Evidence map›Paper›PMID 12835292›Full record

ReviewJournal of clinical pathology2003

Pathogenesis of systemic lupus erythematosus.

C C Mok, C S Lau

Abstract readReview
In one paragraph

Review in Journal of clinical pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 291 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
291citing papers in PubMed, 8 pooled it
–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

291 citing papers in PubMed, 8 syntheses or guidelines pooled it.

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231 more citing papers are in PubMed but not listed here.

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

2 authors.

C C MokDepartment of Medicine and Geriatrics, Tuen Mun Hospital, Tsing Chung Koon Road, New Territories, Hong Kong. ccmok@netvigator.com
C S Lau

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The exact patho-aetiology of systemic lupus erythematosus (SLE) remains elusive. An extremely complicated and multifactorial interaction among various genetic and environmental factors is probably involved. Multiple genes contribute to disease susceptibility. The interaction of sex, hormonal milieu, and the hypothalamo-pituitary-adrenal axis modifies this susceptibility and the clinical expression of the disease. Defective immune regulatory mechanisms, such as the clearance of apoptotic cells and immune complexes, are important contributors to the development of SLE. The loss of immune tolerance, increased antigenic load, excess T cell help, defective B cell suppression, and the shifting of T helper 1 (Th1) to Th2 immune responses leads to B cell hyperactivity and the production of pathogenic autoantibodies. Finally, certain environmental factors are probably required to trigger the disease.

Indexed as

Antibody FormationAutoantibodiesB-LymphocytesCytokinesFemaleGenes, MHC Class IIGenetic Predisposition to DiseaseHLA-DR2 AntigenHLA-DR3 AntigenHumansLupus Erythematosus, SystemicMalePolymorphism, GeneticSelf ToleranceTh1 CellsTh2 CellsAutoantibodiesCytokinesHLA-DR2 AntigenHLA-DR3 Antigen

Identifiers

PMID12835292
PMCPMC1769989

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.