Inadequate Dissociation of Cobalamin From Food Protein

Dietary cobalamin is bioavailable only after proteolytic digestion of food by gastric acid and pepsin. Failure to release cobalamin from food protein can lead to food-cobalamin malabsorption and frank cobalamin deficiency despite the presence of IF.

Congenital Intrinsic Factor Deficiency

Congenital IF deficiency arising from mutations in gastric IF, resulting in complete loss of IF, can be transmitted as an autosomal recessive trait and expressed in homozygotes by the age of 2 years as severe megaloblastic anemia (less than 100 cases reported). Dysfunctional IF may lead to only a mild abnormality in binding to cobalamin and result in a delayed presentation into the second decade.

Loss or Atrophy of Gastric Oxyntic Mucosa

IF deficiency, which arises from atrophy of gastric parietal (oxyntic) mucosal cells, can be caused by total or partial gastrectomy (bariatric surgery); by autoimmune destruction, as observed in adult Addisonian pernicious anemia or, rarely, in a similar disease in children (juvenile pernicious anemia); and after destruction of gastric mucosa by caustic (lye) ingestion.

Total gastrectomy invariably leads to cobalamin deficiency in about 5 years (range, 2 to 10 years); indeed, longitudinal follow-up revealed that all 176 patients developed cobalamin deficiency within 4 years, with earlier clinical presentations occurring in those with lower cobalamin status preoperatively. This condition is often associated with iron deficiency, warranting routine prophylactic cobalamin and parenteral iron replacement.

By contrast, after partial gastrectomy, the degree of cobalamin defi ciency depends on the size of the remaining gastric remnant. Cobalamin deficiency eventually develops in 10% to 20% of patients at 8 years with a minority (about 5%) developing overt clinical manifestations from a combination of decreased IF secretion, hypochlorhydria, intestinal bacterial overgrowth of cobalamin-consuming organisms, and iron defi ciency. It is more common in Billroth II than in Billroth I surgery, and in subtotal than in partial gastrectomy. Morbidly obese patients treated surgically with gastric bypass also have more food-cobalamin malabsorption than patients treated with vertical banded gastroplasty. Even after laparoscopic Roux-en-Y gastric bypass, and despite oral multivitamin supplementation, iron deficiency was seen in one-half of patients and cobalamin deficiency seen in one-quarter at 3 years; therefore all such patients need prophylactic cobalamin and parenteral iron.

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