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Latov N, Kumar G, Vo ML, et al. Elevated Blood Mercury Levels in Idiopathic Axonal Neuropathy. JAMA Neurol. 2015;72(4):474–475. doi:https://doi.org/10.1001/jamaneurol.2015.1
Mercury is an environmental neurotoxin that, in the United States, is most commonly acquired by ingestion of methylmercury in seafood.1 We report that a significant number of patients with idiopathic axonal neuropathy (IAN) have increased blood mercury levels.
The electronic records of all patients with neuropathy newly seen by one of the authors (N.L.) at the Weill Cornell Neuropathy Center from July 1, 2013, to June 30, 2014, were reviewed, with Weill Cornell Neuropathy Center institutional review board approval. Patient consent was waived as most patients were referred for a single visit and not available for follow-up. Neuropathies were classified as previously described.2,3 Blood mercury levels, determined at a commercial laboratory by mass spectroscopy, were considered elevated if greater than 10 µg/L in comparison with normal control individuals.1 Findings in patients with IAN or idiopathic small-fiber axonal neuropathy were compared with those with chronic inflammatory demyelinating neuropathy or diabetes mellitus using the χ2 test.
Of 147 patients who were evaluated, 37 had IAN, 19 had diabetic neuropathy, 32 had chronic inflammatory demyelinating neuropathy, and 37 had small-fiber axonal neuropathy. Blood mercury was tested in 89.6% of the patients. The findings are presented in the Table. Mercury was elevated in 18% of patients with IAN and 9% with small-fiber axonal neuropathy (Figure) compared with none with chronic inflammatory demyelinating neuropathy or diabetic neuropathy, reaching a statistically significant difference between IAN and chronic inflammatory demyelinating neuropathy (P = .02).
Twenty-two of the 147 patients had other causes of neuropathy (2 had celiac disease, 2 had anti–myelin-associated glycoprotein antibodies, 2 had multifocal motor neuropathy, 1 had alcoholic neuropathy, 2 had hereditary neuropathy, 3 had chemotherapy-induced neuropathy, 5 had a low vitamin B1 level, 2 had a low vitamin B12 level, and 3 had a low vitamin B6 level). Of these, 1 with a low vitamin B6 level also had high mercury levels.
Methylmercury from fish is eliminated in the gut and bile rather than the kidneys, so that blood mercury levels are a more accurate indicator of exposure.1,4 In our study, increased levels were found in a significantly higher number of patients with IAN and in some patients with small-fiber axonal neuropathy. Methylmercury toxicity is known to cause axonal neuropathy5,6; however, the concentration and duration of exposure required for neurotoxicity, or whether it caused or contributed to the neuropathy in our patients, is not known. Larger prospective studies are needed to determine whether elevated mercury levels are associated with neuropathy in other patient populations and whether dietary intervention would ameliorate the neuropathy.
Accepted for Publication: January 2, 2015.
Corresponding Author: Norman Latov, MD, PhD, Peripheral Neuropathy Center, Department of Neurology, Cornell University, 1305 York Ave, Ste 217, New York, NY 10021 (email@example.com).
Author Contributions: Dr Latov had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Latov.
Acquisition, analysis, or interpretation of data: All authors.
Drafting of the manuscript: Latov.
Critical revision of the manuscript for important intellectual content: Kumar, Vo, Chin, Carey, Langsdorf, Feuer.
Statistical analysis: Latov, Kumar.
Administrative, technical, or material support: Vo, Chin, Carey, Feuer.
Study supervision: Latov, Feuer.
Conflict of Interest Disclosures: Dr Latov has served as a consultant to Merck, Baxter, CSL Behring, Pfizer, Xenoport, Novartis, and Oncogenex; owns stock in Therapath; is the beneficiary of a research grant from Grifols to Cornell University; and receives book royalties from the American Academy of Neurology. Dr Vo is the beneficiary of a research grant from Grifols to Cornell University. No other disclosures were reported.
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