背景:这项研究的目的是确定吡哆醇缺乏症的患病率,通过磷酸吡哆醛(PLP)水平测量,在住院的患者中,已建立(苯二氮卓耐药)癫痫持续状态(SE)(ESE),并与三个对照组进行比较:没有SE的重症监护病房(ICU)患者(ICU-NOSE),无SE的非ICU住院患者(非ICU),以及有或没有癫痫史的门诊患者(门诊)。
方法:这项回顾性队列研究在北卡罗来纳大学医院和耶鲁纽黑文医院进行。参与者包括在2018年1月至2021年3月期间在临床护理期间测量血清PLP水平的住院患者和门诊患者。获得的第一个PLP水平被归类为正常(>30nmol/L),边际(≤30nmol/L),不足(≤20nmol/L),严重缺乏(≤5nmol/L)。
结果:共纳入293例患者(52eSE,40ICU-noSE,44非ICU,和157门诊病人)。中位年龄为55岁(19-99岁)。eSE组PLP水平中位数(12nmol/L)低于ICU-noSE组PLP水平中位数(22nmol/L,p=0.003),非ICU(16nmol/L,p=0.05),和门诊组(36nmol/L,p<0.001)。eSE患者的边缘和缺陷PLP水平的患病率明显更高(90%和80%,分别)比其他三组的患者(ICU-noSE:70,50%;非ICU:63,54%;门诊病人:38,21%)。纠正危重病的严重程度和收集PLP水平的时机后,这种明显较高的患病率仍然存在。
结论:我们的研究证实了先前的发现,表明在eSE患者中吡哆醇缺乏(通过血清PLP水平测量)的患病率很高,包括使用更严格的吡哆醇缺乏症定义时。eSE患者的患病率高于所有三个对照组的患者(ICU-noSE,非ICU,和门诊)。考虑到吡哆醇的作用,因此PLP,在γ-氨基丁酸的合成及其简单、安全的给药过程中,需要对eSE患者补充吡哆醇进行前瞻性研究.
The objective of this study was to determine the prevalence of pyridoxine deficiency, measured by pyridoxal phosphate (PLP) levels, in patients admitted to the hospital with established (benzodiazepine-resistant) status epilepticus (SE) (eSE) and to compare to three control groups: intensive care unit (ICU) patients without SE (ICU-noSE), non-ICU inpatients without SE (non-ICU), and outpatients with or without a history of epilepsy (outpatient).
This retrospective cohort study was conducted at the University of North Carolina Hospitals and Yale New Haven Hospital. Participants included inpatients and outpatients who had serum PLP levels measured during clinical care between January 2018 and March 2021. The first PLP level obtained was categorized as normal (> 30 nmol/L), marginal (≤ 30 nmol/L), deficient (≤ 20 nmol/L), and severely deficient (≤ 5 nmol/L).
A total of 293 patients were included (52 eSE, 40 ICU-noSE, 44 non-ICU, and 157 outpatient). The median age was 55 (range 19-99) years. The median PLP level of the eSE group (12 nmol/L) was lower than that of the ICU-noSE (22 nmol/L, p = 0.003), non-ICU (16 nmol/L, p = 0.05), and outpatient groups (36 nmol/L, p < 0.001). Patients with eSE had a significantly higher prevalence of marginal and deficient PLP levels (90 and 80%, respectively) than patients in each of the other three groups (ICU-noSE: 70, 50%; non-ICU: 63, 54%; outpatient: 38, 21%). This significantly higher prevalence persisted after correcting for critical illness severity and timing of PLP level collection.
Our study confirms previous findings indicating a high prevalence of pyridoxine deficiency (as measured by serum PLP levels) in patients with eSE, including when using a more restricted definition of pyridoxine deficiency. Prevalence is higher in patients with eSE than in patients in all three control groups (ICU-noSE, non-ICU, and outpatient). Considering the role of pyridoxine, thus PLP, in the synthesis of γ-aminobutyric acid and its easy and safe administration, prospective studies on pyridoxine supplementation in patients with eSE are needed.