Evidence map›Paper›PMID 39118706›Full record

ReviewAnnals of medicine and surgery (2012)2024

Soluble platelet selectin and platelets in COVID-19: a multifaceted connection.

Emmanuel Ifeanyi Obeagu, Getrude Uzoma Obeagu, Patrick Maduabuchi Aja, G I A Okoroiwu, N I Ubosi, Theophilus Pius, Muhammad Ashiru, Kingsley Akaba, Teddy Charles Adias

Abstract readReview
In one paragraph

Review in Annals of medicine and surgery (2012), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Stress-induced hemostasis: mechanisms and implications for health.Annals of medicine and surgery (2012) · 2025
    Review
  8. Article
  9. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Emmanuel Ifeanyi ObeaguDepartment of Medical Laboratory Science, Kampala International University.
Getrude Uzoma ObeaguSchool of Nursing Science, Kampala International University.
Patrick Maduabuchi AjaDepartment of Biochemistry, Faculty of Biomedical Sciences, Kampala International University, Ishaka, Uganda.
G I A OkoroiwuDepartment of Nursing Sciences, Faculty of Allied Health Sciences, Bayero University, Kano, Kano State.
N I UbosiDepartment of Nursing Sciences, Faculty of Allied Health Sciences, Bayero University, Kano, Kano State.
Theophilus PiusDepartment of Medical Laboratory Science, Kampala International University.
Muhammad AshiruDepartment of Nursing Sciences, Faculty of Allied Health Sciences, Bayero University, Kano, Kano State.
Kingsley AkabaDepartment of Haematology, University of Calabar, Calabar, Cross-River State.
Teddy Charles AdiasDepartment of Haematology and Blood Transfusion Science, Faculty of Medical Laboratory Science, Federal University Otuoke, Bayelsa State, Nigeria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The COVID-19 pandemic has brought to light the intricate relationship between platelets, soluble platelet selectin (sP-selectin), and disease pathogenesis. Platelets, traditionally recognized for their role in hemostasis, have emerged as key contributors to the immunothrombotic complications observed in COVID-19 patients. Concurrently, elevated levels of sP-selectin, indicative of platelet activation and endothelial injury, have been consistently identified in COVID-19 patients and have shown associations with disease severity and adverse outcomes. This multifaceted connection underscores the pivotal role of platelets and sP-selectin in orchestrating thromboinflammation, vascular dysfunction, and disease progression in COVID-19. Platelet activation triggers the release of inflammatory mediators and promotes platelet-leukocyte interactions, amplifying the systemic inflammatory response and exacerbating endothelial injury. Additionally, platelet-derived factors contribute to microvascular thrombosis, further exacerbating tissue damage and organ dysfunction in severe COVID-19. Elevated sP-selectin levels serve as biomarkers for disease severity and prognostication, aiding in risk stratification and early identification of patients at higher risk of adverse outcomes. Therapeutic strategies targeting platelet dysfunction and sP-selectin-mediated pathways hold promise in mitigating thromboinflammation and improving outcomes in COVID-19 patients. Antiplatelet agents, platelet inhibitors, and anti-inflammatory therapies represent potential interventions to attenuate platelet activation, inhibit platelet-leukocyte interactions, and alleviate endothelial dysfunction. A comprehensive understanding of the multifaceted connection between platelets, sP-selectin, and COVID-19 pathogenesis offers opportunities for tailored therapeutic approaches aimed at mitigating thromboinflammation and improving patient outcomes in this complex and challenging clinical setting.

Indexed as

COVID-19plateletsoluble platelet selectin

Identifiers

PMID39118706
PMCPMC11305715

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.