Evidence map›Paper›PMID 33993432›Full record

ReviewRheumatology and therapy2021

Cognitive Dysfunction in Systemic Lupus Erythematosus: Immunopathology, Clinical Manifestations, Neuroimaging and Management.

Dominic Seet, Nur Azizah Allameen, Sen Hee Tay, Jiacai Cho, Anselm Mak

Open access · goldAbstract readReview
In one paragraph

Review in Rheumatology and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 2 pooled it
8.8field-weighted citation impact, top 2% 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

38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 78 citations in OpenAlex.

  1. Pooled it
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  12. Review
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  20. Cognitive dysfunction in pediatric systemic lupus erythematosus: current knowledge and future directions.Child neuropsychology : a journal on normal and abnormal development in childhood and adolescence · 2024
    Review
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

5 authors at 2 institutions in 1 country.

Dominic Seet *Division of Rheumatology, Department of Medicine, University Medicine Cluster, National University Health System, 1E Kent Ridge Road, Level 10, NUHS Tower Block, Singapore, 119228, Singapore.
Nur Azizah Allameen *Division of Rheumatology, Department of Medicine, University Medicine Cluster, National University Health System, 1E Kent Ridge Road, Level 10, NUHS Tower Block, Singapore, 119228, Singapore.
Sen Hee TayDivision of Rheumatology, Department of Medicine, University Medicine Cluster, National University Health System, 1E Kent Ridge Road, Level 10, NUHS Tower Block, Singapore, 119228, Singapore.
Jiacai Cho *Division of Rheumatology, Department of Medicine, University Medicine Cluster, National University Health System, 1E Kent Ridge Road, Level 10, NUHS Tower Block, Singapore, 119228, Singapore.
Anselm Mak *Division of Rheumatology, Department of Medicine, University Medicine Cluster, National University Health System, 1E Kent Ridge Road, Level 10, NUHS Tower Block, Singapore, 119228, Singapore. mdcam@nus.edu.sg.ORCID http://orcid.org/0000-0002-4688-7829
National University of Singapore · SGNational University Health System · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cognitive dysfunction (CD) is a common yet often clinically subtle manifestation that considerably impacts the health-related quality of life in patients with systemic lupus erythaematosus (SLE). Given the inconsistencies in CD assessment and challenges in its attribution to SLE, the reported prevalence of CD differs widely, ranging from 3 to 88%. The clinical presentation of CD in SLE is non-specific and may manifest concurrently with overt neuropsychiatric illness such as psychosis or mood disorders or as isolated impairment of attention, working memory, executive dysfunction or processing speed. Despite the lack of standardized and sensitive neuropsychological tests and validated diagnostic biomarkers of CD in SLE, significant progress has been made in identifying pathogenic neural pathways and neuroimaging. Furthermore, several autoantibodies, cytokines, pro-inflammatory mediators and metabolic factors have been implicated in the pathogenesis of CD in SLE. Abrogation of the integrity of the blood-brain barrier (BBB) and ensuing autoantibody-mediated neurotoxicity, complement and microglial activation remains the widely accepted mechanism of SLE-related CD. Although several functional neuroimaging modalities have consistently demonstrated abnormalities that correlate with CD in SLE patients, a consensus remains to be reached as to their clinical utility in diagnosing CD. Given the multifactorial aetiology of CD, a multi-domain interventional approach that addresses the risk factors and disease mechanisms of CD in a concurrent fashion is the favourable therapeutic direction. While cognitive rehabilitation and exercise training remain important, specific pharmacological agents that target microglial activation and maintain the BBB integrity are potential candidates for the treatment of SLE-related CD.

Indexed as

CognitiveGlucocorticoidsImagingLupusNeuropsychiatricSystemic lupus erythematosus

Identifiers

PMID33993432
PMCPMC8217391
OpenAlexW3161157406

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.