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沙利度胺分子的死亡与重生:一例沙利度胺诱发的感觉神经病变

Death and Rebirth of the Thalidomide Molecule: A Case of Thalidomide-Induced Sensory Neuropathy.

作者信息

Kesserwani Hassan

机构信息

Neurology, Flowers Medical Group, Dothan, USA.

出版信息

Cureus. 2021 Feb 4;13(2):e13140. doi: 10.7759/cureus.13140.

DOI:10.7759/cureus.13140
PMID:33728154
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7936918/
Abstract

The thalidomide molecule is a remarkable molecule that exists in a racemic mixture of optical isomers. In the 1950s, due to its teratogenicity, the levorotatory isomer led to its dramatic downfall. However, the molecule with its panoramic mechanisms of action and its uncanny ability to intercalate within the geometry of deoxyribonucleic acid (DNA), led to its remarkable renaissance; thalidomide being United States Food and Drug Administration (FDA)-approved for at least 13 different indications ranging from multiple myeloma to leprosy to glioblastoma. Thalidomide-induced polyneuropathy is usually reversible and is the rate-limiting step in its long-term use. The development of a polyneuropathy is invariably associated with a cumulative dose exceeding 20 grams. However, the polyneuropathy is almost always a sensory neuropathy. Asymmetry, bona fide weakness such as difficulty standing on the heels, a poly-ganglioneuropathy pattern with widespread or patchy numbness and sensory ataxia should raise a red flag and an alternative diagnosis should be considered. We present a typical case of a thalidomide-induced sensory neuropathy in order to highlight the resurgence of thalidomide use in clinical practice. We review the literature and outline the molecular biology of the thalidomide molecule.

摘要

沙利度胺分子是一种存在于旋光异构体消旋混合物中的非凡分子。在20世纪50年代,由于其致畸性,左旋异构体导致了它的急剧衰落。然而,该分子具有全面的作用机制以及奇特的嵌入脱氧核糖核酸(DNA)几何结构的能力,从而使其显著复兴;沙利度胺已获得美国食品药品监督管理局(FDA)批准用于至少13种不同适应症,从多发性骨髓瘤到麻风病再到胶质母细胞瘤。沙利度胺引起的多发性神经病通常是可逆的,并且是其长期使用中的限速步骤。多发性神经病的发生总是与累积剂量超过20克有关。然而,多发性神经病几乎总是感觉性神经病。不对称、真正的无力(如难以足跟站立)、伴有广泛或片状麻木及感觉性共济失调的多神经节神经病模式应引起警惕,应考虑其他诊断。我们呈现一例典型的沙利度胺引起的感觉性神经病病例,以突出沙利度胺在临床实践中的再度应用。我们回顾了文献并概述了沙利度胺分子的分子生物学。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e24e/7936918/ff71faac7336/cureus-0013-00000013140-i03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e24e/7936918/6986d840be4d/cureus-0013-00000013140-i01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e24e/7936918/8332fd8b78f3/cureus-0013-00000013140-i02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e24e/7936918/ff71faac7336/cureus-0013-00000013140-i03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e24e/7936918/6986d840be4d/cureus-0013-00000013140-i01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e24e/7936918/8332fd8b78f3/cureus-0013-00000013140-i02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e24e/7936918/ff71faac7336/cureus-0013-00000013140-i03.jpg

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本文引用的文献

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Polymorphisms in the promotor region of the CRBN gene as a predictive factor for peripheral neuropathy in the course of thalidomide-based chemotherapy in multiple myeloma patients.CRBN 基因启动子区域的多态性可作为多发性骨髓瘤患者基于沙利度胺化疗过程中周围神经病的预测因子。
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Thalidomide as a potent inhibitor of neointimal hyperplasia after balloon injury in rat carotid artery.沙利度胺作为大鼠颈动脉球囊损伤后新生内膜增生的有效抑制剂。
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