Heterogeneous etiologies and mechanisms of bilateral visual impairment in tuberculosis: a retrospective clinical  analysis

Jinli Feng^1#, Ming Fang^2#, Zhuangzhuang Ren^1#, Lihong Wu³, Jun Zhao¹, Shuang Wang¹, Hongfen Wang^1*, Jinming Han^4*, Feng Qiu^1*

¹Senior Department of Neurology, Chinese PLA General Hospital, Beijing 100853, China.

²Department of Anesthesiology, Huashan Hospital Affiliated to Fudan University, Shanghai 200040, China.

³Senior Department of Tuberculosis, Chinese PLA General Hospital, Beijing 100091, China.

⁴Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China.

#co-first author:These authors have contributed equally to this work and share first authorship.

H.W., J.H. and F.Q. were co-corresponding authors.

*Correspondence:

Hongfen Wang; Email: wanghf301@sina.cn

Jinming Han; Email: hanjinming1202@126.com

corresponding author:Feng Qiu; Email: qiufengnet@hotmail.com

Abstract

Objective We aimed to systematically analyze the potential causes of bilateral visual impairment in patients with tuberculosis (TB), and to explore the underlying mechanisms involving infectious, inflammatory, immune-mediated, vascular, metabolic, and drug-related factors, thereby improving clinical awareness of this uncommon complication.

Methods We retrospectively reviewed seven patients with TB who developed bilateral visual decline at the Eighth Medical Center of the Chinese PLA General Hospital between October 2020 and July 2025. Clinical manifestations, neuroimaging features, immunological and nutritional profiles, medication history, therapeutic response, and prognosis were comprehensively analyzed.

Results Among the seven patients, three had tuberculous meningitis, three had pulmonary TB, and one had tuberculous peritonitis. The etiologies of visual impairment were diverse and included: (1) direct invasion of the optic pathway by TB infection; (2) bilateral occipital lobe infarction secondary to tuberculous vasculitis; (3) immune-mediated optic neuropathies triggered by infection—including myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), neuromyelitis optica spectrum disorder (NMOSD), and antibody-negative immune optic neuritis; (4) metabolic optic neuropathy caused by vitamin B1 deficiency; and (5) febuxostat-associated drug-induced neurotoxicity. Following mechanism-oriented individualized treatment, visual acuity was fully recovered in four patients, partially improved in two, and showed no improvement in the one patient with NMOSD.

Conclusion TB-associated visual impairment has complex and heterogeneous etiologies beyond classic anti-TB drug toxicity, including direct infectious involvement, tuberculous vasculitis–related ischemia, infection-triggered immune-mediated demyelination, and nutritional/metabolic disturbances. A mechanism-oriented evaluation integrating clinical features, neuroimaging, antibody testing, nutritional assessment, and careful medication reconciliation may facilitate early targeted management. The potential association between febuxostat exposure and reversible optic neuropathy observed in this series is hypothesis-generating and requires further confirmation.

Keywords: tuberculosis, visual impairment, immune-mediated injury, vasculitis, metabolic abnormalities