Vitamin B6 deficiency is prevalent in primary and secondary myelofibrosis patients

Vitamin B6 deficiency is prevalent in primary and secondary myelofibrosis patients
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DOI:
10.1007/s12185-019-02717-8
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发表时间:
2019-11-01
影响因子:
2.1
通讯作者:
Komatsu, Norio
Komatsu, Norio
中科院分区:
医学4区
文献类型:
--
作者:
Yasuda, Hajime;Tsutsui, Miyuki;Komatsu, Norio

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维生素B6(VB 6)缺乏有助于某些癌症的肿瘤发生和肿瘤进展,并且通常在癌症患者中普遍存在。VB 6也是血红素合成的必需元素,缺乏可导致贫血。原发性骨髓纤维化(PMF)和继发性骨髓纤维化(sMF)是骨髓增生性肿瘤,通常表现为贫血沿着其他血细胞减少。我们进行了一项前瞻性研究,以确定PMF和sMF患者是否患有VB 6缺乏症,以及VB 6缺乏症患者补充VB 6是否改善贫血。分析了12例PMF患者和11例sMF患者。23例患者中共有16例(69.6%)被发现有VB 6缺乏症,但VB 6补充磷酸吡哆醛水合物并没有提高缺乏症患者的血红蛋白水平。没有患者出现维生素B12、铁或铜缺乏。4例患者显示血清叶酸水平低于正常下限,8例患者显示血清锌水平低于正常下限;然而,这些缺陷是边缘性的,不太可能导致贫血。与维生素B6充足的患者相比,维生素B6缺乏的患者血清叶酸水平显着降低,血清铜水平显着升高。需要进一步研究VB 6缺乏与PMF/sMF病因的关系。
Vitamin B6 (VB6) deficiency contributes to oncogenesis and tumor progression in certain cancers, and is prevalent in cancer patients in general. VB6 is also an essential element of heme synthesis, and deficiency can lead to anemia. Primary myelofibrosis (PMF) and secondary myelofibrosis (sMF) are myeloproliferative neoplasms often presenting with anemia along with other cytopenias. We performed a prospective study to determine whether PMF and sMF patients suffer from VB6 deficiency, and whether VB6-deficient patients show improvement of anemias with VB6 supplementation. Twelve PMF patients and 11 sMF patients were analyzed. A total of 16 of 23 patients (69.6%) were found to have VB6 deficiency, but VB6 supplementation with pyridoxal phosphate hydrate did not elevate hemoglobin levels in deficient patients. None of the patients presented with vitamin B12, iron, or copper deficiencies. Four patients showed serum folate levels below the lower limit of normal and eight patients showed serum zinc levels below the lower limit of normal; however, these deficiencies were marginal and unlikely to contribute to anemia. Compared to VB6-sufficient patients, VB6-deficient patients showed significantly lower serum folate levels and higher serum copper levels. Studies elucidating the relationship of VB6 deficiency and etiology of PMF/sMF are warranted.