MAP) is a rare obstetric complication, especially in cases of multiple gestation. We present a case of MAP complicating a dichorionic diamniotic (DCDA) twin pregnancy requiring delivery by emergency cesarean hysterectomy at 30 + 2 weeks of gestation. CASE PRESENTATION: A 36-year-old woman, G3P2, with a DCDA twin pregnancy and known MAP presented to the labour ward at 30 + 2 weeks of gestation with evidence of pre-eclampsia and fulminating HELLP syndrome. Delivery was indicated due to fetal distress, demonstrated by pathological findings on cardiotocography, acutely deranged liver functions and worsening thrombocytopenia. An emergency cesarean hysterectomy was performed with postoperative monitoring in the intensive-care unit. The patient was discharged home on two oral antihypertensive agents. Her platelet count and liver functions were normalized prior to discharge. DISCUSSION: Delivery planning for pregnancies complicated by MAP should commence early in the antenatal period, especially in cases where there is an anticipated risk of preterm delivery, such as multiple pregnancy. Multidisciplinary elective and emergency care plans should be developed and include interventional radiology services when available. Established protocols help to standardize care of these high-risk pregnancies and aid in decision making in emergency scenarios, such as the one presented.

Depletion of Langerhans cells in human papillomavirus type 16-infected skin is associated with E6-mediated down regulation of E-cadherin.

Human papillomavirus type 16 (HPV16) is an oncogenic virus that causes persistent infections in cervical epithelium. The chronic nature of HPV16 infections suggests that this virus actively evades the host immune response. Intraepithelial Langerhans cells (LC) are antigen-presenting cells that are critical in T-cell priming in response to viral infections of the skin. Here we show that HPV16 infection is directly associated with a reduction in the numbers of LC in infected epidermis. Adhesion between keratinocytes (KC) and LC, mediated by E-cadherin, is important in the retention of LC in the skin. Cell surface E-cadherin is reduced on HPV16-infected basal KC, and this is directly associated with the reduction in numbers of LC in infected epidermis. Expression of a single viral early protein, HPV16 E6, in KC reduces levels of cell surface E-cadherin thereby interfering with E-cadherin-mediated adhesion. Through this pathway, E6 expression in HPV16-infected KC may limit presentation of viral antigens by LC to the immune system, thus preventing the initiation of a cell-mediated immune response and promoting survival of the virus.