Fatal lactic acidosis after prolonged linezolid exposure for treatment of multidrug-resistant tuberculosis

Boutoille, David; Grossi, Olivier; Depatureaux, Agnès; Tattevin, Pierre

doi:10.1016/j.ejim.2008.12.002

Cited by 23 publications

(17 citation statements)

References 3 publications

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“…Use of linezolid at half dose (600 mg?day -1 ) helped to reduce bone marrow suppression, but not peripheral and optic neuropathy [124]. Fatal lactic acidosis can also occur after prolonged therapy [125]. A sizeable retrospective study has confirmed these adverse effects [126].…”

Section: Sustained Political Commitmentmentioning

confidence: 80%

Treatment of tuberculosis: update 2010

Yew¹,

Lange²,

Leung³

2010

European Respiratory Journal

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Currently, the standard short-course chemotherapy for tuberculosis comprises a 6-month regimen, with a four-drug intensive phase and a two-drug continuation phase. Alternative chemotherapy using more costly and toxic drugs, often for prolonged durations generally .18 months, is required for multidrug-resistant and extensively drug-resistant tuberculosis. Directly observed treatment, as part of a holistic care programme, is a cost-effective strategy to ensure high treatment success and curtail development of drug resistance in tuberculosis. New antituberculosis drugs are urgently needed to improve the present standard short-course and alternative chemotherapies, by shortening administration durations and increasing cure rates, through the greater potency of these agents. At the same time, the role of adjunctive surgery for drug-resistant tuberculosis has to be better defined. Immunotherapy might improve treatment outcomes of both drug-susceptible and -resistant tuberculosis, and warrants further exploration.

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Section: Sustained Political Commitmentmentioning

confidence: 80%

Treatment of tuberculosis: update 2010

Yew¹,

Lange²,

Leung³

2010

European Respiratory Journal

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“…There is some evidence that polymorphisms in the mitochondrial 16S ribosomal RNA (rRNA) (e.g., A1036G) may contribute to severe linezolid-associated lactic acidosis in adults [33,34]. The prognosis of linezolid-induced lactic acidosis is unclear; in some cases, the outcome was excellent, but there are also some reports of patients with fatal outcome [28,35].…”

Section: Pathophysiologymentioning

confidence: 99%

Drug-induced acid-base disorders

et al. 2014

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The incidence of acid-base disorders (ABDs) is high, especially in hospitalized patients. ABDs are often indicators for severe systemic disorders. In everyday clinical practice, analysis of ABDs must be performed in a standardized manner. Highly sensitive diagnostic tools to distinguish the various ABDs include the anion gap and the serum osmolar gap. Drug-induced ABDs can be classified into five different categories in terms of their pathophysiology: (1) metabolic acidosis caused by acid overload, which may occur through accumulation of acids by endogenous (e.g., lactic acidosis by biguanides, propofol-related syndrome) or exogenous (e.g., glycol-dependant drugs, such as diazepam or salicylates) mechanisms or by decreased renal acid excretion (e.g., distal renal tubular acidosis by amphotericin B, nonsteroidal antiinflammatory drugs, vitamin D); (2) base loss: proximal renal tubular acidosis by drugs (e.g., ifosfamide, aminoglycosides, carbonic anhydrase inhibitors, antiretrovirals, oxaliplatin or cisplatin) in the context of Fanconi syndrome; (3) alkalosis resulting from acid and/or chloride loss by renal (e.g., diuretics, penicillins, aminoglycosides) or extrarenal (e.g., laxative drugs) mechanisms; (4) exogenous bicarbonate loads: milk-alkali syndrome, overshoot alkalosis after bicarbonate therapy or citrate administration; and (5) respiratory acidosis or alkalosis resulting from drug-induced depression of the respiratory center or neuromuscular impairment (e.g

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“…Among the most common side reactions are gastrointestinal disturbances, followed by headache and rash. However, long-term use of this antibiotic can lead to severe toxicity, particularly myelosuppression, peripheral or optic neuropathy, serotonin syndrome (1), and lactic acidosis (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12).…”

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confidence: 99%