ReviewEJHaem2025
Bleeding Complications in JAK2-Variant Essential Thrombocythemia: A Revisit in 2025.
Review in EJHaem, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
3 citing papers in PubMed.
- Ophthalmological and epidemiological profiles of Brazilian patients with philadelphia-negative Myeloproliferative neoplasms.Hematology, transfusion and cell therapy · 2026Article
- A Therapeutic Dilemma: Catastrophic ST-Elevation Myocardial Infarction Following Antiplatelet Therapy Interruption in a Patient With JAK2-Positive Polycythemia Vera.Clinical case reports · 2026Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Essential thrombocythemia (ET) is a myeloproliferative neoplasm characterised by sustained thrombocytosis. Paradoxically, bleeding complications remain an under-recognised clinical challenge. Compared with CALR-mutated patients, those harbouring the JAK2-V617F variant appear more prone to haemorrhage. This may be secondary to acquired von Willebrand syndrome (AvWS) and intrinsic platelet dysfunction. AvWS in ET arises from extreme platelet counts driving the adsorption and proteolysis of high-molecular-weight von Willebrand factor (VWF) multimers, producing a qualitative VWF defect akin to type 2A von Willebrand disease. However, the platelet count threshold for AvWS is variable, and patients with platelet counts below 1000 × 10
Identifiers
What OpenQuestion holds
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.