Cohen H, Weinstein W M, Carmel R
Department of Medicine, University of Southern California School of Medicine, Los Angeles, USA.
Gut. 2000 Nov;47(5):638-45. doi: 10.1136/gut.47.5.638.
The common but incompletely understood entity of malabsorption of food bound cobalamin is generally presumed to arise from gastritis and/or achlorhydria.
To conduct a systematic comparative examination of gastric histology and function.
Nineteen volunteers, either healthy or with low cobalamin levels, were prospectively studied without prior knowledge of their absorption or gastric status.
All subjects underwent prospective assessment of food cobalamin absorption by the egg yolk cobalamin absorption test, endoscopy, histological grading of biopsies from six gastric sites, measurement of gastric secretory function, assay for serum gastrin and antiparietal cell antibodies, and direct tests for Helicobacter pylori infection.
The six subjects with severe malabsorption (group I) had worse histological scores overall and lower acid and pepsin secretion than the eight subjects with normal absorption (group III) or the five subjects with mild malabsorption (group II). However, histological findings, and acid and pepsin secretion overlapped considerably between individual subjects in group I and group III. Two distinct subgroups of three subjects each emerged within group I. One subgroup (IA) had severe gastric atrophy and achlorhydria. The other subgroup (IB) had little atrophy and only mild hypochlorhydria; the gastric findings were indistinguishable from those in many subjects with normal absorption. Absorption improved in the two subjects in subgroup IB and in one subject in group II who received antibiotics, along with evidence of clearing of H pylori. None of the subjects in group IA responded to antibiotics.
Food cobalamin malabsorption arises in at least two different gastric settings, one of which involves neither gastric atrophy nor achlorhydria. Malabsorption can respond to antibiotics, but only in some patients. Food cobalamin malabsorption is not always synonymous with atrophic gastritis and achlorhydria, and hypochlorhydria does not always guarantee food cobalamin malabsorption.
食物结合型钴胺素吸收不良这一常见但尚未完全理解的现象通常被认为源于胃炎和/或胃酸缺乏。
对胃组织学和功能进行系统的比较检查。
19名志愿者，包括健康者或钴胺素水平较低者，在对其吸收或胃部状况不知情的情况下进行前瞻性研究。
所有受试者均通过蛋黄钴胺素吸收试验对食物钴胺素吸收进行前瞻性评估，接受内镜检查、对六个胃部位活检进行组织学分级、测量胃分泌功能、检测血清胃泌素和抗壁细胞抗体，以及进行幽门螺杆菌感染的直接检测。
6名严重吸收不良的受试者（第一组）总体组织学评分更差，胃酸和胃蛋白酶分泌低于8名吸收正常的受试者（第三组）或5名轻度吸收不良的受试者（第二组）。然而，第一组和第三组个体受试者之间的组织学结果以及胃酸和胃蛋白酶分泌有相当大的重叠。第一组中出现了两个各有三名受试者的不同亚组。一个亚组（IA）有严重的胃萎缩和胃酸缺乏。另一个亚组（IB）萎缩程度小，只有轻度胃酸过少；胃部表现与许多吸收正常的受试者难以区分。接受抗生素治疗的IB亚组中的两名受试者和第二组中的一名受试者吸收情况有所改善，同时有幽门螺杆菌清除的证据。IA亚组的受试者均对抗生素无反应。
食物钴胺素吸收不良至少出现在两种不同的胃部情况中，其中一种既不涉及胃萎缩也不涉及胃酸缺乏。吸收不良对抗生素有反应，但仅在部分患者中如此。食物钴胺素吸收不良并不总是萎缩性胃炎和胃酸缺乏的同义词，胃酸过少也不总是保证出现食物钴胺素吸收不良。
