Factors associated with hospital readmissions among patients with COVID-19: A single-center experience.

Identify factors associated with readmission after an index hospital admission for coronavirus disease 2019 (COVID-19) infection in a single center serving an underserved and predominantly minority population. This retrospective descriptive study included 275 patients who tested COVID-19 positive via reverse transcriptase-polymerase chain reaction assay at our institution and who survived the index hospitalization. The main outcomes were 1- and 6-month readmission rates after an index hospitalization for COVID-19. The mortality rate among the readmitted patients was also determined. Factors independently associated with readmission were investigated using multivariable logistic regression. A final sample of 275 patients was included. The mean age was 64.69 ± 14.64 (SD), 133 (48%) were female and 194 (70%) were African American. Their chronic medical conditions included hypertension 203 (74%) and diabetes mellitus 121 (44%). After the hospitalization, 1-month readmission rate was 7.6%, while 6-month readmission rate was 24%. Nine percent of patients who were readmitted subsequently died. Coronary artery disease (CAD) was significantly associated with 6-month readmission odds ratio (OR), 2.15 (95% confidence interval [CI]: 1.04-4.44; p = 0.039) after adjustment for age, gender, ethnicity, and comorbidities. Readmissions were due to cardiac, respiratory, and musculoskeletal symptoms. Hispanic ethnicity was associated with increased readmission OR, 3.16 (95% CI: 1.01-9.88; p = 0.048). No significant difference was found between inflammatory markers or clinical outcomes during the index hospitalization among patients who were readmitted compared to those who were not. A significant number of patients hospitalized for COVID-19 may be readmitted. The presence of CAD is independently associated with high rates of 6-month readmission.

Cytokine and cytokine receptor genes of the adaptive immune response are differentially associated with breast cancer risk in American women of African and European ancestry.

Disparities in breast cancer biology are evident between American women of African ancestry (AA) and European ancestry (EA) and may be due, in part, to differences in immune function. To assess the potential role of constitutional host immunity on breast carcinogenesis, we tested associations between breast cancer risk and 47 single nucleotide polymorphisms (SNPs) in 26 cytokine-related genes of the adaptive immune system using 650 EA (n = 335 cases) and 864 AA (n = 458 cases) women from the Women's Circle of Health Study (WCHS). With additional participant accrual to the WCHS, promising SNPs from the initial analysis were evaluated in a larger sample size (1,307 EAs and 1,365 AAs). Multivariate logistic regression found SNPs in genes important for T helper type 1 (Th1) immunity (IFNGR2 rs1059293, IL15RA rs2296135, LTA rs1041981), Th2 immunity (IL4R rs1801275), and T regulatory cell-mediated immunosuppression (TGFB1 rs1800469) associated with breast cancer risk, mainly among AAs. The combined effect of these five SNPs was highly significant among AAs (P-trend = 0.0005). When stratified by estrogen receptor (ER) status, LTA rs1041981 was associated with ER-positive breast cancers among EAs and marginally among AAs. Only among AA women, IL15 rs10833 and IL15RA rs2296135 were associated with ER-positive tumors, and IL12RB1 rs375947, IL15 rs10833 and TGFB1 rs1800469 were associated with ER-negative tumors. Our study systematically identified genetic variants in the adaptive immune response pathway associated with breast cancer risk, which appears to differ by ancestry groups, menopausal status and ER status.

Innate immunity pathways and breast cancer Risk in African American and European-American women in the Women's Circle of Health Study (WCHS).

African American (AA) women are more likely than European American (EA) women to be diagnosed with early, aggressive breast cancer. Possible differences in innate immune pathways (e.g., inflammatory responses) have received little attention as potential mechanisms underlying this disparity. We evaluated distributions of selected genetic variants in innate immune pathways in AA and EA women, and examined their associations with breast cancer risk within the Women's Circle of Health Study (WCHS). In stage I of the study (864 AA and 650 EA women) we found that genotype frequencies for 35 of 42 tested SNPs (18 candidate genes) differed between AAs and EAs (corroborated by ancestry informative markers). Among premenopausal AA women, comparing variant allele carriers to non-carriers, reduced breast cancer risk was associated with CXCL5-rs425535 (OR=0.61, P=0.02), while among EA women, there were associations with TNFA-rs1799724 (OR =2.31, P =0.002) and CRP-rs1205 (OR=0.54, P=0.01). For postmenopausal women, IL1B-rs1143627 (OR=1.80, P=0.02) and IL1B-rs16944 (OR=1.85, P =0.02) were associated with risk among EA women, with significant associations for TNFA-rs1799724 limited to estrogen receptor (ER) positive cancers (OR=2.0, P =0.001). However, none of the SNPs retained significance after Bonferroni adjustment for multiple testing at the level of P0.0012 (0.05/42) except for TNFA-rs1799724 in ER positive cancers. In a stage II validation (1,365 AA and 1,307 EA women), we extended evaluations for four SNPs (CCL2-rs4586, CRP-rs1205, CXCL5-rs425535, and IL1RN-rs4251961), which yielded similar results. In summary, distributions of variants in genes involved in innate immune pathways were found to differ between AA and EA populations, and showed differential associations with breast cancer according to menopausal or ER status. These results suggest that immune adaptations suited to ancestral environments may differentially influence breast cancer risk among EA and AA women.