TY - JOUR
T1 - Vitamin B6 levels do not correlate with severity of neuropathy in chronic idiopathic axonal polyneuropathy
AU - Stewart, Sarah L.
AU - Thomas, Simone
AU - Höke, Erol
AU - Simpson, David
AU - Singleton, J. Robinson
AU - Höke, Ahmet
N1 - Funding Information:
We thank the patients, their families, and the Foundation of Peripheral Neuropathy for their support of the PNRR. The funding for PNRR is provided by the Foundation for Peripheral Neuropathy. In addition, we thank the neurologists' enrolling patients at the PNRR consortium sites: Drs. Vinay Chaudhry, David Cornblath, Leana Doherty, Lindsey Hayes, Mohammad Khoshnoodi, Brett McCray, Brett Morrison, Michael Polydefkis, Ricardo Roda, and Charlotte Sumner for the Johns Hopkins University, School of Medicine; and Drs Kelsey Barrell, Summer Gibson, Kyle Mahoney, Clark Moser, and Ligia Onofrei for the University of Utah.
Funding Information:
We thank the patients, their families, and the Foundation of Peripheral Neuropathy for their support of the PNRR. The funding for PNRR is provided by the Foundation for Peripheral Neuropathy. In addition, we thank the neurologists' enrolling patients at the PNRR consortium sites: Drs. Vinay Chaudhry, David Cornblath, Leana Doherty, Lindsey Hayes, Mohammad Khoshnoodi, Brett McCray, Brett Morrison, Michael Polydefkis, Ricardo Roda, and Charlotte Sumner for the Johns Hopkins University, School of Medicine; and Drs Kelsey Barrell, Summer Gibson, Kyle Mahoney, Clark Moser, and Ligia Onofrei for the University of Utah.
Funding Information:
The study was supported by the Foundation for Peripheral Neuropathy (FPN) and Dr. Hoke is the chair of the Scientific Advisory Board of the FPN. The officers of the FPN did not have any role in conducting the study or writing the manuscript. The authors do not report any other relevant conflicts of interest.
Publisher Copyright:
© 2021 Peripheral Nerve Society.
PY - 2022/3
Y1 - 2022/3
N2 - Pyridoxine (vitamin B6) toxicity is known to cause a length-dependent, sensory predominant axonal polyneuropathy. There is debate regarding the threshold at which intake levels can cause neurological symptoms through pyridoxine toxicity. We asked if elevated plasma vitamin B6 levels were related to outcome measures in a well-characterized cohort of patients with chronic idiopathic axonal polyneuropathy (CIAP). We included 261 patients enrolled in the Peripheral Neuropathy Research Registry who had a complete dataset including a plasma vitamin B6 value. Patients with vitamin B6 deficiency (0-4.9 μg/L) were excluded. We performed a chi-square test for independence and analyzed the logistic relation of elevated plasma B6 level to nerve conduction studies (NCS), neurological examination findings, and patient-reported symptoms controlling for age and time elapsed since neuropathy symptom onset. Plasma B6 level was not related to neuropathy severity. There was no logistic relation of elevated plasma B6 level to NCS results, examination features including toe strength, vibration sense, and deep tendon reflexes, or patient-reported numbness or pain intensity. This study suggests that moderately elevated plasma B6 levels, even in the 100 to 200 μg/L range, are not associated with significantly worse neuropathy signs or symptoms. Although standard supplementation of B6 does not appear to have a major negative affect on CIAP, this study does not directly answer whether stopping supplementation will have a beneficial effect. Very few patients in the study had vitamin B6 levels >300 μg/L, suggesting that screening for vitamin B6 toxicity may be left to the discretion of the physician.
AB - Pyridoxine (vitamin B6) toxicity is known to cause a length-dependent, sensory predominant axonal polyneuropathy. There is debate regarding the threshold at which intake levels can cause neurological symptoms through pyridoxine toxicity. We asked if elevated plasma vitamin B6 levels were related to outcome measures in a well-characterized cohort of patients with chronic idiopathic axonal polyneuropathy (CIAP). We included 261 patients enrolled in the Peripheral Neuropathy Research Registry who had a complete dataset including a plasma vitamin B6 value. Patients with vitamin B6 deficiency (0-4.9 μg/L) were excluded. We performed a chi-square test for independence and analyzed the logistic relation of elevated plasma B6 level to nerve conduction studies (NCS), neurological examination findings, and patient-reported symptoms controlling for age and time elapsed since neuropathy symptom onset. Plasma B6 level was not related to neuropathy severity. There was no logistic relation of elevated plasma B6 level to NCS results, examination features including toe strength, vibration sense, and deep tendon reflexes, or patient-reported numbness or pain intensity. This study suggests that moderately elevated plasma B6 levels, even in the 100 to 200 μg/L range, are not associated with significantly worse neuropathy signs or symptoms. Although standard supplementation of B6 does not appear to have a major negative affect on CIAP, this study does not directly answer whether stopping supplementation will have a beneficial effect. Very few patients in the study had vitamin B6 levels >300 μg/L, suggesting that screening for vitamin B6 toxicity may be left to the discretion of the physician.
KW - chronic idiopathic axonal polyneuropathy
KW - vitamin B6
UR - http://www.scopus.com/inward/record.url?scp=85122108122&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85122108122&partnerID=8YFLogxK
U2 - 10.1111/jns.12480
DO - 10.1111/jns.12480
M3 - Article
C2 - 34931740
AN - SCOPUS:85122108122
SN - 1085-9489
VL - 27
SP - 31
EP - 37
JO - Journal of the Peripheral Nervous System
JF - Journal of the Peripheral Nervous System
IS - 1
ER -