ArticleOncology letters2025
Splenic infarction secondary to multi-site thrombosis in lung adenocarcinoma with EGFR-L858R mutation: A case report.
Article in Oncology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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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.
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Who cites it
1 citing paper in PubMed.
- Underlying thrombotic conditions in patients with splenic infarction: a 10-year retrospective analysis.Thrombosis journal · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Venous thromboembolism (VTE) is a well-documented complication in lung cancer; however, the culmination of multi-site thrombosis in splenic infarction remains extremely rare. The present case report highlighted the complex interplay between oncogenic drivers and coagulation abnormalities in advanced non-small cell lung cancer (NSCLC). A 37-year-old man with stage IVA (T3N2M1a) EGFR-L858R-mutated lung adenocarcinoma presented with acute left upper quadrant pain. Despite prophylactic anticoagulation with rivaroxaban (10 mg twice daily), imaging indicated progressive thrombosis involving the splenic artery, superior vena cava, and deep veins of the neck and lower extremities. Contrast-enhanced abdominal CT confirmed splenic infarction without secondary abscess formation. The patient underwent intensified anticoagulation with enoxaparin (8,000 IU twice daily) and anti-infective prophylaxis, which achieved spontaneous splenic infarct resolution on follow-up imaging (December 2024 to May 2025). The present case underscored three critical clinical insights: i) The paradoxical thrombotic risk profile associated with EGFR-mutated NSCLC during disease progression; ii) the limitations of current VTE risk assessment tools in advanced malignancies; and iii) the necessity for dynamic anticoagulation strategies in cancer-associated thrombosis. Clinicians are advised to maintain heightened vigilance for thrombotic complications even in genetically defined NSCLC subsets (such as EGFR-L858R mutant lung adenocarcinoma) receiving targeted therapies in the future.
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