Sorted By Test Name - Mayo Medical Laboratories

PA
8683
PCT
83169
Clinical References: Homburger HA: Allergic diseases. In Clinical Diagnosis and Management by
Laboratory Methods. 21st edition. Edited by McPherson RA, Pincus MR. WB Saunders, Publ, New York,
Chapter 53, Part VI, pp. 961-971, 2007
Procainamide, Serum
Clinical Information: Procainamide (PA) is indicated in the treatment of premature ventricular
contractions, ventricular tachycardia, atrial fibrillation, and paroxysmal atrial tachycardia. PA is
contraindicated in patients with complete atrioventricular block. PA is metabolized to an active
metabolite, N-acetylprocainamide (NAPA), with metabolism controlled by genetically determined
enzymes. In patients with normal renal function, fast metabolizers will have a PA:NAPA ratio 2 after 3 hours) are more likely to
develop a positive test for antinuclear antibodies and present with systemic lupus erythematosus-like
symptoms. Patients who have prolonged exposure to procainamide >10.0 mcg/mL or NAPA
concentration >40.0 mcg/mL are very likely to exhibit symptoms of toxicity that are characterized by
hypotension, ventricular fibrillation, widened QRS complex, junctional tachycardia, oliguria, confusion,
nausea, and vomiting. Renal disease, hepatic disease, cardiac failure, and states of low cardiac output
reduce the metabolism and clearance of PA and NAPA. Co-administration of histamine H2 receptor
antagonists, such as cimetidine and ranitidine reduce renal clearance of PA and NAPA resulting in higher
plasma concentrations of each.
Useful For: Monitoring therapy Assessing compliance Evaluating toxicity
Interpretation: Administration of a dose of 50 mg/kg will usually yield the optimal trough
concentration in the range of 4.0 to 8.0 mcg/mL for procainamide and 10.0 to 20.0 mcg/mL for
N-acetylprocainamide.
Reference Values:
PROCAINAMIDE
Therapeutic concentration: 4.0-8.0 mcg/mL
Toxic concentration: >10.0 mcg/mL
N-ACETYLPROCAINAMIDE
Therapeutic concentration: 10.0-20.0 mcg/mL
Toxic concentration: >40.0 mcg/mL
Clinical References: Myerburg RJ, Kessler KM, Kiem I, et al: Relationship between plasma levels
of procainamide, suppression of premature ventricular complexes and prevention of recurrent ventricular
tachycardia. Circulation 1981;64;280-290
Procalcitonin, Serum
Clinical Information: Procalcitonin (ProCT) is a 116 amino acid precursor of calcitonin (CT). ProCT
is processed to an N-terminal 57 amino acid peptide. CT (32 amino acid) and a 21 amino acid C-terminal
peptide, catacalcin (CCP-1). Expression of this group of peptides is normally limited to thyroid C-cells
and, to a small extent, other neuroendocrine cells. CT is the only hormonally active of these peptides. CT
is secreted by C-cells in response to hypercalcemia and inhibits bone resorption by osteoclasts,
minimizing oscillations in serum calcium and calcium loss. During severe systemic inflammation, in
particular related to bacterial infection, the tissue specific control of CT-related peptides expression
breaks down and ProCT and CCP-1 (referred collectively to as ProCT) are secreted in large quantities by
many tissues. CT levels do not change. ProCT may contribute to sepsis-related death. Decreased mortality
after treatment with anti-ProCT antibodies has been demonstrated in animal models of sepsis.
Noninfectious inflammatory stimuli need to be extremely severe to result in ProCT elevations, making it a
more specific marker for severe infections than most other inflammatory markers (cytokines, interleukins,
and acute-phase reactants). ProCT elevations are also more sustained than those of most other markers
and occur in neutropenic patients. This reduces the risk of false-negative results. ProCT becomes
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