Vitamin B12 deficiency is prevalent among patients with plasma cell dyscrasias (PCDs), but the association is poorly understood. Among 501 patients with PCDs, 20% had low B12. Low B12 was more prevalent in patients with preserved renal function. Mean corpuscular volume was not clinically different between patients with low and normal B12 and may not be reliable in PCDs.Background:
Although increased rates of vitamin B12 deficiency have been reported in patients with plasma cell dyscrasias (PCDs), no mechanism has been identified. Excess free light chains (FLCs) could disrupt the renal proximal tubule receptors where B12 is reabsorbed. We sought to characterize the relationship between B12 deficiency and PCDs. We hypothesized that rates of B12 deficiency would be highest in patients with PCDs with high FLC burdens.Methods:
We reviewed the electronic medical records of 501 patients who met inclusion criteria (diagnosed PCD with documented serum B12 and FLC levels) to obtain clinical data recorded prior to patients' lowest B12 levels.Results:
Overall, 20.0% of patients had low vitamin B12. There was an expected negative correlation between estimated glomular filtration rate and FLC (rs = −0.317; P < .001). However, low B12 levels were more prevalent in patients with preserved renal function (P = .047). Low B12 was associated with lower mean corpuscular volume (P = .037).Conclusion:
Higher FLC burden was associated with poor kidney function but not with low B12. Low B12 was seen more commonly in patients with preserved kidney function. Mean corpuscular volume was statistically but not clinically different between patients with low and normal B12 and, therefore, may not be a reliable indicator of B12 deficiency in PCDs. Prospective studies should compare B12 metabolites with FLC levels. Detection of B12 deficiency among patients with PCDs remains important to reduce neurologic dysfunction and cytopenias, sequelae common to B12 deficiency and PCDs.