Clinically significant vitamin B12 deficiency secondary to malabsorption of protein-bound vitamin B12

Abstract

Protein- (chicken serum) bound [⁵⁷Co]cyanocobalamin absorption was evaluated in five hypochlorhydric patients who had developed B₁₂ deficiency despite having normal absorption of unbound crystalline vitamin B₁₂. All five patients had decreased urinary excretion of protein-bound B₁₂ (0.06–0.34%) as compared to twelve normal controls (0.61–5.6%), P<.001. Improvement in protein-bound B₁₂ absorption in four of the five patients occurred with the exogenous administration of hydrochloric acid, pepsin, gastric intrinsic factor, or a combination thereof. Vitamin B₁₂ deficiency developing in the setting of hypochlorhydria may result from deficiency of acid-peptic digestion of B₁₂ bound to protein and/or a relative deficiency of intrinsic factor. This digestive defect is not detected with tests which measure the absorption of unbound crystalline B₁₂ but is detected by a simple test which employs B₁₂ bound to chicken serum as the form of protein-bound B₁₂.