Racial Disparities in the SOFA Score Among Patients Hospitalized with COVID-19

BackgroundSequential Organ Failure Assessment (SOFA) score predicts probability of in-hospital mortality. Many crisis standards of care use SOFA score to allocate medical resources during the COVID-19 pandemic. Research QuestionAre SOFA scores disproportionately elevated among Non-Hispanic Black and Hispanic patients hospitalized with COVID-19, compared to Non-Hispanic White patients? Study Design and MethodsRetrospective cohort study conducted in Yale New Haven Health System, including 5 hospitals with total of 2681 beds. Study population drawn from consecutive patients aged [≥]18 admitted with COVID-19 from March 29th to August 1st, 2020. Patients excluded from the analysis if not their first admission with COVID-19, if they did not have SOFA score recorded within 24 hours of admission, if race and ethnicity data were not Non-Hispanic Black, Non-Hispanic White, or Hispanic, or if they had other missing data. The primary outcomes was SOFA score, with peak score within 24 hours of admission dichotomized as <6 or [≥]6. ResultsOf 2982 patients admitted with COVID-19, 2320 met inclusion criteria and were analyzed, of whom 1058 (45.6%) were Non-Hispanic White, 645 (27.8%) were Hispanic, and 617 (26.6%) were Non-Hispanic Black. Median age was 65.0 and 1226 (52.8%) were female. In univariate logistic screen and in full multivariate model, Non-Hispanic Black patients but not Hispanic patients had greater odds of an elevated SOFA score [≥]6 when compared to Non-Hispanic White patients (OR 1.49, 95%CI 1.11-1.99). InterpretationCrisis standards of care utilizing the SOFA score to allocate medical resources would be more likely to deny these resources to Non-Hispanic Black patients.

Atypical X-chromosome inactivation in an X;1 translocation patient demonstrating Xq28 functional disomy.

X-chromosome inactivation (XCI) is an epigenetic process used to regulate gene dosage in mammalian females by silencing genes on one X-chromosome. While the pattern of XCI is typically random in normal females, abnormalities of the X-chromosome may result in skewing due to disadvantaged cell growth. We describe a female patient with an X;1 translocation [46,X,t(X;1)(q28;q21)] and unusual pattern of XCI who demonstrates functional disomy of the Xq28 region distal to the translocation breakpoint. There was complete skewing of XCI in the patient, along with the atypical findings of an active normal X chromosome and an inactive derivative X. Characterization of the translocation revealed that the patient's Xq28 breakpoint interrupts the DKC1 gene. Molecular analysis of the breakpoint region revealed functional disomy of Xq28 genes distal to DKC1. We propose that atypical XCI occurred in the patient due to a post-inactivation cell selection mechanism likely initiated by disruption of DKC1. As a result, the pattern of XCI is opposite that of the expected for an X;autosome translocation. Therefore, we suggest the phenotypic abnormalities found in the patient are a result of functional disomy in the Xq28 region.