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Mild cobalamin deficiency in older Dutch subjects

Department of Medicine New York Methodist Hospital 50b Sixth Street Brooklyn, NY 11215–9008 Email: rcarmel{at}pol.net

Dear Sir:

The report by van Asselt et al (1) is of great interest and I could not agree more with most of their conclusions. Permit me to add several of our observations in support and extension of theirs. We too have been impressed that half or more of the low cobalamin concentrations in the elderly (and others) cannot be explained by malabsorption (2–4). Because factors other than cobalamin status may affect serum cobalamin concentrations (4), it is important to keep in mind that 25% or more of the low cobalamin concentrations are not accompanied by any metabolic abnormalities and may not represent actual deficiency. Nevertheless, the causes responsible for the low concentrations, especially for the 75% that are associated with metabolic evidence of deficiency, need to be identified. Like van Asselt et al, we have found poor dietary intake of cobalamin to be virtually nonexistent in the elderly (5). Our data also support their observation of an ameliorative effect of cobalamin supplement use on cobalamin status, although it is noteworthy that many of our patients remained mildly deficient despite supplement use (5). Ironically, supplement use also appeared to be highest in subjects who had higher cobalamin intakes from food and, thus, presumably a lesser need for supplementation.

However, a strong word of caution is in order about any automatic equation between atrophic gastritis and food– cobalamin malabsorption. The 2 are not synonymous (3). Half of the patients with severe food– cobalamin malabsorption whom we biopsied and subjected to gastric analysis had neither atrophic gastritis nor achlorhydria (6). Thus, although nearly all patients with atrophic gastritis may have food– cobalamin malabsorption, many without atrophic gastritis may also have food– cobalamin malabsorption. Van Asselt et al might have found a higher prevalence of malabsorption and perhaps even a stronger association with Helicobacter pylori infection had they actually tested absorption directly.

It is too early in our still incomplete understanding of food-cobalamin malabsorption to allow ourselves the liberty of resorting to indirect markers when studying it. In recent years, various authors have proposed not only gastric and duodenal histology but serum gastrin concentrations, holotranscobalamin II concentrations, and other such substitutes for direct testing of food– cobalamin malabsorption. None of these substitutes were ever proven to be satisfactorily specific or sensitive, and at least one of the claims of equivalence has been retracted. I fear that unwarranted methodologic shortcuts will only add confusion to the subject.

As for Dr. Russell's accompanying editorial (7), early answers have begun to appear to his question concerning consequences of elevated methylmalonic acid concentrations (or more precisely, of mild, preclinical cobalamin deficiency). Over the years, we have consistently found electroencephalographic, evoked potential, and P300 potential abnormalities in half or more of our patients with metabolically defined, mild, preclinical cobalamin deficiency (8–10). In most cases, these abnormalities were reversed with cobalamin therapy. Moreover, mild but reversible clinical abnormalities, including neuropathy and memory loss were part of the picture in several patients. The extent of this subtle neurologic dysfunction and its contribution to the risks of mild cobalamin deficiency is an important area for further study.

REFERENCES

1. van Asselt DZB, de Groot LCPGM, van Staveren WA, et al. Role of cobalamin intake and atrophic gastritis in mild cobalamin deficiency in older Dutch subjects. Am J Clin Nutr 1998;68:328–34.[Abstract]
2. Carmel R, Sinow RM, Siegel ME, Samloff IM. Food cobalamin malabsorption occurs frequently in patients with unexplained low serum cobalamin levels. Arch Intern Med 1988; 148:1715–19.[Abstract]
3. Carmel R. Food-cobalamin malabsorption. Baillière's Clin Haematol 1995;8:639–55.[Medline]
4. Carmel R, Montes-Garces R, Wardinsky T, Liebman H. Mild transcobalamin I deficiency is common and may be responsible for many low serum cobalamin levels: observations in a family and survey of 106 patients with low serum cobalamin levels not explained by malabsorption. Blood 1996;88(suppl):646a (abstr).
5. Howard JM, Azen C, Jacobsen DW, Green R, Carmel R. Dietary intake of cobalamin in elderly people who have abnormal serum cobalamin, methylmalonic acid and homocysteine levels. Eur J Clin Nutr 1998;52:582–7.[Medline]
6. Cohen H, Weinstein WM, Marin-Sorensen M, Carmel R. Heterogeneous gastric status in food-cobalamin malabsorption: some patients have normal acid secretion and gastric histology. Am J Clin Nutr 1997;66:206 (abstr).
7. Russell RM. Mild cobalamin deficiency in older Dutch subjects. Am J Clin Nutr 1998;68:222–3.[Medline]
8. Karnaze DS, Carmel R. Neurological and evoked potential abnormalities in subtle cobalamin deficiency states, including those without anemia and with normal absorption of free cobalamin. Arch Neurol 1990;47:1008–12.[Abstract]
9. Carmel R, Gott PS, Waters CH, et al. The frequently low cobalamin levels in dementia usually signify treatable metabolic, neurologic and electrophysiologic abnormalities. Eur J Haematol 1995;54:245–53.[Medline]
10. Gott PS, DeGiorgio CM, Schreiber SS, McCleary CA, Qian D, Carmel R. P300 event-related potentials in elderly patients with subtle preclinical cobalamin (B12) deficiency. J Clin Neurophysiol 1997;14:447 (abstr).

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