Clinical Characteristics and Predictors of Mortality in Obese African-Americans with COVID-19: a Single-Center Retrospective Study.

BACKGROUND: This study aims to add to the body of evidence linking obesity as an established risk factor for COVID-19 infection and also look at predictors of mortality for COVID-19 in the African-Americans (AA) population. METHODS: A retrospective cohort study of patients with confirmed COVID-19 infection was done in a community hospital in New York City. The cohort was divided into two groups, with the non-obese group having a BMI < 30 kg/m2 and the obese group with a BMI ≥ 30 kg/m2. Clinical predictors of mortality were assessed using multivariate regression analysis. RESULTS: Among the 469 (AA) patients included in the study, 56.3% (n = 264) had a BMI < 30 kg/m2 and 43.7% (n = 205) had a BMI ≥ 30 kg/m2. Most common comorbidities were hypertension (n = 304, 64.8%), diabetes (n = 200, 42.6%), and dyslipidemia (n = 74, 15.8%). Cough, fever/chills, and shortness of breath had a higher percentage of occurring in the obese group (67.8 vs. 55.7%, p = 0.008; 58.0 vs. 46.2%, p = 0.011; 72.2 vs. 59.8%, p = 0.005, respectively). In-hospital mortality (41.5 vs. 25.4%, p < 0.001) and mechanical ventilation rates (34.6 vs. 22.7%, p = 0.004) were also greater for the obese group. Advanced age (p = 0.034), elevated sodium levels (p = 0.04), and elevated levels of AST (0.012) were associated with an increase in likelihood of in-hospital mortality in obese group. CONCLUSIONS: Our results show that having a BMI that is ≥ 30 kg/m2 is a significant risk factor in COVID-19 morbidity and mortality. These results highlight the need for caution when managing obese individuals.

Predictors and mortality risk of venous thromboembolism in patients with COVID-19: systematic review and meta-analysis of observational studies.

INTRODUCTION: Novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection resulting in COVID-19 disease is associated with widespread inflammation and a prothrombotic state, resulting in frequent venous thromboembolic (VTE) events. It is currently unknown whether anticoagulation is protective for VTE events. Therefore, we conducted a systematic review to identify predictors of VTE in COVID-19. METHODS: We searched PubMed, EMBASE, Google Scholar, and Ovid databases for relevant observational studies of VTE in COVID-19 disease. The effect size for predictors of VTE was calculated using a random-effects model and presented as forest plots. Heterogeneity among studies was expressed as Q statistics and I2. Bias was assessed using the Newcastle Ottawa Scale for all identified observational studies. Publication bias was assessed with funnel plot analysis. RESULTS: We identified 28 studies involving 6053 patients with suspected or confirmed COVID-19. The overall pooled prevalence of VTE events was 20.7%. Male sex was associated with a higher risk of VTE events, whereas prior history of VTE, smoking, and cancer were not. VTE events were significantly higher in severely ill patients, mechanically ventilated patients, those requiring intensive care admission, and those with a low PaO2/FiO2 ratio (P/F ratio). Chronic comorbidities, including cardiovascular disease, heart failure, renal disease, and pulmonary disease, did not increase the risk of VTE events. Patients with VTE had higher leukocyte counts and higher levels of D-dimer, C-reactive protein, and procalcitonin. The occurrence of VTE was associated with increased length of stay but did not impact mortality. Therapeutic and prophylactic doses of anticoagulation were not protective against VTE. CONCLUSION: VTE in COVID-19 is associated with male gender and severe disease but not with traditional risk factors for VTE. The occurrence of VTE does not appear to be mitigated by either prophylactic or therapeutic anticoagulation. The occurrence of VTE in this population is associated with an increased length of stay but does not appear to impact mortality.

Clinical characteristics and predictors of mortality in African-Americans with COVID-19 from an inner-city community teaching hospital in New York.

There is limited data on the clinical presentation and predictors of mortality in the African-American (AA) patients hospitalized with coronavirus disease 2019 (COVID-19) despite the disproportionately higher burden and mortality. The aim of this study is to report on the clinical characteristics and the predictors of mortality in hospitalized AA patients with COVID-19 infection. In this retrospective cohort review, we included all AA patients with confirmed COVID-19 infection admitted to an inner-city teaching community hospital in New York city. Demographics, clinical presentation, baseline co-morbidities, and laboratory data were compared between survivors and non-survivors. The predictors of mortality were assessed using multivariate logistic regression analysis. Of the 408 (median age, 67 years) patients included, 276 (66.65%, median age 63 years) survived while 132 (33.35%, median age 71 years) died. The most common presenting symptoms were cough, myalgia, fever/chills, shortness of breath, and gastrointestinal symptoms (nausea, vomiting, diarrhea, and abdominal pain), with a prevalence of 62.50%, 43.87%, 53.68%, and 27.21%, respectively. Age (odds ratio [OR], 1.06; confidence interval [CI], 1.04-1.08; P < .001), body mass index (OR, 1.07; CI, 1.04-1.11; P < .001), elevated serum ferritin (OR, 1.99; CI, 1.08-3.66; P < .02), C-reactive protein (OR, 2.42; CI, 1.36-4.33; P < .01), and D-dimers (OR, 3.79; CI, 2.21-6.50; P < .001) at the time of presentation were identified as the independent predictors of mortality. Cough, shortness of breath, fever/chills, gastrointestinal symptoms, and myalgia were the predominant presentation among AAs hospitalized with COVID-19 infection. Advanced age, higher body mass index, elevated serum ferritin, C-reactive protein, and D-dimers are independent predictors of mortality among hospitalized AAs with COVID-19 infection.

Potential contribution of tumor suppressor p53 in the host defense against hepatitis C virus.

UNLABELLED: Infection by hepatitis C virus (HCV) usually results into chronic hepatitis that can ultimately lead to cirrhosis and hepatocellular carcinoma. Type 1 interferons (IFN-alpha/beta) constitute the primary cellular defense against viral infection including HCV. IFN binding to their receptors activates associated Jak1 and Tyk2 kinases, which ultimately leads to phosphorylation and assembly of a signal transducer and activator of transcription protein (STAT)1-STAT2-interferon regulatory factor (IRF)9 trimetric complex called interferon-stimulated gene factor 3 that translocates into the nucleus and binds to the interferon- stimulated response elements (ISRE), leading to transcriptional induction of several antiviral genes, including double-stranded RNA-activated protein kinase (PKR), 2',5'- oligoadenylate synthetase (OAS), and myxovirus resistance protein A (MxA). Understanding the mechanisms of how the virus evades this cellular innate defense and establishes a chronic infection is the key for the development of better therapeutics against HCV infection. Here, we demonstrate that p53 could have a crucial role in the cellular innate defense against HCV. We observed significantly higher levels of HCV RNA replication and viral protein expression in the Huh7 cells when their p53 expressions were knocked down. Moreover, IFN treatment was less effective in inhibiting the HCV RNA replication in the p53-knocked-down (p53kd) Huh7 cells. In fact, the activation of the ISRE and the induction of ISGs were significantly attenuated in the p53kd Huh7 cells and p53 was found to directly interact with IRF9. CONCLUSION: These observations underscore the potential contributions of the tumor suppressor p53 in cellular antiviral immunity against HCV with possible therapeutic implications.