Karnaze D S, Carmel R
Arch Intern Med. 1987 Mar;147(3):429-31.
Serum cobalamin (vitamin B12) levels were analyzed retrospectively in 17 patients with primary degenerative dementia and 11 with specific demonstrable causes of dementia (secondary dementia). The prevalence of low cobalamin levels was significantly increased in primary dementia (29% vs 0% in secondary dementia). Because typical findings of deficiency often seemed absent, we prospectively studied two other patients with primary dementia and low cobalamin levels. Neither of these two had megaloblastic anemia; one had a normal Schilling test while the other's was borderline. Despite this absence of the expected findings, the deoxyuridine suppression test gave biochemical evidence of cobalamin deficiency in both cases. Our survey of 28 patients thus established that low serum cobalamin levels are frequent in primary dementia. Our findings in the two prospectively studied cases (as well as in some of the patients in the survey) indicate that these levels are associated in at least some cases with an atypical deficiency state rather than with disorders such as pernicious anemia. Such atypical deficiency states cannot be identified by classic hematological criteria or by the Schilling test.
对17例原发性退行性痴呆患者和11例有明确可证实病因的痴呆患者（继发性痴呆）的血清钴胺素（维生素B12）水平进行了回顾性分析。原发性痴呆患者中钴胺素水平低的患病率显著升高（原发性痴呆为29%，继发性痴呆为0%）。由于常常似乎没有缺乏的典型表现，我们对另外两名原发性痴呆且钴胺素水平低的患者进行了前瞻性研究。这两名患者均无巨幼细胞贫血；其中一名患者的希林试验结果正常，另一名患者的结果处于临界值。尽管缺乏预期的表现，但脱氧尿苷抑制试验在两例中均给出了钴胺素缺乏的生化证据。我们对28例患者的调查因此确定，血清钴胺素水平低在原发性痴呆中很常见。我们在两例前瞻性研究病例（以及调查中的一些患者）中的发现表明，这些水平至少在某些情况下与非典型缺乏状态相关，而非与恶性贫血等疾病相关。这种非典型缺乏状态无法通过经典血液学标准或希林试验来识别。
