The pathophysiology of diabetic foot: a narrative review.
Level 5 - mechanism / opinion, no new human data
Narrative review without systematic search methodology or original human data
PubMed 37797951 · doi:10.12701/jyms.2023.00731
What was done
The authors synthesized existing literature on the etiology and pathophysiological mechanisms underlying diabetic foot ulcers and Charcot neuroarthropathy. The abstract does not report systematic search methods, databases queried, date ranges, or study inclusion criteria.
What was found
No quantitative findings, sample sizes, or statistical results are reported in the abstract. The review outlines key mechanistic pathways driven by chronic hyperglycemia, including adenosine triphosphate deficiency, polyol pathway activation, oxidative stress, protein kinase C activity, endothelial nitric oxide suppression, sensory-motor-autonomic neuropathies, micro- and macrovascular ischemia, and impaired immune responses to infection.
Why it matters
Synthesizing the multi-system pathophysiology of diabetic foot ulceration provides a conceptual foundation for targeted clinical prevention and therapeutic interventions aimed at preventing major amputations.
Limits
As a narrative review, it lacks systematic search methodology, formal quality assessment of included studies, quantitative pooling, and original empirical data.
Cited by
- supports In diabetes, elevated blood sugar damages the vascular system supplying peripheral nerves, leading to nerve death, tissue necrosis, and increased susceptibility to extremity infections.