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Drugs

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AbAntibody
AbnAbnormal
AFBAcid-fast bacillus
AgAntigen
AIDSAcquired immunodeficiency syndrome
ALTAlanine aminotransferase
ANAAntinuclear antibody
ASTAspartate aminotransferase
CBCComplete blood cell count
CFComplement fixation
CHFCongestive heart failure
CIECounterimmunoelectrophoresis
CKCreatine kinase
CNSCentral nervous system
CSFCerebrospinal fluid
CXRChest x-ray
CYPCytochrome P450
DiffDifferential cell count
EDTAEthylenediaminetetraacetic acid (edetate)
ELISAEnzyme-linked immunosorbent assay
GIGastrointestinal
GNRGram-negative rod
GNCBGram-negative coccobacillus
GPCGram-positive coccus
GVCBGram-variable coccobacillus
HLAHuman leukocyte antigen
IgImmunoglobulin
IMIntramuscular(ly)
INRInternational Normalized Ratio
IVIntravenous(ly)
MinMinute
MNMononuclear cell
MRIMagnetic resonance imaging
NNormal
NegNegative
NPONothing by mouth (nil per os)
PCRPolymerase chain reaction
PMNPolymorphonuclear neutrophil (leukocyte)
POOrally (per os)
PosPositive
PTHParathyroid hormone
RBCRed blood cell
RPRRapid plasma reagin (syphilis test)
SIADHSyndrome of inappropriate antidiuretic hormone (secretion)
SLESystemic lupus erythematosus
T3Triiodothyronine
T4Tetraiodothyronine (thyroxine)
TSHThyroid-stimulating hormone
VVariable
VDRLVenereal Disease Research Laboratory (syphilis test)
WBCWhite blood cell
WkWeek
YrYear
↑Increased
↓Decreased
↔No change

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
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Table 4–1. Therapeutic Drug Monitoring.1...
DrugEffective ConcentrationsHalf-Life (hours)Dosage AdjustmentsComments
Amikacin

Conventional dosing:

 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 dysfunctionConcomitant kanamycin or tobramycin therapy may give falsely elevated amikacin results by immunoassay.
Amitriptyline95–250 ng/mL9–25Drug is highly protein-bound. Patient-specific decrease in protein binding may invalidate quoted therapeutic reference interval for effective concentration.
Carbamazepine4–12 mg/L10–15

Induces its own metabolism.

Metabolite 10,11-epoxide exhibits 13% cross-reactivity by immunoassay. Adverse reactions: skin reactions, myelosuppression.

Cyclosporine100–300 mcg/L (ng/mL) whole blood6–12↓ in renal dysfunction, liver diseaseCyclosporine 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.
Desipramine100–250 ng/mL13–23Drug is highly protein-bound. Patient-specific decrease in protein binding may invalidate quoted therapeutic reference interval for effective concentration.
Digoxin

CHF: 0.5–0.9 ng/mL

Atrial fibrillation: 0.5–2 ng/mL

42; ↑ in uremia, CHF↓ in renal dysfunction, CHF, hypothyroidism; ↑ in hyperthyroidism

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