Diabetic foot complications represent a major global health burden and arise from a multifactorial interaction between neuropathy, ischemia, infection, and impaired wound repair. Increasing evidence suggests that, beyond traditional vascular and metabolic risk factors, endocrine dysregulation plays a central role in shaping vascular dysfunction and tissue vulnerability in patients with diabetes. This narrative review provides an updated overview of the endocrine–vascular axis in the development, progression, and healing of diabetic foot ulcers (DFUs), integrating evidence from experimental and clinical studies identified through targeted searches of PubMed, Embase, and Scopus. We examine how alterations in insulin signaling, relative glucagon excess, adipokine imbalance, dysregulation of stress hormones, and thyroid dysfunction interact with chronic hyperglycemia, dyslipidemia, mitochondrial dysfunction, and low-grade inflammation to impair endothelial homeostasis. These disturbances promote oxidative stress, reduce nitric oxide bioavailability, and compromise microvascular perfusion, thereby creating a pro-ischemic and pro-inflammatory tissue environment that limits angiogenesis, extracellular matrix (ECM) remodeling, immune coordination, and effective wound repair. By linking pathophysiological mechanisms to clinical relevance, this review highlights potential biomarkers of endocrine–vascular dysfunction, implications for risk stratification, and emerging therapeutic perspectives targeting metabolic optimization, endothelial protection, and hormonal modulation. Finally, key knowledge gaps and priority areas for future translational and clinical research are discussed, supporting the development of integrated endocrine-based strategies aimed at improving DFU prevention, healing outcomes, and long-term limb preservation in patients with diabetes.

Chronic rhinosinusitis (CRS) is a prevalent inflammatory disease traditionally defined and assessed by sinonasal symptoms such as nasal obstruction, rhinorrhea, facial pressure, and olfactory dysfunction. However, the burden of CRS extends beyond the sinonasal compartment, including a range of systemic and functional complaints that are not routinely addressed in standard rhinologic practice. Among these, vestibular symptoms, including dizziness, imbalance, and nonspecific disequilibrium, are frequently reported by patients with CRS, yet remain underrecognized and poorly integrated into current diagnostic frameworks and clinical guidelines, despite being captured as a single, psychometrically limited item within the 22-item Sinonasal Outcome Test (SNOT-22). Clinical observations and limited published data, mostly small observational studies and case reports, suggest that vestibular symptoms may fluctuate in parallel with CRS disease activity and may improve following effective medical or surgical control of sinonasal inflammation. Proposed mechanisms include Eustachian tube dysfunction, immune-mediated and neurogenic pathways, trigemino-vestibular interactions, and altered multisensory integration, although current evidence does not establish a causal relationship between CRS disease activity and measurable peripheral vestibular dysfunction. Comparative observations in allergic rhinitis and post-viral upper-airway inflammation situate CRS within a broader inflammatory upper-airway–vestibular interface. This Commentary highlights vestibular dysfunction as an underappreciated extra-sinonasal dimension of CRS with potential clinical and functional relevance. By drawing attention to this clinical blind spot, we aim to encourage more systematic symptom inquiry, interdisciplinary dialogue, and prospective research into the functional consequences of chronic upper-airway inflammation.