Evidence map›Paper›PMID 38038006›Full record

ReviewCurrent vascular pharmacology2024

Endocrine Disorders and Peripheral Arterial Disease - A Series of Reviews Cushing Syndrome-Cortisol Excess.

P Poredoš, G H Schernthaner, A Blinc, D P Mikhailidis, M Jensterle, P Anagnostis, P L Antignani, K Bajuk Studen, M Šabović, M K Ježovnik

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current vascular pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.8field-weighted citation impact, top 24% of its field
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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. Article
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

10 authors at 6 institutions in 5 countries.

P PoredošDepartment of Vascular Diseases, University Medical Centre, Ljubljana, Slovenia.
G H SchernthanerDepartment of Medicine 2, Division of Angiology, Medical University of Vienna, Vienna, Austria.
A BlincDepartment of Vascular Diseases, University Medical Centre, Ljubljana, Slovenia.
D P MikhailidisDepartment of Surgical Biotechnology, Division of Surgery and Interventional Science, University College London Medical School, University College London (UCL) and Department of Clinical Biochemistry, Royal Free Hospital Campus (UCL), London, UK.
M JensterleFaculty of Medicine, Department of Internal Medicine, University of Ljubljana, Ljubljana, Slovenia.
P AnagnostisUnit of Reproductive Endocrinology, 1st Department of Obstetrics and Gynecology, Medical School, Aristotle University of Thessaloniki, Thessaloniki, Greece.
P L AntignaniVascular Centre Nuova Villa Claudia, Rome, Italy.
K Bajuk StudenFaculty of Medicine, Department of Internal Medicine, University of Ljubljana, Ljubljana, Slovenia.
M ŠabovićDepartment of Vascular Diseases, University Medical Centre, Ljubljana, Slovenia.
M K JežovnikThe University of Texas Health Science Center at Houston, Department of Advanced Cardiopulmonary Therapies and Transplantation, Houston, Texas, USA.
Ljubljana University Medical Centre · SIAristotle University of Thessaloniki · GRMedical University of Vienna · ATThe Royal Free Hospital · GBThe University of Texas Health Science Center at Houston · USUniversity of Ljubljana · SI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cushing syndrome (CS), characterised by endogenous or exogenous glucocorticoid hormone excess, is associated with several systemic complications, including impaired glucose metabolism, which often becomes clinically manifest as diabetes mellitus (DM). In addition, CS can harm the arterial wall because of hyperglycaemia, dyslipidaemia, hepatic steatosis, and central obesity. These metabolic disorders promote atherosclerosis by synthesising adipokines, leptin, and proinflammatory cytokines. Lower limb arterial complications in CS are common and significantly impact morbidity and mortality. Furthermore, CS, in combination with DM, is likely to cause more diffuse vascular disease that predominantly affects distal arterial beds. In conclusion, CS promotes atherosclerosis, including peripheral artery disease, by causing functional and morphological deterioration of the arterial vessel wall and increasing the presence of classical risk factors of atherosclerosis.

Indexed as

Cushing SyndromePeripheral Arterial DiseaseAnimalsHumansHydrocortisoneRisk FactorsHydrocortisoneatherogenesiscortisol excessCushing syndromediabetes mellitus.insulin resistancemetabolic syndrome

Identifiers

PMID38038006
OpenAlexW4389224921

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.