{"title":"储存CPDA-1全血细胞因子谱分析。","authors":"R Grunenberg, J Krüger","doi":"10.1159/000223145","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>The pathophysiologic mechanisms of symptoms of nonhemolytic febrile transfusion reactions (NHFTR) are complex and sometimes poorly understood. The prevalence of these reactions especially with platelet transfusions has been attributed more recently to storage-dependent cytokine levels. Until now cytokine concentrations in whole blood (WB) have found very little attention though WB is still relevant to autologous blood and a systematic evaluation of the storage lesion of WB remains of general interest.</p><p><strong>Methods: </strong>Concentrations of interleukins (IL-1beta, IL-6, IL-8), granulocyte-macrophage colony stimulating factor (GM-CSF), and tumor necrosis factors (TNF-alpha, TNF-beta) were analyzed in blood samples drawn from 7 units of WB over a storage period of 35 days. All cytokine concentrations were determined by enzyme immunoassays.</p><p><strong>Results: </strong>IL-1beta, IL-8 increased steadily in all units and TNF-beta in 3 out of 7 from undetectable levels to concentrations of the lower standard ranges. IL-6 and TNF-alpha showed a mean low level plateau. On GM-CSF release storage seemed to have a minor transient effect.</p><p><strong>Conclusions: </strong>It seems questionable that on storage the presence of cytokines in WB reaches concentrations sufficient to explain NHFTR. At present the depletion of leukocytes as the main source of cytokines may not be necessary to be carried to the extreme.</p>","PeriodicalId":13632,"journal":{"name":"Infusionstherapie und Transfusionsmedizin","volume":"22 5","pages":"292-4"},"PeriodicalIF":0.0000,"publicationDate":"1995-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000223145","citationCount":"17","resultStr":"{\"title\":\"Analysis of cytokine profiles of stored CPDA-1 whole blood.\",\"authors\":\"R Grunenberg, J Krüger\",\"doi\":\"10.1159/000223145\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>The pathophysiologic mechanisms of symptoms of nonhemolytic febrile transfusion reactions (NHFTR) are complex and sometimes poorly understood. The prevalence of these reactions especially with platelet transfusions has been attributed more recently to storage-dependent cytokine levels. Until now cytokine concentrations in whole blood (WB) have found very little attention though WB is still relevant to autologous blood and a systematic evaluation of the storage lesion of WB remains of general interest.</p><p><strong>Methods: </strong>Concentrations of interleukins (IL-1beta, IL-6, IL-8), granulocyte-macrophage colony stimulating factor (GM-CSF), and tumor necrosis factors (TNF-alpha, TNF-beta) were analyzed in blood samples drawn from 7 units of WB over a storage period of 35 days. All cytokine concentrations were determined by enzyme immunoassays.</p><p><strong>Results: </strong>IL-1beta, IL-8 increased steadily in all units and TNF-beta in 3 out of 7 from undetectable levels to concentrations of the lower standard ranges. IL-6 and TNF-alpha showed a mean low level plateau. On GM-CSF release storage seemed to have a minor transient effect.</p><p><strong>Conclusions: </strong>It seems questionable that on storage the presence of cytokines in WB reaches concentrations sufficient to explain NHFTR. At present the depletion of leukocytes as the main source of cytokines may not be necessary to be carried to the extreme.</p>\",\"PeriodicalId\":13632,\"journal\":{\"name\":\"Infusionstherapie und Transfusionsmedizin\",\"volume\":\"22 5\",\"pages\":\"292-4\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1995-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1159/000223145\",\"citationCount\":\"17\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Infusionstherapie und Transfusionsmedizin\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1159/000223145\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Infusionstherapie und Transfusionsmedizin","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000223145","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Analysis of cytokine profiles of stored CPDA-1 whole blood.
Background: The pathophysiologic mechanisms of symptoms of nonhemolytic febrile transfusion reactions (NHFTR) are complex and sometimes poorly understood. The prevalence of these reactions especially with platelet transfusions has been attributed more recently to storage-dependent cytokine levels. Until now cytokine concentrations in whole blood (WB) have found very little attention though WB is still relevant to autologous blood and a systematic evaluation of the storage lesion of WB remains of general interest.
Methods: Concentrations of interleukins (IL-1beta, IL-6, IL-8), granulocyte-macrophage colony stimulating factor (GM-CSF), and tumor necrosis factors (TNF-alpha, TNF-beta) were analyzed in blood samples drawn from 7 units of WB over a storage period of 35 days. All cytokine concentrations were determined by enzyme immunoassays.
Results: IL-1beta, IL-8 increased steadily in all units and TNF-beta in 3 out of 7 from undetectable levels to concentrations of the lower standard ranges. IL-6 and TNF-alpha showed a mean low level plateau. On GM-CSF release storage seemed to have a minor transient effect.
Conclusions: It seems questionable that on storage the presence of cytokines in WB reaches concentrations sufficient to explain NHFTR. At present the depletion of leukocytes as the main source of cytokines may not be necessary to be carried to the extreme.