Associations of food-cobalamin malabsorption with ethnic origin, age, Helicobacter pylori infection, and serum markers of gastritis.

OBJECTIVES: Food-cobalamin malabsorption is common in patients with low cobalamin levels. However, characterization of affected subjects has been limited. The aim of this study was to analyze demographic and gastric data in a large study population. METHODS: Data were collected prospectively in 202 subjects (43 volunteers and 159 patients) who underwent the egg yolk-cobalamin absorption test (EYCAT). H. pylori status was determined in 167 of the subjects, serum gastrin and antiparietal cell antibody in 158 and pepsinogen (PG) I and PG II levels in 133. RESULTS: Latin American and black patients had lower EYCAT results than did white or Asian-American ones (p = 0.0001) and had severe food-cobalamin malabsorption (EYCAT < 1%) more often (p = 0.0001). Age correlated inversely with EYCAT results (p = 0.02). H. pylori infection was associated with food-cobalamin malabsorption (p = 0.0001), especially with severe malabsorption where 29/37 subjects (78.4%) were infected. Malabsorption was also associated with higher gastrin levels (p = 0.0001) and lower PG I levels (p = 0.01) and PG I:PG II ratios (p = 0.0001). Multivariate analysis showed that ethnic origin, gastrin levels, H. pylori infection and, to a lesser extent, age were independently associated with the EYCAT results. CONCLUSIONS: Latin American and black patients have food-cobalamin malabsorption more often than do white and Asian-American patients. This association is independent of the malabsorption's association with H. pylori infection, markers of gastritis, such as gastrin, and older age. The patterns of gastric tests suggest that malabsorption may be due to diverse mechanisms, not just atrophic gastritis. The possible role of H. pylori infection in many cases of severe food-cobalamin malabsorption also suggests avenues of treatment and prevention.

High serum cobalamin levels in the clinical setting--clinical associations and holo-transcobalamin changes.

Whereas low cobalamin levels have been studied intensively, systematic information about high levels, especially in the clinical setting, is scarce. Therefore, a prospective comparison was done of 60 patients with high cobalamin levels and 75 with normal levels obtained by a hospital laboratory over a 2.5 month period. Associations with clinical disorders and laboratory test results were examined. Transcobalamin (TC) I and II were measured, especially the holoproteins (TC carrying circulating endogenous cobalamin) which were fractionated with microfine silica powder. High cobalamin levels (> 664 pmol/l; > 900 ng/l) occurred in 94 of 670 consecutive clinically requested assays (14%). The only independently significant associations with a high cobalamin level were renal failure among the clinical disorders (P=0.01), elevated serum creatinine (P=0.0001) and diminished albumin (P=0.0002) levels among laboratory tests. Both holo-TC I and holo-TC II levels were increased in renal failure (P=0.0001) but the increase was relatively greater in holo-TC II. The results indicate that high cobalamin levels are more frequent than low ones in clinical practice and appear to be associated often with renal failure. The elevation of both holo-TC II and holo-TC I suggests that several mechanisms are operative. The accumulation of holo-TC II suggests that cellular uptake of cobalamin by the abundant TC II receptors in the kidney may be impaired. The much better known association of high cobalamin levels with leucocytic disorders is rare, and no association was seen with liver disease.