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1.
Innov Aging ; 6(Suppl 1):785-6, 2022.
Article in English | PubMed Central | ID: covidwho-2212776

ABSTRACT

Older adults and immune-compromised individuals (e.g., cancer survivors) were quickly identified as high-risk groups during the COVID-19 pandemic. Research has examined adverse psychological consequences due to the pandemic in older adults with chronic conditions. However, no research has examined the potential for positive consequences of COVID-19 in older adults with cancer. The current study examined the association between COVID-19 risk, stress, exposure, and perceived post-traumatic growth (PPTG) in adults with cancer. Cancer survivors (n = 231) enrolled in an ongoing longitudinal study completed a one-time COVID-19 experience assessment, including PPTG as a result of the COVID pandemic. Participants (mean age = 68 years) had completed primary treatment for breast, prostate, or colorectal cancer within the past two years. On average, survivors reported modest PPTG related to COVID-19 (mean = 6.03, range = 0–20). Using linear regression, we found that gender, cancer type, and marital status were related to PPTG. Higher COVID-19 risk, more COVID-19 stressors, and higher illness exposure (e.g., having had COVID-19) were significantly positively associated with PPTG scores (ps < .05). In spite of the potential adverse psychological consequences of the COVID-19 pandemic, these results suggest adults with cancer, in our sample, report modest PPTG. Higher COVID-19-related perceived risk, stress, and exposure predicted higher PPTG scores. These findings are interesting in light of studies that suggest PPTG occurs only after time passes from the stressor. Future research could examine how coping with cancer may influence coping with a co-existing or subsequent stressor and its relationship to PPTG.

2.
Infectious Diseases in Clinical Practice ; 30(4):10, 2022.
Article in English | Web of Science | ID: covidwho-1886474

ABSTRACT

Aims This study aimed to investigate the potential of tocilizumab therapy in minimizing mortality and mechanical ventilation (MV) requirements among hospitalized COVID-19 patients. Methods A single-center, retrospective, observational cohort study of 375 patients with severe COVID-19 (from March 1 to April 22, 2020) included 150 patients treated with tocilizumab and 225 consecutive control patients adjusted for age and sex. Both groups received concomitant standard of care treatments in addition to tocilizumab. The statistical methods relied on survival analyses, conditional logistic regression models, and contingency analyses. The outcomes included in-hospital mortality and the MV requirement. Results Tocilizumab associated with improved in-hospital mortality (34.7% vs 46.7%, P = 0.0136) and lower requirement for MV on days 1, 3, and 5 after treatment (P = 0.005, P < 0.0001, and P = 0.0021, respectively). Lower mortality was observed if tocilizumab was administered within 48 hours after admission (P = 0.0226). Older age and low blood oxygen saturation on admission decreased the odds of survival (P < 0.005). Conclusions Our study demonstrates a significant reduction in mortality and decreased requirement of MV with tocilizumab treatment in addition to the standard of care. Early administration of tocilizumab within 48 hours reduces the risk of mortality.

3.
Psycho-Oncology ; 30:73-74, 2021.
Article in English | Web of Science | ID: covidwho-1148535
4.
Pediatric and Developmental Pathology ; 23(6):550, 2020.
Article in English | EMBASE | ID: covidwho-1093937

ABSTRACT

Background: The rarity of placental infection by SARSCoV- 2 suggests the presence of protective measures. SARS-CoV-2 requires coexporession of its receptor, ACE2, and the serine proteinase TMPRSS2 for cellular infection. Both are expressed in the placenta but their protein expression pattern has not been demonstrated to date. Methods: 19 placentas from women with PCR proven SARS-CoV-2 infection were examined for SARS-CoV-2 expression by RNAish and immunohistochemistry (IHC) and for ACE2 and TMPRSS2 by IHC. Gross and histopathology were also reviewed. Two sets of controls were used: 'normal controls' - 122 placentas examined solely for GBS exposure (no other indication for examination) delivered from 2000-2004;and 'abnormal controls' - 130 placentas from neonates with a clinical diagnosis of HIE delivered from 2000-2019. The control placentas were reviewed for gross and histopathology. Results: 2 cases showed placental infection with viral RNA the villous syncytiotrophoblast (ST) and cytotrophoblast (CT) in a patchy distribution in 1 and only focally in the other. The infant with the patchy infection was SARSCoV- 2 PCR positive at 24 hours, the infant with only focal infection was PCR negative. None of the other placentas showed viral infection. All placentas showed robust expression of ACE2 in the trophoblast. The ST and CTexpression was membranous and In most cases ST expression was polarized-strongest, and in many cases only present, on the villous stromal side of the ST. TMPRSS2 was weakly expressed in the placental endothelial cells. Hofbauer cells were negative for both. We did not find a an increase in maternal or fetal vascular malperfusion (MVM or FVM) over controls. We saw MVM at 25%, FVM at 20%, acute chorioamnionitis at 30%, inflammatory pathologies (1 case each of ungradable VUE, intervillositis, Hofbauer cell hyperplasia) at 15%, all within published prevalences and similar to our controls. Conclusion:We did not find increased prevalence of MFM, FVM, infectious, or inflammatory pathology above published our our sets of controls as other have, perhaps due to small sample size. SARS-CoV-2 infection of the placenta is rare and vertical transmission, if it occurs, is even rarer. One mechanism for this is the rare occurrence of maternal SARS-CoV-2 viremia. Another mechanisms might be the unfavorable expression ACE2 and TMPRSS2. We show that their expression is uniquely distinct: ACE2 in the tropohobast and TMPRSS2 in the endothelium. Although we did not detect coexpression we cannot rule out that the vascular-syncytial membranes might coexpress ACE2 and TMPRSS2. We also show that ACE2 expression is polarized in most cases away from the maternal vascular space thereby perhaps limiting SARS-CoV-2 access to ST infection.

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