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Blood, 15 September 2008, Vol. 112, No. 6, pp. 2214-2221.
Prepublished online as a Blood First Edition Paper on July 7, 2008; DOI 10.1182/blood-2008-03-040253.


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Submitted March 27, 2008
Accepted June 24, 2008

How I treat cobalamin (vitamin B12) deficiency

Ralph Carmel*

Medicine, New York Methodist Hospital, Brooklyn, NY, United States

* Corresponding author; email: rac9001{at}nyp.org.

The challenges in medical management of cobalamin deficiency lie in attention to the unique pathophysiology that underlies cobalamin deficiency, more than in the mechanics of therapy. The central physiological principles are that clinically important deficiency is much more likely to occur (and progress) when intrinsic factor-driven absorption fails than when diet is poor, and that most causes take years to produce clinically obvious deficiency. Transient defects have little clinical impact. The key management principle is the importance of follow-up, which requires knowing how the deficiency arose. The virtues of these principles are not always fully appreciated. Recent developments have made diagnosis and management more difficult by diminishing the ability to determine cobalamin absorption status. Clinicians must also grapple with premature medicalization of isolated, mild biochemical changes that added many asymptomatic cases of still undetermined medical relevance to their caseload, often expanded by inflated cobalamin level criteria. The potential for misattribution of cobalamin-unrelated presentations to nongermane cobalamin and metabolite abnormalities has grown. Pathophysiologically based management requires systematic attention to each of its individual components: correctly diagnosing cobalamin deficiency, reversing it, defining its underlying cause, preventing relapse, managing the underlying disorder and its complications, and educating the patient.


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