Can targeted pathological treatments for diabetic peripheral neuropathy reduce complications and hospital burden?

This poster reviews targeted pathological treatments for diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus driven by hyperglycemia-induced damage. This is via the polyol, protein kinase C (PKC), and hexosamine biosynthetic pathways. These pathways contribute to nerve conduction deficits, neuropathic pain, ulceration, sepsis, amputations and an increased hospital burden. A systematic search of PubMed and TRIP databases (post-2000 literature, 23 papers selected) evaluated interventions like aldose reductase inhibitors (e.g., Epalrestat, offering modest sensory and motor nerve improvements but limited reversal), PKC-β inhibitors (e.g., Ruboxistaurin, with inconsistent pain reduction and microvascular effects), NaV1.8 channel blockers (VX-548, reducing daily pain intensity), and Benfotiamine (short-term symptomatic relief without disease modification). While these provide modest symptom relief and minor progression delays, no therapies fully halt or reverse DPN, highlighting the need for larger trials and combination approaches. More research may bring a shift in what is the current focus of treatment: glycemic control/foot surveillance to curb complications and acute care demands.Presented at South West Acute Care Conference, March 2026, University of Southampton Medical School.