Evidence map›Paper›PMID 39202210›Full record

ReviewDiagnostics (Basel, Switzerland)2024

Cardiovascular Risk in Patients with Inflammatory Bowel Diseases-The Role of Endothelial Dysfunction.

Maria A Livzan, Galiya R Bikbavova, Natalya S Lisyutenko, Alisa E Romanyuk, Oxana M Drapkina

Abstract readReview
In one paragraph

Review in Diagnostics (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–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

7 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Acute Coronary Syndrome and Rheumatic Disease.Journal of clinical medicine · 2025
    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

5 authors.

Maria A LivzanDepartment of Faculty Therapy, Omsk State Medical University, 644099 Omsk, Russia.ORCID 0000-0002-6581-7017
Galiya R BikbavovaDepartment of Internal Medicine and Endocrinology, Omsk State Medical University, 644099 Omsk, Russia.
Natalya S LisyutenkoDepartment of Internal Medicine and Endocrinology, Omsk State Medical University, 644099 Omsk, Russia.
Alisa E RomanyukFaculty of Medicine, Omsk State Medical University, 644099 Omsk, Russia.
Oxana M DrapkinaNational Medical Research Center for Therapy and Preventive Medicine, 101990 Moscow, Russia.ORCID 0000-0003-0323-2635

Funding

Russian Science Foundation project No. 23-25-10035
6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) is associated with an increased risk of cardiovascular disease (CVD). Cardiovascular pathology in people with IBD has not been well studied to date, and a direct link between cardiovascular events and IBD has not been established. The mechanisms underlying this association include the parallel and dynamic interaction of inflammation, modulation of the composition of the gut microbiota, endothelial dysfunction, thrombogenicity, and increased endothelial and epithelial permeability. Endothelial dysfunction is a common aspect of the pathogenesis of IBD and atherosclerotic CVD and can be considered one of the most important factors leading to the development and progression of cardiovascular pathology in patients with IBD. The purpose of this literature review is to describe the mechanisms underlying the development of endothelial dysfunction and disorders of the structure and function of the gut-vascular barrier in the pathogenesis of the cardiovascular manifestation of IBD.

Indexed as

Crohn’s diseaseendothelial dysfunctiongut–vascular barrierinflammatory bowel diseaseulcerative colitis

Identifiers

PMID39202210
PMCPMC11353271

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.