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甲卡西酮滥用者的锰诱导帕金森病:暴露和随访的生物标志物。

Manganese-induced parkinsonism in methcathinone abusers: bio-markers of exposure and follow-up.

机构信息

Department of Neurology and Neurosurgery, University of Tartu, Tartu, Estonia.

出版信息

Eur J Neurol. 2013 Jun;20(6):915-20. doi: 10.1111/ene.12088. Epub 2013 Jan 24.

DOI:10.1111/ene.12088
PMID:23347399
Abstract

BACKGROUND AND PURPOSE

Methcathinone abuse is a new cause of manganism. The psychostimulant is prepared from pseudoephedrine using potassium permanganate as an oxidant. We describe the clinical, biological, neuroimaging characteristics and follow-up results in a large Estonian cohort of intravenous methcathinone users.

METHODS

During 2006-2012 we studied 38 methcathinone abusers with a mean age of 33 years. Subjects were rated by the Unified Parkinson's Disease Rating Scale (UPDRS), Hoehn and Yahr (HY), and Schwab and England (SE) rating scales. Twenty-four cases were reassessed 9-70 (20 ± 15) months after the initial evaluation. Manganese (Mn) in plasma and hair was analysed by inductively coupled plasma-atom emission spectrometry. Magnetic resonance imaging (MRI) was performed in 11, and single-photon emission computed tomography (SPECT) with iodobenzamide (IBZM) in eight subjects.

RESULTS

The average total UPDRS score was 43 ± 21. The most severely affected domains in UPDRS Part III were speech and postural stability, the least affected domain was resting tremor. At follow-up there was worsening of HY and SE rating scales. Subjects had a higher mean level of Mn in hair (2.9 ± 3.8 ppm) than controls (0.82 ± 1.02 ppm), P = 0.02. Plasma Mn concentrations were higher (11.5 ± 6.2 ppb) in active than in former users (5.6 ± 1.8 ppb), P = 0.006. Active methcathinone users had increased MRI T1-signal intensity in the globus pallidus, substantia nigra and periaquaductal gray matter. IBZM-SPECT showed normal symmetric tracer uptake in striatum.

CONCLUSION

Methcathinone abusers develop a distinctive hypokinetic syndrome. Though the biomarkers of Mn exposure are characteristic only of recent abuse, the syndrome is not reversible.

摘要

背景与目的

甲卡西酮滥用是锰中毒的一个新病因。该精神兴奋剂是通过使用高锰酸钾将伪麻黄碱制备而成的。我们描述了在爱沙尼亚静脉内使用甲卡西酮的大型队列中,38 例甲卡西酮滥用者的临床、生物学、神经影像学特征和随访结果。

方法

在 2006 年至 2012 年间,我们研究了 38 名平均年龄为 33 岁的甲卡西酮滥用者。采用统一帕金森病评定量表(UPDRS)、Hoehn 和 Yahr(HY)以及 Schwab 和 England(SE)评分量表对受试者进行评分。24 例在初次评估后 9-70(20±15)个月进行了重新评估。通过电感耦合等离子体质谱法(ICP-MS)分析血浆和头发中的锰(Mn)。11 例患者进行了磁共振成像(MRI)检查,8 例患者进行了碘苯甲酰胺(IBZM)单光子发射计算机断层扫描(SPECT)检查。

结果

平均总 UPDRS 评分为 43±21。UPDRS 第三部分中受影响最严重的领域是言语和姿势稳定性,受影响最小的领域是静止性震颤。随访时,HY 和 SE 评分量表均恶化。与对照组(0.82±1.02ppm)相比,受试者头发中的 Mn 水平(2.9±3.8ppm)更高,P=0.02。与前使用者(5.6±1.8ppb)相比,现使用者的血浆 Mn 浓度更高(11.5±6.2ppb),P=0.006。活跃的甲卡西酮使用者的苍白球、黑质和导水管周围灰质的 MRI T1 信号强度增加。IBZM-SPECT 显示纹状体的示踪剂摄取对称正常。

结论

甲卡西酮滥用者会出现独特的运动障碍综合征。尽管 Mn 暴露的生物标志物仅特征性地反映近期滥用,但该综合征是不可逆转的。

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