Loss of vision secondary to toxic optic neuropathy due to gutka overdose: A Case Report

Introduction: Toxic optic neuropathy is defined as the damage caused by a toxin to the optic nerve fibers. There is a vast list of toxins that may lead to optic neuropathies. One of the toxins among this list is tobacco. Gutka being an oral form of tobacco, however, has not been previously related to optic neuropathy. Case presentation: We present a case of a 22-year-old male who presented with decreased far vision and gradually increasing photophobia. He had a history of gutka usage, a form of smokeless tobacco. Investigations revealed a central scotoma on FOV, a swollen optic disc on OCT and deranged Liver function tests. A diagnosis of RIGHT + LEFT optic neuropathy secondary to a chemical toxic was made, which in this case, was gutka. Conclusion: Consumption of gutka can lead to irreversible toxic optic neuropathy.

Management of toxic optic neuropathy via a combination of Wharton’s jelly-derived mesenchymal stem cells with electromagnetic stimulation

Purpose To investigate the effect of the combination of Wharton's jelly derived mesenchymal stem cells (WJ-MSC) and high frequency repetitive electromagnetic stimulation (rEMS) in the therapy of toxic optic neuropathies with severe symptoms after the available current therapy modalities which were unsucessful. Material and methods This prospective, open-label clinical phase-3 study was conducted at Ankara University Faculty of Medicine, Department of Ophthalmology between April 2019 and April 2021. Thirty-six eyes of 18 patients with toxic optic neuropathy (TON) were included in the study. Within 1–3 months after the emergency interventions, patients with various degrees of sequela visual disturbances were studied in this clinical trial. The cases were divided into three groups according to similar demographic characteristics. Group 1: Consists of 12 eyes of 12 patients treated with the WJ-MSC and rEMS combination in one eye. Group 2: Consists of 12 eyes of 12 patients treated with only rEMS in one eye. Group 3: Consists of 12 eyes of six patients treated with only WJ-MSC in both eyes. The course was evaluated by comparing the quantitive functional and structural assessment parameters measured before and at the fourth month of applications in each group. Results The mean best corrected visual acuity (BCVA) delta change percentages of the groups can be ranked as: Group 1 (47%) > Group 3 (32%) > Group 2 (21%). The mean fundus perimetry deviation index (FPDI) delta change percentages of the groups can be ranked as: Group 1 (95%) > Group 2 (33%) > Group 3 (27%). The mean ganglion cell complex (GCC) thickness delta change (decrease in thickness) percentages can be ranked as: Group 1 (− 21%) > Group 3 (− 15%) > Group 2 (− 13%). The visual evoked potential (VEP) P100 latency delta change percentages of the groups can be ranked as: Group 1 (− 18%) > Group 3 (− 10%) > Group 2 (− 8%). The P100 amplitude delta change percentages of the groups can be ranked as: Group 1 (105%) > Group 3 (83%) > Group 2 (24%). Conclusion Toxic optic neuropathies are emergent pathologies that can result in acute and permanent blindness. After poisoning with toxic substances, progressive apoptosis continues in optic nerve axons and ganglion cells. After the proper first systemic intervention in intensive care clinic, the WJ-MSC and rEMS combination seems very effective in the short-term period in cases with TON. To prevent permanent blindness, a combination of WJ-MSC and rEMS application as soon as possible may increase the chance of success in currently untreatable cases. Trial Registration ClinicalTrials.gov ID: NCT04877067.

A Case Report on Reversible Toxic Optic Neuropathy on Long Term Treatment of Linezolid in Extensively Drug-Resistant Tuberculosis Patient

We describe a case of Linezolid-induced severe toxic optic neuropathy in a patient with drug-resistant tuberculosis. Linezolid produced severe toxic optic neuropathy in some who used it for a long time. To the best of our knowledge, the optic neuropathy was completely reversed after omitting Linezolid which is one of the effective drug regimens in his prescription, with significant improvements in eye vision.

Intoksikasi Alkohol Akibat Minuman Keras Oplosan

The incidence of alcoholic liquor poisoning (alcoholic liquor) in Indonesia shows a high number. One of the causes of alcohol poisoning is methanol. Methanol poisoning in Indonesia usually occurs as a result of drinking mixed alcohol liquor. It has been reported a male 23 years old with decreased consciousness after drinking oplosan alcohol suspected to contain methanol. The examination reveals that patients has metabolic acidosis, toxic optic neuropathy (TON) and erosive gastritis. Treatment was acidosis correction, prevent formation of metabolites, hemodialysis with supportive and symptomatic teraphy .Keywords: methanol, poisoning, alcohol mixed liquor

Tacrolimus-induced bilateral optic neuropathy: A case report

Intrduction. Tacrolimus (fujimycin or FK506) is a potent immunosuppressive drug with growing usage. It is usually used in prevention of transplanted organ rejection. Its use is highly valuable, but like other immunosupressants, it has adverse effects. One of them is optic neuropathy. Case report. A 47-year-old white male patients who had received tacrolimus therapy for nine years, after kidney transplantation, developed a subacute, painless vision loss on both eyes. He was thoroughly examined on different possible optic neuropathies and other causes of vision loss. After exclusion of other possible causes, the diagnosis of toxic optic neuropathy was established. His therapy was converted to cyclosporine, by his nephrologist, but his vision had improved only slightly. Conclusion. Toxic optic neuropathies are presented in everyday ophthalmological practice, but they are underestimated. Diagnosis can be demanding, especially when it comes to drugs and substances whose possible toxic effect on the optic nerve is not widely known. Unlike other adverse effects of tacrolimus therapy on nervous system, optic neuropathy can causes great and permanent functional impairment.

RESEARCH OF REPARATIVE MECHANISMS IN THE OPTIC NERVE IN TOXIC NEUROPATHY CAUSED BY Cr (VI)

Intoxication lesions of the optic nerve (toxic optic neuropathy, TON) most often occur under the influence of exogenous factors, including heavy metals. Сell survival under stress have involves heat shock proteins (HSPs). The aim of the research. To assess the optic nerve’s immunoreactivity to heat shock proteins of the HSP70 and HSP90α families and reveal its relationship with the severity of morphological changes in toxic optic neuropathy caused by Cr (VI). Materials and methods. The study was conducted on 48 mature male rats. The experimental groups were given to drink water with Cr(VI) for 20, 40 and 60 days. This type of water is typical for the water basins in the northern districts of the Sumy region. Optic nerves сhanges under the influence of Cr(VI) have investigated by the morphometric method. Neuroglial cells and capillary endothelial cells were assessed by immunohistochemistry by HSP70α and HSP90 expression for intensity and spatial distribution. Results. The data analysis revealed that Cr (VI) has a neurotoxic effect on the optic nerve with the development of edema, which is manifested by the thickening of nerve fibers. The dynamics of HSP70 immunoexpression in the endothelium of the optic nerve capillaries of rats on 20 and 40 experimental days was characterized by stable values and was 1.5 times higher than the control. The maximum number of positively stained cells for the HSP70 marker was detected in endothelial cells of the microvasculature for 60 days – 82.44±12.42 %. HSP70 levels in neuroglia cells of optic nerve have decreased on day 40 (55.66±11.56% p=0.05) and lower than the control (70.44±4.81 %.) group. Optic nerve capillaries was highest immunoactivity on HSP90 in group II endothelial cells – 51.22±14.57% (p=0.05). The activity of HSP90α protein in optic neuroglia cells was characterized by a gradual increase in the duration of the experiment and was higher by 12, 4 % in experimental group III (81.77±21.67 %) compared with control (71.66±4.95 %). Conclusions. Our study provides an insight into the significant difference in the immunoreactivity of heat shock proteins of the HSP70 and HSP90α families in neuroglia and endothelial cells of the optic nerve capillaries under the influence of Cr(VI). The results obtained suggest that Cr (VI) has a neurotoxic effect on the optic nerve with the development of edema, which is manifested by the thickening of nerve fibers. A comparison of the dynamics of the development of the dystrophic process in the optic nerve with the results of the immunohistochemical analysis showed, that an increase in the thickness of nerve fibers is accompanied by an increase in immunoreactive neuroglial cells (HSP90α) and endothelial cells (HSP70).