Evidence map›Paper›PMID 14767982›Full record

ArticleHepatology (Baltimore, Md.)2004

SARS-associated viral hepatitis caused by a novel coronavirus: report of three cases.

Tai-Nin Chau, Kam-Cheong Lee, Hung Yao, Tak-Yin Tsang, Tat-Chong Chow, Yiu-Cheong Yeung, Kin-Wing Choi, Yuk-Keung Tso, Terence Lau, Sik-To Lai and 1 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Hepatology (Baltimore, Md.), 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 228 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
228citing papers in PubMed, 7 pooled it
6.9field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

228 citing papers in PubMed, 7 syntheses or guidelines pooled it, 438 citations in OpenAlex.

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  18. Acute severe hepatitis and COVID-19: case report.The Pan African medical journal · 2024
    Article
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168 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 4 countries.

Tai-Nin ChauDepartment of Medicine and Geriatrics, Princess Margaret Hospital, Hong Kong, SAR China. chautainin@hotmail.com
Kam-Cheong Lee
Hung Yao
Tak-Yin Tsang
Tat-Chong Chow
Yiu-Cheong Yeung
Kin-Wing Choi
Yuk-Keung Tso
Terence Lau
Sik-To Lai
Ching-Lung Lai
Princess Margaret Hospital · NZGTx (United States) · USQueen Mary Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AdultAnti-Inflammatory AgentsApoptosisBiopsyCoronavirusDNA, ViralDrug CombinationsFemaleHepatitis, Viral, HumanHIV Protease InhibitorsHumansLiverLopinavirMethylprednisoloneMiddle AgedMitosisAnti-Inflammatory AgentsDNA, ViralDrug CombinationsHIV Protease InhibitorsLopinavirMethylprednisolonePyrimidinonesRitonavir

Identifiers

PMID14767982
PMCPMC7165792
OpenAlexW2090258227

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.