Ethnic disparities in COVID-19: increased risk of infection or severe disease?
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ABSTRACT:
SUBMITTER: Pan D
PROVIDER: S-EPMC8321429 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:COVID-19 inequities have been well-documented. We evaluated whether higher rates of severe COVID-19 in racial and ethnic minority groups were driven by higher infection rates by evaluating if disparities remained when analyses were restricted to people with infection. We conducted a retrospective cohort study of adults insured through Kaiser Permanente (Colorado, Northwest, Washington), follow-up in March-September 2020. Laboratory results and hospitalization diagnosis codes identified individuals with COVID-19. Severe COVID-19 was defined as invasive mechanical ventilation or mortality. Self-reported race and ethnicity, demographics, and medical comorbidities were extracted from health records. Modified Poisson regression estimated adjusted relative risks (aRRs) of severe COVID-19 in full cohort and among individuals with infection. Our cohort included 1,052,774 individuals, representing diverse racial and ethnic minority groups (e.g., 68,887 Asian, 41,243 Black/African American, 93,580 Hispanic or Latino/a individuals). Among 7,399 infections, 442 individuals experienced severe COVID-19. In the full cohort, severe COVID-19 aRRs for Asian, Black/African American, and Hispanic individuals were 2.09 (95% CI: 1.36, 3.21), 2.02 (1.39, 2.93), and 2.09 (1.57, 2.78), respectively, compared to non-Hispanic Whites. In analyses restricted to individuals with COVID-19, all aRRs were near 1, except among Asian Americans (aRR 1.82 [1.23, 2.68]). These results indicate increased incidence of severe COVID-19 among Black/African American and Hispanic individuals is due to higher infection rates, not increased susceptibility to progression. COVID-19 disparities most likely result from social, not biological, factors. Future work should explore reasons for increased severe COVID-19 risk among Asian Americans. Our findings highlight the importance of equity in vaccine distribution.
| S-EPMC8785693 | biostudies-literature
Project description:: We performed an observational prospective monocentric study in patients living with HIV (PLWH) diagnosed with COVID-19. Fifty-four PLWH developed COVID-19 with 14 severe (25.9%) and five critical cases (9.3%), respectively. By multivariate analysis, age, male sex, ethnic origin from sub-Saharan Africa and metabolic disorder were associated with severe or critical forms of COVID-19. Prior CD4 T cell counts did not differ between groups. No protective effect of a particular antiretroviral class was observed.
| S-EPMC7493770 | biostudies-literature
Project description:BackgroundRacial/ethnic minorities are at higher risk for severe COVID-19. This may be related to social determinants that lead to chronic inflammatory states. The aims of the study were to determine if there are racial/ethnic disparities with inflammatory markers and association of methylprednisolone to in hospital survival.MethodsThis was a secondary analysis of a retrospective cohort study of patients ≥ 18 years of age and admitted for severe COVID-19 pneumonia between March and June 2020 in 13 Hospitals in New Jersey, United States. Patients who received other formulation of corticosteroids were not included. Area under the receiver operating characteristics curves were performed to test for discriminatory ability of each inflammatory makers. Univariate and multivariate Cox regression assessed the association of variables to in hospital survival.ResultsPropensity matched sample (n = 759) between no methylprednisolone (n = 380) and methylprednisolone (n = 379) had 338 Whites, 102 Blacks, 61 Asian/Indians, and 251 non-Black non-White Hispanics. Compared to CRP, area under receiving operating characteristic curve for d-dimer in Hispanics (0.742) was statistically different (DeLong Test P = 0.0041). Multivariate cox regression showed that different variables in Blacks [age ≥ 60 years (HR = 3.71, P = 0.0281), mechanical ventilation (HR = 5.07, P = 0.0281) and creatinine ≥ 1.5 mg/dL (HR = 3.61, P = 0.0007)], Whites [cancer (HR = 1.68, P = 0.0213), qSOFA score of 1 (HR = 1.81, P = 0.0213), qSOFA score of 2 (HR = 5.16, P < 0.0001), qSOFA score of 3 (HR = 11.81, P < 0.0001) and creatinine ≥ 1.5 mg/dL (HR = 2.16, P = 0.0006)], Hispanics [hypertension (HR = 2.52, P = 0.0007), cancer (HR = 2.99, P = 0.0244 and D-dimer ≥ 2 mcg/mL (HR = 2.22, P = 0.0077)], and Asian/Indians [ chronic kidney disease (HR = 6.36, P = 0.0031) and CRP > 20 mg/L (HR = 5.02, P = 0.0032)] were statistically significant for mortality. Low dose and high dose methylprednisolone were significantly associated with prolonged survival in Whites [low dose (HR = 0.37, P < 0.0001) and high dose (HR = 0.48, P < 0.0183)] and Asian/Indians [low dose (HR = 0.13, P = 0.0101) and high dose (HR = 0.15, P = 0.01)]. However, high dose was not associated with improved survival compared to low dose. Methylprednisolone was not associated with prolonged survival in Blacks and Hispanics.ConclusionRacial/Ethnic disparities with inflammatory markers preclude the use of one marker as a predictor of survival. Methylprednisolone is associated with prolonged survival in Asian/Indians and Whites.
| S-EPMC8919360 | biostudies-literature
Project description:Racial/ethnic minorities have experienced higher COVID-19 infection rates than whites, but it is unclear how individual-level housing, occupational, behavioral, and socioeconomic conditions contribute to these disparities in a nationally representative sample. In this study, we assess the extent to which social determinants of health contribute to racial/ethnic differences in COVID-19 infection. Data are from the Understanding America Study's Understanding Coronavirus in America survey (UAS COVID-19 waves 7-29). UAS COVID-19 is one of the only nationally representative longitudinal data sources that collects information on household, work, and social behavioral context during the pandemic. We analyze onset of COVID-19 cases, defined as a positive test or a diagnosis of COVID-19 from a healthcare provider since the previous survey wave, over a year of follow-up (June 2020-July 2021). We consider educational attainment, economic resources, work arrangements, household size, and social distancing as key social factors that may be structured by racism. Cox hazard models indicate that Hispanic people have 48% higher risk of experiencing a COVID-19 infection than whites after adjustment for age, sex, local infection rate, and comorbidities, but we do not observe a higher risk of COVID-19 among Black respondents. Controlling for engagement in any large or small social gathering increases the hazard ratio for Hispanics by 9%, suggesting that had Hispanics had the same social engagement patterns as whites, they may have had even higher risk of COVID-19. Other social determinants-lower educational attainment, working away from home, and number of coresidents-all independently predict higher risk of COVID-19, but do not explain why Hispanic Americans have higher COVID-19 infection risk than whites.
| S-EPMC9162789 | biostudies-literature
Project description:Although there is increasing awareness of disparities in COVID-19 infection risk among vulnerable communities, the effect of behavioral interventions at the scale of individual neighborhoods has not been fully studied. We develop a method to quantify neighborhood activity behaviors at high spatial and temporal resolutions and test whether, and to what extent, behavioral responses to social-distancing policies vary with socioeconomic and demographic characteristics. We define exposure density ([Formula: see text]) as a measure of both the localized volume of activity in a defined area and the proportion of activity occurring in distinct land-use types. Using detailed neighborhood data for New York City, we quantify neighborhood exposure density using anonymized smartphone geolocation data over a 3-mo period covering more than 12 million unique devices and rasterize granular land-use information to contextualize observed activity. Next, we analyze disparities in community social distancing by estimating variations in neighborhood activity by land-use type before and after a mandated stay-at-home order. Finally, we evaluate the effects of localized demographic, socioeconomic, and built-environment density characteristics on infection rates and deaths in order to identify disparities in health outcomes related to exposure risk. Our findings demonstrate distinct behavioral patterns across neighborhoods after the stay-at-home order and that these variations in exposure density had a direct and measurable impact on the risk of infection. Notably, we find that an additional 10% reduction in exposure density city-wide could have saved between 1,849 and 4,068 lives during the study period, predominantly in lower-income and minority communities.
| S-EPMC8020638 | biostudies-literature
Project description:BackgroundThe global coronavirus disease 2019 (COVID-19) has presented significant challenges and created concerns worldwide. Besides, patients who have experienced a SARS-CoV-2 infection could present post-viral complications that can ultimately lead to pulmonary fibrosis. Serum levels of Krebs von den Lungen 6 (KL-6), high molecular weight human MUC1 mucin, are increased in the most patients with various interstitial lung damage. Since its production is raised during epithelial damages, KL-6 could be a helpful non-invasive marker to monitor COVID-19 infection and predict post-infection sequelae.MethodsWe retrospectively evaluated KL-6 levels of 222 COVID-19 infected patients and 70 healthy control. Serum KL-6, fibrinogen, lactate dehydrogenase (LDH), platelet-lymphocytes ratio (PLR) levels and other biological parameters were analyzed. This retrospective study also characterized the relationships between serum KL-6 levels and pulmonary function variables.ResultsOur results showed that serum KL-6 levels in COVID-19 patients were increased compared to healthy subjects (470 U/ml vs 254 U/ml, P <0.00001). ROC curve analysis enabled us to identify that KL-6 > 453.5 U/ml was associated with COVID-19 (AUC = 0.8415, P < 0.0001). KL-6 level was positively correlated with other indicators of disease severity such as fibrinogen level (r = 0.1475, P = 0.0287), LDH level (r = 0,31, P = 0,004) and PLR level (r = 0.23, P = 0.0005). However, KL-6 levels were not correlated with pulmonary function tests (r = 0.04, P = 0.69).ConclusionsKL-6 expression was correlated with several disease severity indicators. However, the association between mortality and long-term follow-up outcomes needs further investigation. More extensive trials are required to prove that KL-6 could be a marker of disease severity in COVID-19 infection.
| S-EPMC9704627 | biostudies-literature
Project description:BackgroundBy mid-May 2020, there were over 1.5 million cases of (SARS-CoV-2) or COVID-19 across the U.S. with new confirmed cases continuing to rise following the re-opening of most states. Prior studies have focused mainly on clinical risk factors associated with serious illness and mortality of COVID-19. Less analysis has been conducted on the clinical, sociodemographic, and environmental variables associated with initial infection of COVID-19.MethodsA multivariable statistical model was used to characterize risk factors in 34,503cases of laboratory-confirmed positive or negative COVID-19 infection in the Providence Health System (U.S.) between February 28 and April 27, 2020. Publicly available data were utilized as approximations for social determinants of health, and patient-level clinical and sociodemographic factors were extracted from the electronic medical record.ResultsHigher risk of COVID-19 infection was associated with older age (OR 1.69; 95% CI 1.41-2.02, p < 0.0001), male gender (OR 1.32; 95% CI 1.21-1.44, p < 0.0001), Asian race (OR 1.43; 95% CI 1.18-1.72, p = 0.0002), Black/African American race (OR 1.51; 95% CI 1.25-1.83, p < 0.0001), Latino ethnicity (OR 2.07; 95% CI 1.77-2.41, p < 0.0001), non-English language (OR 2.09; 95% CI 1.7-2.57, p < 0.0001), residing in a neighborhood with financial insecurity (OR 1.10; 95% CI 1.01-1.25, p = 0.04), low air quality (OR 1.01; 95% CI 1.0-1.04, p = 0.05), housing insecurity (OR 1.32; 95% CI 1.16-1.5, p < 0.0001) or transportation insecurity (OR 1.11; 95% CI 1.02-1.23, p = 0.03), and living in senior living communities (OR 1.69; 95% CI 1.23-2.32, p = 0.001).Conclusionsisk of COVID-19 infection is higher among groups already affected by health disparities across age, race, ethnicity, language, income, and living conditions. Health promotion and disease prevention strategies should prioritize groups most vulnerable to infection and address structural inequities that contribute to risk through social and economic policy.
| S-EPMC7387879 | biostudies-literature
Project description: Not available
| S-BSST563 | biostudies-other
Project description:Individuals infected with the SARS-CoV-2 virus present with a wide variety of phenotypes ranging from asymptomatic to severe and even lethal outcomes. Past research has revealed a genetic haplotype on chromosome 3 that entered the human population via introgression from Neanderthals as the strongest genetic risk factor for the severe COVID-19 phenotype. However, the specific variants along this introgressed haplotype that contribute to this risk and the biological mechanisms that are involved remain unclear. Here, we assess the variants present on the risk haplotype for their likelihood of driving the severe COVID-19 phenotype. We do this by first exploring their impact on the regulation of genes involved in COVID-19 infection using a variety of population genetics and functional genomics tools. We then perform an locus-specific massively parallel reporter assay to individually assess the regulatory potential of each allele on the haplotype in a multipotent immune-related cell line. We ultimately reduce the set of over 600 linked genetic variants to identify 4 introgressed alleles that are strong functional candidates for driving the association between this locus and the severe COVID-19. These variants likely drive the locus’ impact on severity by putatively modulating the regulation of two critical chemokine receptor genes: CCR1 and CCR5. These alleles are ideal targets for future functional investigations into the interaction between host genomics and COVID-19 outcomes.
2023-02-09 | GSE176233 | GEO
Project description:ObjectiveTo investigate whether patients with clozapine treatment are at an increased risk of a more severe COVID-19 infection as compared with patients on other antipsychotic drugs.MethodsIn this register-based cohort study, all residents (age 18 or older) in the Stockholm Region with a psychotic disorder diagnosis and antipsychotic treatment were included (N = 8 233) and followed from 1 March 2020 to 14 January 2021. The exposure was defined as clozapine treatment and the outcome measures (indicating a more severe COVID-19 infection) were: inpatient care, care within intensive care unit or death due to COVID-19 infection. Differences in outcome rates between exposed (n = 966) and unexposed (other antipsychotics; n = 7 267) were examined using Cox proportional hazards models and expressed as hazard ratios (HR) with 95% confidence intervals (CI).ResultsNo statistically significant differences in outcome rates were found between the two groups of patients after adjusting for age, sex and residence in retirement homes. The adjusted HR for the exposed compared to the unexposed was 0.96 (95% CI: 0.54, 1.70) for inpatient care; 1.69 (0.48, 5.93) for care in intensive care unit (ICU); and 0.86 (0.26, 2.80) for death. Regarding inpatient care, additional adjusting for country of birth, living in socioeconomically vulnerable areas, number of care visits during the previous year, and comorbid medical illnesses did not alter the results.ConclusionsOur results may add support to the present guidelines, recommending sustained clozapine treatment during the current COVID-19 pandemic with careful monitoring and readiness to alter drug doses as needed.
| S-EPMC8653206 | biostudies-literature