Altered Expression Levels of CD59, but Not CD55, on Red Blood Cells in Stored Blood.

OBJECTIVE: Red blood cells (RBCs) in storage undergo structural and biochemical changes that may cause functional effects. Studies exploring structural changes affecting the expression levels of CD55 and CD59 on RBCs are limited. The aim of this study was to investigate the pattern of CD55 and CD59 expression on RBCs in stored blood from Arab donors. MATERIALS AND METHODS: Flow-cytometric analysis was performed on RBCs from 92 packed RBC (PRBC) units, stored for varying times, and from 56 nonstored RBC from healthy controls using the commercial REDQUANT kit. RESULTS: The proportions of CD55- and CD59-deficient RBCs from stored PRBC units did not significantly differ when compared with those from healthy controls; however, the mean fluorescent intensity (MFI) of CD59 expression, but not MFI of CD55 expression, on RBCs from stored PRBC units was significantly reduced when compared to the expression of RBCs from healthy controls (p = 0.02). MFI of CD55 expression on RBCs from PRBC units did not significantly differ among the 3 groups of stored RBC; however, there was a statistically significant time-dependent preferential decline in MFI of CD59 expression on RBCs from stored PRBC units (p < 0.01). CONCLUSION: There is a preferential time-dependent decline in the expression of CD59, but not of CD55, on stored RBCs, the in vivo significance of which in relation to the response to PRBC transfusion needs further investigation.

Altered Expression Pattern of CD55 and CD59 on Red Blood Cells in Anemia of Chronic Kidney Disease.

OBJECTIVE: The aim of this study was to investigate the expression pattern of CD55 and CD59 on red blood cells (RBCs) in anemic chronic kidney disease (CKD) patients, and factors that might influence their expression. SUBJECTS AND METHODS: Nighty-one adult anemic CKD patients and 80 healthy controls (HCs) were enrolled. Anemic CKD patients were divided into 3 subgroups based on receiving erythropoietin and renal replacement therapies. Flow cytometric analysis of CD55 and CD59 expression was performed on RBCs from blood samples obtained from CKD patients and HCs. RESULTS: CD59 deficiency was significantly higher among CKD patients than HCs (n = 68, 74.7%, vs. n = 13, 16.3%, respectively; p < 0.001). The median proportions of CD55- and CD59-deficient RBCs in CKD patients were significantly higher compared to HCs (0.34 vs. 0.15, and 4.3 vs. 2.0, p < 0.001 and p < 0.001, respectively). The mean fluorescence intensity (MFI) of CD55 and CD59 expression was significantly lower in CKD patients compared to HCs (1.2 vs. 2.8, and 17.0 vs. 20.3, p < 0.04 and p < 0. 001, respectively). The hemoglobin level was inversely correlated with the proportions of CD55- and CD59-deficient RBCs (r = -0.37, p < 0.001, and r = -0.22, p < 0.02, respectively). The number of CD59-deficient patients was significantly different between the 3 subgroups of CKD patients (p = 0.001), and a significant difference was present in the MFI of CD55 and CD59 expression among the 3 subgroups (p = 0.04 and p = 0.03, respectively). CONCLUSION: The expression pattern of CD55 and CD59 on RBCs is altered in anemic CKD patients, which could play a role in the pathogenesis of anemia in CKD.

Expression pattern of CD55 and CD59 on red blood cells in sickle cell disease.

OBJECTIVES: To investigate the pattern of CD55 and CD59 expression on RBCs of SCD patients, and its association with anemia, biochemical parameters of hemolysis, level of erythropoietin, and pro-inflammatory markers. METHODS: Flow cytometric analysis was performed on RBCs from 71 adult SCD patients and 53 healthy controls, using the commercial REDQUANT kit. RESULTS: CD59 deficiency was significantly higher among SCD patients than among healthy controls. The proportions of CD55-deficient and CD59-deficient RBCs from SCD patients were significantly higher when compared with those from healthy controls (0.17 vs. 0.09 and 2.1 vs. 1.2, respectively). The MFI of CD55 and CD59 expression on RBCs in SCD was significantly reduced when compared to the expression in healthy controls (5.2 vs. 6.4 and 19.4 vs 20.3, respectively). The pattern of CD55 and CD59 expression was not correlated with anemia, biomarkers of hemolysis, erythropoietin level, or other pro-inflammatory markers. DISCUSSION: There is an altered pattern of CD55 and CD59 expression on RBCs of SCD Patients; however, it does not seem to play a causal role in the pathophysiology of anemia, and is unlikely to be influenced by the level of erythropoietin or other inflammatory mediators.

Circulating cell-free DNA in sickle cell disease: is it a potentially useful biomarker?

CONTEXT: Vascular occlusion in sickle cell disease causes increased levels of plasma cell-free DNA as a result of cell death and tissue damage. OBJECTIVES: This study investigates plasma cell-free DNA concentrations in sickle cell disease patients, and aims at exploring the significance of plasma cell-free DNA as a potential biomarker in predicting its complications. DESIGN: Plasma cell-free DNA levels were measured using real-time quantitative polymerase chain reaction to quantitatively measure ß-globin gene in blood samples from 57 sickle cell disease patients with acute vaso-occlusive crisis, 42 patients in steady state, 16 individuals with sickle cell trait, and 40 healthy controls. RESULTS: Plasma cell-free DNA level was significantly elevated in samples from patients with acute vaso-occlusive crisis when compared with those in steady state (P = .002), and was significantly higher both in crisis and in steady state when compared with individuals with sickle cell trait and healthy controls (P < .001). There was no difference in cell-free DNA levels between individuals with sickle cell trait and healthy controls. There was no association between plasma cell-free DNA levels and various clinical complications of sickle cell disease and comorbidity. CONCLUSIONS: Plasma cell-free DNA, as quantified by polymerase chain reaction amplification of the ß-globin and human telomerase reverse transcriptase genes, is increased in sickle cell disease patients in vaso-occlusive crisis and in steady state compared with individuals with sickle cell trait and healthy controls, and may be used as a tool to diagnose and monitor the sickle cell crisis and differentiate post-packed red cell transfusion sickle cell disease patients from individuals with sickle cell trait.

Blood transfusion practice in critically ill patients: a single institutional experience.

OBJECTIVES: To assess the transfusion practice in the intensive care unit (ICU) in a general hospital in Kuwait relative to indications, pretransfusion hemoglobin, red blood cell (RBC) use and outcome. SUBJECTS AND METHODS: 475 patients were admitted to the ICU during the study period (January 2009 to February 2010). Ninety-nine received RBC transfusion. Demographic, clinical and transfusion data were prospectively collected for the 99 patients who were followed up for 30 days, until hospital discharge, or death, whichever occurred first. Indications for RBC transfusion included hemorrhage in 39 patients, improving oxygen-carrying capacity in 55, and hemolysis in 5. RESULTS: Of the 99 transfused patients, 22 (22.22%) were also transfused after discharge from the ICU. Transfusions were more frequent in patients admitted with respiratory failure (30, 30.3%), hemorrhagic shock (24, 24.2%), and septic shock (18, 18.4%). The mean pretransfusion hemoglobin in ICU transfusions was statistically different (70.9 ± 12.7 g/l) from transfusions after discharge (79.7 ± 9.4 g/l) (p < 0.001). Longer ICU stay was associated with more RBC units transfused per transfusion episode per patient (p < 0.001). The Sequential Organ Failure Assessment (SOFA) score was significantly associated with the number of RBC units transfused per patient (p = 0.006). Mortality was significantly associated with Acute Physiology and Chronic Health Evaluation II and SOFA scores, the need and duration for mechanical ventilation, and the length of stay in hospital. CONCLUSION: Intensivists in our center followed a restrictive transfusion practice, by adopting a low pretransfusion hemoglobin threshold. Decisions on RBC transfusions seemed in most cases to be based on a 'transfusion trigger' rather than a physiologic need.