Sorted By Test Name - Mayo Medical Laboratories

NMOC
83936
or neurologic disorders. These enzymes are phosphofructokinase, triosephosphate isomerase,
phosphoglycerate kinase, and glutathione synthase. Kinetic enzyme assays are available for the first 3
disorders. Quantitative measurement of glutathione substitutes for analysis of the enzyme glutathione
synthase.
Useful For: Evaluating patients who have a hemolytic process that is associated with some neurologic
findings
Interpretation: Definitive results and an interpretive report will be provided. Significant abnormal
values typically are 25% of values obtained for a normal individual.
Reference Values:
Definitive results and an interpretive report will be provided.
Clinical References: 1. Fairbanks VF, Klee GG: Biochemical aspects of hematology. In Tietz
Textbook of Clinical Chemistry. 3rd edition. Edited by CA Burtis, ER Ashwood. Philadelphia, WB
Saunders Company, 1999, pp 1642-1644 2. Boulard MR, Meienhofer MC, Bois M, et al: Letter: red-cell
phosphofructokinase deficiency. N Engl J Med 1974;291:978-979 3. Schneider AS, Valentine WN,
Hattori M, Heins HL: Hereditary hemolytic anemia with triosephosphate isomerase deficiency. N Engl J
Med 1965;272:229-235
Neuromyelitis Optica (NMO) Autoantibody, IgG, Spinal Fluid
Clinical Information: Neuromyelitis optica (NMO, also known as Devic's disease and optic-spinal
multiple sclerosis) is a severe idiopathic inflammatory demyelinating disease that selectively affects optic
nerves and the spinal cord, typically spares the brain, and generally follows a relapsing course. Within 5
years, 50% of patients lose functional vision in at least 1 eye or are unable to walk independently. In
North America, the proportion of nonwhite individuals is higher among patients with NMO than among
those with classic multiple sclerosis. During acute attacks, the cerebrospinal fluid contains inflammatory
cells, but often lacks evidence of intrathecal IgG synthesis. Many patients with NMO are misdiagnosed as
having multiple sclerosis, due to earlier misconceptions that NMO was a monophasic disorder, and was
not associated with brain imaging abnormalities. Importantly the prognosis and optimal treatments for the
2 diseases differ. NMO typically has a worse outcome than multiple sclerosis, with frequent and early
relapses. Plasmapheresis is more beneficial for patients with NMO than for those with multiple sclerosis.
Early diagnosis and treatment are important to reduce the morbidity of NMO. Seropositivity for NMO
autoantibody IgG (NMO-IgG) allows early diagnostic distinction between NMO (73% positive; 91%
specific) and multiple sclerosis (0% positive). NMO-IgG is uniformly negative in patients with classical
multiple sclerosis, for which no biomarker is currently recognized. This distinction is important both
prognostically and therapeutically, because optimal treatments differ for NMO (immunosuppression) and
multiple sclerosis (immunomodulation with beta-IFN or glatiramer acetate).
Useful For: Establishing the diagnosis of neuromyelitis optica (NMO) and related disorders (eg,
relapsing transverse myelitis or relapsing optic neuritis), predicting with 60% probability, relapse or
progression to NMO in patients presenting with an initial episode of longitudinally extensive transverse
myelitis. Seropositivity distinguishes these disorders from multiple sclerosis early in the course of disease.
This allows initiation and maintenance of optimal therapy. Serum is the preferred specimen for detection
of NMO-IgG (see #60796 Neuromyelitis Optica (NMO) Evaluation with Reflex, Serum); cerebrospinal
fluid is usually less informative.
Interpretation: A positive value is consistent with NMO or a related disorder, and justifies initiation
of appropriate immunosuppressive therapy at the earliest possible time. Our prospective studies have
revealed that 40% of adult patients with longitudinally-extensive transverse myelitis are seropositive and,
of that group, 60% relapse or progress to NMO within 2 years. No seronegative patient relapsed in up to 7
years of follow-up.
Reference Values:
Negative
Clinical References: 1. Wingerchuk DM, Lennon VA, Pittock SJ, et al: Revised diagnostic criteria
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