Recent developments in the HIV neuropathies
Recent developments in the HIV neuropathies
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DOI：
10.1097/00019052-200306000-00022
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发表时间：
2003-06-01
影响因子：
4.8
通讯作者：
McArthur, JC
中科院分区：
文献类型：
--
作者：
Luciano, CA;Pardo, CA;McArthur, JC
随着高效抗逆转录病毒治疗的引入，周围神经病变已成为HIV感染最常见的神经系统并发症。这些神经病变的频率和频谱正在发生变化，因为各种毒性和免疫因素被新的治疗策略所改变。最近的研究提供了一个更好地了解的危险因素，标志物和相关的致病机制，并彻底审查这些是至关重要的，为提高认识这一重要的和越来越常见的complication.Recent findingsThe联合使用的双脱氧核苷，与免疫介导的机制引发的HIV感染，是至关重要的远端感觉多发性神经病的发展。神经病变的有价值的标志物，如皮肤活检的表皮内神经纤维密度已被验证，并有望成为一个有价值的工具，在检测和监测远端感觉多发性神经病变。病毒学活性标志物也与远端感觉性多发性神经病中神经性疼痛的严重程度相关。在某些情况下，抗逆转录病毒药物增强的病毒抑制实际上可能改善或降低某些类型神经病变的频率。新的证据支持线粒体毒性是双脱氧核苷相关感觉神经病变的主要机制，并且出现了关于预先存在的线粒体缺陷增加风险的问题。确认的治疗仅限于减少症状，需要进一步调查的纠正therapy.SummaryIncreased和改善监测HIV相关的神经病变将允许早期干预，以提高生活质量，防止严重的毒性。更好地了解现行机制将有助于采取更有效的干预措施。
Purpose of reviewWith the introduction of highly active antiretroviral therapy peripheral neuropathies have become the most common neurological complications in HIV infection. The frequency and spectrum of these neuropathies are changing, as the various toxic and immune factors are modified by new treatment strategies. Recent studies have provided a better understanding of the risk factors, markers and relevant pathogenic mechanisms, and a thorough review of these is critical for an improved understanding of this important and increasingly common complication.Recent findingsThe combined use of dideoxynucleosides, in association with immune-mediated mechanisms triggered by HIV infection, are critical in the development of distal sensory polyneuropathy. Valuable markers of neuropathy such as intraepidermal nerve fiber density from skin biopsies have been validated and promise to be a valuable tool in the detection and monitoring of distal sensory polyneuropathy. Markers of virological activity have also been associated with the severity of neuropathic pain in distal sensory polyneuropathy. In some instances, the enhanced viral suppression from antiretroviral agents may actually improve or decrease the frequency of certain types of neuropathy. New evidence supports mitochondrial toxicity as a principal mechanism for dideoxynucleoside-associated sensory neuropathy, and questions arise about enhanced risk with pre-existing mitochondrial defects. Confirmed treatments are limited to the reduction of symptoms, with a need for the further investigation of corrective therapies.SummaryIncreased and improved surveillance for HIV-associated neuropathy will allow earlier interventions to improve quality of life and prevent severe toxicities. A better understanding of the prevailing mechanisms will allow for more effective interventions.