{'fraction_non_alphanumeric': 0.02008407286314806, 'fraction_numerical': 0.0, 'mean_word_length': 5.413173652694611, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Author response: A severe linezolid‐induced rhabdomyolysis and lactic acidosis in Leigh syndrome

Dear Editor, We thank Bindoff and colleagues for the opportunity to clarify some clinical aspects of our case report. The patient was in good clinical condition before the hospitalization for thyroid surgery. No other organs or tissues were affected and, in particular, there was no pre-existing renal or hepatic dysfunction or diabetes. After surgery, for an episode of acute respiratory failure, she was admitted in ICU where she developed the pneumonia. Linezolid was the only new drug added before the episode of lactic acidosis and rhabdomyolysis. She had no muscle rigidity or fever. Mitochondrial toxicity of linezolid has been demonstrated in vitro, in animal models and in humans, even in patients without mitochondrial disease. In our case, as in the patient with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes described by Cope, McFarland, and Schaefer (see the complete reference in our report), the metabolic decompensation occurred after two doses and muscle injury and lactic acidosis progressively resolved after the discontinuation. All these observations led us to consider linezolid as the cause of the described event. We agree that linezolid is an excellent drug for treating methicillin-resistant S. aureus and vancomycinresistant Enterococcus faecium infections and that it is extremely important to avoid denial of therapies which are useful for the treatment of potentially life-threatening conditions. At the same time, our report suggests caution in using linezolid in subjects affected by mitochondrial disease also in absence of a pre-existent lactic acidaemia, especially for the sudden onset of the adverse event that lactate monitoring is not able to predict. Personalized medicine in rare diseases is a challenge that requires systematic sharing of data and clinical experience, like in this case, in order to optimize clinical management. ACKNOWLEDGMENTS Guido Primiano and Serenella Servidei are members of the European Reference Network for Rare Neuromuscular Diseases (ERN-NMD).