"Cytotoxic T Lymphocyte-Associated Antigen-4 (CTLA-4) Gene Single-nucleotide Polymorphism in Primary Immune Thrombocytopenic Purpura in Children"

NCT ID: NCT07014904

Last Updated: 2025-06-17

Basic Information

• Recruitment Status: NOT_YET_RECRUITING
• Total Enrollment: 80 participants
• Study Classification: OBSERVATIONAL
• Study Start Date: 2025-08-20
• Study Completion Date: 2027-07-20

Brief Summary

the investigators aim in this study to investigate the potential association of single gene polymorphisms of CTLA-4 (SNPs; rs: 3087243) using real-time PCR in children with primary ITP.

Detailed Description

Primary immune thrombocytopenia (ITP) is an acquired autoimmune bleeding disorder characterized by isolated thrombocytopenia (platelet count < 100 × 109/L) in the absence of other etiologies. The incidence of the disease is approximately 2-10 per 100,000 adults each year, with a prevalence of 9-20 per 100,000 adults Auto antibody-mediated platelet destruction is the canonical mechanism of platelet destruction in ITP. Platelets coated by anti-glycoprotein (GP) autoantibodies are prematurely destroyed by macrophages via Fcγ receptors (FcγRs) in the reticuloendothelial system. Autoantibodies also accelerate platelet destruction through the induction of complement-dependent cytotoxicity (CDC) and platelet apoptosis Many studies have demonstrated that CD8+ cytotoxic T lymphocytes (CTLs) from peripheral blood or spleen of ITP patients can directly lyse platelets or induce platelet apoptosis through granzyme B and perforin. CTLs and anti-GP autoantibodies can induce the desialylation of platelet surface glycans, leading to premature platelet clearance.

The immune checkpoint pathways are critical modulators of the immune system, allowing immune response initiation and preventing autoimmunity onset. Immune checkpoints, including co-stimulation and co-inhibition signal pathways, are among the central mechanisms that regulate T-cell-mediated immune responses CTLA-4 production is strongly influenced by genetic factors. Single-nucleotide polymorphisms (SNPs) of the CTLA-4-encoding genes are involved in the pathogenesis of many autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) In recent years, it had been shown that thrombocytopenia was associated with the transcription level of CTLA4 and regulation of T-cell activation

Conditions

ITP - Immune Thrombocytopenia

Study Design

• Observational Model Type: CASE_ONLY
• Study Time Perspective: CROSS_SECTIONAL

Study Groups

investigate the potential association of single gene polymorphisms of CTLA-4 (SNPs; rs: 3087243) usi

No interventions assigned to this group

Eligibility Criteria

Exclusion Criteria

Refusal to sign an informed written consent, patient with persistent ITP, patient with chronic ITP, patient with secondary immune thrombocytopenia and patient age < 1 year or > 18 years

• Minimum Eligible Age: 1 Year
• Maximum Eligible Age: 18 Years
• Eligible Sex: ALL
• Accepts Healthy Volunteers: Yes

Sponsors

Sohag University

OTHER

Sponsor Role: lead

Responsible Party

Reham Elsayed Mohamed

Principal Investigator

Responsibility Role: PRINCIPAL_INVESTIGATOR

Central Contacts

Reham Elsayed Mohamed Ail Reham Elsayed Mohamed Ail, MD

Role: CONTACT

Remohelmy1992@gmail.com

01013757753

Douaa Mohammed Sayed Douaa Mohammed Sayed, Prof.Dr

Role: CONTACT

01006261987

Other Identifiers

SOH-Med--25-5-4MD

Identifier Type: -

Identifier Source: org_study_id