Optic Neuropathy from Thiamine Deficiency

Suzuki, Shigeaki; Kumanomido, Takashi; Nagata, Eiichiro; Inoue, Jun; Niikawa, Osamu

doi:10.2169/internalmedicine.36.532

Cited by 20 publications

(11 citation statements)

References 3 publications

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“…This is in agreement with the association between vitamin B1 deficiency and degeneration of ganglion cells of the brain and spinal cord in animal experiments [30], and between vitamin B1 deficiency and a reduced thickness of the retinal ganglion cell layer in rats [31]. Furthermore, a link between vitamin B1 deficiency and other optic neuropathies is well established [32]. Obviously, most participants with a low intake of vitamin B1 in the current study may not have had a manifest vitamin B1 deficiency.…”

Section: Discussionsupporting

confidence: 89%

Nutrient intake and risk of open-angle glaucoma: the Rotterdam Study

et al. 2012

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Open-angle glaucoma (OAG) is the commonest cause of irreversible blindness worldwide. Apart from an increased intraocular pressure (IOP), oxidative stress and an impaired ocular blood flow are supposed to contribute to OAG. The aim of this study was to determine whether the dietary intake of nutrients that either have anti-oxidative properties (carotenoids, vitamins, and flavonoids) or influence the blood flow (omega fatty acids and magnesium) is associated with incident OAG. We investigated this in a prospective population-based cohort, the Rotterdam Study. A total of 3502 participants aged 55 years and older for whom dietary data at baseline and ophthalmic data at baseline and follow-up were available and who did not have OAG at baseline were included. The ophthalmic examinations comprised measurements of the IOP and perimetry; dietary intake of nutrients was assessed by validated questionnaires and adjusted for energy intake. Cox proportional hazard regression analysis was applied to calculate hazard ratios of associations between the baseline intake of nutrients and incident OAG, adjusted for age, gender, IOP, IOP-lowering treatment, and body mass index. During an average follow-up of 9.7 years, 91 participants (2.6%) developed OAG. The hazard ratio for retinol equivalents (highest versus lowest tertile) was 0.45 (95% confidence interval 0.23–0.90), for vitamin B1 0.50 (0.25–0.98), and for magnesium 2.25 (1.16–4.38). The effects were stronger after the exclusion of participants taking supplements. Hence, a low intake of retinol equivalents and vitamin B1 (in line with hypothesis) and a high intake of magnesium (less unambiguous to interpret) appear to be associated with an increased risk of OAG.

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Section: Discussionsupporting

confidence: 89%

Nutrient intake and risk of open-angle glaucoma: the Rotterdam Study

et al. 2012

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“…Ocular manifestations of WE generally include nystagmus, ophthalmoplegia and very rarely visual deterioration and optic neuropathy. We found only two cases of optic neuropathy in nonalcoholic patients in the literature [7,8] . Both cases had thiamine defi ciency induced by parenteral nutrition.…”

Section: Discussionmentioning

confidence: 83%

“…Similar to our case, Van Noort et al [7] reported total visual loss with partial recovery after thiamine supplementation in WE. Sometimes, in WE visual acuity may also be normal despite optic neuropathy [8] .…”

Section: Discussionmentioning

confidence: 99%

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Nonalcoholic Wernicke’s Encephalopathy with Prominent Astasia and Optic Neuropathy

Gökçe

Bülbüloğlu²,

Tuncel³

et al. 2005

Med Princ Pract

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Objective: To present a case with nonalcoholic Wernicke’s encephalopathy (WE) developing astasia and optic neuropathy as major sequelae. Clinical Presentation and Intervention: A 47-year-old woman developed WE following operation for pyloric stenosis. She received total parenteral nutrition before and after operation, but on the second postoperative day she developed visual hallucination and confusion, followed by nystagmus, ophthalmoplegia, apathy, dysarthria and coma. Although the patient has recovered with thiamine treatment, astasia and optic neuropathy persistedas major morbidities. Conclusion: The report shows that astasia and optic neuropathy may be prominent sequelae in some patients with WE.

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“…Suzuki et al have suggested a link between thiamine deficiency and optic neuropathy [9]. It has also been shown that intravenous administration of thiamine in a patient with optic and peripheral neuropathy produced rapid improvement in visual acuity with absence of further episodes of weakness/ataxia [10].…”

Section: Introductionmentioning

confidence: 99%

Sulbutiamine Counteracts Trophic Factor Deprivation Induced Apoptotic Cell Death in Transformed Retinal Ganglion Cells

et al. 2010

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Sulbutiamine is a highly lipid soluble synthetic analogue of vitamin B(1) and is used clinically for the treatment of asthenia. The aim of our study was to demonstrate whether sulbutiamine is able to attenuate trophic factor deprivation induced cell death to transformed retinal ganglion cells (RGC-5). Cells were subjected to serum deprivation for defined periods and sulbutiamine at different concentrations was added to the cultures. Various procedures (e.g. cell viability assays, apoptosis assay, reactive oxygen species analysis, Western blot analysis, flow cytometric analysis, glutathione (GSH) and glutathione-S-transferase (GST) measurement) were used to demonstrate the effect of sulbutiamine. Sulbutiamine dose-dependently attenuated apoptotic cell death induced by serum deprivation and stimulated GSH and GST activity. Moreover, sulbutiamine decreased the expression of cleaved caspase-3 and AIF. This study demonstrates for the first time that sulbutiamine is able to attenuate trophic factor deprivation induced apoptotic cell death in neuronal cells in culture.

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Optic Neuropathy from Thiamine Deficiency

Cited by 20 publications

References 3 publications

Nutrient intake and risk of open-angle glaucoma: the Rotterdam Study

Nutrient intake and risk of open-angle glaucoma: the Rotterdam Study

Nonalcoholic Wernicke’s Encephalopathy with Prominent Astasia and Optic Neuropathy

Sulbutiamine Counteracts Trophic Factor Deprivation Induced Apoptotic Cell Death in Transformed Retinal Ganglion Cells

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