|AIDS||Acquired immunodeficiency syndrome|
|CBC||Complete blood cell count|
|CHF||Congestive heart failure|
|CNS||Central nervous system|
|Diff||Differential cell count|
|EDTA||Ethylenediaminetetraacetic acid (edetate)|
|ELISA||Enzyme-linked immunosorbent assay|
|HLA||Human leukocyte antigen|
|INR||International Normalized Ratio|
|MRI||Magnetic resonance imaging|
|NPO||Nothing by mouth (nil per os)|
|PCR||Polymerase chain reaction|
|PMN||Polymorphonuclear neutrophil (leukocyte)|
|PO||Orally (per os)|
|RBC||Red blood cell|
|RPR||Rapid plasma reagin (syphilis test)|
|SIADH||Syndrome of inappropriate antidiuretic hormone (secretion)|
|SLE||Systemic lupus erythematosus|
|VDRL||Venereal Disease Research Laboratory (syphilis test)|
|WBC||White blood cell|
The basic assumptions underlying therapeutic drug monitoring (Table 4–1) are that drug metabolism varies from patient to patient and that the plasma level of a drug is more closely related to the drug's therapeutic effect or toxicity than is the dosage.
Table 4–1. Therapeutic Drug Monitoring.1 |Favorite Table|Download (.pdf)
Table 4–1. Therapeutic Drug Monitoring.1
|Drug||Effective Concentrations||Half-Life (hours)||Dosage Adjustments||Comments|
Peak: 20–30 mg/L; trough: <10 mg/L
High dose once daily:
Peak: 60 mg/L; trough: undetectable
|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||Drug is highly protein-bound. Patient-specific decrease in protein binding may invalidate quoted therapeutic reference interval for effective concentration.|
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 dysfunction, liver disease||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 the gold standard assays. Monoclonal fluorescence polarization immunoassay (FPIA) and monoclonal chemiluminescence immunoassay also measure cyclosporine reliably; polyclonal immunoassays are less specific owing 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||Drug is highly protein-bound. Patient-specific decrease in protein binding may invalidate quoted therapeutic reference interval for effective concentration.|
CHF: 0.5–0.9 ng/mL
Atrial fibrillation: 0.5–2 ng/mL
|42; ↑ in uremia, CHF||↓ in renal dysfunction, CHF, hypothyroidism; ↑ ...|
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