The clinical pathology of severe acute respiratory syndrome (SARS): a report from China.
Identifieur interne : 003289 ( PubMed/Corpus ); précédent : 003288; suivant : 003290The clinical pathology of severe acute respiratory syndrome (SARS): a report from China.
Auteurs : Yanqing Ding ; Huijun Wang ; Hong Shen ; Zhuguo Li ; Jian Geng ; Huixia Han ; Junjie Cai ; Xin Li ; Wei Kang ; Desheng Weng ; Yaodan Lu ; Dehua Wu ; Li He ; Kaitai YaoSource :
- The Journal of pathology [ 0022-3417 ] ; 2003.
English descriptors
- KwdEn :
- Adrenal Glands (pathology), Adult, Bone Marrow (pathology), Brain (pathology), Female, Humans, Immunohistochemistry (methods), Kidney (pathology), Liver (pathology), Lung (pathology), Lymph Nodes (pathology), Male, Microscopy, Electron, Middle Aged, Myocardium (pathology), Retrospective Studies, Severe Acute Respiratory Syndrome (pathology), Spleen (pathology).
- MESH :
- methods : Immunohistochemistry.
- pathology : Adrenal Glands, Bone Marrow, Brain, Kidney, Liver, Lung, Lymph Nodes, Myocardium, Severe Acute Respiratory Syndrome, Spleen.
- Adult, Female, Humans, Male, Microscopy, Electron, Middle Aged, Retrospective Studies.
Abstract
In order to investigate the clinical pathology of severe acute respiratory syndrome (SARS), the autopsies of three patients who died from SARS in Nan Fang Hospital Guangdong, China were studied retrospectively. Routine haematoxylin and eosin (H&E) staining was used to study all of the tissues from the three cases. The lung tissue specimens were studied further with Macchiavello staining, viral inclusion body staining, reticulin staining, PAS staining, immunohistochemistry, ultrathin sectioning and staining, light microscopy, and transmission electron microscopy. The first symptom was hyperpyrexia in all three cases, followed by progressive dyspnoea and lung field shadowing. The pulmonary lesions included bilateral extensive consolidation, localized haemorrhage and necrosis, desquamative pulmonary alveolitis and bronchitis, proliferation and desquamation of alveolar epithelial cells, exudation of protein and monocytes, lymphocytes and plasma cells in alveoli, hyaline membrane formation, and viral inclusion bodies in alveolar epithelial cells. There was also massive necrosis of splenic lymphoid tissue and localized necrosis in lymph nodes. Systemic vasculitis included oedema, localized fibrinoid necrosis, and infiltration of monocytes, lymphocytes, and plasma cells into vessel walls in the heart, lung, liver, kidney, adrenal gland, and the stroma of striated muscles. Thrombosis was present in small veins. Systemic toxic changes included degeneration and necrosis of the parenchyma cells in the lung, liver, kidney, heart, and adrenal gland. Electron microscopy demonstrated clusters of viral particles, consistent with coronavirus, in lung tissue. SARS is a systemic disease that injures many organs. The lungs, immune organs, and systemic small vessels are the main targets of virus attack, so that extensive consolidation of the lung, diffuse alveolar damage with hyaline membrane formation, respiratory distress, and decreased immune function are the main causes of death.
DOI: 10.1002/path.1440
PubMed: 12845623
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first="Kaitai" last="Yao">Kaitai Yao</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2003">2003</date><idno type="RBID">pubmed:12845623</idno><idno type="pmid">12845623</idno><idno type="doi">10.1002/path.1440</idno><idno type="wicri:Area/PubMed/Corpus">003289</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">003289</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The clinical pathology of severe acute respiratory syndrome (SARS): a report from China.</title><author><name sortKey="Ding, Yanqing" sort="Ding, Yanqing" uniqKey="Ding Y" first="Yanqing" last="Ding">Yanqing Ding</name><affiliation><nlm:affiliation>Department of Pathology, Nan Fang Hospital, First Military Medical University, Guangzhou, Guangdong Province 510515, PR China. dyq@fimmu.com</nlm:affiliation></affiliation></author><author><name sortKey="Wang, Huijun" sort="Wang, Huijun" uniqKey="Wang H" first="Huijun" last="Wang">Huijun Wang</name></author><author><name sortKey="Shen, Hong" sort="Shen, Hong" uniqKey="Shen H" first="Hong" last="Shen">Hong Shen</name></author><author><name sortKey="Li, Zhuguo" sort="Li, Zhuguo" uniqKey="Li Z" first="Zhuguo" last="Li">Zhuguo Li</name></author><author><name sortKey="Geng, Jian" sort="Geng, Jian" uniqKey="Geng J" first="Jian" last="Geng">Jian Geng</name></author><author><name sortKey="Han, Huixia" sort="Han, Huixia" uniqKey="Han H" first="Huixia" last="Han">Huixia Han</name></author><author><name sortKey="Cai, Junjie" sort="Cai, Junjie" uniqKey="Cai J" first="Junjie" last="Cai">Junjie Cai</name></author><author><name sortKey="Li, Xin" sort="Li, Xin" uniqKey="Li X" first="Xin" last="Li">Xin Li</name></author><author><name sortKey="Kang, Wei" sort="Kang, Wei" uniqKey="Kang W" first="Wei" last="Kang">Wei Kang</name></author><author><name sortKey="Weng, Desheng" sort="Weng, Desheng" uniqKey="Weng D" first="Desheng" last="Weng">Desheng Weng</name></author><author><name sortKey="Lu, Yaodan" sort="Lu, Yaodan" uniqKey="Lu Y" first="Yaodan" last="Lu">Yaodan Lu</name></author><author><name sortKey="Wu, Dehua" sort="Wu, Dehua" uniqKey="Wu D" first="Dehua" last="Wu">Dehua Wu</name></author><author><name sortKey="He, Li" sort="He, Li" uniqKey="He L" first="Li" last="He">Li He</name></author><author><name sortKey="Yao, Kaitai" sort="Yao, Kaitai" uniqKey="Yao K" first="Kaitai" last="Yao">Kaitai Yao</name></author></analytic><series><title level="j">The Journal of pathology</title><idno type="ISSN">0022-3417</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adrenal Glands (pathology)</term><term>Adult</term><term>Bone Marrow (pathology)</term><term>Brain (pathology)</term><term>Female</term><term>Humans</term><term>Immunohistochemistry (methods)</term><term>Kidney (pathology)</term><term>Liver (pathology)</term><term>Lung (pathology)</term><term>Lymph Nodes (pathology)</term><term>Male</term><term>Microscopy, Electron</term><term>Middle Aged</term><term>Myocardium (pathology)</term><term>Retrospective Studies</term><term>Severe Acute Respiratory Syndrome (pathology)</term><term>Spleen (pathology)</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Immunohistochemistry</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Adrenal Glands</term><term>Bone Marrow</term><term>Brain</term><term>Kidney</term><term>Liver</term><term>Lung</term><term>Lymph Nodes</term><term>Myocardium</term><term>Severe Acute Respiratory Syndrome</term><term>Spleen</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Female</term><term>Humans</term><term>Male</term><term>Microscopy, Electron</term><term>Middle Aged</term><term>Retrospective Studies</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In order to investigate the clinical pathology of severe acute respiratory syndrome (SARS), the autopsies of three patients who died from SARS in Nan Fang Hospital Guangdong, China were studied retrospectively. Routine haematoxylin and eosin (H&E) staining was used to study all of the tissues from the three cases. The lung tissue specimens were studied further with Macchiavello staining, viral inclusion body staining, reticulin staining, PAS staining, immunohistochemistry, ultrathin sectioning and staining, light microscopy, and transmission electron microscopy. The first symptom was hyperpyrexia in all three cases, followed by progressive dyspnoea and lung field shadowing. The pulmonary lesions included bilateral extensive consolidation, localized haemorrhage and necrosis, desquamative pulmonary alveolitis and bronchitis, proliferation and desquamation of alveolar epithelial cells, exudation of protein and monocytes, lymphocytes and plasma cells in alveoli, hyaline membrane formation, and viral inclusion bodies in alveolar epithelial cells. There was also massive necrosis of splenic lymphoid tissue and localized necrosis in lymph nodes. Systemic vasculitis included oedema, localized fibrinoid necrosis, and infiltration of monocytes, lymphocytes, and plasma cells into vessel walls in the heart, lung, liver, kidney, adrenal gland, and the stroma of striated muscles. Thrombosis was present in small veins. Systemic toxic changes included degeneration and necrosis of the parenchyma cells in the lung, liver, kidney, heart, and adrenal gland. Electron microscopy demonstrated clusters of viral particles, consistent with coronavirus, in lung tissue. SARS is a systemic disease that injures many organs. The lungs, immune organs, and systemic small vessels are the main targets of virus attack, so that extensive consolidation of the lung, diffuse alveolar damage with hyaline membrane formation, respiratory distress, and decreased immune function are the main causes of death.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12845623</PMID><DateCompleted><Year>2003</Year><Month>09</Month><Day>16</Day></DateCompleted><DateRevised><Year>2006</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-3417</ISSN><JournalIssue CitedMedium="Print"><Volume>200</Volume><Issue>3</Issue><PubDate><Year>2003</Year><Month>Jul</Month></PubDate></JournalIssue><Title>The Journal of pathology</Title><ISOAbbreviation>J. Pathol.</ISOAbbreviation></Journal><ArticleTitle>The clinical pathology of severe acute respiratory syndrome (SARS): a report from China.</ArticleTitle><Pagination><MedlinePgn>282-9</MedlinePgn></Pagination><Abstract><AbstractText>In order to investigate the clinical pathology of severe acute respiratory syndrome (SARS), the autopsies of three patients who died from SARS in Nan Fang Hospital Guangdong, China were studied retrospectively. Routine haematoxylin and eosin (H&E) staining was used to study all of the tissues from the three cases. The lung tissue specimens were studied further with Macchiavello staining, viral inclusion body staining, reticulin staining, PAS staining, immunohistochemistry, ultrathin sectioning and staining, light microscopy, and transmission electron microscopy. The first symptom was hyperpyrexia in all three cases, followed by progressive dyspnoea and lung field shadowing. The pulmonary lesions included bilateral extensive consolidation, localized haemorrhage and necrosis, desquamative pulmonary alveolitis and bronchitis, proliferation and desquamation of alveolar epithelial cells, exudation of protein and monocytes, lymphocytes and plasma cells in alveoli, hyaline membrane formation, and viral inclusion bodies in alveolar epithelial cells. There was also massive necrosis of splenic lymphoid tissue and localized necrosis in lymph nodes. Systemic vasculitis included oedema, localized fibrinoid necrosis, and infiltration of monocytes, lymphocytes, and plasma cells into vessel walls in the heart, lung, liver, kidney, adrenal gland, and the stroma of striated muscles. Thrombosis was present in small veins. Systemic toxic changes included degeneration and necrosis of the parenchyma cells in the lung, liver, kidney, heart, and adrenal gland. Electron microscopy demonstrated clusters of viral particles, consistent with coronavirus, in lung tissue. SARS is a systemic disease that injures many organs. The lungs, immune organs, and systemic small vessels are the main targets of virus attack, so that extensive consolidation of the lung, diffuse alveolar damage with hyaline membrane formation, respiratory distress, and decreased immune function are the main causes of death.</AbstractText><CopyrightInformation>Copyright 2003 John Wiley & Sons, Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ding</LastName><ForeName>Yanqing</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Pathology, Nan Fang Hospital, First Military Medical University, Guangzhou, Guangdong Province 510515, PR China. dyq@fimmu.com</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Huijun</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Shen</LastName><ForeName>Hong</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Zhuguo</ForeName><Initials>Z</Initials></Author><Author ValidYN="Y"><LastName>Geng</LastName><ForeName>Jian</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Han</LastName><ForeName>Huixia</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Cai</LastName><ForeName>Junjie</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Xin</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Kang</LastName><ForeName>Wei</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Weng</LastName><ForeName>Desheng</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>Yaodan</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Dehua</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>He</LastName><ForeName>Li</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Yao</LastName><ForeName>Kaitai</ForeName><Initials>K</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Pathol</MedlineTA><NlmUniqueID>0204634</NlmUniqueID><ISSNLinking>0022-3417</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000311" MajorTopicYN="N">Adrenal Glands</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001853" MajorTopicYN="N">Bone 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MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008198" MajorTopicYN="N">Lymph Nodes</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008854" MajorTopicYN="N">Microscopy, Electron</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009206" MajorTopicYN="N">Myocardium</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013154" MajorTopicYN="N">Spleen</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2003</Year><Month>7</Month><Day>8</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2003</Year><Month>9</Month><Day>17</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2003</Year><Month>7</Month><Day>8</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">12845623</ArticleId><ArticleId 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