Plateletpheresis-associated lymphopenia in frequent platelet donors.

More than 1 million apheresis platelet collections are performed annually in the United States. After 2 healthy plateletpheresis donors were incidentally found to have low CD4+ T-lymphocyte counts, we investigated whether plateletpheresis causes lymphopenia. We conducted a cross-sectional single-center study of platelet donors undergoing plateletpheresis with the Trima Accel, which removes leukocytes continuously with its leukoreduction system chamber. We recruited 3 groups of platelet donors based on the total number of plateletpheresis sessions in the prior 365 days: 1 or 2, 3 to 19, or 20 to 24. CD4+ T-lymphocyte counts were <200 cells per microliter in 0/20, 2/20, and 6/20 donors, respectively (P = .019), and CD8+ T-lymphocyte counts were low in 0/20, 4/20, and 11/20 donors, respectively (P < .001). The leukoreduction system chamber's lymphocyte-extraction efficiency was ∼15% to 20% for all groups. Immunophenotyping showed decreases in naive CD4+ T-lymphocyte and T helper 17 (Th17) cell percentages, increases in CD4+ and CD8+ effector memory, Th1, and regulatory T cell percentages, and stable naive CD8+ and Th2 percentages across groups. T-cell receptor repertoire analyses showed similar clonal diversity in all groups. Donor screening questionnaires supported the good health of the donors, who tested negative at each donation for multiple pathogens, including HIV. Frequent plateletpheresis utilizing a leukoreduction system chamber is associated with CD4+ and CD8+ T-cell lymphopenia in healthy platelet donors. The mechanism may be repeated extraction of these cells during plateletpheresis. The cytopenias do not appear to be harmful.

Predictors of Poor Outcomes for COVID-19-Associated Pneumonia in a Minority Population.

Background In December 2019, an unprecedented outbreak of pneumonia of unknown etiology emerged in Wuhan City, Hubei province in China. A novel coronavirus was identified as the causative agent and was subsequently termed COVID-19 by the World Health Organization (WHO). It rapidly became a pandemic, and it has been a significant challenge to healthcare providers to predict outcomes of the infected patients.  Objective  The aim of this study was to investigate the clinical characteristics of patients admitted for COVID-19 infection in an Inner-City Hospital in New York City, to assess the correlation between inflammatory markers and outcomes prediction in a high-risk population. Methods  We identified 235 patients who were admitted to our Hospital in NYC between March 19th and April 25th, 2020 with laboratory confirmed COVID-19 diagnosis with associated pneumonia and who also had documented inflammatory markers (D-dimer, C-reactive protein, lactate dehydrogenase, ferritin, procalcitonin) during their hospital stay.  Results  The study population was predominantly non-Hispanic black. There was no statistically significant difference between survivors and non-survivors by race and/or ethnicity (P = 0.69). Thirty-five percent of the patient population had died by the end of this study and those that died had a higher mean age compared to survivors (69.5 ± 13.6 vs 63.8 ± 15.2, P = 0.004). There is a significant difference in the D-dimer levels in patients who survivedwhen compared to those who died (P = 0.002). A higher proportion of patients that died were admitted to the ICU, (23.7% vs 55.4%, P < 0.0001) and/or intubated (18.4% vs 51.8%, P < 0.0001). Conclusion Our study demonstrated that patients who died had a significantly higher D-dimer (>3,000) when compared with survivors. Higher mean age was associated with increased mortality and admission to ICU and/or intubation.