Parathyroid Hormone
PTHproteinParathyroid hormone dysregulation in acute coronary syndrome reflects systemic mineral metabolic disorder off the atherothrombotic pathway.
Pathway placement
Cascade stepOff-pathway / systemic markers
Confidencelow
RationaleMineral metabolism regulator; associated with ACS but not mechanistic to atherothrombotic cascade.
Druggability
Not assessed (no mapped human gene target).
Type I vs Type II discrimination
ScoresType-II-associated
R — rupture / Type-I—
C — confounder / Type-II58
A — assay feasibility68
E — evidence strength95
T1DI (composite)18
Specificity differential (R−C)-43.3
Confounder panel (Type-II drivers)
1sepsis / systemic inflammationmag 0
2anemia / acute blood lossn/a
3hypovolemia / dehydrationmag 3
4tachyarrhythmian/a
5hypoxemia / respiratory failuren/a
6hypertensive emergencymag 2
7high-demand / peri-operative stressmag 2
Coverage: 4/7 confounders with evidence
Tier: deep-scored (abstract-extracted) · 8 supporting references. 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 or plasma
Collection tube
Serum separator (gold/red-top, SST) · K2/K3-EDTA (lavender-top)
Method / principle
Sandwich immunoassay (ELISA) — research-grade unless a cleared assay exists
Reagent / substrate
Matched anti-target antibody pair (capture + labeled detection)
Platform
ELISA microplate or multiplex (Luminex/MSD)
Turnaround · availability
Send-out / research · Research-grade (no universal clinical assay)
Literature evidence(1)
- Increase of renal resistive index and mineral metabolism disorder in patients with acute coronary syndrome with preserved renal function.European review for medical and pharmacological sciences · 2020 · PMID 33275237 · doi