PhD Scientific Days 2024

Poster Session M - Cardiovascular Medicine and Research 1.

Cytokine Patterns of Thrombotic Thrombocytopenic Purpura (TTP) and COVID-19

Előadó neve

Dr. Demeter, Flóra

Neptun code

DBWYCM

Előadó munkahelye

Semmelweis University, Department of Internal Medicine and Hematology

Előadó telefonszáma

06202552023

Előadó e-mail címe

flora.demeter@gmail.com

Az előadás címe

Cytokine Patterns of Thrombotic Thrombocytopenic Purpura (TTP) and COVID-19

Szerző(k) neve és munkahelye

Flóra Demeter¹

1: Semmelweis University, Department of Internal Medicine and Hematology

Bemutatás módja

Poszter

Szekció

Poster Session M - Cardiovascular Medicine and Research 1.

Language of the presentation

English

Preferred session

Cardiovascular Medicine and Research

Összefoglaló szövege

Thrombotic thrombocytopenic purpura (TTP) is a thrombotic microangiopathy characterized by life-threatening acute episodes alternating with phases of remission. Recently, the concept of immunothrombosis (IT) has emerged as a driving force of several diseases including TTP and COVID-19. Cytokines are vital regulators of inflammation, thus the analysis of their patterns is crucial to understand immunothrombotic diseases (ITDs). Unlike the extensive research on the COVID-19 cytokine storm, limited data exists on the baseline cytokine patterns of TTP patients, with no studies directly comparing remission to acute phase, making it our primary focus. Moreover, we aimed to compare cytokine patterns of TTP and COVID-19 to identify disease-specific or general IT characteristics.
Plasma concentrations of 33 soluble mediators (SMs: cytokines, chemokines, soluble receptors and growth factors) were measured by bead-based LEGENDplex™ analysis, using 3 commercially available kits. We collected 80 cytrate plasma samples: 32 from COVID-19 patients divided into 3 severity groups (12 Covid 2: hospitalized, no O2 need; 13 Covid 3: hospitalized, O2 on nasal cannula/mask; 7 Covid 4: intensive care unit), 32 TTP sample pairs from 16 patients in remission and acute phases, and 16 healthy controls. Statistical analyses included the Mann-Whitney, Wilcoxon, or Jonckheere tests, and principal component analysis (PCA).
6 SMs, mainly governing the adaptive immune response, were undetectable in all patient groups. In TTP, 11 SMs (mainly inflammatory cytokines) decreased in both remission and the acute phase, while 1 decreased and two elevated only in the latter. In COVID-19, 12 key proinflammatory SMs increased (with 11 showing a severity trend), while 3 decreased with severity trend. In severe COVID-19, 18 SMs exceeded acute TTP levels, with just 1 was higher in acute TTP. PCA identified CXCL10, IL-1RA, VEGF, STREM-1, IL-18 and CCL4 as the main discriminators between the two groups.
Adaptive immunity appears to be less engaged than the innate response in both COVID-19 and TTP. Despite categorizing TTP as an ITD, its cytokine pattern suggests a distinct pathomechanism from COVID-19. Our findings support labeling TTP as thromboinflammatory rather than immunothrombotic (as in COVID-19), to highlight thrombosis rather than inflammation as the driving force.

Supported by HUN-REN-SU.

University

Semmelweis University

Supervisor

Dr. László Cervenak

Publication of my abstract

I give consent to the publication of my abstract on the website of the congress.

Kind

Szabad

Status

elfogadva

Accepted presentation method

poszter

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

7484

Start

16:50

End

16:53