The Resected Terminal Ileum
A 38-year-old woman with Crohn's disease has 90 cm of her terminal ileum removed. Three months later she reports watery diarrhoea, pale bulky stools that float, 6 kg weight loss, and tingling in her fingers and toes. Investigations: haemoglobin 9.2 g/dL, MCV 106 fL, serum vitamin B12 low, serum calcium and 25-hydroxyvitamin D low, faecal fat markedly raised. Serum folate, fasting glucose and stool elastase are normal. Her BMI has fallen from 22 to 18.5. She has been eating boiled polished rice and avoiding all visible fat because 'fat makes the diarrhoea worse', and she asks why she cannot simply take a vitamin tablet instead of monthly injections. Her surgeon remarks that the operation was 'only in the last part of the small intestine, where nothing much is absorbed anyway'.
1. Explain why the surgery produced a macrocytic anaemia and fatty stools. Link each finding to one specific absorptive step.
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Macrocytic anaemia - vitamin B12. Dietary B12 is freed from food proteins by gastric acid and pepsin, transferred to intrinsic factor secreted by parietal cells, and the B12–intrinsic factor complex is taken up by cubilin receptors that are confined to the terminal ileum. Resecting that segment removes the only uptake site. B12 is the cofactor for methionine synthase, which regenerates tetrahydrofolate; without it, thymidylate and DNA synthesis stall, so the erythroid precursor's nucleus matures more slowly than its cytoplasm. The result is a large cell with a high MCV and low haemoglobin - macrocytic, not microcytic.
Steatorrhoea - bile salts. Bile salts are reabsorbed actively only in the terminal ileum and recycled in the enterohepatic circulation. Losing that segment depletes the bile salt pool below the critical micellar concentration, so micelles do not form, long-chain fatty acids and fat-soluble vitamins are not absorbed, and fat appears in stool. Low vitamin D and calcium follow the same defect.
Why folate and glucose are normal: folate has broad jejunal absorption, and glucose is absorbed as monosaccharide in the jejunum. The lesion is site-specific, which is exactly why only B12, fat and fat-soluble vitamins are affected.
2. Correct the surgeon's statement that 'nothing much is absorbed in the last part of the small intestine'. Use at least three substances handled there, and explain one consequence beyond anaemia and fatty stools.
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The terminal ileum is not a passive conduit; it is a specialised absorptive surface.
- Vitamin B12 - the sole site of intrinsic factor–dependent, receptor-mediated uptake. Losing it guarantees B12 deficiency once liver stores fall.
- Bile salts - active sodium-dependent reabsorption here returns bile salts to the liver, cycling the 3–5 g pool several times a day. Lose the site and the pool shrinks.
- Fat-soluble vitamins (A, D, E, K) - absorbed in micelles that depend on that bile salt pool; vitamin K deficiency can prolong prothrombin time.
- Water and electrolytes - the ileum is a major salvage site for fluid, so resection contributes to the diarrhoea.
A consequence often missed: unabsorbed fatty acids and bile salts reaching the colon increase colonic permeability to oxalate, and calcium that would have bound oxalate is bound to fat instead. Oxalate absorption rises, and the patient is at risk of calcium oxalate kidney stones. There is also a 'bile salt diarrhoea' component, because bile salts stimulate colonic chloride and water secretion. So the correct statement is that the terminal ileum handles a small number of substances, but they are ones no other segment can substitute for.
3. Why can she not simply take an ordinary multivitamin tablet? Under what reasoning would high-dose oral B12 work, and what else should be added to her plan?
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An ordinary multivitamin contains roughly 2–5 µg of B12, and that dose can only be absorbed by the intrinsic factor–cubilin route in the terminal ileum, which she no longer has. So a standard tablet is effectively swallowed and excreted.
There is, however, a second route: about 1–2% of any oral dose is absorbed by passive diffusion across the intestinal mucosa without intrinsic factor. That fraction is tiny, but it scales with the dose. At 1,000 µg daily, roughly 10 µg is absorbed - more than the 2 µg daily requirement - which is why high-dose oral regimens are used in some patients. The choice between oral and intramuscular therapy then depends on reliability: injections bypass the gut entirely and are preferred when there is neurological involvement (her tingling), continuing diarrhoea, or doubt about adherence. The argument is quantitative, not a matter of which route is 'stronger'.
Her plan also needs: replacement of vitamin D and calcium; a diet that is not fat-free, since fat-soluble vitamin absorption is already marginal (medium-chain triglycerides help because they enter portal blood without micelles or chylomicrons); and monitoring of B12, folate and haemoglobin.