Immune ThrombocytopeniaNCT07298733
The Value of Interleukin-1β and Interleukin-33 Genetic Expression in the Pathogenesis and Differentiation of Primary ITP and SLE-Related Thrombocytopenia
An observational study of Immune Thrombocytopenia and System; Lupus Erythematosus, run by Sohag University.
Trial summary
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. Read more about this study
- Who is it for?
- Ages 18 to 60 years
- Conditions the study is for
- Immune Thrombocytopenia, System; Lupus Erythematosus
- What is being tested?
- measuring gene expression
- How many people
- 300 participants
- Where
- No sites listed yet
- Study dates
- 1 Jan 2026to 31 Dec 2026
- Phase
- Observational
- Are there results?
- Not yet: the study is under way
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 60 years
- All sexes
- Adult
Study population: It's a cross sectional study that will be carried out in the period from November 2025 to November 2026. * Groups: 1. Group A: Patients with newly diagnosed or chronic primary ITP. 2. Group B: Patients with SLE-associated thrombocytopenia. 3. Group C: Healthy controls (age- and sex-matched). 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. All patients will be subjected to : Sample Collection: * 5 ml peripheral blood collected under sterile conditions. * Separation of PBMCs (peripheral blood mononuclear cells). Laboratory Methods: 1. RNA Extraction: from PBMCs. 2. cDNA Synthesis: using reverse transcriptase. 3. Gene Expression Analysis: using Quantitative Real-Time PCR (qRT-PCR)
Who may be able to join
- • Adults (18-60 years).
- Diagnosed primary ITP
- Diagnosed SLE with thrombocytopenia
Who cannot join
- • Patients on recent immunosuppressive therapy (<4 weeks).
- Co-existing infections, malignancies, or other autoimmune cytopenias
Trial locations and contacts
No sites are listed yet. Contact the study team or a site near you to ask about taking part.
About this study
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
Read the detailed description
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.
- Being tested
- measuring gene expression
- Keywords
- gene expression, ITP, inflammation, autoimmune
- Medical subject headings
- Purpura, Thrombocytopenic, Idiopathic, Lupus Erythematosus, Systemic, Inflammation
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
measuring gene expressionDiagnostic 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)
| Study group | Role | What they receive |
|---|---|---|
| Systemic lupus erythematosis | patients proved with SLE Receives: Diagnostic Test: measuring gene expression | |
| Idiopathic thrombocytopenic purpura | patients proved with ITP Receives: Diagnostic Test: measuring gene expression | |
| Normal controls | normal persons showing no disease matching age and gender Receives: Diagnostic Test: measuring gene expression |
What is being measured
The primary outcome is the main question the study is designed to answer.
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
- 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)
Measured: January 2026 to August 2026
2. To correlate cytokine expression levels with platelet counts and disease activity scores.
- 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)
Measured: January 2026 to August 2026
3. To assess the potential of IL-1β and IL-33 as diagnostic biomarkers for differentiating ITP from SLE-thrombocytopenia.
- 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)
Measured: June 2026 to august 2026
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted23 Dec 2025
- Study start1 Jan 2026 (estimated)
- Primary completion1 Aug 2026 (estimated)
- Study completion31 Dec 2026 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for Immune ThrombocytopeniaStudies of the same condition, open and under way.
- More trials run by Sohag UniversityThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Case-control
- Time perspective
- Cross-sectional
- Enrolment
- 300 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Sohag University
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Noha Saber Shafik, Sohag University
- Investigators
- Marwa Z elsayed, Lecturer, Principal investigator, faculty of Medicine Sohag universitySamar M Kamal, lecturer, Study chair, fauculty of Medicine , Sohag university
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT07298733
- Sponsor's protocol ID
- Soh-Med-25-10-10PD
- Status last verified
- Dec 2025
- First submitted
- 9 Dec 2025
- Last updated
- 23 Dec 2025
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Study at a glance
From the registry record, last updated by the sponsor on 23 Dec 2025. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- The Value of Interleukin-1β and Interleukin-33 Genetic Expression in the Pathogenesis and Differentiation of Primary ITP and SLE-Related Thrombocytopenia
- ClinicalTrials.gov ID
- NCT07298733
- Acronym / sponsor ID
- Soh-Med-25-10-10PD
- Keywords
- gene expression, ITP, inflammation, autoimmune
- Study type
- Observational
- Recruitment status
- Not yet recruiting
- Enrolment
- 300 participants (estimated)
- Lead sponsor
- Sohag UniversityUniversity, hospital or other
- Study start
- 1 Jan 2026 (estimated)
- Primary completion
- 1 Aug 2026 (estimated)
- Study completion
- 31 Dec 2026 (estimated)
- First posted
- 23 Dec 2025 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
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
Detailed description
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.
Study design
- Observational model
- Case-control
- Time perspective
- Cross-sectional
- Number of arms
- 3
| Arm | Type | Receives |
|---|---|---|
| Systemic lupus erythematosis | – | Diagnostic Test: measuring gene expressionpatients proved with SLE |
| Idiopathic thrombocytopenic purpura | – | Diagnostic Test: measuring gene expressionpatients proved with ITP |
| Normal controls | – | Diagnostic Test: measuring gene expressionnormal persons showing no disease matching age and gender |
Who may qualify
- Ages
- 18 to 60 years
- Sex
- All
- Age groups
- Adult
- Study population
- It's a cross sectional study that will be carried out in the period from November 2025 to November 2026. * Groups: 1. Group A: Patients with newly diagnosed or chronic primary ITP. 2. Group B: Patients with SLE-associated thrombocytopenia. 3. Group C: Healthy controls (age- and sex-matched). 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. All patients will be subjected to : Sample Collection: * 5 ml peripheral blood collected under sterile conditions. * Separation of PBMCs (peripheral blood mononuclear cells). Laboratory Methods: 1. RNA Extraction: from PBMCs. 2. cDNA Synthesis: using reverse transcriptase. 3. Gene Expression Analysis: using Quantitative Real-Time PCR (qRT-PCR)
Key inclusion criteria (3 listed)
- • Adults (18-60 years).
Key exclusion criteria (2 listed)
- • Patients on recent immunosuppressive therapy (<4 weeks).
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| measuring gene expression* 5 ml peripheral blood collected under sterile conditions. * Separation of PBMCs (peripheral blood mononuclear cells). for : 1. RNA Extraction: from PBMCs. 2. cDNA Synthesis: using reverse transcriptase. 3. Gene Expression Analysis using Quantitative Real-Time PCR (qRT-PCR) | Diagnostic test | Idiopathic thrombocytopenic purpura, Normal controls, Systemic lupus erythematosis |
Primary outcome
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: 1. RNA Extraction: from PBMCs. 2. cDNA Synthesis: using reverse transcriptase. 3. 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: 1. RNA Extraction: from PBMCs. 2. cDNA Synthesis: using reverse transcriptase. 3. 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: 1. RNA Extraction: from PBMCs. 2. cDNA Synthesis: using reverse transcriptase. 3. Gene Expression Analysis: * Quantitative Real-Time PCR (qRT-PCR)
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 23 Dec 2025.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part.
Marwa Z elsayed, Lecturer principal investigator
faculty of Medicine Sohag university
Samar M Kamal, lecturer study chair
fauculty of Medicine , Sohag university
Questions about this trial
What is this clinical trial studying?
An observational study of Immune Thrombocytopenia and System; Lupus Erythematosus, run by Sohag University.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 3 inclusion and 2 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: opening soon, as of the sponsor's last update on 23 Dec 2025. Status can change between updates, so confirm with the study contact before making plans.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
Contact Noha S Shafik, professor (01067261504, nohasaber@med.sohag.edu.eg), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
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). The study lists 3 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 23 Dec 2025.