SARS-Associated viral hepatitis caused by a novel coronavirus: Report of three cases
Identifieur interne : 000776 ( PascalFrancis/Checkpoint ); précédent : 000775; suivant : 000777SARS-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 :
- Hepatology : (Baltimore, Md.) [ 0270-9139 ] ; 2004.
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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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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">SARS-Associated viral hepatitis caused by a novel coronavirus: Report of three cases</title>
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<series><title level="j" type="main">Hepatology : (Baltimore, Md.)</title>
<title level="j" type="abbreviated">Hepatology : (Baltim. Md.)</title>
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<term>Coronavirus</term>
<term>Gastroenterology</term>
<term>Report</term>
<term>Severe acute respiratory syndrome</term>
<term>Viral hepatitis A</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term>
<term>Hépatite virale A</term>
<term>Etude cas</term>
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<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>
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<fA11 i1="01" i2="1"><s1>CHAU (Tai-Nin)</s1>
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<fA11 i1="02" i2="1"><s1>LEE (Kam-Cheong)</s1>
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<fA11 i1="03" i2="1"><s1>HUNG YAO</s1>
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<fA11 i1="04" i2="1"><s1>TSANG (Tak-Yin)</s1>
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<fA11 i1="05" i2="1"><s1>CHOW (Tat-Chong)</s1>
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<fA11 i1="06" i2="1"><s1>YEUNG (Yiu-Cheong)</s1>
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<fA11 i1="07" i2="1"><s1>CHOI (Kin-Wing)</s1>
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<fA11 i1="08" i2="1"><s1>TSO (Yuk-Keung)</s1>
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</fA11>
<fA14 i1="01"><s1>Department of Medicine and Geriatrics and Department of Pathology, Princess Margaret Hospital</s1>
<s3>HKG</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>10 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Hong Kong DNA Chips Ltd.</s1>
<s3>HKG</s3>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Medicine, Queen Mary Hospital, University of Hong Kong</s1>
<s3>HKG</s3>
<sZ>11 aut.</sZ>
</fA14>
<fA20><s1>302-310</s1>
</fA20>
<fA21><s1>2004</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>19427</s2>
<s5>354000113465180080</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2004 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>45 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>04-0357484</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Hepatology : (Baltimore, Md.)</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>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.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B13</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B05C02C</s0>
</fC02>
<fC02 i1="03" i2="X"><s0>002B05C02G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Syndrome respiratoire aigu sévère</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Severe acute respiratory syndrome</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Síndrome respiratorio agudo severo</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Hépatite virale A</s0>
<s5>03</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Viral hepatitis A</s0>
<s5>03</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Hepatitis vírica A</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Etude cas</s0>
<s5>05</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Case study</s0>
<s5>05</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Estudio caso</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Compte rendu</s0>
<s5>08</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Report</s0>
<s5>08</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Informe</s0>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Gastroentérologie</s0>
<s5>09</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Gastroenterology</s0>
<s5>09</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Gastroenterología</s0>
<s5>09</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Virose</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Viral disease</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Virosis</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Infection</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Infection</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Infección</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Appareil respiratoire pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Respiratory disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Poumon pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Lung disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Pulmón patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Appareil digestif pathologie</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Digestive diseases</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Aparato digestivo patología</s0>
<s5>40</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Foie pathologie</s0>
<s5>41</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Hepatic disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Hígado patología</s0>
<s5>41</s5>
</fC07>
<fN21><s1>208</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
<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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