Ibrutinib effect in acquired von Willebrand syndrome secondary to Waldenström macroglobulinemia
The pathological increase of clonal IgM in Waldenström macroglobulinemia can be associated with acquired von Willebrand syndrome and can be a major risk of bleeding symptoms in this subgroup of patients with Waldenström macroglobulinemia. The Bruton tyrosine kinase inhibitor ibrutinib is one of the...
| Main Authors: | , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
SAGE Publishing
2021-08-01
|
| Series: | Therapeutic Advances in Hematology |
| Online Access: | https://doi.org/10.1177/20406207211039326 |
| _version_ | 1818910809584041984 |
|---|---|
| author | María Poza Rodrigo Íñiguez Irene Zamanillo Sara Redondo Rafael Alonso Joaquín Martínez-López Ana Jiménez-Ubieto |
| author_facet | María Poza Rodrigo Íñiguez Irene Zamanillo Sara Redondo Rafael Alonso Joaquín Martínez-López Ana Jiménez-Ubieto |
| author_sort | María Poza |
| collection | DOAJ |
| description | The pathological increase of clonal IgM in Waldenström macroglobulinemia can be associated with acquired von Willebrand syndrome and can be a major risk of bleeding symptoms in this subgroup of patients with Waldenström macroglobulinemia. The Bruton tyrosine kinase inhibitor ibrutinib is one of the approved treatments for symptomatic Waldenström macroglobulinemia. However, some controversy exists regarding the use of ibrutinib in these patients with high risk of bleeding because of its antiaggregant effect that could increase the risk of bleeding. Here, we present the case of a patient with Waldenström macroglobulinemia with associated acquired von Willebrand syndrome and progressively significant bleeding symptoms, who experienced a rapid increase in von Willebrand factor with ibrutinib treatment, despite only reaching a partial response in IgM levels similar to those reached with other previous treatments. We suggest that the control over the monoclonal protein is not the only mechanism that explains the good response, improvement in the bleeding symptoms and von Willebrand factor levels. This fact could be explained by the reduced glycoprotein Ib receptor expression induced by ibrutinib and the consequent von Willebrand factor increase in peripheral blood. |
| first_indexed | 2024-12-19T22:48:42Z |
| format | Article |
| id | doaj.art-cbb3befc6d664c8a9d79c5cf541c22a6 |
| institution | Directory Open Access Journal |
| issn | 2040-6215 |
| language | English |
| last_indexed | 2024-12-19T22:48:42Z |
| publishDate | 2021-08-01 |
| publisher | SAGE Publishing |
| record_format | Article |
| series | Therapeutic Advances in Hematology |
| spelling | doaj.art-cbb3befc6d664c8a9d79c5cf541c22a62022-12-21T20:02:53ZengSAGE PublishingTherapeutic Advances in Hematology2040-62152021-08-011210.1177/20406207211039326Ibrutinib effect in acquired von Willebrand syndrome secondary to Waldenström macroglobulinemiaMaría PozaRodrigo ÍñiguezIrene ZamanilloSara RedondoRafael AlonsoJoaquín Martínez-LópezAna Jiménez-UbietoThe pathological increase of clonal IgM in Waldenström macroglobulinemia can be associated with acquired von Willebrand syndrome and can be a major risk of bleeding symptoms in this subgroup of patients with Waldenström macroglobulinemia. The Bruton tyrosine kinase inhibitor ibrutinib is one of the approved treatments for symptomatic Waldenström macroglobulinemia. However, some controversy exists regarding the use of ibrutinib in these patients with high risk of bleeding because of its antiaggregant effect that could increase the risk of bleeding. Here, we present the case of a patient with Waldenström macroglobulinemia with associated acquired von Willebrand syndrome and progressively significant bleeding symptoms, who experienced a rapid increase in von Willebrand factor with ibrutinib treatment, despite only reaching a partial response in IgM levels similar to those reached with other previous treatments. We suggest that the control over the monoclonal protein is not the only mechanism that explains the good response, improvement in the bleeding symptoms and von Willebrand factor levels. This fact could be explained by the reduced glycoprotein Ib receptor expression induced by ibrutinib and the consequent von Willebrand factor increase in peripheral blood.https://doi.org/10.1177/20406207211039326 |
| spellingShingle | María Poza Rodrigo Íñiguez Irene Zamanillo Sara Redondo Rafael Alonso Joaquín Martínez-López Ana Jiménez-Ubieto Ibrutinib effect in acquired von Willebrand syndrome secondary to Waldenström macroglobulinemia Therapeutic Advances in Hematology |
| title | Ibrutinib effect in acquired von Willebrand syndrome secondary to Waldenström macroglobulinemia |
| title_full | Ibrutinib effect in acquired von Willebrand syndrome secondary to Waldenström macroglobulinemia |
| title_fullStr | Ibrutinib effect in acquired von Willebrand syndrome secondary to Waldenström macroglobulinemia |
| title_full_unstemmed | Ibrutinib effect in acquired von Willebrand syndrome secondary to Waldenström macroglobulinemia |
| title_short | Ibrutinib effect in acquired von Willebrand syndrome secondary to Waldenström macroglobulinemia |
| title_sort | ibrutinib effect in acquired von willebrand syndrome secondary to waldenstrom macroglobulinemia |
| url | https://doi.org/10.1177/20406207211039326 |
| work_keys_str_mv | AT mariapoza ibrutinibeffectinacquiredvonwillebrandsyndromesecondarytowaldenstrommacroglobulinemia AT rodrigoiniguez ibrutinibeffectinacquiredvonwillebrandsyndromesecondarytowaldenstrommacroglobulinemia AT irenezamanillo ibrutinibeffectinacquiredvonwillebrandsyndromesecondarytowaldenstrommacroglobulinemia AT sararedondo ibrutinibeffectinacquiredvonwillebrandsyndromesecondarytowaldenstrommacroglobulinemia AT rafaelalonso ibrutinibeffectinacquiredvonwillebrandsyndromesecondarytowaldenstrommacroglobulinemia AT joaquinmartinezlopez ibrutinibeffectinacquiredvonwillebrandsyndromesecondarytowaldenstrommacroglobulinemia AT anajimenezubieto ibrutinibeffectinacquiredvonwillebrandsyndromesecondarytowaldenstrommacroglobulinemia |