Abstract
Are NO Precursors Truly Effective in MELAS?
Highlights
nitric oxide (NO) deficiency in mitochondrial disorders (MIDs) is most likely a secondary phenomenon and not the primary causative mechanism that leads to clinical manifestations in MIDs
Stroke-like episodes are the clinical manifestation of a stroke-like lesion (SLL) on MRI, which is clearly distinguishable from an ischemic lesion
The main difference between the 2 is that SLLs are not confined to a vascular territory, whereas ischemic stroke is restricted to the vascular territory of the occluded artery
Summary
NO deficiency in mitochondrial disorders (MIDs) is most likely a secondary phenomenon and not the primary causative mechanism that leads to clinical manifestations in MIDs. The authors mention a number of therapeutic options available for patients with MID. Many options are not addressed, those which may significantly prolong life in these patients.[4] These include oral anticoagulation, heart failure therapy, antiarrhythmic therapy with drugs or implantation of a pacemaker, a cardiac resychronisation therapy (CRT) system, or an implantable cardioverter defibrillator, and invasive or noninvasive mechanical ventilation.[4] In this respect, it is necessary to mention idebenone as an approved drug for the treatment of patients with Leber hereditary optic neuropathy, which has been shown to improve color vision, increase cellspecific ATP production, and decrease oxidative stress.[5]
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