Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Autoimmune thrombocytopenia.

B H Chong1, S-J Ho

  • 1Department of Medicine, Centre of Vascular Research, St George Clinical School, University of New South Wales, NSW, Australia. beng.chong@unsw.edu.au

Journal of Thrombosis and Haemostasis : JTH
|August 17, 2005
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Clinical relevance of nitrated beta 2-glycoprotein I in antiphospholipid syndrome: Implications for thrombosis risk.

Journal of autoimmunity·2021
Same author

Quantification of NETs-associated markers by flow cytometry and serum assays in patients with thrombosis and sepsis.

International journal of laboratory hematology·2018
Same author

Activation of tumour cell ECM degradation by thrombin-activated platelet membranes: potentially a P-selectin and GPIIb/IIIa-dependent process.

Clinical & experimental metastasis·2015
Same author

Recommendations for the use of the non-obese diabetic/severe combined immunodeficiency mouse model in autoimmune and drug-induced thrombocytopenia: communication from the SSC of the ISTH.

Journal of thrombosis and haemostasis : JTH·2015
Same author

Beware of NK cells in pre-clinical metastasis models.

Clinical & experimental metastasis·2013
Same author

EGFR and the complexity of receptor crosstalk in the cardiovascular system.

Current molecular medicine·2012
Same journal

The Natural Mutation Arg221aTrp in Human α-Thrombin Abrogates Physiological Na<sup>+</sup> Binding and Preferentially Hinders the Protease Anticoagulant Functions.

Journal of thrombosis and haemostasis : JTH·2026
Same journal

A historical review of the biological, semantic and clinical aspects of aspirin resistance.

Journal of thrombosis and haemostasis : JTH·2026
Same journal

Association between Thrombus Neutrophil Extracellular Traps Content and Ischemic Stroke Recurrence.

Journal of thrombosis and haemostasis : JTH·2026
Same journal

Peptide-Mediated Inhibition of Surface-Initiated Thrombogenesis.

Journal of thrombosis and haemostasis : JTH·2026
Same journal

Growth differentiation factor-15 and bleeding risk in patients with venous thromboembolism.

Journal of thrombosis and haemostasis : JTH·2026
Same journal

Physiological Anticoagulant Deficiencies: Pathogenesis, Diagnosis, and Clinical Implications.

Journal of thrombosis and haemostasis : JTH·2026
See all related articles

Idiopathic thrombocytopenic purpura (ITP) is an autoimmune platelet destruction disorder. Treatment focuses on maintaining safe platelet counts, with splenectomy as a key option for persistent cases.

Area of Science:

  • Hematology
  • Immunology
  • Autoimmune Diseases

Background:

  • Idiopathic thrombocytopenic purpura (ITP) is an autoimmune disorder characterized by platelet destruction.
  • Platelets are primarily targeted by antibodies against GPIIb/IIIa and GPIb/IX, with recent evidence implicating cytotoxic T cells.
  • Diagnosis involves excluding other causes of thrombocytopenia.

Purpose of the Study:

  • To outline the diagnostic criteria and treatment strategies for Idiopathic Thrombocytopenic Purpura (ITP).
  • To discuss management options for mild and severe ITP cases, including refractory patients.
  • To highlight the role of splenectomy and future therapeutic prospects.

Main Methods:

  • Diagnosis by exclusion of other thrombocytopenia causes.

Related Experiment Videos

  • Treatment initiation based on platelet count thresholds (<30 x 10(9) L(-1)).
  • Consideration of corticosteroids, IVIG, anti-D, and splenectomy.
  • Main Results:

    • Mild ITP cases (platelets >30 x 10(9) L(-1)) often require no treatment.
    • Corticosteroids, IVIG, or anti-D are used for persistent low platelet counts.
    • Splenectomy is highly effective for ITP unresponsive to initial therapies.

    Conclusions:

    • Management of ITP aims to maintain safe platelet levels with minimal adverse effects.
    • Splenectomy is the most effective treatment for ITP after 3-6 months of failed spontaneous remission.
    • Refractory ITP presents a management challenge with limited options; thrombopoietic agents offer future promise.