List new articles about thrombose after covid vaccines
Executive summary
A concise set of recently published studies and reviews documents that rare thrombotic events—most notably vaccine‑induced immune thrombotic thrombocytopenia (VITT or TTS)—were observed after adenoviral COVID‑19 vaccines and, less commonly, reported after mRNA vaccines; large population studies and systematic reviews quantify risk and emphasize that COVID‑19 infection itself carries a higher thrombotic risk [1] [2] [3]. The most recent comparative and mechanistic work through 2025 refines understanding of which platforms carry higher relative risk and explores clinical features and outcomes across vaccine types [4] [5].
1. Recent comprehensive updates and systematic reviews — what to read first
For consolidated, evidence‑based overviews, an update on thromboembolic events after COVID vaccination synthesizes the literature on VTE, arterial events and VITT and notes rare but measurable TTS signals especially after adenoviral vaccines (ChAdOx1‑S, Ad26.COV2.S) with VAERS estimates and platform differences [1], while a systematic review of 286 patients catalogs clinical presentations, timing (mean ~11 days), platelet findings and that most reported events in early series were linked to AstraZeneca (ChAdOx1) [6]; an earlier systematic review and exploratory analysis also discusses hypothesized mechanisms linking vaccines to VITT [7].
2. Population and cohort studies quantifying the risk in the real world
Large population‑based analyses provide context: a Catalonia study compared post‑vaccine thrombosis and thrombocytopenia rates with background and with SARS‑CoV‑2 infection, offering direct population estimates [2], and an international network cohort across five European countries and the US observed a pooled ~30% increased risk of thrombocytopenia after a first ChAdOx1‑S dose and a trend toward increased venous thrombosis with thrombocytopenia after Ad26.COV2.S versus BNT162b2 [3]; self‑controlled case‑series from England likewise identified rare thrombocytopenia and thromboembolic signals after ChAdOx1 that prompted policy changes [8].
3. Case series, clinical cohorts and mechanistic reporting to understand severity and timing
Clinically detailed case and multicenter cohort studies remain essential: early NEJM and Lancet reports documented clusters of severe cerebral venous thrombosis with thrombocytopenia occurring about 7–10 days after ChAdOx1 vaccination and helped define VITT as a syndrome [9] [10], while case compilations and surveillance summaries counted possible CVST and splanchnic events across vaccine recipients and cautioned about voluntary‑reporting limits [11]; smaller case series document rare thrombotic events after mRNA vaccines but emphasize far lower counts compared with adenoviral vectors [12] [13].
4. Newer comparative and risk‑benefit analyses through 2024–2025
More recent work refines prior signals: a 2024 risk‑benefit and causal‑pathway analysis examined thromboembolic risks after mRNA vaccines and reported studies finding increased risks for thromboembolism, ischemic stroke and CVST after first doses in some cohorts, while reiterating the necessity of weighing vaccine benefits against infection risks [5]; a 2025 Communications Medicine comparison found VITT remains rare and reported no strong evidence of clinically relevant differences in VITT cases between Ad26 and ChAdOx1 when carefully compared, updating prior platform‑specific impressions [4].
5. How to read these articles together — balance, limitations and policy implications
Taken together, the literature shows a reproducible, rare syndrome of VITT after adenoviral‑vector COVID vaccines with clear clinical features and measurable signals in surveillance and cohort data that shaped regulatory restrictions [9] [3] [14], while signals after mRNA vaccines are substantially rarer and more contested in magnitude and causality [12] [5]; these studies also repeatedly stress that SARS‑CoV‑2 infection itself produces a higher and more frequent thrombotic burden, and many data sources rely on passive reporting or heterogeneous case definitions, limiting direct incidence comparisons without careful methodological reading [1] [2] [11].