巴西疫情爆发 8 年来所报告的先天性寨卡综合征临床病理结果分析

Dhaara Shah, Dhairavi Shah, Olivia Mua, Rana Zeine
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引用次数: 0

摘要

目的:始于巴西的寨卡病毒疫情从2015年2月持续到2016年11月,并发展成为国际公共卫生紧急事件。受寨卡病毒感染的孕妇所生的一组婴儿患有先天性寨卡综合征(CZS),最初定义为严重小头畸形、视网膜瘢痕、关节畸形和肌张力过高。本研究探讨了迄今为止描述的所有 CZS 临床病理结果的性质、范围和严重程度,并按系统进行了汇编和分析。它回顾了监测疾病进展的研究,并提出了 CZS 分期的分类方案。此外,还讨论了与 CZS 发病机制有关的致畸细胞和分子机制。方法:通过WorldCat.org和ProQuest Central数据库进行文献检索,对2015-2016年CZS爆发的系列病例研究进行系统回顾。结果收录了 26 篇报告,描述了 2016 年至 2023 年间 CZS 病例(包括死胎)的放射学、眼科学、听力学、整形外科和实验室检测结果。CZS神经病理学包括产前和产后小头畸形、脑钙化、四肢瘫痪、癫痫、脑室肥大、脑实质减少、皮质发育畸形和睡眠脑电图紊乱。视力障碍是由于视网膜和视神经病变造成的。传导性和感音神经性听力障碍稳定。肌张力过高、肌张力过低和痉挛伴有足部、髋部、膝部和肩部畸形,导致关节畸形和关节活动受限。免疫器官增大,白细胞计数增加,细胞因子失调。颅面畸形影响了中面部,并导致牙齿萌出延迟。其他研究提出,这些全身性致畸效应可能是由于胎儿多个祖细胞系受到经胎盘寨卡病毒感染所致。结论与 CZS 相关的大脑、眼睛、肌肉骨骼和免疫功能损害造成了从中度到重度不等的残疾,并显著增加了特定年龄的死亡率。有必要开展进一步的研究,以评估进展情况、划分阶段、阐明介导寨卡致畸的确切分子机制、制定合适的治疗策略以及设计支持性社会政策。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Analysis of congenital Zika syndrome clinicopathologic findings reported in the 8 years since the Brazilian outbreak
Aim: A Zika virus outbreak that began in Brazil, developed into an international public health emergency that extended from February 2015 until November 2016. Zika-infected pregnant women gave birth to a cohort of infants with congenital Zika syndrome (CZS) originally defined by severe microcephaly, retinal scarring, joint deformities, and hypertonia. This study examines the nature, extent, and severity of all CZS clinicopathologic findings described to date, compiled and analyzed by system. It reviews studies monitoring disease progression and proposing classification schemes for CZS stages. The teratogenic cellular and molecular mechanisms implicated in CZS pathogenesis are also discussed. Methods: A systematic review was conducted by literature search through WorldCat.org and ProQuest Central databases to identify studies on case series from the 2015–2016 CZS outbreak. Results: Twenty-six reports were included describing radiologic, ophthalmologic, audiologic, orthopedic, and laboratory test results in CZS cases including stillborns between 2016 and 2023. CZS neuropathology included prenatal and postnatal microcephaly, cerebral calcifications, quadriparesis, epilepsy, ventriculomegaly, reduced cerebral parenchyma, malformation of cortical development, and sleep electroencephalogram disturbances. Visual deficits were due to retinal and optic nerve lesions. Conductive and sensorineural hearing deficits were stable. Hypertonia, hypotonia, and spasticity with foot, hip, knee, and shoulder deformities resulted in arthrogryposis and restricted joint mobility. There was enlargement of immune organs, increased leukocyte counts, and cytokine dysregulation. Oro-craniofacial deformities affected the midface and caused dental eruption delay. Additional studies proposed that these systemic teratogenic effects could be attributable to transplacental Zika virus infection of multiple fetal progenitor cell lineages. Conclusions: The CZS-associated impairments in brain, eye, musculoskeletal, and immunologic functions caused disabilities that varied from moderate to severe, and significantly increased age-specific mortality rates. Further research is warranted to assess progression, classify stages, elucidate the precise molecular mechanisms mediating Zika teratogenicity, develop suitable therapeutic strategies, and design supportive social policies.
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