Sorted By Test Name - Mayo Medical Laboratories

NEURF
88846
FNMYC
87862
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 McPherson RA, Pincus MR. WB Saunders, Publ, New York,
Chapter 53, Part VI, pp. 961-971, 2007
Neuraminidase, Fibroblasts
Clinical Information: A deficiency of the enzyme neuraminidase results in sialidosis, an autosomal
recessive lysosomal storage disorder. There are 2 sialidosis phenotypes. Type 1 is characterized by a
cherry-red spot on the retina, progressive decreased acuity, impaired color vision, or night blindness.
Neurologic problems include poorly controlled myoclonus (sudden brief involuntary muscle
contractions), painful neuropathy, and delayed nerve conduction. The majority of type I patients have
been Italian. Type II sialidosis is distinguished from type I by the presence of abnormal somatic features,
including coarse facies and dysotosis multiplex. Type II can generally be subdivided into an infantile
form, juvenile form, and congenital (or hydropic) form. In addition to primary neuraminidase deficiency
disorders, there are also patients with a similar clinical disorder who suffer from a combined deficiency of
neuraminidase and beta-galactosidase. To date, the human alpha-neuraminidase defect is sialidosis
patients has not been well characterized. This situation is complicated by the fact that neuraminidase is
unstable and quickly destroyed by freezing, sonication, solubilization, and most purification procedures.
Useful For: As an aid in the diagnosis of sialidosis
Interpretation: Patient specimens with >23% of co-run normal control activity are considered to be
normal. Specimens with 17% to 23% of co-run normal activity are in an indeterminate range; molecular
confirmation is recommended, if clinically indicated. Specimens with 23% of the co-run normal control of the day
Clinical References: Thomas GH: Disorders of glycoprotein degradation: alpha-mannosidosis,
beta-mannosidosis, fucosidosism and sialidosis. In The Metabolic Basis of Inherited Disease, 8th edition.
Edited by CR Scriver, AL Beuadet, WS Sly, DE Valle. Chapter 140. 2001, pp 3507
Neuroblastoma, 2p24 (MYCN) Amplification, FISH
Clinical Information: Neuroblastoma is a solid tumor that occurs in early childhood and is usually
found in the adrenal glands, but rarely is found in other areas of the body. Approximately 25% of all
neuroblastomas have amplification of the MYCN oncogene, located on chromosome 2 at p24.1.
Amplification of the MYCN oncogene correlates with an unfavorable prognosis and aggressive disease.
Useful For: As a prognostic factor for patients with neuroblastoma As an aid to treatment decisions in
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