Carmel R
University of Southern California School of Medicine, Los Angeles 90033, USA.
Baillieres Clin Haematol. 1995 Sep;8(3):639-55. doi: 10.1016/s0950-3536(05)80224-0.
Food-cobalamin malabsorption is marked by the inability to release cobalamin from food, which therefore cannot be taken up by intrinsic factor for absorption. The defect is not detectable by classical clinical tests like the Schilling test which are all based on the absorption of free, crystalline cobalamin. Tests of food-cobalamin absorption have been devised, the most popular ones using cobalamin bound to eggs or to chicken serum. The disparity between the abnormal results of these tests and the normal results with the Schilling test defines the disorder of food-cobalamin malabsorption. Release of cobalamin from food requires acid and pepsin, and most food-cobalamin malabsorptive states can be traced to gastric defects. However, other mechanisms may also play a role. The malabsorption is limited to food cobalamin and any free cobalamin, presumably including recycled biliary cobalamin, will be absorbed normally, which may explain its frequently insidious nature. The effect on cobalamin status covers a broad spectrum. At one extreme, some individuals, perhaps in the earliest stages, have normal cobalamin status, while at the other extreme may be found deficiency every bit as severe as in the most florid case of pernicious anaemia. Most often, however, the deficiency is mild, frequently marked by only a low serum cobalamin level, mild evidence of metabolic insufficiency and, sometimes, minimal clinical sequelae. Moreover, in some cases the gastric defect progresses and intrinsic factor secretion is affected, thus transforming into classical pernicious anaemia; this is not inevitable, however, and probably occurs in only a minority of patients. The course of food-cobalamin malabsorption is therefore a varied one. Nevertheless, it may be the most common cause of subtle or mild cobalamin deficiency and it is also sometimes associated with severe deficiency. Its identification and treatment need to be considered more widely in the clinical setting.
食物性钴胺素吸收不良的特征是无法从食物中释放钴胺素，因此钴胺素无法被内因子摄取以供吸收。这种缺陷无法通过像希林试验这样的传统临床检测方法检测出来，因为这些检测方法都是基于游离结晶钴胺素的吸收情况。人们已经设计出了食物性钴胺素吸收试验，其中最常用的是使用与鸡蛋或鸡血清结合的钴胺素。这些试验的异常结果与希林试验的正常结果之间的差异定义了食物性钴胺素吸收不良这种病症。从食物中释放钴胺素需要胃酸和胃蛋白酶，大多数食物性钴胺素吸收不良状态可追溯到胃部缺陷。然而，其他机制可能也起作用。这种吸收不良仅限于食物中的钴胺素，任何游离钴胺素，大概包括循环的胆汁钴胺素，都会被正常吸收，这可能解释了其常见的隐匿性。对钴胺素状态的影响范围很广。在一个极端情况下，一些个体，可能处于最早阶段，钴胺素状态正常，而在另一个极端则可能发现与最严重的恶性贫血病例一样严重的缺乏症。然而，大多数情况下，缺乏症是轻微的，通常仅表现为血清钴胺素水平低、代谢不足的轻微迹象，有时还有最小的临床后遗症。此外，在某些情况下，胃部缺陷会进展并影响内因子分泌，从而转变为典型的恶性贫血；然而，这并非不可避免，可能仅发生在少数患者中。因此，食物性钴胺素吸收不良的病程是多样的。尽管如此，它可能是轻微或轻度钴胺素缺乏最常见的原因，有时也与严重缺乏有关。在临床环境中，需要更广泛地考虑其识别和治疗。
