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CERE
8364
patients with multiple sclerosis (MS). Oligoclonal banding in CSF is also positive in approximately 80%
of patients with MS. The use of CSF index plus oligoclonal banding has been reported to increase the
sensitivity to over 90%. The index is independent of the activity of the demyelinating process.
Reference Values:
CSF index: 0.00-0.85
CSF IgG: 0.0-8.1 mg/dL
CSF albumin: 0.0-27.0 mg/dL
Serum IgG
0-4 months: 100-334 mg/dL
5-8 months: 164-588 mg/dL
9-14 months: 246-904 mg/dL
15-23 months: 313-1,170 mg/dL
2-3 years: 295-1,156 mg/dL
4-6 years: 386-1,470 mg/dL
7-9 years: 462-1,682 mg/dL
10-12 years: 503-1,719 mg/dL
13-15 years: 509-1,580 mg/dL
16-17 years: 487-1,327 mg/dL
> or =18 years: 767-1,590 mg/dL
Serum albumin: 3,200-4,800 mg/dL
CSF IgG/albumin: 0.00-0.21
Serum IgG/albumin: 0.0-0.4
CSF IgG synthesis rate: 0-12 mg/24 hours
Clinical References: 1. Tourtellotte WW, Walsh MJ, Baumhefner RW, et al: The current status of
multiple sclerosis intra-blood-brain-barrier IgG synthesis. Ann NY Acad Sci 1984;436:52-67 2. Bloomer
LC, Bray PF: Relative value of three laboratory methods in the diagnosis of multiple sclerosis. Clin Chem
1981;27:2011-2013 3. Hische EA, van der Helm HJ: Rate of synthesis of IgG within the blood-brain
barrier and the IgG index compared in the diagnosis of multiple sclerosis. Clin Chem 1987;33:113-114 4.
Swanson JW: Multiple Sclerosis: update in diagnosis and review of prognostic factors. Mayo Clin Proc
1989;64:577-586 5. Markowitz H, Kokmen E: Neurologic diseases and the cerebrospinal fluid
immunoglobulin profile. Mayo Clin Proc 1983;58:273-274
Ceruloplasmin, Serum
Clinical Information: Ceruloplasmin is an acute phase protein and a transport protein. This
blue-colored glycoprotein belongs to the alpha 2-globulin electrophoretic fraction and contains 8 copper
atoms per molecule. Incorporation of copper into the structure occurs during the synthesis of
ceruloplasmin in the hepatocytes. After secretion from the liver, ceruloplasmin migrates to
copper-requiring tissue where the copper is liberated during catabolism of the ceruloplasmin molecule. In
addition to transporting copper, ceruloplasmin has a catalytic function in the oxidation of iron (Fe[2+] to
Fe[3+]), polyamines, catecholamines, and polyphenols. Decreased concentrations occur during recessive
autosomal hepatolenticular degeneration (Wilson disease). On a pathochemical level, the disease, which is
accompanied by reduced ceruloplasmin synthesis, occurs as a consequence of missing Cu(2+)
incorporation into the molecule due to defective metallothionein. This results in pathological deposits of
copper in the liver (with accompanying development of cirrhosis), brain (with neurological symptoms),
cornea (Kayser-Fleischer ring), and kidneys (hematuria, proteinuria, aminoaciduria). In homozygous
carriers, ceruloplasmin levels are severely depressed. Heterozygous carriers exhibit either no decrease at
all or just a mild decrease. The rare Menkes syndrome is a genetically caused copper absorption disorder
with concomitant lowering of the ceruloplasmin level. Protein loss syndromes and liver cell failures are
the most important causes of acquired ceruloplasmin depressions. As ceruloplasmin is a sensitive acute
phase reactant, increases occur during acute and chronic inflammatory processes. Great increases can lead
to a green-blue coloration of the sera. See Wilson Disease Testing Algorithm in Special Instructions.
Refer to The Diagnosis of Wilson Disease Mayo Medical Laboratories Communique 2005 Feb;30(2) for
more information regarding diagnostic strategy.
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