Sorted By Test Name - Mayo Medical Laboratories

CTSA
81979
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
Ceramide Trihexoside/Sulfatide Accumulation in Urine
Sediment, Urine
Clinical Information: Fabry disease is an X-linked recessive lysosomal storage disorder caused by a
deficiency of the enzyme alpha-galactosidase A (alpha-Gal A). Reduced enzyme activity results in
accumulation of glycosphingolipids in the lysosomes throughout the body, in particular, the kidney, heart,
and brain. Severity and onset of symptoms are dependent on the residual enzyme activity. Males with
1% activity may present with either
of 2 variant forms of Fabry disease (renal or cardiac) with onset of symptoms later in life. Individuals with
the renal variant typically present in the third decade of life with the development of renal insufficiency
and, ultimately, end-stage renal disease. Individuals with the renal variant may or may not share other
symptoms with the classic form of Fabry disease. Individuals with the cardiac variant are often
asymptomatic until they present with cardiac findings such as cardiomyopathy, mitral insufficiency, or
conduction abnormalities in the fourth decade. The cardiac variant is not associated with renal failure.
Variant forms of Fabry disease may be underdiagnosed. Females who are carriers of Fabry disease can
have clinical presentations ranging from asymptomatic to severely affected, and may have alpha-Gal A
activity in the normal range. Individuals with Fabry disease, regardless of the severity of symptoms, may
show an increased excretion of ceramide trihexoside in urine. Metachromatic leukodystrophy (MLD) is an
autosomal recessive lysosomal storage disorder caused by a deficiency of the arylsulfatase A enzyme,
which leads to the accumulation of various sulfatides in the brain, nervous system, and visceral organs,
including the kidney and gallbladder. The 3 clinical forms of MLD are late-infantile, juvenile, and adult,
depending on age of onset. All result in progressive neurologic changes and leukodystrophy demonstrated
on magnetic resonance imaging. Late-infantile MLD is the most common (50%-60% of cases) and
typically presents between 1 and 2 years of age with hypotonia, clumsiness, diminished reflexes, and
slurred speech. Progressive neurodegeneration occurs with a typical disease course of 3 to 10 years.
Juvenile MLD (20%-30% of cases) is characterized by onset between 4 and 14 years. Typical presenting
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