Transfusion · 2026
Acute pain transfusion reaction in a patient with thalassemia: In-depth characterization of short- and long-term phenotypes.
СтатьяКлинический случайНазвание и аннотация: Перевод в очереди
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Tzafa Georgia, Delicou Sophia, Barla Ioanna, Theocharaki Konstantina, Kondi Aggeliki, Velentzas Athanassios D, Simantiris Nikolaos, Stylianaki Elli-Anna, Mpekoulis George, Pavlou Efthymia, Vassilaki Niki, Kostopoulos Ioannis V, Xydaki Aikaterini, Nomikou Efrosyni, Aggeli Ioanna-Katerina, Thomaidis Nikolaos, Gikas Evangelos, Samiotaki Martina, Zoidakis Jerome, Politis Constantina, Antonelou Marianna H
Аннотация
BACKGROUND: Acute pain transfusion reaction (APTR) is a rare, under-recognized condition of unknown etiology. It can cause significant distress in recipients, necessitating symptomatic management and, occasionally, hospitalization.
STUDY DESIGN AND METHODS: Here, we present an APTR event in an adult subject with transfusion-dependent thalassemia (TDT). Patient and returned red blood cell (RBC) unit samples from this one, and additionally from preceding and subsequent transfusions, were compared with patient and unit reference groups, matched for genetic profile and storage duration, respectively, using laboratory, morphological, and multi-omics approaches.
RESULTS: The patient had a pre-transfusion hemoglobin concentration of 10.7 g/dL and evidence of coagulation and fibrinolysis. Following APTR, the patient RBCs showed acute oxidative stress, increased adhesiveness, phosphatidylserine exposure, and membrane-specific proteostatic failure. Multi-omics analyses revealed overexpression of biological response modifiers, like gamma-aminobutyric acid derivatives, RANTES/DARC, and ongoing ephrin-B reverse signaling. The implicated RBC unit displayed advanced storage lesions with overexpression of ophthalmate and STEAP3, among others, metabolic aging not matching its "chronological age", and differential expression of potential immune mediators and neuromodulators. Functional enrichment analysis linked the differential proteome profile of the unit with RBC dysfunction and neuropathy. APTR-related pathologies showed only partial resolution over a two-week period, indicating sustained disturbances in proteostasis and hypercoagulability, as evidenced, among other markers, by thrombospondin binding to patient RBCs.
DISCUSSION: This study identified a series of patient and RBC unit stress markers and conditions potentially linked to APTR. These hypothesis-generating variables and molecular signatures may facilitate prospective evaluation and mechanistic investigation of suspected APTR cases.
STUDY DESIGN AND METHODS: Here, we present an APTR event in an adult subject with transfusion-dependent thalassemia (TDT). Patient and returned red blood cell (RBC) unit samples from this one, and additionally from preceding and subsequent transfusions, were compared with patient and unit reference groups, matched for genetic profile and storage duration, respectively, using laboratory, morphological, and multi-omics approaches.
RESULTS: The patient had a pre-transfusion hemoglobin concentration of 10.7 g/dL and evidence of coagulation and fibrinolysis. Following APTR, the patient RBCs showed acute oxidative stress, increased adhesiveness, phosphatidylserine exposure, and membrane-specific proteostatic failure. Multi-omics analyses revealed overexpression of biological response modifiers, like gamma-aminobutyric acid derivatives, RANTES/DARC, and ongoing ephrin-B reverse signaling. The implicated RBC unit displayed advanced storage lesions with overexpression of ophthalmate and STEAP3, among others, metabolic aging not matching its "chronological age", and differential expression of potential immune mediators and neuromodulators. Functional enrichment analysis linked the differential proteome profile of the unit with RBC dysfunction and neuropathy. APTR-related pathologies showed only partial resolution over a two-week period, indicating sustained disturbances in proteostasis and hypercoagulability, as evidenced, among other markers, by thrombospondin binding to patient RBCs.
DISCUSSION: This study identified a series of patient and RBC unit stress markers and conditions potentially linked to APTR. These hypothesis-generating variables and molecular signatures may facilitate prospective evaluation and mechanistic investigation of suspected APTR cases.