TY - JOUR
T1 - Pharmacometabolomics of L-carnitine treatment response phenotypes in patients with septic shock
AU - Puskarich, Michael A.
AU - Finkel, Michael A.
AU - Karnovsky, Alla
AU - Jones, Alan E.
AU - Trexel, Julie
AU - Harris, Brooke N.
AU - Stringer, Kathleen A.
N1 - Publisher Copyright:
Copyright © 2015 by the American Thoracic Society
PY - 2015/1/1
Y1 - 2015/1/1
N2 - Rationale: Sepsis therapeutics have a poor history of success in clinical trials, due in part to the heterogeneity of enrolled patients. Pharmacometabolomics could differentiate drug response phenotypes and permit a precision medicine approach to sepsis. Objectives: To use existing serum samples from the phase 1 clinical trial of L-carnitine treatment for severe sepsis to metabolically phenotype L-carnitine responders and nonresponders. Methods: Serum samples collected before (T0) and after completion of the infusion (T24, T48) from patients randomized to either L-carnitine (12 g) or placebo for the treatment of vasopressor-dependent septic shock were assayed by untargeted 1H-nuclear magnetic resonance metabolomics. The normalized, quantified metabolite data sets of L-carnitine- and placebotreated patients at each time point were compared by analysis of variance with post-hoc testing for multiple comparisons. Pathway analysis was performed to statistically rank metabolic networks. Measurements and Main Results: Thirty-eight metabolites were identified in all samples. Concentrations of 3-hydroxybutyrate, acetoacetate, and 3-hydroxyisovalerate were different at T0 and over time in L-carnitine-treated survivors versus nonsurvivors. Pathway analysis of pretreatment metabolites revealed that synthesis and degradation of ketone bodies had the greatest impact in differentiating L-carnitine treatment response. Analysis of all patients based on pretreatment 3-hydroxybutyrate concentration yielded distinct phenotypes. Using the T0 median 3-hydroxybutyrate level (153 μM), patients were categorized as either high or low ketone. L-carnitine-treated low-ketone patients had greater use of carnitine as evidenced by lower post-treatment L-carnitine levels. The L-carnitine responders also had faster resolution of vasopressor requirement and a trend toward a greater improvement in mortality at 1 year (P = 0.038) compared with patients with higher 3-hydroxybutyrate. Conclusions: The results of this preliminary study, which were not readily apparent from the parent clinical trial, show a unique metabolite profile of L-carnitine responders and introduce pharmacometabolomics as a viable strategy for informing L-carnitine responsiveness. The approach taken in this study represents a concrete example for the application of precision medicine to sepsis therapeutics that warrants further study.
AB - Rationale: Sepsis therapeutics have a poor history of success in clinical trials, due in part to the heterogeneity of enrolled patients. Pharmacometabolomics could differentiate drug response phenotypes and permit a precision medicine approach to sepsis. Objectives: To use existing serum samples from the phase 1 clinical trial of L-carnitine treatment for severe sepsis to metabolically phenotype L-carnitine responders and nonresponders. Methods: Serum samples collected before (T0) and after completion of the infusion (T24, T48) from patients randomized to either L-carnitine (12 g) or placebo for the treatment of vasopressor-dependent septic shock were assayed by untargeted 1H-nuclear magnetic resonance metabolomics. The normalized, quantified metabolite data sets of L-carnitine- and placebotreated patients at each time point were compared by analysis of variance with post-hoc testing for multiple comparisons. Pathway analysis was performed to statistically rank metabolic networks. Measurements and Main Results: Thirty-eight metabolites were identified in all samples. Concentrations of 3-hydroxybutyrate, acetoacetate, and 3-hydroxyisovalerate were different at T0 and over time in L-carnitine-treated survivors versus nonsurvivors. Pathway analysis of pretreatment metabolites revealed that synthesis and degradation of ketone bodies had the greatest impact in differentiating L-carnitine treatment response. Analysis of all patients based on pretreatment 3-hydroxybutyrate concentration yielded distinct phenotypes. Using the T0 median 3-hydroxybutyrate level (153 μM), patients were categorized as either high or low ketone. L-carnitine-treated low-ketone patients had greater use of carnitine as evidenced by lower post-treatment L-carnitine levels. The L-carnitine responders also had faster resolution of vasopressor requirement and a trend toward a greater improvement in mortality at 1 year (P = 0.038) compared with patients with higher 3-hydroxybutyrate. Conclusions: The results of this preliminary study, which were not readily apparent from the parent clinical trial, show a unique metabolite profile of L-carnitine responders and introduce pharmacometabolomics as a viable strategy for informing L-carnitine responsiveness. The approach taken in this study represents a concrete example for the application of precision medicine to sepsis therapeutics that warrants further study.
KW - 3-hydroxybutyric acid
KW - Individualized medicine
KW - Ketone bodies
KW - Nuclear magnetic resonance
KW - Sepsis
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U2 - 10.1513/AnnalsATS.201409-415OC
DO - 10.1513/AnnalsATS.201409-415OC
M3 - Article
C2 - 25496487
AN - SCOPUS:84922469698
SN - 2325-6621
VL - 12
SP - 46
EP - 56
JO - Annals of the American Thoracic Society
JF - Annals of the American Thoracic Society
IS - 1
ER -