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GRHMS
50037
proteins) followed by respiratory disease (rhinitis and asthma) in older children and adults due to
sensitivity to inhalant allergens (dust mite, mold, and pollen inhalants).
Useful For: Testing for IgE antibodies may be useful to establish the diagnosis of an allergic disease
and to define the allergens responsible for eliciting signs and symptoms. Testing also may be useful to
identify allergens which may be responsible for allergic disease and/or anaphylactic episode, to confirm
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 McPherson RA, Pincus MR. WB Saunders, Publ, New York,
Chapter 53, Part VI, pp. 961-971, 2007
GRHPR Gene, Full Gene Analysis
Clinical Information: Primary hyperoxaluria type 2 (PH2) is a hereditary disorder of glyoxylate
metabolism caused by deficiency of the hepatic enzyme glyoxylate reductase/hydroxypyruvate reductase
(GRHPR). Absence of GRHPR activity results in excess oxalate and usually L-glycerate excreted in the
urine leading to nephrolithiasis (kidney stones) and sometimes renal failure. Onset of PH2 is typically in
childhood or adolescence with symptoms related to kidney stones. In some cases, kidney failure may be
the initial presenting feature. Nephrocalcinosis, as seen by renal ultrasound, is observed less frequently in
individuals with PH2 than primary hyperoxaluria type 1 (PH1). End-stage renal disease (ESRD) is also
less common and of later onset than PH1; however, once ESRD develops, oxalate deposition in other
organs such as bone, retina, and myocardium can occur. While, the exact prevalence and incidence of
PH2 are not known, it is thought that PH2 is less common than PH1, which has an estimated prevalence
rate of 1 to 3 per million population and an incidence of 0.1 per million/year. Biochemical testing is
indicated in patients with possible primary hyperoxaluria. Measurement of urinary oxalate in a timed,
24-hour urine collection is strongly preferred, with correction to adult body surface area in pediatric
patients (HYOX/86213 Hyperoxaluria Panel, Urine; OXU/8669 Oxalate, Urine). In very young children
(incapable of performing a timed collection), random urine oxalate to creatinine ratios may be used for
determination of oxalate excretion. In patients with reduced kidney function, POXA/81408 Oxalate,
Plasma is also recommended. Urinary excretion of oxalate of >1.0 mmol/1.73 m(2)/24 hours is strongly
suggestive of, but not diagnostic for, primary hyperoxaluria, as there are other forms of inherited (PH1
and non-PH1/PH2) hyperoxaluria and secondary hyperoxaluria that may result in similarly elevated urine
oxalate excretion rates. An elevated urine glycerate in the presence of hyperoxaluria is suggestive of PH2.
Caution is warranted in interpretation of urine oxalate excretion in patients with reduced kidney function
as urine oxalate concentrations may be lower due to reduced glomerular filtration rate. Historically, the
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