Evidence map›Paper›PMID 39132510›Full record

ArticleMedComm2024

An autoantibody profile identified by human genome-wide protein arrays in rheumatoid arthritis.

Xu Liu, Xiaoying Zhang, Yu-Jian Kang, Fei Huang, Shuang Liu, Yixue Guo, Yingni Li, Changcheng Yin, Mingling Liu, Qimao Han and 11 more

Abstract read
In one paragraph

Article in MedComm, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Article
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

21 authors.

Xu LiuDepartment of Rheumatology and Immunology Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135) Beijing China.ORCID https://orcid.org/0000-0003-4107-894X
Xiaoying ZhangDepartment of Rheumatology and Immunology Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135) Beijing China.
Yu-Jian KangChongqing Key Laboratory of Intelligent Oncology for Breast Cancer Cancer Hospital School of Medicine Chongqing University Chongqing China.
Fei HuangGeneral Medical Department Huazhong University of Science and Technology Union Shenzhen Hospital Shenzhen China.
Shuang LiuDepartment of Rheumatology and Immunology First Affiliated Hospital of Kunming Medical University. Kunming China.
Yixue GuoDepartment of Rheumatology and Immunology Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135) Beijing China.
Yingni LiDepartment of Rheumatology and Immunology Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135) Beijing China.
Changcheng YinBeijing Protein Innovation B-8, Airport Industrial Zone Beijing China.
Mingling LiuDepartment of Rheumatology the First Affiliated Hospital of Guangzhou University of Chinese Medicine Guangzhou China.
Qimao HanDepartment of Rheumatology The First Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine. No.24 Heping Road Xiangfang District Harbin China.
Qingwen WangDepartment of Rheumatism and Immunology Peking University Shenzhen Hospital Shenzhen China.
Hua YeDepartment of Rheumatology and Immunology Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135) Beijing China.
Haihong YaoDepartment of Rheumatology and Immunology Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135) Beijing China.
Chun LiDepartment of Rheumatology and Immunology Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135) Beijing China.
Jiahe LiDepartment of Rheumatology and Immunology Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135) Beijing China.
Wangzha PingcuoDepartment of Rheumatology and Immunology Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135) Beijing China.
Yan ZhangDepartment of Rheumatology and Immunology Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135) Beijing China.
Yin SuDepartment of Rheumatology and Immunology Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135) Beijing China.
Ge GaoState Key Laboratory of Protein and Plant Gene Research, School of Life Sciences Biomedical Pioneering Innovative Center (BIOPIC) & Beijing Advanced Innovation Center for Genomics (ICG) Center for Bioinformatics (CBI) Peking University Beijing China.
Zhanguo LiDepartment of Rheumatology and Immunology Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135) Beijing China.
Xiaolin SunDepartment of Rheumatology and Immunology Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135) Beijing China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Precise diagnostic biomarkers of anticitrullination protein antibody (ACPA)-negative and early-stage RA are still to be improved. We aimed to screen autoantibodies in ACPA-negative patients and evaluated their diagnostic performance. The human genome-wide protein arrays (HuProt arrays) were used to define specific autoantibodies from the sera of 182 RA patients and 261 disease and healthy controls. Statistical analysis was performed with SPSS 17.0. In Phase I study, 51 out of 19,275 recombinant proteins covering the whole human genome were selected. In Phase II validation study, anti-ANAPC15 (anaphase promoting complex subunit 15) exhibited 41.8% sensitivity and 91.5% specificity among total RA patients. There were five autoantibodies increased in ACPA-negative RA, including anti-ANAPC15, anti-LSP1, anti-APBB1, anti-parathymosin, and anti-UBL7. Anti-parathymosin showed the highest prevalence of 46.2% (

Indexed as

anticitrullination protein antibody (ACPA)autoantibodyHuProt arrayrheumatoid arthritis

Identifiers

PMID39132510
PMCPMC11317183

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.