Actual Incidence of Transfusion-Related Adverse Reactions Compared with Transfusion-Related Signs or Symptoms and by Each Blood Product / 대한수혈학회지

BACKGROUND: Transfusion-related adverse reaction is detected based on patients' adverse signs or symptoms during or after transfusion. We analyzed the actual incidence of transfusion-related adverse reactions by investigating diagnosed cases among reported signs or symptoms, and reexamined our transfusion-related adverse reaction reporting system. METHODS: From January to June, 2015, there were 4,234 cases of transfusion and 18,191 units of blood product were used. During transfusion, patients' signs or symptoms were checked and reported by the medical team at least three times, 5 minutes after transfusion started, during transfusion, and after transfusion, using the electronic reporting system in the blood bank. A laboratory medicine doctor investigated reported signs or symptoms by reviewing patients' electronic medical records, diagnosed transfusion-related adverse reaction by textbook definition, and surveyed actual incidence. In addition, incidence of transfusion-related signs or symptoms and transfusionrelated adverse reaction by each blood product was determined. RESULTS: Out of 1,091 transfusion-related signs or symptoms, only 226 cases (20.71%) were diagnosed with transfusion-related adverse reaction. Among these, most common cases were febrile nonhemolytic reaction with incidence of 0.91%, followed by allergic reaction with 0.32%. The incidence of transfusion-related adverse reaction by each blood product was highest for leukocyte-reduced red blood cells 3.41% and apheresis platelets 2.59%. Febrile nonhemolytic reaction was mainly related to red blood cells and allergic reaction was mainly related to platelets. CONCLUSION: The actual incidence of transfusion-related adverse reaction was only 20% of transfusion-related signs or symptoms. Therefore, reforming the reporting system and transfusion-related clinical inspection and education are required.

Role of TGF-beta in Survival of Phagocytizing Microglia: Autocrine Suppression of TNF-alpha Production and Oxidative Stress

Microglia are recognized as residential macrophageal cells in the brain. Activated microglia play a critical role in removal of dead or damaged cells through phagocytosis activity. During phagocytosis, however, microglia should survive under the harmful condition of self-producing ROS and pro-inflammatory mediators. TGF-beta has been known as a classic anti-inflammatory cytokine and controls both initiation and resolution of inflammation by counter-acting inflammatory cytokines. In the present study, to understand the self-protective mechanism, we studied time-dependent change of TNF-alpha and TGF-beta production in microglia phagocytizing opsonized-beads (i.e., polystyrene microspheres). We found that microglia phagocytized opsonized-bead in a time-dependent manner and simultaneously produced both TNF-alpha and TGF-beta. However, while TNF-alpha production gradually decreased after 6 h, TGF-beta production remained at increased level. Microglial cells pre-treated with lipopolysaccharides (a strong immunostimulant, LPS) synergistically increased the production of TNF-alpha and TGF-beta both. However, LPS-pretreated microglia produced TNF-alpha in a more sustained manner and became more vulnerable, probably due to the marked and sustained production of TNF-alpha and reduced TGF-beta. Intracellular oxidative stress appears to change in parallel with the microglial production of TNF-alpha. These results indicate TGF-beta contributes for the survival of phagocytizing microglia through autocrine suppression of TNF-alpha production and oxidative stress.