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Objective: To investigate the relationship between preeclampsia and SARS-CoV-2 infection during pregnancy. Methods: This was a retrospective cohort study of pregnant women between March and October 2020. Pregnant patients admitted to 14 obstetrical centers in Michigan, USA formed the study population. Of the N = 1458 participants, 369 had SARS-CoV-2 infection (cases). Controls were uninfected pregnancies that were delivered in the same obstetric unit within 30 days of the index case. Robust Poisson regression was used to estimate relative risk (RR) of preterm and term preeclampsia and preeclampsia involving placental lesions. The analysis included adjustment for relevant clinical and demographic risk factors.Results: SARS-CoV-2 infection during pregnancy increased the risk of preeclampsia [adjusted aRR = 1.69 (1.26–2.26)], preeclampsia involving placental lesions [aRR = 1.97(1.14–3.4)] and preterm preeclampsia 2.48(1.48–4.17). Although the highest rate of preeclampsia was observed in patients infected with SARS-CoV-2 who were symptomatic (18.4%), there was increased risk even in asymptomatic SARS-CoV-2 infected patients (14.2%) relative to non-infected controls (8.7%) (p < 0.05). This association with symptomatology was also noted with preterm preeclampsia for which the rate doubled from 2.7% in controls to 5.2% in asymptomatic cases and reached 11.8% among symptomatic cases (p < 0.05). The rate of preterm preeclampsia among cases of pregnant people self-identified as Black reached 10.1% and was almost double the rate of the reminder of the group of infected pregnancies (5.3%), although the rate among uninfected was almost the same (2.7%) for both Black and non-Black groups (interaction p = 0.05).Conclusions: Infection with SARS-CoV-2 increases the risk of preeclampsia even in the absence of symptoms, although symptomatic persons are at even higher risk. Racial disparities in the development of preterm preeclampsia after SARS-CoV-2 infection may explain discrepancies in prematurity between different populations. [ABSTRACT FROM AUTHOR]

In critically ill patients with COVID-19, established therapies in the setting of respiratory failure include invasive mechanical ventilation and extracorporeal membrane oxygenation (ECMO). This case report describes a pregnant woman in her 30s who was hospitalised at 35 weeks gestation with moderate COVID-19 disease. Her condition worsened following delivery, and she required intubation, maximum ventilatory support and ECMO. Because of the severe and irreversible nature of her lung disease, she ultimately underwent bilateral lung transplantation. This case showcases lung transplantation as an alternative life-saving option for patients with severe COVID-19 associated respiratory failure refractory to ECMO and mechanical ventilation. Further studies are needed to develop a multidisciplinary approach for patient selection for transplantation within the context of COVID-19 and to assess long-term outcomes. [ABSTRACT FROM AUTHOR]

Background. Evans syndrome (ES) is a chronic autoimmune disease characterized by autoimmune hemolytic anemia along with immune thrombocytopenic purpura. Few case reports of ES in pregnancy have been published, and ES may be difficult to distinguish from other diagnoses more common in pregnancy. Guidelines for treatment of ES are not well-defined. Case. A 23-year-old multigravid woman in active labor was found to have severe anemia and thrombocytopenia. She was diagnosed with ES and started on immunosuppressive treatments for persistent immune thrombocytopenic purpura. In the postpartum period, she was found to have coronavirus (COVID-19) infection and acute pulmonary embolism. Conclusion. Evans syndrome is a challenge to diagnose in pregnancy and poses important considerations for intrapartum and postpartum management. [ABSTRACT FROM AUTHOR]

Previous studies have suggested that children with neurofibromatosis type 1 are shorter than their unaffected counterparts as an effect of a germline NF1 gene mutation. The pathophysiology of this effect is still uncertain. The purpose of this study was to characterize longitudinal growth in children with neurofibromatosis type 1 in order to assess growth velocity and its influence on stature. Longitudinal height data were collected for 188 patients with a confirmed clinical diagnosis of neurofibromatosis type 1. Children with neurofibromatosis type 1 had population mean heights statistically different from the general population, with a reduced peak height velocity during pubertal growth. In addition, there were no significant differences in the timing of peak height velocity during puberty between the general population and those with neurofibromatosis type 1. These data demonstrate that short stature in neurofibromatosis type 1 is due in part to subnormal height acquisition during puberty. [ABSTRACT FROM AUTHOR]