Evidence map›Paper›PMID 41821730›Full record

SynthesisFrontiers in endocrinology2026

Unveiling the hidden link: diabetes mellitus as a catalyst for orbital apex syndrome.

Shu Xin Gao, Jie Gao

Abstract readSystematic Review
In one paragraph

Synthesis in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Shu Xin GaoGeneral Practice Department, Cangzhou Central Hospital, Cangzhou, China.
Jie GaoGeneral Practice Department, Cangzhou Central Hospital, Cangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Orbital Apex Syndrome (OAS) is a disease of multiple brain nerves at the orbital apex leading to vision loss and neurological impairments. Diabetes Mellitus (DM), a metabolic disorder with cardiovascular, immunological and neurological effects, is involved in OAS pathogenesis. However, the association between DM and OAS is not well studied. DM and OAS are poorly understood and may not be diagnosed correctly, especially when outbreaks such as COVID-19 are being investigated. Methods: A systematic review of 33 studies published between 2000 and 2025 was conducted to analyze DM-related OAS epidemiology, pathophysiology, clinical phenotypes, and treatment outcomes, focusing on the mechanistic links, pandemic trends, and glycemic control effect on therapeutic effectiveness. Results: Chronic hyperglycemia induced orbital apex microvascular damage (endothelial dysfunction, thrombosis, vascular senescence), immunosuppression induced opportunistic infections (mostly mucormycosis), and diabetic neuropathy induced neuromuscular dysfunction. During COVID-19, diabetic patients had the highest OAS incidence (more than 70% of cases involved rhino-orbital mucormycosis). Optimal glycemic control is associated with a 32% higher antifungal treatment effectiveness and a 28% lower rate of surgical complications. Epidemiological data showed that DM was the main predisposing factor, with 71.4%-81.8% infectious OAS cases occurred in diabetic populations. Conclusion: DM is underreported as a critical catalyst for OAS with complications directly increasing severity and progression. Routine DM screening (e.g., glycated hemoglobin monitoring) and integrated glycemic management are essential for OAS prevention and treatment. Long-term studies on inflammatory factors and personalized multidisciplinary care are needed to address mechanistic gaps and improve visual and neurological outcomes in high-risk diabetic patients.

Indexed as

COVID-19Diabetes ComplicationsDiabetes MellitusOrbital DiseasesHumansSARS-CoV-2Syndromediabetes mellitusdiabetic fungal infectionsdiabetic microvascular damageorbital apex syndromepathophysiological mechanisms

Identifiers

PMID41821730
PMCPMC12975586

What OpenQuestion 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 OpenQuestion graph.