ReviewCurrent opinion in hematology2014
Advances in the pathophysiology and treatment of heparin-induced thrombocytopenia.
Review in Current opinion in hematology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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
17 citing papers in PubMed, 36 citations in OpenAlex.
- Reduced induction of anti-PF4/heparin antibody in RA patients after total knee arthroplasty.Arthritis research & therapy · 2016Trial
- TENDYNE mitral valve implantation complicated by heparin-induced thrombocytopenia in a patient with NSCLC: a case report.European heart journal. Case reports · 2026Article
- Case Report: Confirmed and suspected heparin-induced thrombocytopenia during therapeutic plasma exchange in neuromyelitis optica spectrum disorder: a single-centre case series.Frontiers in immunology · 2026Article
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- Risk factors of gastrointestinal bleeding after cardiopulmonary bypass in children: a retrospective study.Frontiers in cardiovascular medicine · 2023Article
- Use of a whole-cell ELISA to detect additional antibodies in setting of suspected heparin-induced thrombocytopenia.European journal of haematology · 2019Article
- The Clinical Utility of the Heparin Neutralization Assay in the Diagnosis of Heparin-Induced Thrombocytopenia.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis · 2018Article
- Synthesis and biocompatibility of an argatroban-modified polysulfone membrane that directly inhibits thrombosis.Journal of materials science. Materials in medicine · 2018Article
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- Anti-miR-148a regulates platelet FcγRIIA signaling and decreases thrombosis in vivo in mice.Blood · 2015Article
- What's new about heparin-induced thrombocytopenia type II.Intensive care medicine · 2015Article
- The significance and management of thrombocytopenia in antiphospholipid syndrome.Current rheumatology reports · 2015Review
- Restoration of adrenal function after bilateral adrenal damage due to heparin-induced thrombocytopenia (HIT): a case report.Journal of medical case reports · 2015Article
- Catastrophic APS in the context of other thrombotic microangiopathies.Current rheumatology reports · 2015Review
- Missing Cells: Pathophysiology, Diagnosis, and Management of (Pan)Cytopenia in Childhood.Frontiers in pediatrics · 2015Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
purpose of reviewTo review the recent developments in understanding the pathophysiology of heparin-induced thrombocytopenia (HIT) and in applying this knowledge to the treatment of patients with suspected and proven HIT. RECENT
findingsHIT pathophysiology is dynamic and complex. HIT pathophysiology is initiated by four essential components--heparin (Hep), platelet factor 4 (PF4), IgG antibodies against the Hep-PF4 complex, and platelet FcγRIIa. HIT is propagated by activated platelets, monocytes, endothelial cells, and coagulation proteins. Insights into the unique HIT antibody response continue to emerge, but without consensus as to the relative roles of B cells, T cells, and antigen-presenting cells. Platelet activation via FcγRIIa, the sine qua non of HIT, has become much better appreciated. Therapy remains challenging for several reasons. Suspected HIT is more frequent than proven HIT, because of the widespread use of Hep and the inadequacies of current diagnostic tests and scoring systems. In proven HIT, approved treatments reduce but do not eliminate thrombosis, and have substantial bleeding risk. Rational novel therapeutic strategies, directed at the initiating steps in HIT pathophysiology and with potential combinations staged over time, are in various phases of development. SUMMARY: Progress continues in understanding the breadth of molecular and cellular players in HIT. Translation to improved diagnosis and treatment is needed.
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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.