|Amikacin || |
Conventional dosing: Peak: 20–30 mg/L; trough: < 10 mg/L
High dose once daily:
Peak: 60 mg/L; trough: < 5 mg/L
|2–3; ↑ in uremia ||↓in renal dysfunction ||Concomitant kanamycin or tobramycin therapy may give falsely elevated amikacin results by immunoassay. |
|Amitriptyline ||95–250 ng/mL ||9–25 ||No data on dose adjustments in patients with renal or hepatic dysfunction; use with caution ||Drug is highly protein-bound. Patient-specific decrease in protein binding may invalidate quoted therapeutic reference interval for effective concentration. |
|Carbamazepine ||4–12 mg/L ||10–15 ||↓(75% of dose) in severe renal dysfunction; use with caution in hepatic dysfunction || |
Induces its own metabolism.
Metabolite 10,11-epoxide exhibits 13% cross-reactivity by immunoassay. Adverse reactions: skin reactions, myelosuppression.
|Cyclosporine ||100–300 mcg/L (ng/mL) whole blood ||6–12 ||↓in renal or hepatic dysfunction ||Cyclosporine is lipid-soluble (20% bound to leukocytes; 40% to erythrocytes; 40% in plasma, highly bound to lipoproteins); the binding is temperature-dependent in vitro and concentration-dependent in vivo. HPLC and LC-tandem mass spectrometry methods are highly specific for parent drug and considered as the gold standard assays. Monoclonal fluorescence polarization immunoassay (FPIA) and monoclonal chemiluminescence immunoassay also measure cyclosporine reliably; polyclonal immunoassays are less specific due to cross-reaction with drug metabolites. Anticonvulsants and rifampin increase metabolism. Erythromycin, ketoconazole, and calcium channel blockers decrease metabolism. The main adverse reaction is concentration-related nephrotoxicity. |
|Desipramine ||100–250 ng/mL ||13–23 ||No data on dose adjustments in patients with renal or hepatic dysfunction; use with caution ||Drug is highly protein-bound. Patient-specific decrease in protein binding may invalidate quoted therapeutic reference interval for effective concentration. |
|Digoxin || |
HF: 0.5–0.9 mcg/L
Atrial fibrillation: 0.5–2 mcg/L
|36–42; ↑ in uremia, HF || |
↓in renal dysfunction, HF, hypothyroidism
↑ in hyperthyroidism
Bioavailability of digoxin tablets is 50–90%.
Specimen must not be drawn within 4 hours of an intravenous dose or 6 hours of an oral dose.
Dialysis does not remove a significant amount.
Hypokalemia potentiates toxicity.
Digitalis toxicity is a clinical and not a laboratory diagnosis.
Digibind (digoxin-specific antibody) therapy of digoxin overdose can interfere with measurement of digoxin levels depending on the digoxin assay.
Elimination reduced by amiodarone, quinidine, and verapamil.
|Ethosuximide ||40–100 mg/L || |
|No data on dose adjustments in patients with renal or hepatic dysfunction; use with caution ||Levels used primarily to assess clinical response and compliance. Toxicity is rare and does not correlate well with plasma concentrations. |
|Gentamicin || |
Conventional dosing: Peak: 4–8 mg/L; trough: < 2 mg/L
High dose once daily: Peak: 20 mg/L; trough: undetectable
|2–3; ↑ in uremia (7.3 during dialysis) ||↓in renal dysfunction || |
Draw peak specimen (conventional dosing) 30 minutes after end of 30- to 60-min infusion.
Draw trough just before next dose.
In uremic patients, some penicillins (eg, carbenicillin, ticarcillin, piperacillin) may decrease gentamicin half-life from 46 hours to 22 hours, posing a risk of reduced antibacterial efficacy.
The main adverse reactions are CNS, otic, and renal toxicities.
|Imipramine ||180–350 ng/mL ||10–16 ||No data ...|