Evidence map›Paper›PMID 36998631›Full record

ArticleOpen forum infectious diseases2023

Blood and Site of Disease Inflammatory Profiles Differ in Patients With Pericardial Tuberculosis and Human Immunodeficiency Virus Type 1.

Hygon Mutavhatsindi, Elsa Du Bruyn, Sheena Ruzive, Patrick Howlett, Maddalena Cerrone, Alan Sher, Katrin D Mayer-Barber, Daniel L Barber, Mpiko Ntsekhe, Robert J Wilkinson and 1 more

Open access · goldFull text read
In one paragraph

Article in Open forum infectious diseases, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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 2 institutions in 3 countries.

Hygon MutavhatsindiWellcome Centre for Infectious Disease Research in Africa, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory, South Africa.ORCID https://orcid.org/0000-0001-6605-6275
Elsa Du BruynWellcome Centre for Infectious Disease Research in Africa, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory, South Africa.ORCID https://orcid.org/0000-0002-5088-2158
Sheena RuziveWellcome Centre for Infectious Disease Research in Africa, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory, South Africa.
Patrick HowlettWellcome Centre for Infectious Disease Research in Africa, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory, South Africa.ORCID https://orcid.org/0000-0003-2381-7067
Maddalena CerroneWellcome Centre for Infectious Disease Research in Africa, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory, South Africa.ORCID https://orcid.org/0000-0002-6900-6086
Alan SherImmunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.ORCID https://orcid.org/0000-0001-7053-2895
Katrin D Mayer-BarberInflammation and Innate Immunity Unit, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.ORCID https://orcid.org/0000-0002-0311-3233
Daniel L BarberT Lymphocyte Biology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.ORCID https://orcid.org/0000-0001-7008-7509
Mpiko NtsekheWellcome Centre for Infectious Disease Research in Africa, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory, South Africa.ORCID https://orcid.org/0000-0002-0851-7675
Robert J WilkinsonWellcome Centre for Infectious Disease Research in Africa, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory, South Africa.ORCID https://orcid.org/0000-0002-2753-1800
Catherine RiouWellcome Centre for Infectious Disease Research in Africa, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory, South Africa.ORCID https://orcid.org/0000-0001-9679-0745
University of Cape Town · ZANational Institutes of Health · US

Funding

Immune Regulation in Mycobacterial InfectionsZIAAI001171 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI BARBER, DANIEL · 2012 to 2025
$16.7M
Innate inflammatory responses during pulmonary infectionsZIAAI001207 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MAYER-BARBER, KATRIN · 2015 to 2025
$13.6M
HIV-associated Tuberculosis Training Program (HATTP)D43TW010559 · FIC · UNIVERSITY OF CAPE TOWN · PI Graeme Ayton Meintjes · 2017 to 2026
$3.0M
Contribution of the CD153/CD30 axis to Mycobacterium tuberculosis control in humansR21AI148027 · NIAID · UNIVERSITY OF CAPE TOWN · PI RIOU, CATHERINE · 2019 to 2020
$291k
FIC NIH HHS D43 TW010559NIAID NIH HHS R21 AI148027Wellcome Trust
6 · The paper itself

Abstract

Background: To better understand the pathogenesis of pericardial tuberculosis (PCTB), we sought to characterize the systemic inflammatory profile in people with human immunodeficiency virus type 1 (HIV-1) with latent TB infection (LTBI), pulmonary TB (PTB), or PCTB. Methods: Using Luminex, we measured the concentration of 39 analytes in pericardial fluid (PCF) and paired plasma from 18 PCTB participants, and plasma from 16 LTBI and 20 PTB participants. Follow-up plasma samples were also obtained from PTB and PCTB participants. HLA-DR expression on Results: Assessment of the overall systemic inflammatory profile by principal component analysis showed that the inflammatory profile of active TB participants was distinct from the LTBI group, while PTB patients could not be distinguished from those with PCTB. When comparing the inflammatory profile between PCF and paired blood, we found that the concentrations of most analytes (25/39) were elevated at site of disease. However, the inflammatory profile in PCF partially mirrored inflammatory events in the blood. After TB treatment completion, the overall plasma inflammatory profile reverted to that observed in the LTBI group. Lastly, HLA-DR expression showed the best performance for TB diagnosis compared to previously described biosignatures built from soluble markers. Conclusions: Our results show that the inflammatory profile in blood was comparable between PTB and PCTB. However, at the site of infection (PCF), inflammation was significantly elevated compared to blood. Additionally, our data emphasize the potential role of HLA-DR expression as a biomarker for TB diagnosis.

Indexed as

diagnosisinflammatory profilepericardial tuberculosissite of diseasetreatment response

Identifiers

PMID36998631
PMCPMC10043131
OpenAlexW4323660588

What Socratic holds

Textfull text, public
LicenceCC BY
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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.