Screening out the Exposome to Improve Transfusion Quality.
Screening out the Exposome to Improve Transfusion Quality.
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DOI：
10.1097/hs9.0000000000000605
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发表时间：
2021-07
期刊：
影响因子：
6.6
通讯作者：
Vinchi F
中科院分区：
文献类型：
--
作者：
DeSimone RA;Vinchi F
DeSimone and Vinchi Screening out the Exposome glycolysis and function under physiological and pathological conditions. One blood donor in the study had ranitidine detected, and RBCs from this donor showed, as predicted, elevated S1P metabolism and S1P-regulated glycolysis with a decrease in several metabolic storage lesion markers, including markers of poor posttransfusion recovery such as hypoxanthine, arachidonic acid, and 12-hydroxyeicosatetraeonic acid. The authors further confirmed their findings by showing that ranitidine boosted S1P levels and glycolysis in a dose-dependent fashion in human and murine wild-type RBCs, but not in Sphk1-KO RBCs. Lastly, a proteome integral solubility alteration assay suggested a number of potential interactions of ranitidine with human RBCs, including hemoglobin subunits and several enzymes involved in redox homeostasis, glutathione synthetase, guanosine monophosphate metabolism, structural homeostasis, vesiculation, and protein degradation.The authors’ findings have several implications for the field of transfusion medicine. As the blood donor population ages in the United States, donors will progressively be exposed to more and more medications to maintain health. It is important to understand how drugs impact RBC physiology and metabolism as units from these donors are used routinely for transfusion. In their study, a striking 65.1% of FDA-approved medications showed a significant effect on RBC metabolism. Although the authors present an example of a medication that may enhance RBC storage, which can have implications for improving RBC storage and quality, it is also important to be mindful of medications with potential detrimental effects on RBC metabolism. Decreased transfusion efficacy has important implications for all patients, but especially for those receiving chronic transfusions throughout their lifespan such as in sickle cell disease or thalassemia. Every additional transfusion in these patients can be associated with alloantibody formation, which can make future blood more difficult to obtain, as well as transfusion reactions and increased iron overload. Although blood donor recruitment continues to be challenging, the age of personalized transfusion medicine is exhilarating, and these recent findings suggest that we will soon be able to provide units with enhanced efficacy and safety by screening out harmful donor exposures.
