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Ruhnke, Leo [Verfasser:in]; Stölzel, Friedrich [Verfasser:in]; Wagenführ, Lisa [Verfasser:in]; Altmann, Heidi [Verfasser:in]; Platzbecker, Uwe [Verfasser:in]; Herold, Sylvia [Verfasser:in]; Rump, Andreas [Verfasser:in]; Schröck, Evelin [Verfasser:in]; Bornhäuser, Martin [Verfasser:in]; Schetelig, Johannes [Verfasser:in]; von Bonin, Malte [Verfasser:in]

Case Report: ANXA2 Associated Life-Threatening Coagulopathy With Hyperfibrinolysis in a Patient With Non-APL Acute Myeloid Leukemia

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  • Medientyp: E-Artikel
  • Titel: Case Report: ANXA2 Associated Life-Threatening Coagulopathy With Hyperfibrinolysis in a Patient With Non-APL Acute Myeloid Leukemia
  • Beteiligte: Ruhnke, Leo [Verfasser:in]; Stölzel, Friedrich [Verfasser:in]; Wagenführ, Lisa [Verfasser:in]; Altmann, Heidi [Verfasser:in]; Platzbecker, Uwe [Verfasser:in]; Herold, Sylvia [Verfasser:in]; Rump, Andreas [Verfasser:in]; Schröck, Evelin [Verfasser:in]; Bornhäuser, Martin [Verfasser:in]; Schetelig, Johannes [Verfasser:in]; von Bonin, Malte [Verfasser:in]
  • Erschienen: Lausanne: Frontiers Research Foundation, [2023]
  • Erschienen in: Frontiers in oncology ; 11, (2021)
  • Sprache: Englisch
  • Schlagwörter: ANXA2 ; coagulopathy ; disseminated intravascular coagulation ; WES ; acute promyelocytic leukemia ; PDPN ; acute myeloid leukemia ; hyperfibrinolysis
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: Patients with acute promyelocytic leukemia (APL) often present with potentially lifethreateninghemorrhagic diathesis. The underlying pathomechanisms of APLassociatedcoagulopathy are complex. However, two pathways considered to be APLspecifichad been identified: 1) annexin A2 (ANXA2)-associated hyperfibrinolysis and 2)podoplanin (PDPN)-mediated platelet activation and aggregation. In contrast, sincedisseminated intravascular coagulation (DIC) is far less frequent in patients with non-APL acute myeloid leukemia (AML), the pathophysiology of AML-associated hemorrhagicdisorders is not well understood. Furthermore, the potential threat of coagulopathy in non-APL AML patients may be underestimated. Herein, we report a patient with non-APL AMLpresenting with severe coagulopathy with hyperfibrinolysis. Since his clinical courseresembled a prototypical APL-associated hemorrhagic disorder, we hypothesizedpathophysiological similarities. Performing multiparametric flow cytometry (MFC) andimmunofluorescence imaging (IF) studies, we found the patient’s bone-marrowmononuclear cells (BM-MNC) to express ANXA2 - a biomarker previously thought to beAPL-specific. In addition, whole-exome sequencing (WES) on sorted BM-MNC (leukemiaassociatedimmunophenotype (LAIP)1: ANXAlo, LAIP2: ANXAhi) demonstrated high intratumorheterogeneity. Since ANXA2 regulation is not well understood, further research todetermine the coagulopathy-initiating events in AML and APL is indicated. Moreover,ANXA2 and PDPN MFC assessment as a tool to determine the risk of life-threatening DICin AML and APL patients should be evaluated.
  • Zugangsstatus: Freier Zugang
  • Rechte-/Nutzungshinweise: Namensnennung (CC BY)