ReviewJournal of clinical medicine2023
Autoimmune Heparin-Induced Thrombocytopenia.
Review in Journal of clinical medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Guidelines on the Use of Therapeutic Apheresis in Clinical Practice-Evidence-Based Approach From the Writing Committee of the American Society for Apheresis: The Tenth Special Issue.Journal of clinical apheresis · 2026Guideline
- Classification of Platelet-Activating Anti-Platelet Factor 4 Disorders.International journal of laboratory hematology · 2026Review
- [Analysis of Clinical Characteristics and Diagnostic Indicators in Patients With Heparin-induced Thrombocytopenia After Cardiac Surgery].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026Article
- Autoimmune heparin-induced thrombocytopenia following cardiac surgery.BMJ case reports · 2026Article
- Translational immunothrombosis in autoimmune Heparin-Induced thrombocytopenia: targeting the FcγRIIa-Syk-BTK and complement pathways.Clinical and experimental medicine · 2026Review
- The hidden threat: understanding anti-PF4 disorders without proximate heparin exposure.Frontiers in immunology · 2026Review
- Argatroban-Associated Adverse Events: An Analysis Based on FDA Adverse Event Reporting System (FAERS).Cardiovascular toxicology · 2025Article
- Platelet factor 4 modulates endothelial cell antimicrobial activity to enhance bacterial clearance and improve sepsis outcomes.bioRxiv : the preprint server for biology · 2025Article
- Thrombocytopenia and Anemia After Cardiac Surgery.American journal of hematology · 2025Article
- Article
- Emerging Thrombotic Disorders Associated with Virus-Based Innovative Therapies: From VITT to AAV Gene Therapy-Related Thrombotic Microangiopathy.Thrombosis and haemostasis · 2025Review
- Anti-Platelet factor 4 immunothrombosis-not just heparin and vaccine triggers.Research and practice in thrombosis and haemostasis · 2025Review
- Advances in our understanding of anti-PF4 related immunothrombosis.Frontiers in immunology · 2025Review
- Demystifying autoimmune HIT: what it is, when to test, and how to treat.Hematology. American Society of Hematology. Education Program · 2024Review
- Approaches to management of HIT in complex scenarios, including cardiac surgery.Hematology. American Society of Hematology. Education Program · 2024Review
- Recurrent Stent Thrombosis Following Myocardial Infarction Associated With VITT-Like Antibodies.JACC. Case reports · 2024Article
- High-Dose Immunoglobulin Therapy for Multiple Thromboembolism in Persisting Heparin-Induced Thrombocytopenia.Cureus · 2024Article
- Low Incidence of Anti-PF4/Heparin Antibodies in Patients with Acute Myelogenous Leukemia.Mediterranean journal of hematology and infectious diseases · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autoimmune thrombocytopenia (aHIT) is a severe subtype of heparin-induced thrombocytopenia (HIT) with atypical clinical features caused by highly pathological IgG antibodies ("aHIT antibodies") that activate platelets even in the absence of heparin. The clinical features of aHIT include: the onset or worsening of thrombocytopenia despite stopping heparin ("delayed-onset HIT"), thrombocytopenia persistence despite stopping heparin ("persisting" or "refractory HIT"), or triggered by small amounts of heparin (heparin "flush" HIT), most cases of fondaparinux-induced HIT, and patients with unusually severe HIT (e.g., multi-site or microvascular thrombosis, overt disseminated intravascular coagulation [DIC]). Special treatment approaches are required. For example, unlike classic HIT, heparin cessation does not result in de-escalation of antibody-induced hemostasis activation, and thus high-dose intravenous immunoglobulin (IVIG) may be indicated to interrupt aHIT-induced platelet activation; therapeutic plasma exchange may be required if high-dose IVIG is ineffective. Also, aHIT patients are at risk for treatment failure with (activated partial thromboplastin time [APTT]-adjusted) direct thrombin inhibitor (DTI) therapy (argatroban, bivalirudin), either because of APTT confounding (where aHIT-associated DIC and resulting APTT prolongation lead to systematic underdosing/interruption of DTI therapy) or because DTI inhibits thrombin-induced protein C activation. Most HIT laboratories do not test for aHIT antibodies, contributing to aHIT under-recognition.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.