Reply to the letter titled “More likely than through head trauma, is LHON triggered by mitochondrion-toxic drugs or oxidative stress”

Abstract

I would like to thank Dr. Finsterer for his interest in my recently published article in Documenta Ophthalmologica, a case report involving Leber’s hereditary optic neuropathy (LHON) triggered after ocular and head trauma [1]. I admit to some shortcomings of my report, and I agree with his opinion. Generally, as he mentioned, LHON can be triggered by mitochondria-toxic agents or oxidative stress. In this case, the patient received intravenous (IV) steroid and oral NSAIDs during the hospitalization period as treatment for traumatic optic neuropathy and orbital contusion. The patient did not receive potentially mitochondrion-toxic drugs including antibiotics, anti-seizure drugs (e.g. valproic acid), certain analgesics (e.g. fentanyl), statins/fibrates, antifungal agents, or certain anesthetics (e.g. propofol). In addition, previous review papers have presented several other environmental factors implicated in LHON, including exposure to cigarette smoke, alcohol and chemical toxins, head trauma, acute physical illness, psychological stress, and antiretroviral and anti-tuberculous drugs [2–4]. Some previous reports have suggested head or ocular trauma rarely as a trigger of LHON [5, 6]. On history-taking and medical record review of the patient, he had no evidence of drug administration as stated above. The specific mechanism for trauma in relation to the activation of LHON in healthy carriers is still unclear. It was hard to reveal the mechanism of conversion of LHON following head and ocular trauma in this case report. I don’t think that the cause of LHON activation is trauma alone. There is a possibility that the intracellular organs including mitochondria may be damaged by trauma, and the oxidative stress may be increased after trauma, inducing retinal ganglion cell (RGC) apoptosis and triggering LHON. Overall, I appreciate Dr. Finsterer pointing out the shortcomings of this case report. To my knowledge, no mitochondria-toxic agent was prescribed to the patient. I also think that oxidative stress has a major role in triggering LHON activation. Unfortunately, I cannot investigate the exact relationship between trauma and LHON activation or the specific mechanism associated with oxidative stress during traumatic injury in optic nerve tissue and retinal ganglion cells in this report. I want to suggest the probability that a head or eye trauma could be one of the triggering factors for This reply refers to the article available at https://doi.org/10. 1007/s10633-020-09815-7.