Frenkel E P, Yardley D A
Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas, USA.
Hematol Oncol Clin North Am. 2000 Oct;14(5):1079-100, viii. doi: 10.1016/s0889-8588(05)70172-6.
Classically, deficiency of folic acid (folate) or vitamin B12 (cobalamin) was recognized by the presence of a macrocytic anemia resulting from megaloblastic changes in the bone marrow. A markedly changing paradigm has identified both new mechanisms for altered folate and cobalamin status and new sequelae and clinical interrelationships that include altered mechanisms of absorption, a changing pattern of neurologic deficits, an increased risk of vascular occlusive lesions, and an important relationship with the mechanisms of neoplastic transformation. Several of these newer characterizations relate to issues of neoplasia in the nonpregnant woman and to issues in pregnancy, such as the potential for developmental abnormalities of the fetal nervous system.
传统上,叶酸或维生素B12缺乏是通过骨髓巨幼细胞改变导致的大细胞性贫血来识别的。一个显著变化的范例已经确定了叶酸和钴胺素状态改变的新机制,以及新的后遗症和临床相互关系,包括吸收机制改变、神经功能缺损模式变化、血管闭塞性病变风险增加,以及与肿瘤转化机制的重要关系。其中一些新特征与非孕妇的肿瘤形成问题以及妊娠问题有关,比如胎儿神经系统发育异常的可能性。