ArticleCase reports in hematology2025
Supercharged Hypercoagulability: A Case of Heparin-Induced Thrombocytopenia With Thrombosis in a Patient With Double Heterozygous Factor V Leiden and Prothrombin Mutations.
Article in Case reports in hematology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Factor V Leiden (FVL) and the prothrombin 20210A gene mutation are two common genetic predispositions to hypercoagulability. We present a complex case of recurrent venous thromboembolism (VTE) in a 50-year-old woman with double heterozygosity for FVL and prothrombin G20210A, complicated by heparin-induced thrombocytopenia (HIT) and May-Thurner syndrome. Following a recent orthopedic surgery and a sedentary postoperative course, the patient developed extensive bilateral deep vein thrombosis (DVT) and a saddle pulmonary embolism. Initial anticoagulation with heparin was complicated by progressive thrombocytopenia and confirmed HIT, prompting transition to bivalirudin and subsequently argatroban. Despite therapeutic anticoagulation and multiple interventional procedures, the patient experienced repeated thrombotic events. After increasing the therapeutic aPTT goal for argatroban, she ultimately stabilized and was successfully transitioned to oral apixaban. This case highlights the synergistic risk posed by the combination of inherited thrombophilia, structural venous abnormalities, and acquired prothrombotic conditions. It provides insight into the complex nature of proper anticoagulation strategies in these individual cases. Our use of argatroban with higher aPTT goals may provide guidance in future cases of refractory VTE. Further studies are needed to better understand the optimal therapies and management for patients with hereditary and acquired thrombophilia.
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.