Abstract

The recent rise in the use of linezolid to treat a variety of resistant pathogens has uncovered many side effects. Some patients develop lactic acidosis, myelosuppression, optic or peripheral neuropathies, and myopathies. We evaluated an elderly patient who presented to the Emergency Room with linezolid toxicity and a novel neurologic complication characterized by bilateral globi pallidi necrosis. Mitochondrial ribosome inhibition was described to be the predisposing factor. The patient belongs to the mitochondrial J1 haplotype known to be associated with side effects of the drug. We recommend based on the molecular profile of the illness pretreatment considerations and complication management.

Highlights

  • A 74 years old Caucasian man presented to the Emergency Department because of altered level of consciousness

  • It is used to treat a variety of gram-positive infections, including methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant enterococci (VRE), Nocardia infections and multidrug-resistant tuberculosis

  • We have shown that all mitochondrial respiratory chain complexes activities, but complex II, are depressed in the patient, with more severe loss in Complexes IV and V (Figures 2C–E)

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Summary

INTRODUCTION

A 74 years old Caucasian man presented to the Emergency Department because of altered level of consciousness He had undergone a recent right knee prosthesis implantation and had been on antibiotic therapy for 5 weeks for prosthesis infection. The patient was in shock with a mean arterial pressure of 54 mmHg and severe metabolic acidosis (pH = 6.9) with respiratory alkalosis. His anion gap was 37, with a serum bicarbonate level of 4 mmol/L and a markedly elevated serum lactic acid level of 21 mmol/L. The patient’s serum lactic acid level normalized on day 7 of hospitalization His pancytopenia progressively improved and normalized on day 9 with a reticulocyte count of 6.2%. The patient’s symptoms improve drastically with rehabilitation

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