M Multi-Organ Histopathological Changes in SARS COV2 Infection: A Systematic Review and Meta-analysis

Maream Mohammed Ali Al-Haboobi, Rihab Hameed Al-Mudhafar
{"title":"M Multi-Organ Histopathological Changes in SARS COV2 Infection: A Systematic Review and Meta-analysis","authors":"Maream Mohammed Ali Al-Haboobi, Rihab Hameed Al-Mudhafar","doi":"10.36330/kmj.v20i1.15435","DOIUrl":null,"url":null,"abstract":"Background: The World Health Organization has officially acknowledged the emergence of Coronavirus Disease 2019 (COVID-19), attributed to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, as a rapidly escalating global public health issue and declared it a pandemic. SARS-CoV-2 infection can lead to varied and multiorgan pathologies, with the most notable impacts occurring in the lungs (characterized by phases of diffuse alveolar damage, microthrombi, and bronchopneumonia), heart (involving lymphocytic myocarditis), kidney (resulting in acute tubular injury), and vasculature (involving microthrombi and deep vein thrombi). Objectives: To summarize, resolve contradiction and provide solid evidence on multiorgan histopathological changes caused by SARS-CoV2 infection.   Material and method: Histological data obtained from autopsy and biopsy studies were gathered following the guidelines of the Preferred Reporting Items for Systematic Review (PRISMA). An extensive electronic search was conducted on databases such as PubMed, Science Direct, Scopus, and Google Scholar, covering the period from database inception to March 2022. The collected studies underwent a systematic literature search, and a thorough critical review was performed. Result: After excluding studies that did not meet the eligibility criteria, a total of 58 articles were included in the review. We estimate the histopathological findings of 13 organ. For the pool proportion of exudative, proliferative and fibrotic phase of diffuse alveolar damage of lung is (70.666%, 56.126% and 33.031%) respectively. For liver steotosis is 35.808%. For acute tubular injury of kidney is 74.872%. For adrenal cortical necrosis is 13.113%. For brain gliosis is 13.865%. For heart necrosis is 5.477%. For gastrointestinal tract the pool proportion of inflammatory cells infiltration is 6.171%. For placental infarction is 25.684%. For orchitis is 29.019%. For perivascular inflammation of skin is 35.176%. For lymphocytic depletion of white pulp of spleen is 69.204%. For hemophagiocytosis of lymph node is 7.022%. For bone marrow fibrosis is 8.473%. Conclusion: COVID-19 is characterized as a multiorgan infection closely associated with a hyperinflammatory state, believed to initiate with diffuse alveolar damage and immuno-thrombotic microangiopathy. The extensive activation of the immune system and microvascular damage may contribute to indirect harm to other organs, although the direct impact of the virus on these tissues cannot be ruled out.","PeriodicalId":507092,"journal":{"name":"Kufa Medical Journal","volume":"3 5","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Kufa Medical Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.36330/kmj.v20i1.15435","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Background: The World Health Organization has officially acknowledged the emergence of Coronavirus Disease 2019 (COVID-19), attributed to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, as a rapidly escalating global public health issue and declared it a pandemic. SARS-CoV-2 infection can lead to varied and multiorgan pathologies, with the most notable impacts occurring in the lungs (characterized by phases of diffuse alveolar damage, microthrombi, and bronchopneumonia), heart (involving lymphocytic myocarditis), kidney (resulting in acute tubular injury), and vasculature (involving microthrombi and deep vein thrombi). Objectives: To summarize, resolve contradiction and provide solid evidence on multiorgan histopathological changes caused by SARS-CoV2 infection.   Material and method: Histological data obtained from autopsy and biopsy studies were gathered following the guidelines of the Preferred Reporting Items for Systematic Review (PRISMA). An extensive electronic search was conducted on databases such as PubMed, Science Direct, Scopus, and Google Scholar, covering the period from database inception to March 2022. The collected studies underwent a systematic literature search, and a thorough critical review was performed. Result: After excluding studies that did not meet the eligibility criteria, a total of 58 articles were included in the review. We estimate the histopathological findings of 13 organ. For the pool proportion of exudative, proliferative and fibrotic phase of diffuse alveolar damage of lung is (70.666%, 56.126% and 33.031%) respectively. For liver steotosis is 35.808%. For acute tubular injury of kidney is 74.872%. For adrenal cortical necrosis is 13.113%. For brain gliosis is 13.865%. For heart necrosis is 5.477%. For gastrointestinal tract the pool proportion of inflammatory cells infiltration is 6.171%. For placental infarction is 25.684%. For orchitis is 29.019%. For perivascular inflammation of skin is 35.176%. For lymphocytic depletion of white pulp of spleen is 69.204%. For hemophagiocytosis of lymph node is 7.022%. For bone marrow fibrosis is 8.473%. Conclusion: COVID-19 is characterized as a multiorgan infection closely associated with a hyperinflammatory state, believed to initiate with diffuse alveolar damage and immuno-thrombotic microangiopathy. The extensive activation of the immune system and microvascular damage may contribute to indirect harm to other organs, although the direct impact of the virus on these tissues cannot be ruled out.
M SARS COV2 感染的多器官组织病理学变化:系统回顾和元分析
背景:世界卫生组织已正式确认,由严重急性呼吸系统综合征冠状病毒 2(SARS-CoV-2)病毒引起的 2019 年冠状病毒病(COVID-19)的出现是一个迅速升级的全球公共卫生问题,并宣布其为大流行病。SARS-CoV-2 感染可导致多种多器官病变,最显著的影响发生在肺部(以弥漫性肺泡损伤、微血栓和支气管肺炎为特征)、心脏(涉及淋巴细胞性心肌炎)、肾脏(导致急性肾小管损伤)和血管(涉及微血栓和深静脉血栓)。目标:总结、解决SARS-CoV2感染引起的多器官组织病理学变化的矛盾,并提供确凿证据。 材料与方法按照系统性综述首选报告项目(PRISMA)的指导原则,收集从尸检和活检研究中获得的组织学数据。在 PubMed、Science Direct、Scopus 和 Google Scholar 等数据库中进行了广泛的电子检索,检索时间从数据库建立之初到 2022 年 3 月。对收集到的研究进行了系统的文献检索,并进行了全面的严格审查。结果在排除了不符合资格标准的研究后,共有 58 篇文章被纳入综述。我们估计了 13 个器官的组织病理学结果。肺弥漫性肺泡损伤的渗出期、增殖期和纤维化期的总比例分别为(70.666%、56.126% 和 33.031%)。肝脏脂肪变性为 35.808%。肾脏急性肾小管损伤为 74.872%。肾上腺皮质坏死为 13.113%。脑胶质增生为 13.865%。心脏坏死为 5.477%。胃肠道炎症细胞浸润池比例为 6.171%。胎盘梗塞为 25.684%。睾丸炎为 29.019%。皮肤血管周围炎症为 35.176%。脾脏白髓淋巴细胞耗竭为 69.204%。淋巴结嗜血细胞增多为 7.022%。骨髓纤维化为 8.473%。结论COVID-19 的特点是与高炎症状态密切相关的多器官感染,据信其起因是弥漫性肺泡损伤和免疫血栓性微血管病变。免疫系统的广泛激活和微血管损伤可能会对其他器官造成间接伤害,尽管不能排除病毒对这些组织的直接影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信