Leber’s Hereditary Optic Neuropathy Precipitated by Tadalafil Use for Erectile Dysfunction

Cornish, Kurt Spiteri; Barras, Christopher W.

doi:10.3109/08820538.2010.541320

Cited by 6 publications

(5 citation statements)

References 13 publications

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“…However, the NO pathway was not evaluated in this study; instead, a possible link with the activation of Ca 2+ -activated potassium channels mediated by cGMP was speculated [ 176 ]. Nevertheless, the beneficial effects of PDE5i to treat PMD are still poorly understood, since preclinical studies [ 177 , 178 ] and case reports [ 179 ] gave controversial results; further investigations on the mechanisms need to be implemented.…”

Section: “One-size-fits-all” Approachesmentioning

confidence: 99%

Therapeutic Approaches to Treat Mitochondrial Diseases: “One-Size-Fits-All” and “Precision Medicine” Strategies

et al. 2020

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Primary mitochondrial diseases (PMD) refer to a group of severe, often inherited genetic conditions due to mutations in the mitochondrial genome or in the nuclear genes encoding for proteins involved in oxidative phosphorylation (OXPHOS). The mutations hamper the last step of aerobic metabolism, affecting the primary source of cellular ATP synthesis. Mitochondrial diseases are characterized by extremely heterogeneous symptoms, ranging from organ-specific to multisystemic dysfunction with different clinical courses. The limited information of the natural history, the limitations of currently available preclinical models, coupled with the large variability of phenotypical presentations of PMD patients, have strongly penalized the development of effective therapies. However, new therapeutic strategies have been emerging, often with promising preclinical and clinical results. Here we review the state of the art on experimental treatments for mitochondrial diseases, presenting “one-size-fits-all” approaches and precision medicine strategies. Finally, we propose novel perspective therapeutic plans, either based on preclinical studies or currently used for other genetic or metabolic diseases that could be transferred to PMD.

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Section: “One-size-fits-all” Approachesmentioning

confidence: 99%

Therapeutic Approaches to Treat Mitochondrial Diseases: “One-Size-Fits-All” and “Precision Medicine” Strategies

et al. 2020

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“…The majority of these are known for interfering with mitochondrial respiratory function (De Marinis ; Ikeda et al. ; Cornish & Barras ).…”

Section: Environmental Factors and Lhon Expressionmentioning

confidence: 99%

“…There are, however, many more substances that are under suspicion to trigger LHON: cyanides, meth-anol, pesticides, phosphodiesterase type 5 inhibitors, antibiotics such as ethambutol, chloramphenicol, linezolid, aminoglycosides and antiretroviral drugs (for HIV). The majority of these are known for interfering with mitochondrial respiratory function (De Marinis 2001;Ikeda et al 2006;Cornish & Barras 2011).…”

Section: Environmental Factors and Lhon Expressionmentioning

confidence: 99%

Toxic optic neuropathies: an updated review

Grzybowski

Zülsdorff²,

Wilhelm

et al. 2014

Acta Ophthalmologica

160

132

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ABSTRACT.Toxic optic neuropathy (TON) is caused by the damage to the optic nerve through different toxins, including drugs, metals, organic solvents, methanol and carbon dioxide. A similar clinical picture may also be caused by nutritional deficits, including B vitamins, folic acid and proteins with sulphur-containing amino acids. This review summarizes the present knowledge on disease-causing factors, clinical presentation, diagnostics and treatment in TON. It discusses in detail known and hypothesized relations between drugs, including tuberculostatic drugs, antimicrobial agents, antiepileptic drugs, antiarrhythmic drugs, disulfiram, halogenated hydroquinolones, antimetabolites, tamoxifen and phosphodiesterase type 5 inhibitors and optic neuropathy.Key words: adalimumab optic neuropathy -antitumor necrosis factor alpha optic neuropathycuban epidemic optic neuropathy -ethambutol optic neuropathy -infliximab optic neuropathy -Leber's hereditary optic neuropathy -nutritional optic neuropathy -tobaccoalcohol amblyopia -toxic optic neuropathy Acta Ophthalmol. 2015: 93: 402-410

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“…Several substances known to interfere with the function of the mitochondrial respiratory chain are under suspicion of triggering LHON in mutation carriers. These include antibiotics such as ethambutol, chloramphenicol, linezolid, aminoglycosides; antiretroviral drugs; as well as cyanides, methanol, pesticides, and phosphodiesterase type 5 inhibitors [25][26][27][28][29][30].…”

Section: Discussionmentioning

confidence: 99%

Sulthiame impairs mitochondrial function in vitro and may trigger onset of visual loss in Leber hereditary optic neuropathy

Reinert

Pacheu-Grau

Catarino

et al. 2021

Orphanet J Rare Dis

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Background Leber hereditary optic neuropathy (LHON) is the most common mitochondrial disorder and characterized by acute or subacute painless visual loss. Environmental factors reported to trigger visual loss in LHON mutation carriers include smoking, heavy intake of alcohol, raised intraocular pressure, and some drugs, including several carbonic anhydrase inhibitors. The antiepileptic drug sulthiame (STM) is effective especially in focal seizures, particularly in benign epilepsy of childhood with centrotemporal spikes, and widely used in pediatric epileptology. STM is a sulfonamide derivate and an inhibitor of mammalian carbonic anhydrase isoforms I–XIV. Results We describe two unrelated patients, an 8-year-old girl and an 11-year-old boy, with cryptogenic focal epilepsy, who suffered binocular (subject #1) or monocular (subject #2) visual loss in close temporal connection with starting antiepileptic pharmacotherapy with STM. In both subjects, visual loss was due to LHON. We used real-time respirometry in fibroblasts derived from LHON patients carrying the same mitochondrial mutations as our two subjects to investigate the effect of STM on oxidative phosphorylation. Oxygen consumption rate in fibroblasts from a healthy control was not impaired by STM compared with a vehicle control. In contrast, fibroblasts carrying the m.14484T>C or the m.3460G>A LHON mutation displayed a drastic reduction of the respiration rate when treated with STM compared to vehicle control. Conclusions Our observations point to a causal relationship between STM treatment and onset or worsening of visual failure in two subjects with LHON rather than pure coincidence. We conclude that antiepileptic medication with STM may pose a risk for visual loss in LHON mutation carriers and should be avoided in these patients.

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Leber’s Hereditary Optic Neuropathy Precipitated by Tadalafil Use for Erectile Dysfunction

Cited by 6 publications

References 13 publications

Therapeutic Approaches to Treat Mitochondrial Diseases: “One-Size-Fits-All” and “Precision Medicine” Strategies

Therapeutic Approaches to Treat Mitochondrial Diseases: “One-Size-Fits-All” and “Precision Medicine” Strategies

Toxic optic neuropathies: an updated review

Sulthiame impairs mitochondrial function in vitro and may trigger onset of visual loss in Leber hereditary optic neuropathy

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