Evidence map›Paper›PMID 25336464›Full record

Trial reportJournal of the American Heart Association2014

Depletion of B-cells with rituximab improves endothelial function and reduces inflammation among individuals with rheumatoid arthritis.

Priscilla Y Hsue, Rebecca Scherzer, Carl Grunfeld, John Imboden, Yuaner Wu, Gus Del Puerto, Elaine Nitta, Judy Shigenaga, Amanda Schnell Heringer, Peter Ganz and 1 more

Registry-linked trialOpen access · goldAbstract readClinical Trial
In one paragraph

Trial report in Journal of the American Heart Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00844714 (Cardiovascular Risk Markers in Patients With Rheumatoid Arthritis), which is not on this map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
5.1field-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.

NCT00844714 nacompletednot on this map

Cardiovascular Risk Markers in Patients With Rheumatoid Arthritis: Effect of Rituximab Therapy

TypeinterventionalSponsorUniversity of California, San FranciscoRan2009 to 2014Enrolled20ConditionsEndothelial Function, Rheumatoid Arthritis, InflammationArmsRituxan
3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.

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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

11 authors at 3 institutions in 1 country.

Priscilla Y HsueDivision of Cardiology, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, CA (P.Y.H., Y.W., E.N., A.S.H., P.G.).
Rebecca ScherzerSan Francisco Veterans Affairs Medical Center, Department of Medicine UCSF, University of California, San Francisco, CA (R.S., C.G., J.S.).
Carl GrunfeldSan Francisco Veterans Affairs Medical Center, Department of Medicine UCSF, University of California, San Francisco, CA (R.S., C.G., J.S.).
John ImbodenDivision of Rheumatology, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, CA (J.I., G.P., J.G.).
Yuaner WuDivision of Cardiology, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, CA (P.Y.H., Y.W., E.N., A.S.H., P.G.).
Gus Del PuertoDivision of Rheumatology, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, CA (J.I., G.P., J.G.).
Elaine NittaDivision of Cardiology, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, CA (P.Y.H., Y.W., E.N., A.S.H., P.G.).
Judy ShigenagaSan Francisco Veterans Affairs Medical Center, Department of Medicine UCSF, University of California, San Francisco, CA (R.S., C.G., J.S.).
Amanda Schnell HeringerDivision of Cardiology, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, CA (P.Y.H., Y.W., E.N., A.S.H., P.G.).
Peter GanzDivision of Cardiology, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, CA (P.Y.H., Y.W., E.N., A.S.H., P.G.).
Jonathan GrafDivision of Rheumatology, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, CA (J.I., G.P., J.G.).
University of California, San Francisco · USSan Francisco General Hospital · USSan Francisco VA Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIndividuals with rheumatoid arthritis (RA) are at increased risk for cardiovascular disease, partly due to systemic inflammation and endothelial dysfunction. B-cells play an important pathogenic role in the inflammatory process that drives RA disease activity. Rituximab, a chimeric murine/human monoclonal antibody that depletes B-cells, is an effective therapy for RA. The purpose of this study was to determine whether B-cell depletion with rituximab reduces systemic inflammation and improves macrovascular (brachial artery flow-mediated dilation, FMD) and microvascular (reactive hyperemia) endothelial function in RA patients. METHODS AND

resultsRA patients received a single course of rituximab (1000 mg IV infusion at baseline and on day 15). FMD, reactive hyperemia, inflammatory markers, and clinical assessments were performed at baseline, week 12, and week 24. Twenty patients (95% female, median age 54 years) completed the study. Following treatment, FMD improved from a baseline of 4.5±0.4% to 6.4±0.6% at 12 weeks (mean±SE; P<0.0001), followed by a decline at week 24; a similar pattern was observed for hyperemic velocity. Significant decreases in RA disease scores, high-sensitivity C-reactive protein, erythrocyte sedimentation rate, and circulating CD19+ B-cells were sustained through week 24. Cholesterol and triglycerides became significantly although modestly elevated during the study.

conclusionsDepletion of B-cells with rituximab improved macrovascular and microvascular endothelial function and reduced systemic inflammation, despite modest elevation in lipids. Given these results, rituximab should be evaluated in the future for its possible role in reducing excess cardiovascular risk in RA. CLINICAL

trial registrationURL http://ClinicalTrials.gov. Unique identifier: NCT00844714.

Indexed as

AdultAntibodies, Monoclonal, Murine-DerivedArthritis, RheumatoidBiomarkersB-LymphocytesC-Reactive ProteinDose-Response Relationship, DrugDrug Administration ScheduleEndothelium, VascularFemaleFollow-Up StudiesHumansInflammationInfusions, IntravenousMaleMiddle AgedAntibodies, Monoclonal, Murine-DerivedBiomarkersC-Reactive ProteinRituximabB‐cellsendothelial functioninflammationrheumatoid arthritis

Identifiers

PMID25336464
PMCPMC4323827
OpenAlexW2114701446

What Socratic holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

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.