TABLE 4.

Clinical and genetic characteristics of patients included in the study sorted according to clinical severity and percentage of variation in mitochondrial protein synthesis in PBMC^a

Code	Clinical manifestation(s)	Polymorphism(s) in:		Haplotype	% change in PBMC mitochondrial protein synthesis
		12S rRNA	16S rRNA
P1	Asymptomatic			H*	−75.80
P2	Asymptomatic			H*	−67.00
P3	Asymptomatic	m.961T→G		H*	−88.48
P4	Asymptomatic	m.709G→A		H*	−17.74
P5	Asymptomatic	m.1189T→C	m.1811A→G, m.2706A→G	UK	−90.06
P6	Asymptomatic		m.2706A→G, m.3010G→A	No N	−54.63
P7	Asymptomatic	m.1598G→A	m.1703C→T, m.1719G→A, m.2706A→G	N*	−58.18
P8	Anemia			H5	−99.13
P9	Hyperlactatemia			H*	−78.08
P10	Hyperlactatemia		m.2098G→A	H*	−84.89
P11	Hyperlactatemia		m.2706A→G, m.3197T→C	U5	−1.96
P12	Hyperlactatemia	m.980T→C	m.1811A→G, m.2523C→T, m.2706A→G	U1811/U*	−47.19
P13	Hyperlactatemia, asthenia	m.709G→A	m.1888G→A, m.2706A→G, m.2850T→C	T (JT, no J)
P14	Hyperlactatemia, gastrointestinal discomfort	m.1189T→C	m.1811A→G, m.2706A→G	UK	−54.74
P15	Vomiting, anemia		m.2092C→T	H*
P16	Sickness and vomiting, asthenia, anemia	m.709G→A, m.930G→A	m.1888G→A, m.2706A→G	T (JT, no J)	−12.29
P17	Hyperlactatemia, anemia, asthenia		m.3010G→A	H1	−10.60
P18	Thrombocytopenia		m.1700T→C, m.2706A→G, m.3197T→C	U5
P19	Lactic acidosis, gastrointestinal discomfort, sickness and vomiting, anemia, thrombocytopenia	961insC	m.2706A→G, m.3197T→C	U5	−50.70

^aIn addition to the polymorphisms and mutations depicted here, all the patients presented m.750A→G and m.1438A→G polymorphisms with respect to the mitochondrial DNA Cambridge reference sequence containing these 2 rare variations. Despite identical antibiotic exposures for all the patients, clinical manifestations of linezolid toxicity ranged from asymptomatic individuals to patients presenting as many as 5 secondary effects. None of them showed clinical signs of peripheral neuropathy, which has usually been described upon linezolid treatment for extended periods, longer than the currently approved 28-day period. The distributions of mitochondrial haplogroups and polymorphisms in the cohort of linezolid-treated patients resembled the standard distributions observed in European populations.