Mayo Test Catalog, (Sorted By Test Name) - Mayo Medical ...

WSCR
81163
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
3 3.50-17.4 Positive
4 17.5-49.9 Strongly positive
5 50.0-99.9 Strongly positive
6 > or =100 Strongly positive Reference values
apply to all ages.
Clinical References: Homburger HA: Allergic diseases. In Clinical Diagnosis and Management by
Laboratory Methods. 21st edition. Edited by RA McPherson, MR Pincus. New York, WB Saunders
Company, 2007, Chapter 53, Part VI, pp 961-971
Williams Syndrome, 7q11.23 Deletion, FISH
Clinical Information: Williams syndrome (WS) is a genetic disorder that occurs in 1/20,000 to
1/50,000 live births. Although WS is typically a sporadic disorder, familial cases have been reported. WS
is characterized by a variable combination of cardiovascular abnormalities, connective tissue
abnormalities, distinct facial features, infantile hypercalcemia, mental retardation, and characteristic social
interactions such as extreme friendliness and attention-deficit hyperactivity disorder. Isolated congenital
narrowing of the ascending aorta is common in WS patients and results in a separate syndrome called
supravalvular aortic stenosis (SVAS). WS is a contiguous gene deletion syndrome, caused by deletion of
several genes on chromosome 7q. One gene that often is deleted in WS is the elastin gene, which causes
SVAS and other cardiovascular disease in these patients. This association was described by Ewart et al
(1993) who identified hemizygosity of the elastin gene in WS and SVAS. The elastin gene, ELN, has
been mapped to 7q11.23 (Williams syndrome chromosome region, and is reportedly hemizygous in up to
96% of patients with WS. The deletion of an elastin gene locus cannot be detected by conventional
high-resolution chromosome analysis in the vast majority of cases due to the small size of this deletion.
Nickerson et al used molecular methods to detect a deletion of the elastin gene in 91% (39/43) of WS
patients.
Useful For: Detecting deletions of the elastin gene at 7q11.23 Diagnosis of Williams syndrome, when
used in combination with high-resolution chromosome studies and clinical evaluation
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