乙胺丁醇视神经毒性结构-功能损害与危险因素研究进展OA

Ethambutol-induced optic neurotoxicity is a major cause of irreversible visual impairment during anti-tuberculosis treatment,clinically characterized by subacute,bilateral symmetric and painless visual dysfunction.Its pathogenic mechanism stems from the chelation of copper and zinc ions by ethambutol and its metabolite 2,2'-(ethylenediamino)-dibutyric acid,which triggers dual mitochondrial-lysosomal dysfunction,adenosine triphosphate depletion and axonal transport blockage,ultimately leading to the apoptosis of retinal ganglion cells.At the subclinical stage,thickness changes in the retinal nerve fiber layer and the retinal ganglion cell inner plexiform layer,as well as prolonged P100 latency of visual evoked potentials,occur synchronously;the earlier decrease in macular vascular density suggests impaired ocular blood flow.These changes not only provide critical evidence for the early diagnosis of ethambutol-induced optic neurotoxicity but also offer important clues for exploring its pathogenesis.Moreover,risk factors for this condition include a daily dosage of≥15 mg/kg,a treatment course exceeding 6 months,chronic kidney disease,advanced age and smoking,all of which significantly increase the incidence risk.Clinicians'proficient grasp of the relevant pathogenesis,ocular changes and risk factors will facilitate early diagnosis and treatment,and to the greatest extent prevent irreversible visual impairment in patients.To reduce irreversible visual impairment while ensuring the efficacy of anti-tuberculosis therapy,this article systematically summarizes the pathogenesis,structural and functional damage characteristics,and high-risk factors of ethambutol-induced optic neurotoxicity,aiming to provide evidence-based basis and research directions for its early clinical identification and precise prevention and control.