Pyridoxine deficiency in adult patients with status epilepticus☆
Introduction
An 8-year-old girl admitted for status epilepticus had seizures refractory to multiple AED's, VNS placement, ketamine infusion, and propofol infusion. She had a low pyridoxine level of 5 ng/mL. An improvement in the EEG was seen within 24 h after starting pyridoxine supplementation. The patient died of complications secondary to hypothermia protocol and metabolic acidosis. In light of her short but impressive response to pyridoxine, we decided to look at pyridoxine levels in our adult patients with status epilepticus (SE).
Section snippets
Methods
We obtained IRB approval to evaluate our patients admitted to the Ochsner Medical Center, Jefferson Campus, neurological ICU for SE. The patients were admitted between January 2014 and February 2015. Eighty-one adult patients with SE were identified with documented pyridoxine levels. For comparison purposes, we looked at serum pyridoxine levels in outpatients with epilepsy from the past three years (n = 132). A level of 10 ng/mL and below was chosen as a low pyridoxine level.
Results
Upon review of the data, all but six of the patients admitted for SE had low levels of pyridoxine of which seventeen patients had undetectable levels. When this was compared to the outpatient population, a larger proportion of patients (n = 80) had normal levels of pyridoxine. None of the patients in the outpatient group had undetectable levels. The mean pyridoxine was 4.7 ng/ml in the group with status epilepticus and 25.2 ng/ml in the outpatient group. This difference is statistically significant
Pyridoxine
Albert Svent-Gyorgy first isolated pyridoxine in 1934 [1]. Pyridoxine is found in animal and plant-derived food [2]. The standard vitamin B6 supplement is pyridoxine hydrochloride (HCL) which is inexpensive. Pyridoxine is a water soluble vitamin and is absorbed by the upper small intestine. It is then transported to the liver where it is first oxidized to pyridoxal and then undergoes phosphorylation to pyridoxal 5′-phosphate (P5P) in the liver. The metabolic active coenzyme form of vitamin B6
Conclusion
A selective pyridoxine deficiency was seen in 94% of patients with status epilepticus (compared to 39% in the outpatients) which leads us to believe that there is a relationship between status epilepticus and pyridoxine levels. The difference in mean pyridoxine level in the group with status epilepticus was statistically significant to the comparison group. Further studies on the effect of pyridoxine on status epilepticus control are needed.
Conflicts of interest
None.
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The B-vitamins
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This paper is part of the Special Issue based on The 5th London-Innsbruck Colloquium on Status Epilepticus and Acute Seizures (Volume 49).