Shashank Kraleti1, Izoumrod Soultanova. 1. College of Medicine, Department of Family and Preventive Medicine, University of Arkansas for Medical Sciences, USA.
Abstract
OBJECTIVE: To describe a patient who developed pancytopenia and lactic acidosis after receiving linezolid therapy. CASE SUMMARY: A 32-year-old man with past medical history of heart failure, hypertension received a 14-day course of linezolid for treatment of empyema with broncho-pleural fistula. During his follow up visit, he was found to be septic and further evaluation showed pancytopenia, acidosis and elevated liver enzymes. With the exclusion of other possible etiologies, the time course to development of these laboratory abnormalities correlated with the use of linezolid. Antibiotics were switched subsequently and the labs improved after reaching a nadir on the fourth day after stopping linezolid. DISCUSSION: Linezolid was noted to cause time and dose-dependent reversible myelosuppression in preclinical studies. There are several case reports of throinbocytopenia occurring with linezolid use, but only few cases of pancytopenia and lactic acidosis are reported. Exact mechanism of toxicity is unknown, but many hypothesize it to be similar to chloramphenicol marrow toxicity because of the cross-reactivity to mitochondrial ribosomes. CONCLUSIONS: Clinicians should be aware of linezolid as a drug capable of causing pancytopenia, lactic acidosis and elevated liver enzymes. While recovery is usually complete following withdrawal of the drug, we need to still monitor for these rare but severe complications; and consider treating only for a shorter duration, if possible.
OBJECTIVE: To describe a patient who developed pancytopenia and lactic acidosis after receiving linezolid therapy. CASE SUMMARY: A 32-year-old man with past medical history of heart failure, hypertension received a 14-day course of linezolid for treatment of empyema with broncho-pleural fistula. During his follow up visit, he was found to be septic and further evaluation showed pancytopenia, acidosis and elevated liver enzymes. With the exclusion of other possible etiologies, the time course to development of these laboratory abnormalities correlated with the use of linezolid. Antibiotics were switched subsequently and the labs improved after reaching a nadir on the fourth day after stopping linezolid. DISCUSSION: Linezolid was noted to cause time and dose-dependent reversible myelosuppression in preclinical studies. There are several case reports of throinbocytopenia occurring with linezolid use, but only few cases of pancytopenia and lactic acidosis are reported. Exact mechanism of toxicity is unknown, but many hypothesize it to be similar to chloramphenicolmarrow toxicity because of the cross-reactivity to mitochondrial ribosomes. CONCLUSIONS: Clinicians should be aware of linezolid as a drug capable of causing pancytopenia, lactic acidosis and elevated liver enzymes. While recovery is usually complete following withdrawal of the drug, we need to still monitor for these rare but severe complications; and consider treating only for a shorter duration, if possible.