When Glycaemic Control Comes Too Fast: Treatment‐Induced Neuropathy of Diabetes and Charcot Neuro‐Osteoarthropathy as Emerging Iatrogenic Complications of Rapid Metabolic Correction

PURPOSE OF REVIEW: Diabetes therapeutics can lower glycated haemoglobin (HbA1c) by several percentage points within weeks. While long-term microvascular risk is reduced by improved glycaemia, abrupt metabolic transitions may destabilise tissues adapted to chronic hyperglycemia. We review treatment-induced neuropathy of diabetes (TIND) and active Charcot neuro-osteoarthropathy (CNO) as two neurovascular complications reported after rapid glycaemic correction, and we propose a unifying 'metabolic tempo' framework for prevention and early detection. RECENT FINDINGS: TIND is an acute, painful small-fibre and autonomic neuropathy occurring within 2-8 weeks after large HbA1c reductions, frequently coinciding with early worsening of retinopathy and nephropathy. Human in vivo nerve imaging demonstrates epineurial arteriovenous shunting and proliferative, leaky microvessels, supporting a microvascular dysregulation/ischaemia-reperfusion model. For CNO, causal evidence linking rapid glycaemic improvement to disease onset remains limited and mainly observational; however, multiple case reports (including pregnancy, post-transplantation, and major weight loss contexts) and retrospective cohorts suggest that major glycaemic 'deceleration' may cluster in the months preceding active CNO in susceptible patients with long-standing neuropathy. SUMMARY: Rapid glycaemic correction should not be avoided when urgently needed, but 'tempo-aware' strategies may be warranted in microvascularly fragile patients (very high baseline HbA1c, established neuropathy/retinopathy, kidney disease, or major weight loss). We outline pragmatic risk stratification, surveillance, and interdisciplinary pathways (neurology-podiatry-ophthalmology-nephrology) to reduce delayed diagnosis and prevent deformity and disability.