SARS-CoV-2 vaccine immunogenicity is commonly evaluated by measuring antibody titers against the SARS-CoV-2 Spike (S) protein. Previously, inferior humoral vaccination responses in patients with lymphoid malignancies have been shown. 1 This can be attributed to immune defects caused by disease or treatment. NHL and CLL treated with CD20-and MM with CD38-directed therapies, leads to longlasting B-or plasma-cell depletion, respectively. CLL and MM are associated with hypogammaglobulinemia and aberrations in T-cell function. T-cell immunity is vital for viral clearance and long-lasting protection against COVID-19 after vaccination. 2 Moreover, high CD8 + T-cells contribute to COVID-19 survival in hematological patients. 3 Studies investigating T-cell responses after vaccination in patients with lymphoid malignancies are, however, scarce and results are conflicting. This leaves a knowledge gap, underlining the urgency of an in-depth and reproducible analysis of functional SARS-CoV-2 specific T-cell responses following vaccination in hematological patients. Patients. Adult patients diagnosed with CLL, NHL, or MM at two tertiary care centers in the Netherlands undergoing SARS-CoV-2 vaccination were included in the study. Serological and T-cell responses
Vitamin C is an important micronutrient for various immune cells. It increases phagocytic cell function and is necessary for T and natural killer (NK) cell development. Patients in need of an autologous hematopoietic stem cell transplantation (HSCT) are often vitamin C-depleted. We therefore hypothesized that vitamin C supplementation could improve immune recovery in autologous HSCT patients. This blinded, placebo-controlled trial included 44 patients randomized to receive vitamin C or a placebo. The following outcome measures used were clinical and immunological parameters, among others: time to neutrophil recovery, serum, and intracellular vitamin C values. Twenty-one patients received vitamin C, and 23 received a placebo. The time to neutrophil recovery did not differ between the two groups at 11.2 days (p = 0.96). There were no differences in hospitalization time (19.7 vs. 19.1 days, p = 0.80), the incidence of neutropenic fever (57% vs. 78%, p = 0.20), or 3-month overall survival (90.5% vs. 100%, p = 0.13). Bacteremia seemed to occur less in the vitamin C group (10% vs. 35%, p = 0.07). Our study shows no benefit from vitamin C supplementation on neutrophil recovery and hospitalization, despite possible lower rates of bacteremia in the vitamin C group. Therefore, we do not advise vitamin C supplementation in this treatment group.
Patients referred for evaluation of bleeding symptoms occasionally have a prolonged platelet function analyser (PFA) closure time, without evidence for von Willebrand disease or impaired platelet aggregation. The aim of this study was to establish a shear-dependent platelet function defect in these patients. Patients were included based on high bleeding score and prior PFA prolongation. Common tests of von Willebrand factor (VWF) and platelet function and exome sequencing were performed. Microfluidic analysis of shear-dependent collagen-induced wholeblood thrombus formation was performed. In 14 PFA-only patients, compared to healthy volunteers, microfluidic tests showed significantly lower platelet adhesion and thrombus formation parameters. This was accompanied by lower integrin activation, phosphatidylserine exposure and P-selectin expression. Principal components analysis indicated VWF as primary explaining variable of PFA prolongation, whereas conventional platelet aggregation primarily explained the reduced thrombus parameters under shear. In five patients with severe microfluidic abnormalities, conventional platelet aggregation was in the lowest range of normal. No causal variants in Mendelian genes known to cause bleeding or platelet disorders were identified. Multiparameter assessment of whole-blood thrombus formation under shear indicates single or combined effects of low-normal VWF and low-normal platelet aggregation in these patients, suggesting a shear-dependent platelet function defect, not detected by static conventional haemostatic tests.
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