Macrocytic anemia due to stasis of the contents of the small intestine is a well known clinical entity. It has been reported in association with improperly drained intestinal segments at all levels of the small bowel, including partially obstructed afferent loops after gastrectomy,1 multiple jejunal diverticula,1–3 and with poorly draining ileal segments.4, 5 There is now strong evidence that bacterial overgrowth in such intestinal segments plays a major role in the etiology of the hematologic syndrome.2, 4–7 At present, however, the exact mechanism by which this bacterial proliferation leads to a malabsorption or malutilization of vitamin B12 is still not clear. In an effort to throw further light on this matter, segments of jejunum were interposed into the colon. We hoped by this technique to provide some information on two separate but related aspects the relationship of bacterial proliferation to malabsorption. First, because the segment of small intestine subjected to continuous fecal contamination would be out of the upper alimentary stream, any defect in absorption of vitamin B12 could then be considered to occur as a result of a circulating substance such as a toxin. Second, it could be observed whether prolonged bacterial contamination of the mucosa of the upper intestinal tract could cause recognizable histologic changes suggestive of a malabsorptive defect.
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Hermann et al. (1964) studied this question.
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