Kass L
Department of Internal Medicine, University of Michigan, Ann Arbor.
CRC Crit Rev Clin Lab Sci. 1978;9(1):1-47. doi: 10.3109/10408367809150914.
Although readily treatable with vitamin B12, pernicious anemia continues to captivate investigative endeavors of those interested in the pathophysiology and pathogenesis of this disorder. Notable advances have been made in understanding properties of intrinsic factor, vitamin B12-binding proteins, structure and de novo synthesis of vitamin B12, mechanism of action of vitamin B12-dependent enzymes in man, and metabolic consequences of reduced activities of these enzymes in pernicious anemia. Similarly, newer morphological observations have given information regarding pathogenesis of some of the cytological abnormalities found in megaloblasts, and recent cytochemical studies have shed light on abnormalities of nuclear and cytoplasmic constituents in vitamin B12-deficient cells. Both cellular and humoral factors may contribute to immune-mediated processes in pernicious anemia, although as yet, it has not been established with certainty that pernicious anemia is an autoimmune disorder. As we look ahead, it will be important to define the process or processes responsible for atrophic gastritis, which is the pathophysiological basis of pernicious anemia. Likewise, advances in biophysics used in the study of cell membranes, cell surface phenomena, and metallic ion transport may find applicability in the study of pernicious anemia and perhaps provide further insights into metabolic abnormalities responsible for the development of megaloblastosis.
尽管恶性贫血可用维生素B12轻易治愈，但它仍继续吸引着那些对该疾病的病理生理学和发病机制感兴趣的人的研究努力。在理解内因子的特性、维生素B12结合蛋白、维生素B12的结构和从头合成、人体中维生素B12依赖性酶的作用机制以及这些酶活性降低在恶性贫血中的代谢后果方面已经取得了显著进展。同样，更新的形态学观察提供了有关巨幼细胞中发现的一些细胞学异常的发病机制的信息，最近的细胞化学研究揭示了维生素B12缺乏细胞中核和细胞质成分的异常。细胞和体液因素都可能促成恶性贫血中的免疫介导过程，尽管到目前为止，尚未确定恶性贫血是一种自身免疫性疾病。展望未来，确定导致萎缩性胃炎（恶性贫血的病理生理学基础）的一个或多个过程将很重要。同样，用于研究细胞膜、细胞表面现象和金属离子转运的生物物理学进展可能在恶性贫血的研究中得到应用，并可能为导致巨幼细胞形成的代谢异常提供进一步的见解。
