A patient undergoes an ileal resection for Crohn's disease. He subsequently develops fat malabsorption and vitamin B12 deficiency. The mechanism of vitamin B12 (cobalamin) malabsorption after ileal resection is:

• A Reduced gastric intrinsic factor production due to feedback inhibition from the absent ileum
• B Increased bacterial overgrowth in the blind loop consuming B12 before absorption
• C Loss of the specialized ileal cubilin/amnionless receptor complex (cubam receptor) that is the exclusive site for IF-B12 complex absorption in the terminal ileum ✓
• D B12 is absorbed in the jejunum; ileal resection affects fat but not B12

Explanation

Vitamin B12 absorption requires intrinsic factor (IF, secreted by gastric parietal cells) to form an IF-B12 complex in the stomach/duodenum. This complex is then exclusively absorbed in the terminal ileum via specific receptors: the cubam complex (cubilin + amnionless proteins) recognizes IF-B12 and mediates endocytosis. The terminal ileum is the only site in the GI tract with these receptors—absorption cannot occur elsewhere. Following ileal resection, the cubam receptor is absent, so IF-B12 cannot be absorbed regardless of normal IF production. Patients require parenteral (IM) B12 supplementation. Fat malabsorption occurs because bile salts are also absorbed in the terminal ileum; without enterohepatic recirculation, fat digestion is impaired.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.