Evidence map›Paper›PMID 29870500›Full record

ReviewCurrent opinion in rheumatology2018

Drug-induced lupus erythematosus: an update on drugs and mechanisms.

Ye He, Amr H Sawalha

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Current opinion in rheumatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 3 pooled it
5.2field-weighted citation impact, top 4% 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

65 citing papers in PubMed, 3 syntheses or guidelines pooled it, 166 citations in OpenAlex.

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5 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 at 2 institutions in 2 countries.

Ye HeDivision of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Amr H SawalhaDivision of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Central South University · CNUniversity of Michigan–Ann Arbor · US

Funding

Role of DNA methylation in lupusR01AI097134 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Amr H Sawalha · 2013 to 2026
$4.5M
KIR+CD11ahiCD4+ T cells in Systemic AutoimmunityU19AI110502 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RICHARDSON, BRUCE C. · 2014 to 2018
$2.6M
NIAID NIH HHS R01 AI097134NIAID NIH HHS U19 AI110502
6 · The paper itself

Abstract

purpose of reviewRapid introduction of newly developed drugs in the absence of clear understanding of the pathophysiologic mechanisms behind drug-induced lupus erythematosus (DILE) can sometimes make DILE difficult to recognize in clinical practice. The purpose of this review is to summarize drugs most recently reported to be involved in DILE and discuss the current landscape of diverse mechanisms involved. RECENT

findingsA large number of proton pump inhibitor (PPI)-induced subacute cutaneous lupus erythematosus cases have been reported, suggesting a shift over time in the spectrum of drugs implicated in DILE. Twenty-two articles comprising 29 DILE case reports published within the last 2 years are summarized in this review, including 12 (41.4%) systemic DILE. Antitumor necrosis factor (anti-TNF) drugs were the most frequently (41.7%) reported to introduce systemic DILE in these cases. Chemotherapeutic drugs were the most common drug class (54.5%) involved in subacute cutaneous lupus erythematosus, with an observed higher incidence in female patients. Enhanced neutrophil extracellular trap (NET) formation induced by procainamide and hydralazine could be a new mechanism contributing to the pathogenesis of DILE. SUMMARY: The list of drugs implicated in triggering DILE is expanding as new drugs with novel mechanisms of action are being developed. It is important to recognize culprit drugs that may induce lupus erythematosus, as discontinuation usually results in improvement of drug-induced manifestations. Characterizing the mechanisms involved might help better understand the cause of idiopathic autoimmunity.

Indexed as

AutoimmunityGenetic Predisposition to DiseaseHumansHydralazineImmunologic FactorsLupus Erythematosus, CutaneousLupus Erythematosus, SystemicProcainamideTumor Necrosis Factor-alphaHydralazineImmunologic FactorsProcainamideTumor Necrosis Factor-alpha

Identifiers

PMID29870500
PMCPMC7299070
OpenAlexW2806711256

What OpenQuestion holds

Textmetadata
LicenceTDM
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.