Kurumazaki Mayuna, Ogawa Noriko, Kobayashi Mariko, Ikejiri Fumiyoshi, Kanasaki Keizo
Department of Internal Medicine 1, Shimane University Faculty of Medicine, Japan.
Okuizumo Town Hospital, Japan.
Intern Med. 2025 Aug 1;64(15):2338-2343. doi: 10.2169/internalmedicine.4723-24. Epub 2025 Jan 15.
We herein report a 56-year-old man with severe hypocalcemia during ruxolitinib therapy for myelofibrosis transitioning from Janus kinase 2 mutation-positive polycythemia vera. Blood transfusions were administered every one to two weeks for ruxolitinib-induced anemia. Blood tests revealed hypocalcemia with low tartrate-resistant acid phosphatase-5b, 25-hydroxyvitamin D (25 (OH) D), and 1,25-dihydroxyvitamin D (1,25 (OH) D) levels within the lower reference range. Intact-parathyroid hormone levels were relatively low compared to calcium levels. Severe hypocalcemia with ruxolitinib is rare and may be caused by a combination of factors, impaired vitamin D activation due to liver or renal insufficiency, accumulation of calcium-chelating agents from blood transfusions, and inadequate compensatory response to PTH.
我们在此报告一名56岁男性,在接受芦可替尼治疗骨髓纤维化(由Janus激酶2突变阳性的真性红细胞增多症转变而来)期间出现严重低钙血症。因芦可替尼引起的贫血,每1至2周进行一次输血。血液检查显示低钙血症,抗酒石酸酸性磷酸酶-5b、25-羟基维生素D(25(OH)D)和1,25-二羟基维生素D(1,25(OH)₂D)水平处于参考范围下限。与钙水平相比,完整甲状旁腺激素水平相对较低。芦可替尼导致的严重低钙血症较为罕见,可能由多种因素共同引起,包括肝肾功能不全导致维生素D活化受损、输血中钙螯合剂的蓄积以及对甲状旁腺激素的代偿反应不足。