Not Yet Recruiting

NCT Number: NCT07298733

The Value of Interleukin-1β and Interleukin-33 Genetic Expression in the Pathogenesis and Differentiation of Primary ITP and SLE-Related Thrombocytopenia

Primary immune thrombocytopenia (ITP) is an autoimmune- mediated acquired bleeding disorder, defined as a platelet count less than 100×109/L without other causes of isolated thrombocytopenia. The etiology of ITP is complex and heterogeneous, and as no specific biomarkers are indicating its presence, ITP remains a diagnosis of exclusion. The heterogeneous nature of ITP is evident in the differences in clinical presentation and response to regular treatment among patients and the multiple mechanisms that have been forwarded to account for it, such as autoantibodies, T cell dysregulation, and impaired megakaryocytes. Except primary ITP, all forms of immune-mediated thrombocytopenia is defined as secondary ITP. Secondary ITP has several causes, including autoimmune diseases such as systemic lupus erythematosus

Not Yet Recruiting

Trial opening soon.

Get Notified

Key information

Conditions

Immune Thrombocytopenia Autoimmune Diseases Blood Coagulation Disorders Blood Platelet Disorders Connective Tissue Diseases Cytopenia Hematologic Diseases Hemic and Lymphatic Diseases Hemorrhage Hemorrhagic Disorders Immune System Diseases Inflammation Lupus Erythematosus, Systemic Pathologic Processes Pathological Conditions, Signs and Symptoms Purpura Purpura, Thrombocytopenic Purpura, Thrombocytopenic, Idiopathic Signs and Symptoms Skin Manifestations Skin and Connective Tissue Diseases System; Lupus Erythematosus Thrombocytopenia Thrombotic Microangiopathies

Age range

18 year–60 year

Sex eligibility

All sexes

Study type

Observational

About this study

SLE is a complex autoimmune disease and is usually associated with hematological abnormality , including thrombocytopenia, the prevalence of which in SLE\\patients has been reported to be 7-30%. Conversely, the prevalence of SLE in all ITP cases in adults is approximately 5%, making SLE the most common cause of secondary ITP. In the early stages, when there are only thrombocytopenia symptoms, it is sometimes difficult to determine what form of ITP is present in patients with SLE. SLE-associated thrombocytopenia (SLE- TP) is defined as a platelet count less than 100×109/L in the absence of any other identifiable cause.

The pathogenesis of thrombocytopenia in SLE is heterogeneous and multifactorial. However, it is widely accepted that an increased platelet clearance mediated by autoantibodies against platelets contributes to the pathogenesis, which is analogous to the mechanism of ITP. Differing from primary ITP, the clinical treatment for thrombocytopenia secondary to an identifiable cause is often targeted to the ongoing disorder. However, there are no specific biomarkers to differentiate SLE-TP from ITP.

The family of interleukin (IL)-1 cytokines is a family of protein molecules consisting of 11 members, including IL-1α (IL-1F1), IL-1β (IL-1F2), IL-1 receptor antagonist (IL-1Ra, IL-1F3), IL-18 (IL-1F4), IL-36Ra (IL-1F5), IL- 36α (IL-1F6), IL-37 (IL-1F7), IL-36β (IL-1F8), IL-36γ (IL-1F9), IL-38 (IL-1F10), and IL-33 (IL-1F11).

This cytokine family plays a crucial role as major proinflammatory and immunoregulatory mediators in a wide range of autoinflammatory, infectious, tumor, and autoimmune diseases that act through the receptors of the Toll-like/IL-1 receptor superfamily. The production of inflammatory cytokines such as IL-1, IL- 18, and IL-36 acts by activating target cells through the receptor superfamily then amplifying the immune response.

However, antagonists such as IL-1Ra, the receptor antagonist of IL-1α and IL-1β, act as inhibitors of IL-1 dependent inflammation. The blocking of IL-1, particularly of IL-1β, has recently become the standard therapy for autoinflammatory diseases. Moreover, IL-1β, a driver of tumor-promoting inflammation in cancer, can be targeted in patients using an IL-1 receptor antagonist acting as a checkpoint inhibitor. Several studies have suggested abnormal changes in IL-18, and IL-18-binding protein (IL-18BP) were involved in the pathogenesis of SLE and ITP .

Furthermore, recent studies demonstrate that IL-1 may also take part in inflammatory pathologies and auto-immune diseases by participating in the development of T-helper 17 (Th17) cells and increased numbers of Th17 cells have been reported in patients with SLE and ITP.

Who can participate

Only the study team can determine whether someone qualifies for participation.

Inclusion criteria

• Adults (18-60 years).

Diagnosed primary ITP
Diagnosed SLE with thrombocytopenia

Exclusion criteria

• Patients on recent immunosuppressive therapy (<4 weeks).

Co-existing infections, malignancies, or other autoimmune cytopenias

Treatment and study plan

measuring gene expression

Diagnostic Test

5 ml peripheral blood collected under sterile conditions.
Separation of PBMCs (peripheral blood mononuclear cells). for :

RNA Extraction: from PBMCs.
cDNA Synthesis: using reverse transcriptase.
Gene Expression Analysis using Quantitative Real-Time PCR (qRT-PCR)

Primary outcomes

1. To evaluate and compare the expression levels of IL-1β and IL-33 in patients with primary ITP and those with SLE-associated thrombocytopenia

Time frame: January 2026 to August 2026
- 5 ml peripheral blood collected under sterile conditions.
- Separation of PBMCs (peripheral blood mononuclear cells).
Laboratory Methods:
- RNA Extraction: from PBMCs.
- cDNA Synthesis: using reverse transcriptase.
- Gene Expression Analysis:
- Quantitative Real-Time PCR (qRT-PCR)
2. To correlate cytokine expression levels with platelet counts and disease activity scores.

Time frame: January 2026 to August 2026
- 5 ml peripheral blood collected under sterile conditions.
- Separation of PBMCs (peripheral blood mononuclear cells).
Laboratory Methods:
- RNA Extraction: from PBMCs.
- cDNA Synthesis: using reverse transcriptase.
- Gene Expression Analysis:
- Quantitative Real-Time PCR (qRT-PCR)
3. To assess the potential of IL-1β and IL-33 as diagnostic biomarkers for differentiating ITP from SLE-thrombocytopenia.

Time frame: June 2026 to august 2026
- 5 ml peripheral blood collected under sterile conditions.
- Separation of PBMCs (peripheral blood mononuclear cells).
Laboratory Methods:
- RNA Extraction: from PBMCs.
- cDNA Synthesis: using reverse transcriptase.
- Gene Expression Analysis:
- Quantitative Real-Time PCR (qRT-PCR)

Study contacts

Contact information is provided by the study sponsor or research team.

Dina H Mohmad, lecturer

CONTACT

[email protected]

01119886946

Noha S Shafik, professor

CONTACT

[email protected]

01067261504

Sponsors and collaborators

Lead sponsor

Sohag University

Other

Registry information

Important dates

Study start: 2026
Primary completion: 2026
Study completion: 2026
First posted: Dec 23, 2025
Registry last updated: Dec 23, 2025

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

Published trials that share one or more normalized conditions with this study.

Not Yet Recruiting