Evidence map›Paper›PMID 31798280›Full record

ArticleWorld journal of gastroenterology2019

Serum amyloid A levels in patients with liver diseases.

Zi-Ying Yuan, Xing-Xin Zhang, Yu-Jing Wu, Zhi-Ping Zeng, Wei-Min She, Shi-Yao Chen, Yuan-Qing Zhang, Jin-Sheng Guo

Open access · bronzeAbstract read
In one paragraph

Article in World journal of gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Serum amyloid A concentrations, COVID-19 severity and mortality: An updated systematic review and meta-analysis.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2021
    Pooled it
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  7. Serum amyloid A in HFpEF and cardiometabolic diseases.Basic research in cardiology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 1 country.

Zi-Ying YuanDepartment of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Xing-Xin ZhangDepartment of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Yu-Jing WuDepartment of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Zhi-Ping ZengDepartment of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Wei-Min SheDepartment of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Shi-Yao ChenDepartment of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Yuan-Qing ZhangThe First Affiliated Hospital, Yunnan Institute of Digestive Disease, Kunming Medical University, Kunming 650000, Yunnan Province, China.
Jin-Sheng GuoDepartment of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai 200032, China. guo.jinsheng@zs-hospital.sh.cn.
Fudan University · CNZhongshan Hospital · CNKunming Medical University · CNSun Yat-sen University · CNThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSerum amyloid A (SAA) is an acute phase protein mainly synthesized by the liver. SAA induces inflammatory phenotype and promotes cell proliferation in activated hepatic stellate cells, the major scar forming cells in the liver. However, few studies have reported on the serum levels of SAA in human liver disease and its clinical significance in various liver diseases.

aimTo investigate the serum levels of SAA in patients with different liver diseases and analyze the factors associated with the alteration of SAA levels in chronic hepatitis B (CHB) patients.

methodsTwo hundred and seventy-eight patients with different liver diseases and 117 healthy controls were included in this study. The patients included 205 with CHB, 22 with active autoimmune liver disease (AILD), 21 with nonalcoholic steatohepatitis (NASH), 14 with drug-induced liver injury (DILI), and 16 with pyogenic liver abscess. Serum levels of SAA and other clinical parameters were collected for the analysis of the factors associated with SAA level. Mann-Whitney

resultsAll patients with active liver diseases had higher serum SAA levels than healthy controls and the inactive CHB patients, with the highest SAA level found in patients with pyogenic liver abscess (398.4 ± 246.8 mg/L). Patients with active AILD (19.73 ± 24.81 mg/L) or DILI (8.036 ± 5.685 mg/L) showed higher SAA levels than those with active CHB (6.621 ± 6.776 mg/L) and NASH (6.624 ± 4.891 mg/L). Single (

conclusionSerum level of SAA is a sensitive biomarker for inflammatory activity of pyogenic liver abscess. It may also be a weak marker reflecting milder inflammatory status in the liver of patients with CHB and other active liver diseases.

Indexed as

AdultBiomarkersCase-Control StudiesChronic DiseaseC-Reactive ProteinFemaleHumansLiver Abscess, PyogenicLiver DiseasesMaleMiddle AgedSerum Amyloid A ProteinBiomarkersC-Reactive ProteinSerum Amyloid A ProteinChronic hepatitis BInflammationLiver diseasesPyogenic liver abscessSerum amyloid A

Identifiers

PMID31798280
PMCPMC6881510
OpenAlexW2991297835

What OpenQuestion holds

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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.