Reference Range: No Growth

< 15 U/mL: Negative
≥ 15 U/mL: Positive

< 15 U/mL: Negative
≥ 15 U/mL: Positive

No acid-fast bacilli isolated

< 15 U/mL: Negative
≥ 15 U/mL: Positive

See report

  Panel Gene List
ACTA2, ADAMTS2, AEBP1, ALDH18A1, ATP6V0A2, ATP6V1E1, ATP7A, 
B3GALT6, B3GAT3, B4GALT7, BGN, CBS, CHST14, COL1A1, COL1A2, COL2A1, COL3A1, 
COL4A1, COL5A1, COL5A2, COL9A1, COL9A2, COL9A3, COL11A1, COL11A2, COL12A1, DSE, 
EFEMP2, ELN, FBLN5, FBN1, FBN2, FKBP14, FLNA, LOX, LTBP4, MAT2A, MED12, MFAP5, 
MYH11, MYLK, NOTCH1, PLOD1, PRDM5, PRKG1, PYCR1, RIN2, SKI, SLC2A10, SLC39A13, 
SMAD2, SMAD3, SMAD4, TAB2, TGFB2, TGFB3, TGFBR1, TGFBR2, TNXB, ZNF469

Negative

See Report
 
TAT: 11- 15 Days

≤ 4 mg/L

No organisms observed

Not Detected

16542-50426 pg/mL

Negative

Levels >1000 pg/mL suggestive of pathologic parathyroid lesion

See Report

Pathologists interpretation

Healthy individuals with intact, functioning thyroid: < or = 33 ng/mL
The reference ranges listed below, however, are for thyroid cancer follow up of athyrotic patients and apply to unstimulated and stimulated thyroglobulin (Tg) measurements. Ranges are based on best practice guidelines and the literature, which includes Mayo Clinic studies, and represent clinical decision levels.
 
Decision levels for thyroid cancer patients, who are not completely athyrotic (ie, patient has some remnant normal thyroid tissue), have not been established, but are likely to be somewhat higher: remnant normal thyroid tissue contributes to serum Tg concentrations 0.2-1.0 ng/mL per gram of remnant tissue, depending on the thyroid-stimulating hormone (TSH) level.
 
Tg <0.2 ng/mL: Tg levels must be interpreted in the context of TSH levels, serial Tg measurements, and radioiodine ablation status. Undetectable Tg levels in athyrotic individuals on suppression therapy indicate a minimal risk (<1%-2%) of clinically detectable recurrent papillary/follicular thyroid cancer.
 
Tg > or = 0.2 ng/mL to 2.0 ng/mL: Tg levels must be interpreted in the context of TSH levels, serial Tg measurements, and radioiodine ablation status. Tg levels of 0.2-2.0 ng/mL in athyrotic individuals on suppressive therapy indicate a low risk of clinically detectable recurrent papillary/follicular thyroid cancer.
 
Tg 2.1 ng/mL to 9.9 ng/mL: Tg levels must be interpreted in the context of TSH levels, serial Tg measurements and radioiodine ablation status. Tg levels of 2.1-9.9 ng/mL in athyrotic individuals on suppression therapy indicate an increased risk of clinically detectable recurrent papillary/follicular thyroid cancer.
 
Tg > or = 10 ng/mL: Tg levels must be interpreted in the context of TSH levels, serial Tg measurements and radioiodine ablation status. Tg levels of 10 ng/mL or above in athyrotic individuals on suppressive therapy indicate a significant (>25%) risk of clinically detectable recurrent papillary/follicular thyroid cancer.

This test should not be used for blood donor screening, associated re-entry protocols, or for screening Human Cell, Tissues and Cellular and Tissue-Based Products (HCT/P).

Test                                                       Reference Range

Rubella Antibody IgM                              19.9 AU/mL or less- Not Detected

CMV Antibody IgM                                  29.9 AU/mL or less-Not Detected

Toxoplasma gondii Ab, IgM                        7.9 AU/mL or less- Not Detected

PHENYLALANINE            27.0-107.0 nmol/mL

TYROSINE

                         <4 weeks: 40.0-280.0 nmol/mL

                  > or =4 weeks: 25.0-150.0 nmol/mL

The quantitative results of phenylalanine and tyrosine with

age-dependent reference values are reported without added

interpretation. When applicable, reports of abnormal results

may contain an interpretation based on available clinical information.

 A phenylalanine:tyrosine ratio higher than 3 is considered abnormal.

Phenylketonuria (PKU) is the most frequent inherited disorder of amino acid metabolism (about 1:10,000-1:15,000) and was the first successfully treated inborn error of metabolism. It is inherited in an autosomal recessive manner and is caused by a defect in the enzyme phenylalanine hydroxylase (PAH), which converts the essential amino acid phenylalanine to tyrosine. Deficiency of PAH results in decreased levels of tyrosine and an accumulation of phenylalanine in blood and tissues. Untreated, PKU leads to severe brain damage with intellectual impairment, behavior abnormalities, seizures, and spasticity. The level of enzyme activity differentiates classic PKU (PAH activity <1%) from other milder forms; however, all are characterized by increased levels of phenylalanine (hyperphenylalaninemia). Treatment includes the early introduction of a diet low in phenylalanine. Some patients may also benefit from adjuvant tetrahydrobiopterin (BH4) supplementation (a cofactor for PAH), or enzyme substitution therapy.

No mutation detected

The assay will not consistently detect germline mosaicism below 50% or rule out the presence of large chromosomal aberrations, including rearrangements, inversions that do not change copy number of genomic regions. The assay does not detect repeat expansions. Possible intergenic variant interactions are not commented on. False positive or false negative results may occur for reasons that include: insufficient information available about rare genetic variants, sex chromosome abnormalities, pseudogene interference, blood transfusions, bone marrow transplantation, somatic or tissue-specific mosaicism, mislabeled samples, or erroneous representation of family relationships. Variants that do not alter an amino acid composition of a protein may be difficult to assess for pathogenicity since they may produce abnormalities in structures not assessed by conventional analysis paradigms, eg, mRNA expression and processing.1 Interpretation of the clinical significance of gene variations is limited by information about the variant that is available at the time of reporting, and by the quality and quantity of clinical information provided with the sample. As the understanding of human genetic diversity improves, the interpretation of the clinical significance of variants may change.
This test was developed and its performance characteristics determined by Labcorp. It has not been cleared or approved by the Food and Drug Administration

Females: Not applicable
 
PROSTATE-SPECIFIC ANTIGEN (PSA) Males:

 
PERCENT FREE PSA
Males:
When PSA is in the range of 4-10 ng/mL

 
PROSTATE HEALTH INDEX (phi)
Males:
When PSA is in the range of 4-10 ng/mL

Calculation of prostate health index (phi) as a part of a reflex test when PSA concentrations are between 4 and 10 ng/mL
Prostate-specific antigen (PSA) is a glycoprotein produced by the prostate gland, the lining of the urethra, and the bulbourethral gland. Normally, very little PSA is secreted in the blood. In conditions of increased glandular size and tissue damage, PSA is released into circulation. Measurement of serum PSA is useful for determining the extent of prostate cancer and assessing the response to prostate cancer treatment. PSA is also used as a screening tool for prostate cancer detection, although its use in screening has become controversial in recent years. While an elevated serum PSA is associated with prostate cancer, a number of benign conditions, such as benign prostatic hyperplasia (BPH) and prostatitis might lead to elevated serum PSA concentrations. As a consequence PSA lacks specificity for prostate cancer detection.
 
Several PSA isoforms have been identified that can further increase the specificity of PSA for prostate cancer. In particular, the [-2] form of proPSA (p2PSA) shows improved performance over either total or free PSA for prostate cancer detection on biopsy. The prostate health index (phi) is a formula that combines all 3 PSA forms (total PSA, free PSA, and p2PSA) into a single score. phi is calculated using the following formula: (p2PSA/free PSA) x square root of PSA.
 
In a multicenter study that compared the performance of PSA, free PSA, p2PSA, and phi in men undergoing prostate biopsy due to a serum PSA concentration between 4 and 10 ng/mL, phi was the best predictor of any prostate cancer, high-grade cancer, and clinically significant cancer. At 95% clinical sensitivity, the clinical specificity of phi was 16.0%, compared to 8.4% for free PSA and 6.5% for PSA.