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PHMA
82736
valproic acid is that the total concentration of phenytoin decreases due to increased clearance but the free
fraction increases; the free concentration of phenytoin, which is the active form remains virtually the
same. Thus, no dosage adjustment is needed when valproic acid is added to maintain the same
pharmacologic effect, but the total concentration of phenytoin decreases. In contrast to the valproic acid
situation, in renal failure, there is not the same opportunity for the free phenytoin fraction to be cleared.
The end result is that both the total and free concentration of phenytoin increase, with the free
concentration increasing faster than the total. Dosage must be reduced to avoid toxicity. The free
phenytoin level is the best indicator of adequate therapy in renal failure. Toxicity is a constant possibility
because of the manner in which phenytoin is metabolized. Small increases in dose can lead to very large
increases in blood concentration, resulting in early signs of toxicity such as nystagmus, ataxia, and
dysarthria. Severe toxicity occurs when the blood concentration is >30 mcg/mL and is typified by tremor,
hyperreflexia, and lethargy. The outcome of phenytoin toxicity is not as serious as phenobarbital because
phenytoin is not a central nervous system sedative.
Useful For: Monitoring for appropriate therapeutic concentration Assessing compliance or toxicity
Interpretation: Dose should be adjusted to achieve steady-state blood concentrations between 10
mcg/mL to 20 mcg/mL.
Reference Values:
Therapeutic concentration: 10.0-20.0 mcg/mL
Toxic concentration: > or =30.0 mcg/mL
Clinical References: 1. Richens A: Clinical pharmacokinetics of phenytoin. Clin Pharmacokinet
1979;4:153-169 2. Moyer TP: Therapeutic drug monitoring. In Tietz Textbook of Clinical Chemistry. 4th
edition. Edited by CA Burtis, ER Ashwood. WB Saunders Company, Philadelphia, 2005, pp 1237-1285
Phoma betae, IgE
Clinical Information: Clinical manifestations of immediate hypersensitivity (allergic) diseases are
caused by the release of proinflammatory mediators (histamine, leukotrienes, and prostaglandins) from
immunoglobulin E (IgE)-sensitized effector cells (mast cells and basophils) when cell-bound IgE
antibodies interact with allergen. In vitro serum testing for IgE antibodies provides an indication of the
immune response to allergen(s) that may be associated with allergic disease. The allergens chosen for
testing often depend upon the age of the patient, history of allergen exposure, season of the year, and
clinical manifestations. In individuals predisposed to develop allergic disease(s), the sequence of
sensitization and clinical manifestations proceed as follows: eczema and respiratory disease (rhinitis and
bronchospasm) in infants and children less than 5 years due to food sensitivity (milk, egg, soy, and wheat
proteins) followed by respiratory disease (rhinitis and asthma) in older children and adults due to
sensitivity to inhalant allergens (dust mite, mold, and pollen inhalants).
Useful For: Testing for IgE antibodies may be useful to establish the diagnosis of an allergic disease
and to define the allergens responsible for eliciting signs and symptoms. Testing also may be useful to
identify allergens which may be responsible for allergic disease and/or anaphylactic episode, to confirm
sensitization to particular allergens prior to beginning immunotherapy, and to investigate the specificity of
allergic reactions to insect venom allergens, drugs, or chemical allergens.
Interpretation: Detection of IgE antibodies in serum (Class 1 or greater) indicates an increased
likelihood of allergic disease as opposed to other etiologies and defines the allergens that may be
responsible for eliciting signs and symptoms. The level of IgE antibodies in serum varies directly with the
concentration of IgE antibodies expressed as a class score or kU/L.
Reference Values:
Class IgE kU/L Interpretation
0 Negative
1 0.35-0.69 Equivocal
2 0.70-3.49 Positive
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