Evidence map›Paper›PMID 39337495›Full record

ArticleInternational journal of molecular sciences2024

Anti-Inflammatory Cytokine Profiles in Thrombotic Thrombocytopenic Purpura-Differences Compared to COVID-19.

Flóra Demeter, György Bihari, Dorina Vadicsku, György Sinkovits, Erika Kajdácsi, Laura Horváth, Marienn Réti, Veronika Müller, Zsolt Iványi, János Gál and 12 more

Abstract readComparative Study
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

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

8 citing papers in PubMed.

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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

22 authors.

Flóra DemeterDepartment of Internal Medicine and Haematology, Semmelweis University, 1088 Budapest, Hungary.ORCID 0000-0003-0149-2871
György BihariDepartment of Internal Medicine and Haematology, Semmelweis University, 1088 Budapest, Hungary.
Dorina VadicskuDepartment of Internal Medicine and Haematology, Semmelweis University, 1088 Budapest, Hungary.
György SinkovitsDepartment of Internal Medicine and Haematology, Semmelweis University, 1088 Budapest, Hungary.ORCID 0000-0002-5355-7318
Erika KajdácsiDepartment of Internal Medicine and Haematology, Semmelweis University, 1088 Budapest, Hungary.
Laura HorváthDepartment of Internal Medicine and Haematology, Semmelweis University, 1088 Budapest, Hungary.
Marienn RétiDepartment of Haematology and Stem Cell Transplantation, Central Hospital of Southern Pest National Institute of Haematology and Infectious Diseases, 1097 Budapest, Hungary.ORCID 0000-0002-4682-5628
Veronika MüllerDepartment of Pulmonology, Semmelweis University, 1083 Budapest, Hungary.ORCID 0000-0002-1398-3187
Zsolt IványiDepartment of Anaesthesiology and Intensive Therapy, Semmelweis University, 1085 Budapest, Hungary.
János GálDepartment of Anaesthesiology and Intensive Therapy, Semmelweis University, 1085 Budapest, Hungary.
László GopcsaDepartment of Haematology and Stem Cell Transplantation, Central Hospital of Southern Pest National Institute of Haematology and Infectious Diseases, 1097 Budapest, Hungary.
Péter ReményiDepartment of Haematology and Stem Cell Transplantation, Central Hospital of Southern Pest National Institute of Haematology and Infectious Diseases, 1097 Budapest, Hungary.
Beáta SzathmáryDepartment of Infectology, Central Hospital of Southern Pest, National Institute of Haematology and Infectious Diseases, 1097 Budapest, Hungary.
Botond LakatosDepartment of Infectology, Central Hospital of Southern Pest, National Institute of Haematology and Infectious Diseases, 1097 Budapest, Hungary.
János SzlávikDepartment of Infectology, Central Hospital of Southern Pest, National Institute of Haematology and Infectious Diseases, 1097 Budapest, Hungary.
Ilona BobekDepartment of Anaesthesiology and Intensive Therapy, Central Hospital of Southern Pest, National Institute of Haematology and Infectious Diseases, 1097 Budapest, Hungary.ORCID 0000-0003-2187-4666
Zita Z ProhászkaDepartment of Internal Medicine and Haematology, Semmelweis University, 1088 Budapest, Hungary.
Zsolt FörhéczDepartment of Internal Medicine and Haematology, Semmelweis University, 1088 Budapest, Hungary.
Tamás MassziDepartment of Internal Medicine and Haematology, Semmelweis University, 1088 Budapest, Hungary.
István Vályi-NagyDepartment of Haematology and Stem Cell Transplantation, Central Hospital of Southern Pest National Institute of Haematology and Infectious Diseases, 1097 Budapest, Hungary.
Zoltán ProhászkaDepartment of Internal Medicine and Haematology, Semmelweis University, 1088 Budapest, Hungary.
László CervenakDepartment of Internal Medicine and Haematology, Semmelweis University, 1088 Budapest, Hungary.

Funding

Ministry of Innovation and Technology of Hungary, European Union TKP2021-EGA-24 (MOLORKIV)National Research, Development, and Innovation Fund of Hungary TKP2021-EGA-08
6 · The paper itself

Abstract

Thromboinflammation/immunothrombosis plays a role in several diseases including thrombotic thrombocytopenic purpura (TTP) and COVID-19. Unlike the extensive research that has been conducted on COVID-19 cytokine storms, the baseline and acute phase cytokine profiles of TTP are poorly characterized. Moreover, we compared the cytokine profiles of TTP and COVID-19 to identify the disease-specific/general characteristics of thromboinflammation/immunothrombosis. Plasma concentrations of 33 soluble mediators (SMs: cytokines, chemokines, soluble receptors, and growth factors) were measured by multiplex bead-based LEGENDplex™ immunoassay from 32 COVID-19 patients (32 non-vaccinated patients in three severity groups), 32 TTP patients (remission/acute phase pairs of 16 patients), and 15 control samples. Mainly, the levels of innate immunity-related SMs changed in both diseases. In TTP, ten SMs decreased in both remission and acute phases compared to the control, one decreased, and two increased only in the acute phase compared to remission, indicating mostly anti-inflammatory changes. In COVID-19, ten pro-inflammatory SMs increased, whereas one decreased with increasing severity compared to the control. In severe COVID-19, sixteen SMs exceeded acute TTP levels, with only one higher in TTP. PCA identified CXCL10, IL-1RA, and VEGF as the main discriminators among their cytokine profiles. The innate immune response is altered in both diseases. The cytokine profile of TTP suggests a distinct pathomechanism from COVID-19 and supports referring to TTP as thromboinflammatory rather than immunothrombotic, emphasizing thrombosis over inflammation as the driving force of the acute phase.

Indexed as

COVID-19CytokinesPurpura, Thrombotic ThrombocytopenicSARS-CoV-2AdultAgedFemaleHumansImmunity, InnateInflammationMaleMiddle AgedCytokinesCOVID-19cytokinesimmunothrombosisinflammationsevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2)thromboinflammationthrombotic thrombocytopenic purpura

Identifiers

PMID39337495
PMCPMC11432022

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Registered trials

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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.