Regulatory molecular mechanisms governing immunothrombotic adversities in heparin-induced thrombocytopenia: validation of novel therapeutic strategies

Regulatory molecular mechanisms governing immunothrombotic adversities in heparin-induced thrombocytopenia: validation of novel therapeutic strategies - HIT-CXCR7

Status

Active, not recruiting

Phases

Unknown

Study type

Observational

Source

DRKS

Registry ID

DRKS00039816

Enrollment

Registered

2026-06-08

Start date

2026-07-01

Completion date

Unknown

Last updated

2026-06-22

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

D69.53

Interventions

Group 1: The following samples will be collected: • 2 tubes, each containing 5.4 ml of citrated blood • 1 tube containing 10 ml of serum

Eligibility

Sex/Gender

All

Age

18 Years to No maximum

Inclusion criteria

Inclusion criteria: • Hospitalized patients with acute HIT type II (with (n=20) and without thrombosis (n=20)) • Age = 18 years • Written informed consent to participate in the study. • Patients who are unable to provide informed consent may also be included. Individuals with acute HIT are frequently in a clinical condition that transiently limits their decision-making capacity. • For patients who are temporarily unable to provide consent, informed consent will be obtained from the legally authorized representative. As soon as the patient regains the ability to consent, they will be asked to confirm or withdraw their participation in the study

Exclusion criteria

Exclusion criteria: • Patients younger than 18 years • Pregnancy or breastfeeding • Patients who lack the capacity to provide informed consent and for whom no legal representative is available • Patients who decline to participate or withdraw consent at any stage • Patients with severe coagulation disorders unrelated to HIT (e.g., disseminated intravascular coagulation) • Patients in whom blood sampling is medically contraindicated (e.g., severe anemia, critical hemodynamic instability, or other conditions judged unsuitable by the treating physician)

Design outcomes

Primary

Measure	Time frame
a. To evaluate the therapeutic potential of CXCR7 activation in regulating platelet-driven thrombo-inflammatory responses in HIT (in vitro and ex vivo) b. To investigate molecular mechanisms underlying increased thrombotic risk in HIT using phosphoproteomic and lipidomic profiling, with focus on CXCR7–cAMP signaling. c. To compare the efficacy of a CXCR7 agonist with iloprost, a clinically established antiplatelet therapy, in preclinical murine models of HIT.	—

Measure

Time frame

a. To evaluate the therapeutic potential of CXCR7 activation in regulating platelet-driven thrombo-inflammatory responses in HIT (in vitro and ex vivo) b. To investigate molecular mechanisms underlying increased thrombotic risk in HIT using phosphoproteomic and lipidomic profiling, with focus on CXCR7–cAMP signaling. c. To compare the efficacy of a CXCR7 agonist with iloprost, a clinically established antiplatelet therapy, in preclinical murine models of HIT.

—

Secondary

Measure	Time frame
d. To analyze CXCR7 expression on platelets and neutrophils in HIT patients, and assess its potential as a novel therapeutic target ex vivo.	—

Countries

Germany

Contacts

Public ContactMadhumita Chatterjee

Institut für Klinische und Experimentelle Transfusionsmedizin (IKET)

Madhumita.Chatterjee@med.uni-tuebingen.de+49-(0)7071-29-81601

Outcome results

None listed

Source: DRKS (via WHO ICTRP) · Data processed: Jun 29, 2026