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Diagnosing Cobalamin-Deficiency Polyneuropathy Can Be Difficult

  • Authors:
  • CME Released: 9/18/2003
  • Valid for credit through: 9/18/2004, 11:59 PM EST
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Target Audience and Goal Statement

This article is intended for primary care physicians, neurologists, and other specialists who care for patients with neuropathy.

The goal of this activity is to provide the latest medical news to physicians and other healthcare professionals in order to enhance patient care.

Upon completion of this activity, participants will be able to:

  • Describe the challenges of diagnosing Cbl deficiency.
  • Evaluate the characteristics of Cbl-deficiency polyneuropathy.


This article may discuss investigational products or unapproved uses of products regulated by the U.S. Food and Drug Administration.


  • Laurie Barclay, MD

    Laurie Barclay is a freelance reviewer and writer for Medscape.


    Disclosure: Dr. Barclay has reported no significant financial interests.

CME Author(s)

  • Charles P Vega, MD

    Associate Professor, Residency Director, Department of Family Medicine, University of California, Irvine


    Disclosure: Dr. Vega has disclosed that he serves on the speakers bureaus of Pfizer and Lilly.

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Diagnosing Cobalamin-Deficiency Polyneuropathy Can Be Difficult


CME Released: 9/18/2003

Valid for credit through: 9/18/2004, 11:59 PM EST


Sept. 18, 2003 -- A cohort study published in the September issue of the Archives of Neurology sheds new light on the association of cobalamin (Cbl) deficiency and polyneuropathy (PN).

"Diagnosing Cbl deficiency as a cause of PN is problematic, as the frequency of both disorders increases with age, and serum Cbl levels can be difficult to interpret," write David S. Saperstein, MD, from the University of Kansas Medical Center in Kansas City, and colleagues. "Identifying Cbl deficiency in patients with PN does not necessarily prove that Cbl deficiency is the cause of the PN.... These uncertainties pose problems for the clinician attempting to determine how aggressively to pursue the diagnosis and treatment of Cbl deficiency in patients presenting with what appears to be CSPN [cryptogenic sensory/sensorimotor polyneuropathy]."

In this cohort survey from an academic neuromuscular clinic, 324 patients with PN were identified during a two-year period. Based on low serum Cbl levels or elevated serum methylmalonic acid or homocysteine levels, 27 patients (8%; 95% confidence interval, 5% - 11%) were diagnosed as having Cbl deficiency, including 12 with normal Cbl levels but elevated serum metabolite levels.

Whether Cbl deficiency was defined using low Cbl levels or elevated serum metabolite levels, features favoring Cbl deficiency over CSPN were concomitant involvement of the upper and lower extremities, symptom onset in the hands, and sudden onset ( P < .005). Of 12 Cbl-deficient patients with normal serum Cbl levels, six (50%) had autoimmune pernicious anemia.

Parenteral replacement therapy in Cbl-deficient patients caused little objective improvement, but these patients showed less progression than did those with CSPN ( P = .02).

Study limitations include retrospective design not allowing sufficient assessment of treatment response, inconsistent follow-up, and small sample size.

"This study highlights the challenges of proving that Cbl deficiency is the cause for PN and identifies clinical features that suggest Cbl-deficiency PN. Testing of serum metabolite levels may identify Cbl deficiency in some patients with normal serum Cbl levels," the authors write. "It is possible that Cbl replacement therapy needs to be started early for significant improvement in PN symptoms and findings to occur.... A larger prospective study with more structured and prolonged monitoring of treatment response and more use of evoked potentials and spinal imaging is needed to definitively address many of these uncertainties."

Arch Neurol. 2003;60:1296-1301