Volume 25, August 2021, Pages 150-155  https://doi.org/10.1016/j.preghy.2021.05.019Get rights and content Acute pulmonary edema is a rare, life threatening complication affecting approximately 0.08% of women during pregnancies and even more common during the immediate post-partum period [1]. The pathophysiological changes related to this phenomenon are related to an endothelial damage, abnormal hemodynamics [2], [3] resulting in diastolic dysfunction [4], [5], increased cardiac preload [6], [7], [8] and afterload [3], [9] which are all common in preeclampsia with severe features [10]. It was suggested that contributing factors are advanced maternal age, obesity, cesarean delivery, tocolytic therapy, pre-pregnancy cardiac disease, iatrogenic fluid overload, and parity [1], [7]. In low cardiac output, high peripheral vascular resistance scenario, the use of negative inotropic anti-hypertensive medications such as labetalol have been suggested to make hemodynamics worse, contributing to the development of acute pulmonary edema [11], [12]. Increasing the use of non-steroidal anti-inflammatory drugs (NSAIDS), which can cause fluid retention may also be a contributing factor [13]. The age at which women experience their first pregnancy has increased throughout the decades mostly attributed to advances in artificial reproductive technology (ART) [14], [15], [16], [17]. Advanced maternal age is an independent risk factor for the development of cardiovascular diseases [18] owing to vascular stiffness and endothelial dysfunction [19], [20], [21], both of which contribute to the development of hypertension [22], [23]. Moreover, artificial reproductive technology (ART) and even more so oocyte donation, frequently seen at advanced age, are independent risk factors for developing hypertensive pregnancy disorders [24], [25]. Therefore, pregnant women at advanced age that develop preeclampsia are distinct obstetric high risk group for hemodynamic deterioration and development of acute pulmonary edema [15], [18], [26]. As pulmonary edema is a life-threatening condition, our objective was to describe the clinical, epidemiological and cardiovascular hemodynamic of advanced maternal age women with preeclampsia that developed acute pulmonary edema in order to predict and possibly prevent this complication. This was a retrospective cohort descriptive study of women at advanced age with preeclampsia that developed acute pulmonary edema in a single university affiliated tertiary hospital between the years 2011 and 2019. The study participants were identified through the hospital's medical records from all advanced maternal age women above 45 years who delivered a live born or stillborn infant after 20 weeks gestation and who had diagnosed with preeclampsia [27]. Diagnosis of pulmonary edema was Overall, during the study period 90,540 women delivered in our hospital, of them, 540 women (0.6%) above age 45 years gave birth. Of those, 67 women (12.4%) had preeclampsia in which 4 women (6%) were complicated with acute pulmonary edema (Fig. 1). All four women were nulliparous and had conceived through IVF with oocyte donation, none of them smoked during pregnancy, had history of cardiac disease, pregestational diabetes or chronic hypertension, and none used antihypertensive medication We presented case series of four nulliparous women at the fifth decade of life with diagnosis of preeclampsia that developed acute pulmonary edema in the post-partum period. Cardiovascular assessments, including echocardiography and stress test were performed prior to initiating ART, and in all four women, these assessments were unremarkable. All four women deteriorated hemodynamically, presenting with acute pulmonary edema in the early post partum period characterized by dyspnea, hypertensive The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
To investigate the role of glycemic control in development of preeclampsia (PE) in women with type 1 diabetes mellitus (T1DM). An observational case-control study comparing 244 women with type 1 diabetes and 488 controls was conducted. Among women with T1DM HbA1c, average daily glucose values, fasting, preprandial, 1-hour and 2-hour postprandial glucose levels, and daily 3 meals postprandial glucose areas were evaluated. Uterine artery pulsatility indices (PI) at 16, 20, 24 weeks‘ gestation were obtained. Data analysis included rates of PE in both groups, and association between glycemic control, uterine artery PI and development of PE among women with T1DM. PE developed in 13.1% of diabetic women and in 3.5% of women in the control group (odds ratio 4.2; 95% CI 2.2–8.1). In multivariate logistic regression analysis, HbA1c in the 1st trimester, mean daily glucose level in the 1st and 2nd trimester, daily 3 meal postprandial glucose area in the 1st and 2nd trimester, and the uterine arteries PI at 24 weeks’ gestation were found to be associated with development of PE. The uterine arteries PI showed a significant positive correlation with the 3 meal postprandial glucose area at 16, 20, 24 weeks. In women with T1DM, poor glycemic control early in pregnancy is associated with an increased risk of subsequent PE. An association between poor placentation, as indicated by the increased PI of uterine arteries, and a maternal metabolic factor, that is the 3 meal post-prandial glucose area, has been shown, supporting the increased rate of PE among women with T1DM. Preeclampsia is associated with maternal morbidity and mortality during pregnancy, and also an increased cardiovascular disease (CVD) risk later in life. During preeclampsia, alterations in secreted placental factors leading to systemic maternal endothelial dysfunction are evident. However, little is known about the associated endothelial intracellular signaling. STAT3 is a latent cytoplasmic transcription factor involved in endothelial cell differentiation, survival, and angiogenesis. We aimed to test if preeclampsia and preeclampsia-related placental factors could alter serum-induced STAT3(Y705) activation in endothelial cells. Furthermore, if altered serum-induced endothelial STAT3 (Y705) activation is related to post-preeclamptic CVD risk. HUVECs were used as a model of maternal endothelium. Experiments entailed addition of 20% human pregnancy serum as well as addition of recombinant PlGF, sFLT1 and VEGF-A165a to the cells. Levels of pSTAT3(Y705) related to STAT3 levels were evaluated by immunoblotting analysis. Our results show that preeclamptic serum induces significantly lower STAT3(Y705) phosphorylation compared with uncomplicated pregnancy serum (P = 0.0089) in endothelial cells. Furthermore, STAT3(Y705) phosphorylation was not changed upon addition of PlGF, sFLT1, or VEGF-A165a together with pregnancy sera compared with sera alone. Finally, sera from women with previous preeclampsia and current hypertension and carotid atherosclerotic plaques show significantly lower STAT3(Y705) phosphorylation capabilities compared with healthy women with previous uncomplicated pregnancies 8–18 years after deliveries (P = 0.029). Reduction in serum-induced endothelial STAT3(Y705) activation may play an important role in the preeclampsia-associated endothelial dysfunction. Additionally, reduced endothelial STAT3(Y705) phosphorylation may contribute to increased post-preeclamptic CVD risk 8–18 years after delivery. Pre-eclampsia (PE) accounts for 14.8% of maternal deaths in South Africa. Tenascin C (TN-C) is an anti-inflammatory cytokine expressed in the extracellular matrix and may be dysregulated in the hyperinflammatory PE microenvironment. This study examined serum TN-C in normotensive pregnant (n = 36) and pre-eclamptic (n = 36) HIV positive and negative women using an immunoassay. TN-C was significantly upregulated in PE vs normotensive pregnant women (p = 0.0075) and HIV-positive vs negative pregnant women (p = 0.0009). TN-C levels across all groups was statistically different (p < 0.0001). This study demonstrates an elevation of TN-C in HIV-associated PE. The potential benefit of TN-C as a biomarker to detect PE development requires investigation. The share of Klebsiella pneumoniae in infections has been recently increasing. Multidrug-resistant strains that produce more than one antibiotic resistance mechanism are also increasingly isolated. Contamination of the organs preservation fluid occurs quite often, but the isolated microorganisms are mainly saprophytic bacteria that are part of the skin microbiota (coagulase-negative Staphylococcus, Corynebacterium spp). The following case describes a K. pneumoniae blood infection in a patient after liver transplantation. Susceptibility of the strains to chosen antimicrobials was determined using the automated method. For strain isolated from blood, it was confirmed by loop-mediated isothermal amplification of genetic material. The large interferon-inducible anti-angiogenic pro-inflammatory GTPase Guanylate Binding Protein-1 (GBP-1) is produced and secreted by activated endothelial cells and is highly induced by inflammatory cytokines and inhibited by angiogenic growth factors. During pregnancy a generalized mild inflammatory response is observed. During preeclampsia this generalized inflammatory response is even further activated and activation of the endothelium occurs. We hypothesized that GBP-1 is increased in healthy pregnancy and will be even further increased during preeclampsia. In the first experiment, plasma and placentas were collected from healthy and preeclamptic pregnancies. Plasma was also collected from non-pregnant women. For the second experiment longitudinal blood samples from women with a healthy or preeclamptic pregnancy were collected from the end of the first trimester until birth and one sample postpartum. The plasma GBP-1 levels were measured by ELISA and GBP-1 mRNA and protein levels in the placenta were tested by qPCR and immunohistochemistry. During pregnancy higher plasma concentrations of GBP-1 compared with non-pregnant women were observed. Surprisingly, during preeclampsia, plasma GBP-1 levels were lower than in control pregnancies and similar to the level of non-pregnant controls. Placental GBP-1 mRNA levels were not different between healthy and preeclamptic pregnancies and GBP-1 protein was virtually undetectable in the trophoblast by immunohistochemistry in placental tissue. Evaluation of longitudinal samples showed that plasma GBP-1 concentrations increased towards the end of pregnancy in healthy pregnancies, but not in preeclampsia. In line with our hypothesis, we found higher GBP-1 plasma levels during healthy pregnancy. However, plasma GBP-1 did not further increase during preeclampsia, but was stable. Further studies are needed to evaluate why GBP-1 does not increase during preeclampsia. Two cases of advanced alkaptonuria (AKU) with co-existing osteoporosis are described. Case 1 developed multiple non-vertebral fragility fractures, while Case 2 developed vertebral fragility fractures, both refractory to bisphosphonates. Difficulties in diagnosing osteoporosis in AKU complicated by extensive calcifying and ossifying spondylosis are discussed. Both patients continued to fracture despite nitisinone therapy for metabolic control of AKU, as well as bisphosphonate antiresorptive therapy for osteoporosis. Subsequently the patients were treated with teriparatide 20 μg subcutaneous injections daily for two years, leading to reduction in fractures soon after commencing therapy in both cases. Markers of bone remodelling P1NP and CTX were stimulated. No complications due hypercalcaemia or calcification were encountered in either case. We conclude that teriparatide is an effective adjunct in the treatment of AKU when bisphosphonates prove ineffective. |
What causes pulmonary edema in preeclampsia
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