View clinical trials related to Purpura.
Filter by:TTP is a rare and serious blood disorder, characterized by the formation of small clots (micro thrombi) within the circulation and can be fatal. The formation of blood clots occurs primarily in the smaller blood vessels, the arterioles and capillaries, associated with multisystem organ involvement, especially the brain and kidneys. TTP has an incidence of approximately 1-3 people/million of the population/year. TTP is due to a decrease in an enzyme, ADAMTS 13 that is released by cells lining blood vessels (endothelial cells). ADAMTS 13 'cleaves' or breaks down very large von Willebrand Factor (vWF) strands. vWF is used in blood clotting. Deficiency or inhibition of the enzyme, results in release of the ultra large vWF into the circulation. Platelets bind to these ultra large vWF multimers, promoting blood clot formation and platelet consumption (thrombocytopenia). In more then 70% of TTP cases no precipitating cause can be found and the majority of these patients have antibodies against ADAMTS 13. Plasma Exchange (PEX) was introduced in the management of TTP in 1977 and the mortality of TTP patients has since decreased from approximately 90% to 15-20%. PEX is essential in TTP treatment as plasma contains the missing enzyme ADAMTS 13. Rituximab (licensed and internationally used monoclonal antibody) selectively acts on white blood cells known as B-lymphocytes or B cells that produce the antibody to ADAMTS 13. By inhibiting ADAMTS 13 antibody production, ADAMTS 13 activity increases, resulting in remission. Rituximab has been used in our institutions in patients with acute TTP that are refractory to standard treatment - PEX. The resulting remission has been dramatic, with a non-toxic side effect profile and no patients to date has relapsed (longest follow-up 19 months) following Rituximab therapy. Therefore, we plan to use Rituximab with PEX in patients who present with acute TTP.
In this study we want to investigate if combination therapy with rituximab (R) + dexamethasone (DXM) is superior to monotherapy with DXM in patients with newly diagnosed idiopathic thrombocytopenic purpura (ITP). Before treatment molecular studies - gene expression profiling - are performed to characterize at the molecular level those patients responding adequately to the treatment as compared to those obtaining a minor or no responses. The hypothesis is that combination therapy is superior to monotherapy as defined above. Using gene expression studies up-front the hypothesis is that this method may be able to predict the response to treatment.
Phase II, multi-center, 3 part, staggered cohort, open-label and double blind, randomized, placebo controlled study involving 3 age-determined cohorts (Cohort 1: between 12 and 17 years old; Cohort 2: between 6 and 11 years old; Cohort 3: between 1 and 5 years old). Daily dosing with eltrombopag will begin with 5 patients in the oldest age cohort in an open label fashion, and a review of safety, pharmacokinetic and platelet count data will be performed regularly. If no safety concerns are identified after 12 weeks, 18 additional patients will be randomised to placebo or eltrombopag (2:1 randomisation). After 7 weeks of randomized treatment, all patients will receive eltrombopag in an open label fashion. The total duration of treatment with eltrombopag will be 24 weeks. If at the time of the aforementioned 12 week review of the first 5 patients no safety issues are identified, dosing will begin in the next lower age cohort with an initial group of 5 patients. The same procedure will be followed in terms of safety review and subsequent enrolment and randomisation of the additional patients. Initiation of the younger age cohort will take place once data from the previous has been evaluated. Doses will be adjusted according to platelet counts and tolerability. The study will include a review of the safety data by a Data Safety Monitoring Board.
Multicentric non-randomized phase II opened prospective study (10 centres involved). Primary endpoint: - To evaluate the kinetics of B-cell depletion by rituximab and its pharmacokinetics in patients treated with rituximab in association with plasma exchanges. Secondary endpoints: - To evaluate the tolerance of rituximab, the volume of plasma and the number of plasma exchange sessions required to achieve a durable complete remission, and to determinate the duration of B-cell depletion. - To evaluate the incidence of persistent severe acquired ADAMTS13 deficiency following treatment with rituximab, as well as the incidence of relapses.
The purpose of this study is to evaluate changes in bone marrow morphology (structure) after long-term exposure to romiplostim.
This is a single-center, prospective, controlled study with one eltrombopag treatment group and 2 control groups, one on standard steroid treatment, and another one untreated. The aim of the study is to determine the effect of Thrombopoietin Receptor (MPL) agonists on shear-induced platelet activation.
This study was conducted in conjunction with the 2 phase 3 studies of AMG 531 (20030105 and 20030212) and an open-label extension study (20030213) and compared pretreatment and posttreatment bone marrow samples for the purpose of studying morphologic changes.
This was a phase II multi-center, randomized, open-label study with two parallel study groups to evaluate the efficacy and safety of PG2 in ITP patients.
An open-label, dose-adjustment extension study to evaluate the safety and efficacy of eltrombopag for treatment of subjects with ITP who have previously been enrolled in the eltrombopag trial TRA108109 (NCT00540423).
This study is designed to compare the efficacy and safety of higher doses of Rituxan with a regimen combining standard doses of Rituxan + CVP in patients with chronic ITP who did not respond to or relapsed after standard doses of Rituxan. Patients eligible for this protocol will be stratified into two subgroups according to their initial response to Rituxan.