Linezolid/sodium bicarbonate
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Various toxicities following drug toxicity and lack of efficacy: case report A 9-year-old girl developed lactic acidosis, peripheral neuropathy and worsening of previously present bone marrow suppression during the treatment with linezolid for Mycobacterium abscessus infection. Later, she exhibited lack of efficacy with sodium bicarbonate during treatment of lactic acidosis. The girl was diagnosed with common B-cell-precursor acute lymphoblastic leukemia (BCP-ALL) at the age of 2 years. Initially she received treatment according to the international protocol AIEOP-BFM-2009 and achieved remission. Five years after achieving remission, she suffered a late isolated bone marrow relapse. Consequently, she underwent allogeneic hematopoietic stem cell transplant (HSCT) from an unrelated donor. Her post-transplant course was complicated by severe chronic graft-versus-host disease (GVHD), which required long-term immunosuppressive treatment with prednisone, budesonide and sirolimus. Two years later (at the age of 9 years), she was hospitalised due to sudden chest pain radiating to the left shoulder and haematemesis. Based on examinations, Mycobacterium abscessus (subspecies: massiliense) infection was diagnosed. Hence, she started receiving combined IV antimicrobial treatment that included linezolid 810 mg/day (divided in 3 doses) along with amikacin and meropenem. Additionally treatments included posaconazole (as antifungal) and antiviral treatment with valaciclovir. Mild bone marrow suppression was noted at the time of hospital admission. Her plasma lactate level was monitored twice weekly, and no signs of acidosis were noted. On day 46 of linezolid therapy, she complained of abdominal pain, anorexia, nausea and vomiting. Initially, GVHD exacerbation was suspected, and the dose of prednisone was increased. On day 51, altered consciousness was noted with tachycardia (160 beats/min), repeated vomiting and kussmaul breathing. Laboratory tests showed severe lactic acidosis, electrolyte imbalance, hypoalbuminaemia, aminoaciduria elevated transaminases and lactate levels with normal renal parameters, CRP level and procalcitonin level. Based on the examinations, previously suspected GVHD exacerbation was ruled out and linezolid-induced lactic acidosis was diagnosed. Consequently, the girl’s linezolid therapy was stopped. Other drugs (amikacin and valaciclovir) were also stopped. Intense alakalisation was started with sodium bicarbonate, but lactic acidosis persisted [route and dosage not stated]. Her consciousness, HR and lactic acidosis normalised after decrease in serum linezolid levels (6.2 mg/L after 16 hours of last administration). At the same time, worsening of bone marrow suppression was noted. Leukocytic cytochrome-c oxidase (COX) activity normalised after her condition stabilised clinically and lactate level dropped. Peripheral neuropathy of her left leg persisted. Smolka V, et al. Severe linezolid-induced lactic acidosis in a child with acute lymphoblastic leukemia: A case report. Journal of Infection and Chemoth
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