Study Results
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
Get a concise snapshot of the trial, including recruitment status, study phase, enrollment targets, and key timeline milestones.
NOT_YET_RECRUITING
42 participants
OBSERVATIONAL
2024-01-01
2025-02-01
Brief Summary
Review the sponsor-provided synopsis that highlights what the study is about and why it is being conducted.
Related Clinical Trials
Explore similar clinical trials based on study characteristics and research focus.
Longitudinal Cohort of Pediatric Primary Immune Thrombocytopenia (ITP)
NCT06107582
Prognostic Value of CD Markers in Immune Thrombocytopenic Purpura
NCT04311593
Study of T Cells and Natural Killer Cells Expression in Patients With Immune Thrombocytopenic Purpura
NCT05093257
Association of Platelet Parameters With Bleeding Severity in Children With ITP
NCT03810352
Anti-CD38 Antibody Treating Pediatric Primary Immune Thrombocytopenia (ITP)
NCT06168851
Detailed Description
Dive into the extended narrative that explains the scientific background, objectives, and procedures in greater depth.
B lymphocytes play a critical role in immune responses through antibody production, antigen presentation to T cells, and cytokine secretion. CD4+ T helper cells play a crucial role in supporting B cell development into antibody-secreting plasma cells. Furthermore, evidence of auto reactive CD4+ T cells targeting platelet epitopes has been reported.
It was found that there is clonal expansion of a particular subset of CD8+ T cells, known as terminally differentiated effector memory T cells (TEMRA cells), in refractory ITP. Furthermore, CD8+ T cells induce platelet activation and apoptosis in an antibody-independent mechanism for refractory thrombocytopenia that may be amenable to therapeutic targeting. IFN-γ is an important cytokine involved in host defence and immune regulation. It is primarily produced by T helper, cytotoxic T, and natural killer cells. Dysregulated secretion of IFN-γ has been implicated in the development of autoimmune disorders. Initial studies on ITP focused on the role of autoantibodies. Therefore, drug discovery efforts have focused on suppressing aberrant humoral immunity through B cell depletion, disruption of immunoreceptor, and inhibition of autoantibody activity. By comparing the marker expression in different treatment response groups, the investigator can potentially identify markers that may serve as predictive or prognostic indicators of treatment response. This information could be valuable for guiding treatment decisions and optimizing patient outcomes in pediatric ITP.
Conditions
See the medical conditions and disease areas that this research is targeting or investigating.
Study Design
Understand how the trial is structured, including allocation methods, masking strategies, primary purpose, and other design elements.
CASE_ONLY
CROSS_SECTIONAL
Study Groups
Review each arm or cohort in the study, along with the interventions and objectives associated with them.
Respondents to second-line therapy
Immune markers in ITPpatients Respondant to second line therapy
complete blood count, CD3+ , CD4+ , CD8+, CD16+, CD56+, IFN-γ.
1. Full history
2. Thorough clinical examinations
3. Laboratory investigations will include:
1. complete blood count with focus on platelet count, platelet distribution width and mean platelet volume. Platelet count will be confirmed by direct blood film and blood smear.
2. Measurements of CD3+, CD4+, CD8+ and natural killer cells (CD16+, CD56+) will be conducted using flow cytometry.
3. Serum IFN-γ levels will be determined using an ELISA kit.
4. Response to the treatment will be assessed according to The International Working Group criteria which defines Response as platelet count ≥ 30 x 10⁹/L and \>2-fold increase in platelet count from baseline and absence of bleeding, measured on 2 occasions greater than 7 days apart. No response is characterized by a platelet count \<30 x 10⁹/L or a less than 2-fold increase in platelet count from baseline, or the presence of bleeding.
Non-Respondents to second-line therapy
Immune markers in ITPpatients nonrespondant to second line therapy
complete blood count, CD3+ , CD4+ , CD8+, CD16+, CD56+, IFN-γ.
1. Full history
2. Thorough clinical examinations
3. Laboratory investigations will include:
1. complete blood count with focus on platelet count, platelet distribution width and mean platelet volume. Platelet count will be confirmed by direct blood film and blood smear.
2. Measurements of CD3+, CD4+, CD8+ and natural killer cells (CD16+, CD56+) will be conducted using flow cytometry.
3. Serum IFN-γ levels will be determined using an ELISA kit.
4. Response to the treatment will be assessed according to The International Working Group criteria which defines Response as platelet count ≥ 30 x 10⁹/L and \>2-fold increase in platelet count from baseline and absence of bleeding, measured on 2 occasions greater than 7 days apart. No response is characterized by a platelet count \<30 x 10⁹/L or a less than 2-fold increase in platelet count from baseline, or the presence of bleeding.
Interventions
Learn about the drugs, procedures, or behavioral strategies being tested and how they are applied within this trial.
complete blood count, CD3+ , CD4+ , CD8+, CD16+, CD56+, IFN-γ.
1. Full history
2. Thorough clinical examinations
3. Laboratory investigations will include:
1. complete blood count with focus on platelet count, platelet distribution width and mean platelet volume. Platelet count will be confirmed by direct blood film and blood smear.
2. Measurements of CD3+, CD4+, CD8+ and natural killer cells (CD16+, CD56+) will be conducted using flow cytometry.
3. Serum IFN-γ levels will be determined using an ELISA kit.
4. Response to the treatment will be assessed according to The International Working Group criteria which defines Response as platelet count ≥ 30 x 10⁹/L and \>2-fold increase in platelet count from baseline and absence of bleeding, measured on 2 occasions greater than 7 days apart. No response is characterized by a platelet count \<30 x 10⁹/L or a less than 2-fold increase in platelet count from baseline, or the presence of bleeding.
Eligibility Criteria
Check the participation requirements, including inclusion and exclusion rules, age limits, and whether healthy volunteers are accepted.
Inclusion Criteria
Exclusion Criteria
17 Years
ALL
No
Sponsors
Meet the organizations funding or collaborating on the study and learn about their roles.
Assiut University
OTHER
Responsible Party
Identify the individual or organization who holds primary responsibility for the study information submitted to regulators.
Gehad Mahmoud Abdelsalam
Principle Investigator
Principal Investigators
Learn about the lead researchers overseeing the trial and their institutional affiliations.
Khaled I El-sayeh, M.D.
Role: STUDY_DIRECTOR
Assiut University
Mostafa M Embaby, M.D.
Role: STUDY_DIRECTOR
Assiut University
Azhar A Mohammed, M.D.
Role: STUDY_DIRECTOR
Assiut University
Central Contacts
Reach out to these primary contacts for questions about participation or study logistics.
References
Explore related publications, articles, or registry entries linked to this study.
Kayal L, Jayachandran S, Singh K. Idiopathic thrombocytopenic purpura. Contemp Clin Dent. 2014 Jul;5(3):410-4. doi: 10.4103/0976-237X.137976.
Zufferey A, Kapur R, Semple JW. Pathogenesis and Therapeutic Mechanisms in Immune Thrombocytopenia (ITP). J Clin Med. 2017 Feb 9;6(2):16. doi: 10.3390/jcm6020016.
Cancro MP. The BLyS/BAFF family of ligands and receptors: key targets in the therapy and understanding of autoimmunity. Ann Rheum Dis. 2006 Nov;65 Suppl 3(Suppl 3):iii34-6. doi: 10.1136/ard.2006.058412.
Kuwana M, Kaburaki J, Kitasato H, Kato M, Kawai S, Kawakami Y, Ikeda Y. Immunodominant epitopes on glycoprotein IIb-IIIa recognized by autoreactive T cells in patients with immune thrombocytopenic purpura. Blood. 2001 Jul 1;98(1):130-9. doi: 10.1182/blood.v98.1.130.
Malik A, Sayed AA, Han P, Tan MMH, Watt E, Constantinescu-Bercu A, Cocker ATH, Khoder A, Saputil RC, Thorley E, Teklemichael A, Ding Y, Hart ACJ, Zhang H, Mitchell WA, Imami N, Crawley JTB, Salles-Crawley II, Bussel JB, Zehnder JL, Adams S, Zhang BM, Cooper N. The role of CD8+ T-cell clones in immune thrombocytopenia. Blood. 2023 May 18;141(20):2417-2429. doi: 10.1182/blood.2022018380.
Pollard KM, Cauvi DM, Toomey CB, Morris KV, Kono DH. Interferon-gamma and systemic autoimmunity. Discov Med. 2013 Sep;16(87):123-31.
HARRINGTON WJ, MINNICH V, HOLLINGSWORTH JW, MOORE CV. Demonstration of a thrombocytopenic factor in the blood of patients with thrombocytopenic purpura. J Lab Clin Med. 1951 Jul;38(1):1-10. No abstract available.
Shulman NR, Marder VJ, Weinrach RS. Similarities between known antiplatelet antibodies and the factor responsible for thrombocytopenia in idiopathic purpura. Physiologic, serologic and isotopic studies. Ann N Y Acad Sci. 1965 Jun 30;124(2):499-542. doi: 10.1111/j.1749-6632.1965.tb18984.x. No abstract available.
van Leeuwen EF, van der Ven JT, Engelfriet CP, von dem Borne AE. Specificity of autoantibodies in autoimmune thrombocytopenia. Blood. 1982 Jan;59(1):23-6.
Ghanima W, Khelif A, Waage A, Michel M, Tjonnfjord GE, Romdhan NB, Kahrs J, Darne B, Holme PA; RITP study group. Rituximab as second-line treatment for adult immune thrombocytopenia (the RITP trial): a multicentre, randomised, double-blind, placebo-controlled trial. Lancet. 2015 Apr 25;385(9978):1653-61. doi: 10.1016/S0140-6736(14)61495-1. Epub 2015 Feb 5.
Mahevas M, Azzaoui I, Crickx E, Canoui-Poitrine F, Gobert D, Languille L, Limal N, Guillaud C, Croisille L, Jeljeli M, Batteux F, Baloul S, Fain O, Pirenne F, Weill JC, Reynaud CA, Godeau B, Michel M. Efficacy, safety and immunological profile of combining rituximab with belimumab for adults with persistent or chronic immune thrombocytopenia: results from a prospective phase 2b trial. Haematologica. 2021 Sep 1;106(9):2449-2457. doi: 10.3324/haematol.2020.259481.
Newland AC, Sanchez-Gonzalez B, Rejto L, Egyed M, Romanyuk N, Godar M, Verschueren K, Gandini D, Ulrichts P, Beauchamp J, Dreier T, Ward ES, Michel M, Liebman HA, de Haard H, Leupin N, Kuter DJ. Phase 2 study of efgartigimod, a novel FcRn antagonist, in adult patients with primary immune thrombocytopenia. Am J Hematol. 2020 Feb;95(2):178-187. doi: 10.1002/ajh.25680. Epub 2019 Dec 10.
Faul F, Erdfelder E, Lang AG, Buchner A. G*Power 3: a flexible statistical power analysis program for the social, behavioral, and biomedical sciences. Behav Res Methods. 2007 May;39(2):175-91. doi: 10.3758/bf03193146.
Rodeghiero F, Stasi R, Gernsheimer T, Michel M, Provan D, Arnold DM, Bussel JB, Cines DB, Chong BH, Cooper N, Godeau B, Lechner K, Mazzucconi MG, McMillan R, Sanz MA, Imbach P, Blanchette V, Kuhne T, Ruggeri M, George JN. Standardization of terminology, definitions and outcome criteria in immune thrombocytopenic purpura of adults and children: report from an international working group. Blood. 2009 Mar 12;113(11):2386-93. doi: 10.1182/blood-2008-07-162503. Epub 2008 Nov 12.
Other Identifiers
Review additional registry numbers or institutional identifiers associated with this trial.
ITPIMMUNEMARKERS
Identifier Type: -
Identifier Source: org_study_id
More Related Trials
Additional clinical trials that may be relevant based on similarity analysis.