{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,7]],"date-time":"2026-03-07T00:08:24Z","timestamp":1772842104549,"version":"3.50.1"},"reference-count":14,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2025,8,26]],"date-time":"2025-08-26T00:00:00Z","timestamp":1756166400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,11,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and objectives<\/jats:title>\n                    <jats:p>Due to its potentially better long-term haematologic tolerance compared to linezolid, tedizolid represents an attractive option for prolonged antibiotic therapy in complicated\/chronic Gram-positive infections. However, there is little information regarding the risk of peripheral neurological toxicity, representing another obstacle to the extended use of oxazolidinones. Reporting neurologic adverse events occurring during tedizolid therapy for chronic implant-associated infections.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Patients and methods<\/jats:title>\n                    <jats:p>Patients experiencing tedizolid-associated neurologic adverse events were retrospectively described in a case series.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Five patients (four males; age range, 65\u201375\u2005years) receiving tedizolid (200\u2005mg q24h) as long-term suppressive therapy for chronic implant-associated infection presented with peripheral neuropathy. In four cases, tedizolid was used after discontinuation of linezolid for toxicity, including one case of neuropathy. Three had at least one additional risk factor for neuropathy (including two diabetes, one of them with diabetes-related nephropathy). Neuropathic symptoms [paraesthesia (n\u200a=\u200a2), worsening of pre-existing neuropathy (n\u200a=\u200a2), dysesthesias (n\u200a=\u200a1)] appeared after a median of 12.4 (IQR, 8.2\u201313.3) months of tedizolid treatment. Electromyoneurography (EMNG) confirmed axonal sensory polyneuropathy in all but one patient for which EMNG was still within normal ranges, but compatible with incipient neurotoxicity. Tedizolid was stopped in all patients, three patients required specific treatment for neuropathic pain. At last follow-up [2.4 (IQR, 1\u20132.5) years from tedizolid discontinuation], clinical recovery from neuropathy was noted in three patients. The two patients with persistent neuropathy symptoms were diabetic; one showed EMNG improvement.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Prolonged used of tedizolid may be associated with peripheral neurologic toxicity, which should be monitored in at-risk patients.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/jac\/dkaf315","type":"journal-article","created":{"date-parts":[[2025,8,13]],"date-time":"2025-08-13T11:49:48Z","timestamp":1755085788000},"page":"2918-2922","source":"Crossref","is-referenced-by-count":1,"title":["Peripheral neuropathy during long-term suppressive therapy with tedizolid: a case series"],"prefix":"10.1093","volume":"80","author":[{"given":"Tomaso","family":"Beringheli","sequence":"first","affiliation":[{"name":"Centre de r\u00e9f\u00e9rence pour la prise en charge des infections ost\u00e9o-articulaires complexes (CRIOAc Lyon, 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