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SARS-Associated viral hepatitis caused by a novel coronavirus: Report of three cases

Identifieur interne : 005A70 ( Main/Exploration ); précédent : 005A69; suivant : 005A71

SARS-Associated viral hepatitis caused by a novel coronavirus: Report of three cases

Auteurs : Tai-Nin Chau [Hong Kong] ; Kam-Cheong Lee [Hong Kong] ; HUNG YAO [Hong Kong] ; Tak-Yin Tsang [Hong Kong] ; Tat-Chong Chow [Hong Kong] ; Yiu-Cheong Yeung [Hong Kong] ; Kin-Wing Choi [Hong Kong] ; Yuk-Keung Tso [Hong Kong] ; Terence Lau [Hong Kong] ; Sik-To Lai [Hong Kong] ; Ching-Lung Lai [Hong Kong]

Source :

RBID : Pascal:04-0357484

Descripteurs français

English descriptors

Abstract

Liver impairment is commonly reported in up to 60% of patients who suffer from severe acute respiratory syndrome (SARS). Here we report the clinical course and liver pathology in three SARS patients with liver impairment. Three patients who fulfilled the World Health Organization case definition of probable SARS and developed marked elevation of alanine aminotransferase were included. Percutaneous liver biopsies were performed. Liver specimens were examined by light and electron microscopy, and immunohistochemistry. Reverse-transcriptase polymerase chain reaction (RT-PCR) using enhanced real-time PCR was applied to look for evidence of SARS-associated coronavirus infection. Marked accumulation of cells in mitosis was observed in two patients and apoptosis was observed in all three patients. Other common pathologic features included ballooning of hepatocytes and mild to moderate lobular lymphocytic infiltration. No eosinophilic infiltration, granuloma, cholestasis, fibrosis, or fibrin deposition was noted. Immunohistochemical studies revealed 0.5% to 11.4% of nuclei were positive for proliferative antigen Ki-67. RT-PCR showed evidence of SARS-associated coronavirus in the liver tissues, but not in the sera of all 3 patients. However, electron microscopy could not identify viral particles. No giant mitochondria, micro- or macro-vesicular steatosis was observed. In conclusion, hepatic impairment in patients with SARS is due to SARS-associated coronavirus infection of the liver. The prominence of mitotic activity of hepatocytes is unique and may be due to a hyperproliferative state with or without disruption of cell cycle by the coronavirus. With better knowledge of pathogenesis, specific therapy may be targeted to reduce viral replication and modify the disease course.


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<term>ADN viral (analyse)</term>
<term>Adulte</term>
<term>Adulte d'âge moyen</term>
<term>Anti-inflammatoires (usage thérapeutique)</term>
<term>Apoptose</term>
<term>Association médicamenteuse</term>
<term>Biopsie</term>
<term>Coronavirus (génétique)</term>
<term>Coronavirus (isolement et purification)</term>
<term>Femelle</term>
<term>Foie (anatomopathologie)</term>
<term>Foie (virologie)</term>
<term>Humains</term>
<term>Hépatites virales humaines (anatomopathologie)</term>
<term>Hépatites virales humaines (traitement médicamenteux)</term>
<term>Hépatites virales humaines (virologie)</term>
<term>Inhibiteurs de protéase du VIH (usage thérapeutique)</term>
<term>Lopinavir</term>
<term>Mitose</term>
<term>Méthylprednisolone (usage thérapeutique)</term>
<term>Pyrimidinones (usage thérapeutique)</term>
<term>Ritonavir (usage thérapeutique)</term>
<term>Syndrome respiratoire aigu sévère ()</term>
<term>Syndrome respiratoire aigu sévère (anatomopathologie)</term>
<term>Syndrome respiratoire aigu sévère (traitement médicamenteux)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en">
<term>DNA, Viral</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en">
<term>Anti-Inflammatory Agents</term>
<term>HIV Protease Inhibitors</term>
<term>Methylprednisolone</term>
<term>Pyrimidinones</term>
<term>Ritonavir</term>
</keywords>
<keywords scheme="MESH" qualifier="analyse" xml:lang="fr">
<term>ADN viral</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr">
<term>Foie</term>
<term>Hépatites virales humaines</term>
<term>Syndrome respiratoire aigu sévère</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en">
<term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en">
<term>Hepatitis, Viral, Human</term>
<term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en">
<term>Coronavirus</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr">
<term>Coronavirus</term>
</keywords>
<keywords scheme="MESH" qualifier="isolation & purification" xml:lang="en">
<term>Coronavirus</term>
</keywords>
<keywords scheme="MESH" qualifier="isolement et purification" xml:lang="fr">
<term>Coronavirus</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en">
<term>Hepatitis, Viral, Human</term>
<term>Liver</term>
<term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr">
<term>Hépatites virales humaines</term>
<term>Syndrome respiratoire aigu sévère</term>
</keywords>
<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr">
<term>Anti-inflammatoires</term>
<term>Inhibiteurs de protéase du VIH</term>
<term>Méthylprednisolone</term>
<term>Pyrimidinones</term>
<term>Ritonavir</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr">
<term>Foie</term>
<term>Hépatites virales humaines</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en">
<term>Hepatitis, Viral, Human</term>
<term>Liver</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Adult</term>
<term>Apoptosis</term>
<term>Biopsy</term>
<term>Drug Combinations</term>
<term>Female</term>
<term>Humans</term>
<term>Lopinavir</term>
<term>Middle Aged</term>
<term>Mitosis</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr">
<term>Adulte</term>
<term>Adulte d'âge moyen</term>
<term>Apoptose</term>
<term>Association médicamenteuse</term>
<term>Biopsie</term>
<term>Femelle</term>
<term>Humains</term>
<term>Lopinavir</term>
<term>Mitose</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Hépatite virale A</term>
<term>Etude cas</term>
<term>Coronavirus</term>
<term>Compte rendu</term>
<term>Gastroentérologie</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">Liver impairment is commonly reported in up to 60% of patients who suffer from severe acute respiratory syndrome (SARS). Here we report the clinical course and liver pathology in three SARS patients with liver impairment. Three patients who fulfilled the World Health Organization case definition of probable SARS and developed marked elevation of alanine aminotransferase were included. Percutaneous liver biopsies were performed. Liver specimens were examined by light and electron microscopy, and immunohistochemistry. Reverse-transcriptase polymerase chain reaction (RT-PCR) using enhanced real-time PCR was applied to look for evidence of SARS-associated coronavirus infection. Marked accumulation of cells in mitosis was observed in two patients and apoptosis was observed in all three patients. Other common pathologic features included ballooning of hepatocytes and mild to moderate lobular lymphocytic infiltration. No eosinophilic infiltration, granuloma, cholestasis, fibrosis, or fibrin deposition was noted. Immunohistochemical studies revealed 0.5% to 11.4% of nuclei were positive for proliferative antigen Ki-67. RT-PCR showed evidence of SARS-associated coronavirus in the liver tissues, but not in the sera of all 3 patients. However, electron microscopy could not identify viral particles. No giant mitochondria, micro- or macro-vesicular steatosis was observed. In conclusion, hepatic impairment in patients with SARS is due to SARS-associated coronavirus infection of the liver. The prominence of mitotic activity of hepatocytes is unique and may be due to a hyperproliferative state with or without disruption of cell cycle by the coronavirus. With better knowledge of pathogenesis, specific therapy may be targeted to reduce viral replication and modify the disease course.</div>
</front>
</TEI>
<affiliations>
<list>
<country>
<li>Hong Kong</li>
</country>
</list>
<tree>
<country name="Hong Kong">
<noRegion>
<name sortKey="Chau, Tai Nin" sort="Chau, Tai Nin" uniqKey="Chau T" first="Tai-Nin" last="Chau">Tai-Nin Chau</name>
</noRegion>
<name sortKey="Choi, Kin Wing" sort="Choi, Kin Wing" uniqKey="Choi K" first="Kin-Wing" last="Choi">Kin-Wing Choi</name>
<name sortKey="Chow, Tat Chong" sort="Chow, Tat Chong" uniqKey="Chow T" first="Tat-Chong" last="Chow">Tat-Chong Chow</name>
<name sortKey="Hung Yao" sort="Hung Yao" uniqKey="Hung Yao" last="Hung Yao">HUNG YAO</name>
<name sortKey="Lai, Ching Lung" sort="Lai, Ching Lung" uniqKey="Lai C" first="Ching-Lung" last="Lai">Ching-Lung Lai</name>
<name sortKey="Lai, Sik To" sort="Lai, Sik To" uniqKey="Lai S" first="Sik-To" last="Lai">Sik-To Lai</name>
<name sortKey="Lau, Terence" sort="Lau, Terence" uniqKey="Lau T" first="Terence" last="Lau">Terence Lau</name>
<name sortKey="Lee, Kam Cheong" sort="Lee, Kam Cheong" uniqKey="Lee K" first="Kam-Cheong" last="Lee">Kam-Cheong Lee</name>
<name sortKey="Tsang, Tak Yin" sort="Tsang, Tak Yin" uniqKey="Tsang T" first="Tak-Yin" last="Tsang">Tak-Yin Tsang</name>
<name sortKey="Tso, Yuk Keung" sort="Tso, Yuk Keung" uniqKey="Tso Y" first="Yuk-Keung" last="Tso">Yuk-Keung Tso</name>
<name sortKey="Yeung, Yiu Cheong" sort="Yeung, Yiu Cheong" uniqKey="Yeung Y" first="Yiu-Cheong" last="Yeung">Yiu-Cheong Yeung</name>
</country>
</tree>
</affiliations>
</record>

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