The Amelioration of Myelofibrosis with Thrombocytopenia by a JAK1/2 Inhibitor, Ruxolitinib, in a Post-polycythemia Vera Myelofibrosis Patient with a <i>JAK2</i> Exon 12 Mutation
-
- Ikeda Kazuhiko
- Department of Hematology, Fukushima Medical University, Japan Department of Transfusion and Transplantation Immunology, Fukushima Medical University, Japan
-
- Ueda Koki
- Department of Hematology, Fukushima Medical University, Japan
-
- Sano Takahiro
- Department of Hematology, Fukushima Medical University, Japan
-
- Ogawa Kazuei
- Department of Hematology, Fukushima Medical University, Japan
-
- Ikezoe Takayuki
- Department of Hematology, Fukushima Medical University, Japan
-
- Hashimoto Yuko
- Department of Pathology and Diagnostic Pathology, Fukushima Medical University, Japan
-
- Morishita Soji
- Department of Transfusion Medicine and Stem Cell Regulation, Juntendo University Graduate School of Medicine, Japan
-
- Komatsu Norio
- Department of Hematology, Juntendo University School of Medicine, Japan
-
- Ohto Hitoshi
- Department of Transfusion and Transplantation Immunology, Fukushima Medical University, Japan
-
- Takeishi Yasuchika
- Department of Cardiovascular Medicine, Fukushima Medical University, Japan
この論文をさがす
抄録
<p>Less than 5% of patients with polycythemia vera (PV) show JAK2 exon 12 mutations. Although PV patients with JAK2 exon 12 mutations are known to develop post-PV myelofibrosis (MF) as well as PV with JAK2V617F, the role of JAK inhibitors in post-PV MF patients with JAK2 exon 12 mutations remains unknown. We describe how treatment with a JAK1/2 inhibitor, ruxolitinib, led to the rapid amelioration of marrow fibrosis, erythrocytosis and thrombocytopenia in a 77-year-old man with post-PV MF who carried a JAK2 exon 12 mutation (JAK2H538QK539L). This case suggests that ruxolitinib is a treatment option for post-PV MF in patients with thrombocytopenia or JAK2 exon 12 mutations. </p>
収録刊行物
-
- Internal Medicine
-
Internal Medicine 56 (13), 1705-1710, 2017
一般社団法人 日本内科学会