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一名肝硬化患者在接受JAK1/2抑制剂治疗骨髓纤维化期间发生严重低钙血症

Severe Hypocalcemia During JAK1/2 Inhibitor Therapy for Myelofibrosis in a Patient with Liver Cirrhosis.

作者信息

Kurumazaki Mayuna, Ogawa Noriko, Kobayashi Mariko, Ikejiri Fumiyoshi, Kanasaki Keizo

机构信息

Department of Internal Medicine 1, Shimane University Faculty of Medicine, Japan.

Okuizumo Town Hospital, Japan.

出版信息

Intern Med. 2025 Aug 1;64(15):2338-2343. doi: 10.2169/internalmedicine.4723-24. Epub 2025 Jan 15.

Abstract

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.

摘要

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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6783/12393966/1bfdc8c5aed5/1349-7235-64-15-2338-g001.jpg

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