ABSTRACT
Objective: Describe incidental tomographic in the sample, correlating them with risk factors for chest diseases and sociodemographic data. Method(s): This is a retrospective and observational study covering 162 patients admitted to the COVID sector of the HU/UFJF, from April 1, 2020, to July 7, 2021, with a confirmed laboratory diagnosis of COVID-19. The variables were described in absolute and relative frequencies. The comparison of the correlation between the outcome variable (the tomographic findings) for independent samples was performed using Pearson's chi-square test (without correction) or Fisher's test when relevant. Result(s): Of the 162 patients, 15.4% had a solitary pulmonary nodule;14.8% had multiple pulmonary nodules;1.8%, lung mass;3.1%, mediastinal mass, and 9.3% had mediastinal adenomegaly. Findings such as excavations, pleural effusion, emphysema, PTE, pneumothorax, chronic interstitial disease, cavitation, aneurysms, and significant atheromatosis, classified in this study in the "Other" category showed impressive results, with an overall prevalence of 81.5%. This study demonstrated that 34% of patients had two or more types of incidental CT findings and that 88.3% of patients had at least some type of incidental CT finding. Conclusion(s): The pandemic of SARS-CoV-2 infections has brought a series of challenges and lessons learned to healthcare teams around the world. The massive implementation of highly sensitive diagnostic methods, such as chest tomography, ends up bringing an additional challenge, which is to deal with incidental findings, making good clinical reasoning necessary to avoid unnecessary investigations and not leave without diagnosis and treatment of diseases in early and asymptomatic stages.Copyright © 2023 Faculdade de Medicina de Ribeirao Preto - U.S.P.. All rights reserved.
ABSTRACT
Preeclampsia (PE), new onset hypertension (HTN) during pregnancy, is associated with placental ischemia and chronic inflammation that includes increased CD4+ T cells, B cells secreting agonistic autoantibodies against the angiotensin II type 1 receptor (AT1AA), and activation of the complement system. Previous studies have shown AT1-AA is produced in patients with COVID-19 infection. Interestingly, having had COVID-19 during pregnancy is associated with increased incidence of developing a PE phenotype during pregnancy. We have previously shown an important role for B cell depletion or AT1AA inhibition to attenuate HTN in rat models of PE. Collectively, this data suggests B cells contribute to PE development and that B cells may increase incidence of PE in patients with a history (Hx) of COVID-19 during pregnancy through production of the AT1AA. We hypothesize B cells from PE or CV Hx PE patients produce AT1AA resulting in HTN and complement activation in pregnancy. Placental B cells were isolated from normal pregnant (NP), PE, normotensive (NT) CV Hx, or PE CV Hx patients at delivery. B cells were transferred i.p. into pregnant athymic rats at gestation (GD) 12. On GD18, carotid catheters were inserted. On GD19, blood pressure was measured and tissues collected. PE B cell recipients had increased Mean Arterial Pressure (MAP) (115+/-3 mmHg n=6) compared to NP B cell recipients (97+/-4 mmHg n=6 p<0.05). PE B cell recipients had increased AT1AA (20+/-2 DELTABPM n=4) compared to NP B cell recipients (6+/-1 DELTABPM n=4 p<0.05). PE B cell recipients had increased markers of complement activation such as reduced plasma C4 (1302+/-169 mug/mL n=4) and C3 (516+/-45 mug/mL n=4) compared to recipients of NP B cells (2348+/-338 mug/mL n=4 p<0.05) and (790+/-66 mug/mL n=4 p<0.05) respectively. CV Hx PE B cell recipients had elevated MAP (108+/-3 mmHg n=4) compared to CV Hx NT B cell recipients (101+/-7 mmHg n=4) and increased AT1AA (24+/-3 DELTABPM n=3) compared to CV Hx NT B cell Recipients (4+/-1 DELTABPM n=4 p<0.05). Collectively, this study demonstrates an important role for B cells to cause HTN during pregnancy;and indicates that B cells contribute to a higher incidence of PE in women with a Hx of CV infection during pregnancy possibly by secreting AT1-AA.