James B. Bussel

ORCID: 0000-0002-2884-9247
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About
Contact & Profiles
Research Areas
  • Platelet Disorders and Treatments
  • Blood groups and transfusion
  • Autoimmune Bullous Skin Diseases
  • Chronic Lymphocytic Leukemia Research
  • Immunodeficiency and Autoimmune Disorders
  • Blood disorders and treatments
  • Blood properties and coagulation
  • Renal Diseases and Glomerulopathies
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Heparin-Induced Thrombocytopenia and Thrombosis
  • Cell Adhesion Molecules Research
  • Complement system in diseases
  • Monoclonal and Polyclonal Antibodies Research
  • Immune Cell Function and Interaction
  • Multiple Myeloma Research and Treatments
  • Lymphoma Diagnosis and Treatment
  • Venous Thromboembolism Diagnosis and Management
  • T-cell and B-cell Immunology
  • Hemoglobinopathies and Related Disorders
  • Blood Coagulation and Thrombosis Mechanisms
  • Erythrocyte Function and Pathophysiology
  • Hemophilia Treatment and Research
  • Glycosylation and Glycoproteins Research
  • Acute Myeloid Leukemia Research
  • Chronic Myeloid Leukemia Treatments

Weill Cornell Medicine
2016-2025

NewYork–Presbyterian Hospital
2016-2025

Cornell University
2016-2025

New York Hospital Queens
2016-2025

Presbyterian Hospital
2016-2025

Leiden University Medical Center
2024

Claritas Genomics (United States)
2022

University of Pennsylvania
1991-2021

Assuta Medical Center
2020

New York State Department of Health
1971-2018

Over the last decade, there have been numerous developments and changes in treatment practices for management of patients with immune thrombocytopenia (ITP). This article is an update International Consensus Report published 2010. A critical review was performed to identify all relevant articles between 2009 2018. An expert panel screened, reviewed, graded studies formulated updated consensus recommendations based on new data. The final document provides diagnosis ITP adults, during...

10.1182/bloodadvances.2019000812 article EN cc-by-nc-nd Blood Advances 2019-11-26

The pathogenesis of chronic idiopathic thrombocytopenic purpura (ITP) involves antibody-mediated platelet destruction and reduced production. Stimulation production may be an effective treatment for this disorder.We conducted a trial in which 118 adults with ITP counts less than 30,000 per cubic millimeter who had relapses or whose count was refractory to at least one standard were randomly assigned receive the oral thrombopoietin-receptor agonist eltrombopag (30, 50, 75 mg daily) placebo....

10.1056/nejmoa073275 article EN New England Journal of Medicine 2007-11-28

Most current treatments for chronic immune thrombocytopenic purpura (ITP) act by decreasing platelet destruction. In a phase 1–2 study, we administered thrombopoiesis-stimulating protein, AMG 531, to patients with ITP.

10.1056/nejmoa054626 article EN New England Journal of Medicine 2006-10-18

Cases of apparent secondary immune thrombocytopenia (ITP) after SARS-CoV-2 vaccination with both the Pfizer and Moderna versions have been reported reached public attention. Public alarm was heightened following death first identified patient from an intracranial hemorrhage, which on Internet, then in USA Today1 The New York Times.2 Described below, we collected a series cases very low platelet counts occurring within 2 weeks order to enhance our understanding possible relationship, if any,...

10.1002/ajh.26132 article EN American Journal of Hematology 2021-02-19

THE production of antiplatelet antibodies and removal IgG-coated platelets by the mononuclear phagocyte system play an important part in pathogenesis immune thrombocytopenic purpura. The coating with immunoglobulin results their spleen liver, presumably receptors for Fc fragment IgG (Fcγ).1 , 2 Prolongation Fcγ-receptor-mediated clearance opsonized red cells after splenectomy1 3 infusions high doses intravenous gamma globulin,4 5 conjunction favorable clinical responses to these therapies,...

10.1056/nejm198605083141907 article EN New England Journal of Medicine 1986-05-08

Spleen tyrosine kinase (Syk) signaling is central to phagocytosis-based, antibody-mediated platelet destruction in adults with immune thrombocytopenia (ITP). Fostamatinib, an oral Syk inhibitor, produced sustained on-treatment responses a phase 2 ITP study. In two parallel, 3, multicenter, randomized, double-blind, placebo-controlled trials (FIT1 and FIT2), patients persistent/chronic were randomized 2:1 fostamatinib (n = 101) or placebo 49) at 100 mg BID for 24 weeks dose increase...

10.1002/ajh.25125 article EN cc-by-nc American Journal of Hematology 2018-04-26
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