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Vitamin B12 Deficiency
The physiology of vitamin B12 absorption is complex. Vitamin B12 is liberated from dietary sources by acid and pepsin. R factor is released in saliva and binds to free vitamin B12 to protect it from degradation. In the duodenum, R factor is cleaved by proteases, allowing vitamin B12 to bind to intrinsic factor produced by the stomach. This complex then moves to the ileum, where it is absorbed by ileal intrinsic factor receptors. Luminal bacteria can bind vitamin B12 and use it in their metabolic activities, which may interfere with normal transluminal uptake.
Theoretically, patients with pouches have a high risk of vitamin B12 deficiency, as the ileal pouch created from the distal ileum inherently has fecal stasis, adaptive mucosal changes (colonic metaplasia), and small bowel bacterial overgrowth with subsequent microbial binding and utilization of luminal vitamin B12; these patients also have poor oral intake and dietary restrictions.7 In one study, 25% of IPAA patients had vitamin B12 deficiency without evidence of malabsorption, as indicated by normal Schilling tests.11Vitamin B12 deficiency can be corrected with oral supplementation, implicating poor intake as a major mechanism of the condition.11 However, in another study that examined patients with IPAA, 56% of patients with vitamin B12 deficiency also had bile salt deconjugation, as determined by 14C-glycocholic acid breath testing and fecal bile acid secretion.12 These findings suggest that bacterial overgrowth is the potential causative mechanism.12 Small bowel bacterial overgrowth is thought to occur due to anatomic and motility changes, particularly loss of the ileocecal valve from the creation of the pouch reservoir.7Although small bowel bacterial overgrowth diagnosed via breath testing was not reported to be associated with chronic pouchitis, the suitability of the breath test currently used in patients with intact colons is controversial in the setting of IPAA.13
It is unclear whether pouch surgery itself has a positive or negative impact on vitamin B12 metabolism. In a cross-sectional study, vitamin B12 deficiency occurred in 13% of UC patients preoperatively and in only 3% of IPAA patients.14 Although a possible explanation for this finding could be the improved general nutritional status of the patients, this improvement may be secondary to backwash ileitis, which resolves postoperatively. The latter explanation implicates villous changes as having a role in metabolic abnormalities. Villous atrophy is indeed known to occur in patients with IPAA and may be the result of physiologic adaptation (colonic metaplasia of the ileal mucosa) or chronic pouchitis.15,16 Atrophy may result in abnormal vitamin B12 absorption and deficiency in this population.
