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HYOX
86213
Results Expressed as a Percentage of
CD19+ B Cells
Percentage Absolute Count (Cells/mcL)
CD19+ CD27+ 6.3-52.8 18.0-145.0
CD19+ CD27+ IgM+ IgD+ 1.7-29.3 4.0-85.0
CD19+ CD27+ IgM- IgD- 2.3-26.5 7.0-61.0
CD19+ CD27+ IgM+ IgD- 0-5.3 0-12.0
CD19+ IgM+ 26.0-78.0 37.0-327.0
CD19+ CD38+ IgM- 4.1-42.2 7.0-153.0
CD19+ CD38+ IgM+ 1.2-50.7 2.0-139.4
CD19+ CD21+ 92.1-99.6 85.0-533.0
CD19+ CD21- 0.2-8.6 0.3-22.0 B-CELL CD40 EXPRESSION
BY FLOW CYTOMETRY Present
(normal) X-LINKED HYPER IgM
SYNDROME Present An interpretive
report will be provided.
Clinical References: 1. Gulino AV, Notarangelo LD: Hyper-IgM syndromes. Curr Opin Rheumatol
2003;15:422-429 2. Durandy A, Peron S, Fischer A: Hyper-IgM syndromes. Curr Opin Rheumatol
2006;18:369-376 3. Lee W-I, Torgerson TR, Schumacher MJ, et al: Molecular analysis of a large cohort
of patient with hyper immunoglobulin M (IgM) syndrome. Blood 2005;105:1881-1890 4. Erdos M,
Durandy A, Marodi L: Genetically acquired class-switch recombination defects: the multi-faced
hyper-IgM syndrome. Immunol Letter 2005;97:1-6 5. Carmichael KF, Abayomi A: Analysis of diurnal
variation of lymphocyte subsets in healthy subjects and its implication in HIV monitoring and treatment.
15th Intl Conference on AIDS, Bangkok, Thailand, 2004, Abstract # B11052 6. Dimitrov S, Benedict C,
Heutling D, et al: Cortisol and epinephrine control opposing circadian rhythms in T-cell subsets. Blood
2009 (prepublished online March 17, 2009) 7. Dimitrov S, Lange T, Nohroudi K, Born J: Number and
function of circulating antigen presenting cells regulated by sleep. Sleep 2007;30:401-411 8. Kronfol Z,
Nair M, Zhang Q, et al: Circadian immune measures in healthy volunteers: relationship to
hypothalamic-pituitary-adrenal axis hormones and sympathetic neurotransmitters. Pyschosomatic
Medicine 1997;59:42-50 9. Malone JL, Simms TE, Gray GC, et al: Sources of variability in repeated
T-helper lymphocyte counts from HIV 1-infected patients: total lymphocyte count fluctuations and
diurnal cycle are important. J AIDS 1990;3:144-151 10. Paglieroni TG, Holland PV: Circannual variation
in lymphocyte subsets, revisited. Transfusion 1994;34:512-516
Hyperoxaluria Panel, Urine
Clinical Information: Increased urinary oxalate frequently leads to renal stone formation.
Identification of the cause of increased urinary oxalate is important in the evaluation of the individual
with renal oxalate stones or renal insufficiency due to hyperoxaluria and has important implications in
therapy, management and prognosis. Hyperoxalurias have been classified as primary (genetically
determined) and secondary. Type I (PH1), a autosomal recessive deficiency of peroxisomal
alanine:glyoxylate aminotransferase due to mutations in the AGXT gene, is characterized by increased
urinary oxalic, glyoxylic, and glycolic acids. PH1 manifestations include deposition of calcium oxalate
in the kidneys (nephrolithiasis, nephrocalcinosis), and end-stage renal disease. Calcium oxalate deposits
can be found in other tissues such as the heart and eyes, and lead to a variety of additional symptoms.
Age of onset is variable with a small percentage of patients presenting in the first year of life with
failure to thrive, nephrocalcinosis, and metabolic acidosis. Approximately half of affected individuals
show manifestations of PH1 in late childhood or early adolescence, and the remainder present in
adulthood with recurrent renal stones. Some PH1 individuals respond to supplementary pyridoxine
therapy. Hyperoxaluria type II (PH 2) is due to a defect in GRHPR gene resulting in a deficiency of the
enzyme hydroxypyruvate reductase. PH2 is autosomal recessive and identified by an increase in urinary
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