Glucocorticoid steroid metabolites
metaboliteStress-induced glucocorticoid metabolites reflect acute systemic perturbation and hemodynamic stress during Type 1 MI.
Pathway placement
Cascade stepMyocardial injury (shared endpoint)
Confidencemedium
RationaleAcute stress-hormone metabolites specific to thrombotic MI pathophysiology.
Also acts inSystemic / off-pathway
Druggability
Not assessed (no mapped human gene target).
Type I vs Type II discrimination
ScoresLow-confidence (proxy)
R — rupture / Type-I23
C — confounder / Type-II54
A — assay feasibility42
E — evidence strength20
T1DI (composite)3
Specificity differential (R−C)-31.1
Confounder panel (Type-II drivers)
No confounder evidence retrieved.
Tier: light (literature co-occurrence proxy — lower confidence). See the discrimination table for all markers.
Assay & specimen
Class-level default (no specific cleared assay)— generic method inferred from analyte class; confirm against a specific product insert before use.
Specimen
Serum, plasma or urine
Collection tube
Serum separator (gold/red-top, SST) · Lithium heparin (green-top) · Sterile urine container
Method / principle
LC-MS/MS (targeted metabolomics) or enzymatic colorimetric where available
Reagent / substrate
Stable-isotope-labeled internal standard (MS); or enzyme-coupled Trinder reagent
Platform
LC-MS/MS; some automated chemistry
Turnaround · availability
Send-out / research · Specialized / research
Literature evidence(1)
- Systems characterization of differential plasma metabolome perturbations following thrombotic and non-thrombotic myocardial infarction.Journal of proteomics · 2017 · PMID 28341595 · doi