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Reported otolaryngologic-cutaneous relationships arise through distinct mechanisms, including direct infectious spread, shared inflammatory predisposition, local sensory-neuroimmune signaling, and neuropathic-like symptoms without nerve injury. This structured narrative review evaluates clinical and translational evidence for these categories and distinguishes neurogenic inflammation from neuropathic pain and itch. PubMed/MEDLINE was searched through August 12, 2026, with supplementary targeted association searches on September 1, 2026. Acute bacterial rhinosinusitis may cause periorbital or orbital cellulitis through direct anatomic spread. Associations of chronic rhinosinusitis with rosacea and allergic rhinitis with atopic dermatitis or eczema remain observational and do not establish causality or temporal sequence. Sensory-neuropeptide signaling is best established for pruritus and remains suggestive for rosacea. Intense or persistent nociceptor activation can amplify neurogenic inflammation and produce burning, stinging, itch, or allodynia that resembles neuropathic symptoms without the somatosensory lesion required for neuropathic disease. Clinical evaluation should classify findings as infectious, shared inflammatory or atopic, neurogenic inflammatory, neuropathic-like, or neuropathic and should direct treatment to the established disorder. Human evidence does not support targeted treatment of a shared otolaryngologic-cutaneous neuroimmune pathway.
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Islam et al. (2026) studied this question.
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