TEST DIRECTORY
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There are currently 28 names in this directory beginning with the letter V.
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Expected Turnaround Time
2 - 4 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Information
Related Documents
Specimen Requirements
Specimen
Serum
Volume
0.2 mL
Container
Red-top tube or gel-barrier tube
Storage Instructions
Room temperature
Stability Requirements
| Temperature | Period |
|---|---|
| Room temperature | 14 days |
| Refrigerated | 14 days |
| Frozen | 3 months |
| Freeze/thaw cycles | Stable x3 |
Test Details
Methodology
Thermo Fisher ImmunoCAP®
Vaginitis Plus (VG+), NuSwab®
Expected Turnaround Time
3 - 4 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Information
Related Documents
For more information, please view the literature below.
LABupdate: Candida Species Identification by NAA
Microbiology Specimen Collection and Transport Guide
NuSwab℠: Smart Testing Has Arrived
Protect Your Patients From the Consequences of Untreated Chlamydia, Gonorrhea, and Trichomonas: Easily Detected and Easily Treated
The Most Accurate Results Come From the Best Specimens
Trichomonas vaginalis: Detect More Infections With Nucleic Acid Amplification
Specimen Requirements
Specimen
Vaginal swab
Volume
One swab
Minimum Volume
One swab
Container
Aptima® vaginal or unisex swab
Collection
Vaginal swab: Collect vaginal fluid sample using the Gen-Probe® Aptima® swab by contacting the swab to the lower third of the vaginal wall and rotating the swab for 10 to 30 seconds to absorb fluid. Immediately place the swab into the transport tube and carefully break the swab shaft against the side of the tube. Tightly screw on the cap.
Storage Instructions
Maintain specimen at room temperature or refrigerate (2°C to 30°C). Stable at room temperature or refrigerated for 30 days.
Causes for Rejection
Specimen with incorrect patient identification; unlabeled specimen; inappropriate specimen transport conditions; specimens received after prolonged delay (usually >72 hours); specimen leaked in transit; specimen in expired transport or incorrect transport device; specimens with inappropriate source for test requested; specimen with fixative or additives; Aptima® urine transport; Aptima® swab transport >30 days from collection; Aptima® swab specimen without a swab; cleaning swab (white-shaft swab) in Aptima® swab transport; any non−Gen-Probe® swab submitted in Aptima® transport device; transport device with multiple swabs; bloody or grossly mucoid specimens; bacterial swabs; specimen in ProbeTec™ UPT transport; ProbeTec™ Q-swabs
Test Details
Use
This test is intended to be used as an aid to the diagnosis of bacterial vaginosis (BV) in women with a clinical presentation consistent with this disorder. The BV test utilizes semiquantitative PCR analysis of the three most predictive marker organisms (Atopobium vaginae, BVAB-2, and Megasphaera-1) to generate a total score that correlates directly with the presence or absence of BV. In this test system, samples with a total score of 0 to 1 are considered negative for BV, samples with a score of 3 to 6 are positive for BV, and samples with a score of 2 are indeterminate for BV. Used to detect the presence of Candida albicans and Candida glabrata DNA in vaginal samples as an aid to the diagnosis of vulvovaginal candidiasis in symptomatic women. Also used in the diagnosis of Chlamydia trachomatis, Neisseria gonorrhoeae, and Trichomonas vaginalis infections.
Limitations
This test was developed, and its performance characteristics determined, by LabCorp. It has not been cleared or approved by the US Food and Drug Administration (FDA). The FDA has determined that such clearance or approval is not necessary.
Methodology
Nucleic acid amplification (NAA)
Valproic Acid, Serum or Plasma
Synonyms
- Depacon®
- Depakene®
- Depakote®
- Stavzor™
- Valproate
Expected Turnaround Time
1 - 3 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Documents
Specimen Requirements
Specimen
Serum or plasma
Volume
1 mL
Minimum Volume
0.3 mL
Container
Red-top tube or green-top (heparin) tube. Do not use a gel-barrier tube. The use of gel-barrier tubes is not recommended due to slow absorption of the drug by the gel. Depending on the specimen volume and storage time, the decrease in drug level due to absorption may be clinically significant.
Collection
Transfer separated serum or plasma to a plastic transport tube. Oral: peak: one to four hours after dose (influenced by meals); trough: immediately prior to next dose (possibly more useful than peak values).
Storage Instructions
Room temperature
Stability Requirements
| Temperature | Period |
|---|---|
| Room temperature | 14 days |
| Refrigerated | 14 days |
| Frozen | 14 days |
| Freeze/thaw cycles | Stable x3 |
Causes for Rejection
Gel-barrier tube; hemolysis; lipemia
Test Details
Use
Valproate (valproic acid; divalproex sodium, a compound containing sodium valproate and valproic acid) controls absence, myoclonic, and tonic-clonic seizures in generalized, idiopathic, and symptomatic epilepsy. It is most useful in typical absence seizures. Valproate is as effective as ethosuximide in patients with absence seizures alone and is variably effective in atypical absence seizures. Although some clinicians prefer valproate for absence seizures, the American Academy of Pediatrics (Committee on Drugs, 1982) recommended that it be reserved for use when therapeutic failure or intolerance to ethosuximide occurs, because valproate causes rare but potentially fatal hepatotoxicity. Many neurologists consider valproate the drug of choice for patients with both absence and other generalized seizure types, including tonic-clonic convulsions. Its efficacy is about the same as in patients with the latter type alone.
Valproate is an alternative drug in the treatment of complex partial seizures but may be considered for initial therapy in patients with partial and secondarily generalized seizures.
Valproate is the drug of choice in myoclonic epilepsy, with or without generalized tonic-clonic seizures, including juvenile myoclonic epilepsy of Janz, that begins in adolescence or early adulthood. Photosensitive myoclonus is usually easily controlled. Valproate also is effective in the treatment of benign myoclonic epilepsy, postanoxic myoclonus, and, with clonazepam, in severe progressive myoclonic epilepsy that is characterized by tonic-clonic seizures as well. It also may be preferred in certain stimulus-sensitive (reflex, startle) epilepsies.
Although valproate may be effective for infantile spasms, it is relatively contraindicated in children whose spasms are due to hyperglycinemia or other underlying metabolic (mitochondrial) abnormalities. In general, atonic and akinetic seizures in patients with Lennox-Gastaut syndrome are difficult to control, but valproate is the drug of choice for treatment of mixed seizure types. Since this drug has been useful in some patients who are refractory to all other antiepileptic drugs, it may warrant a trial in nearly all nonresponsive patients regardless of seizure type.
Methodology
Immunoassay (IA)
Reference Interval
Therapeutic: 50−100 μg/mL
Critical Value
Potentially toxic: >120 μg/mL
Additional Information
Hepatotoxicity may be fatal, but is idiosyncratic and not preventable by routinely monitoring liver enzymes. Hepatotoxicity occurs in very young children, most often those on multiple anticonvulsants.1 Valproate-induced cytopenias may be dose-related and warrant monitoring of complete blood counts during therapy.2 Encephalopathy with hyperammonemia without liver function test abnormalities may occur.3 Pregnant women in first month are at risk for neural tube defects.
Valproate is absorbed rapidly and completely following oral administration; peak plasma concentrations usually occur within two hours after ingestion of liquid preparations and three to four hours after ingestion of the delayed-release tablet preparation, divalproex sodium, which contains sodium valproate and valproic acid. Food delays absorption but does not affect bioavailability.
The plasma protein binding of valproate is saturable within the usual therapeutic range (approximately 90% at 75 μg/mL). Usual effective plasma concentrations range from 50−120 μg/mL.4 With a daily dose of more than 500 mg, plasma concentrations may not increase proportionately because clearance increases with an increase in the free fraction. Daily fluctuations (up to two times higher) in free fraction and clearance also occur as a result of displacement by free fatty acids or circadian influences; thus, when plasma concentrations are being monitored, samples should be taken at a uniform time. Many neurologists recommend measuring trough concentrations.
Valproate is eliminated almost exclusively by hepatic metabolism. The metabolic fate is complex. A variety of conjugation and oxidative processes are involved, including entry into pathways (eg, beta oxidation) normally reserved for endogenous fatty acids. As the dose is increased, mitochondrial beta oxidation becomes saturated and increased glucuronidation occurs.
Metabolites may contribute to both antiepileptic and hepatotoxic effects. The antiepileptic activity of valproate (including the time course) is poorly correlated with steady-state valproate plasma concentrations. One unsaturated metabolite, 2-n-propyl-4-pentenoic acid (4-ene-VPA), has been proposed as a key hepatotoxic metabolite. The formation of this metabolite is increased by concomitant use of phenytoin, phenobarbital, carbamazepine, and other drugs that induce cytochrome P450. Due to inhibition of the same enzyme system, valproic acid may cause elevated levels of clomipramine with resultant seizures when the two agents are co-administered.5
The half-life of valproate in adults is 12 to 16 hours. In epileptic patients receiving polytherapy, the half-life is approximately nine hours, although five hours has also been reported. The half-lives in school-age children and young adolescents are well within the range of values in adults. Elimination half-lives are longer in neonates and generally shorter during middle and late infancy. Although hepatic clearance is reduced, the half-life in geriatric patients is approximately 15 hours. This has been attributed to the larger free fraction observed in this age group, especially in those with hypoalbuminemia.
Vanadium, Urine
Expected Turnaround Time
3 - 7 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Specimen Requirements
Specimen
Urine (random)
Volume
10 mL
Minimum Volume
1 mL
Container
Metal-free plastic urine container or metal-free transport tube
Collection
Use metal-free or acid washed containers for collection; transfer an aliquot of urine to a metal-free transfer tube
Storage Instructions
Submission/transport (<3 days): Room temperature. For storage beyond three days, specimen should be refrigerated or frozen.
Causes for Rejection
Use of non−metal-free collection containers or tubes
Test Details
Use
Evaluate exposure to vanadium
Methodology
Inductively coupled plasma/mass spectrometry (ICP/MS); spectrophotometry (SPEC)
Reference Interval
• Unexposed population: <1.0 ng/mL
• Exposed: Biological exposure index (BEI): 50 µg/g creatinine (end of shift)
Vancomycin, Serum, Peak and Trough
Synonyms
- Vancocin®
Special Instructions
Peak levels should be ordered using test 070327. Trough levels should be ordered using test 070328. Peak and trough levels may be ordered together as a profile on the same request form using test 717314. Please label tubes appropriately as “peak” and “trough.”
Expected Turnaround Time
Within 1 day
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Specimen Requirements
Stability Requirements
| Temperature | Period |
|---|---|
| Room temperature | 3 days |
| Refrigerated | 14 days |
| Frozen | 14 days |
| Freeze/thaw cycles | Stable x3 |
Varicella Zoster Virus (VZV) Antibodies, IgG
Synonyms
- Chickenpox Titers
- Herpes Zoster Antibodies
- VZV IgG
Expected Turnaround Time
1 - 2 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Documents
Specimen Requirements
Specimen
Serum
Volume
0.5 mL
Minimum Volume
0.2 mL
Container
Red-top tube or gel-barrier tube
Storage Instructions
Room temperature
Stability Requirements
| Temperature | Period |
|---|---|
| Room temperature | 14 days |
| Refrigerated | 14 days |
| Frozen | 14 days |
| Freeze/thaw cycles | Stable x4 |
Causes for Rejection
Hemolysis; lipemia; gross bacterial contamination
Test Details
Use
Diagnose VZV infection; determine adult susceptibility to infection
Methodology
Chemiluminescent immunoassay (CLIA)
Reference Interval
• Negative: <135 index
• Equivocal: 135−165 index
• Positive: >165 index
Additional Information
Although most cases of varicella or zoster are clinically unambiguous, serology may be occasionally useful in the differential diagnosis of other blistering illnesses or when infection shows an unusual complication, such as hepatitis. It may also be important to establish whether an individual is susceptible when clinical history is unclear, or when varicella immune globulin may be needed, as in the immunocompromised host or cancer patient on toxic chemotherapy. Zoster is more common with aging and may occur in the face of significant antibody titers, demonstrating that cell-mediated immunity is also significant.
Varicella Zoster Virus (VZV), DNA PCR
Synonyms
- VZV, DNA by Real-time PCR
Expected Turnaround Time
4 - 5 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Documents
Specimen Requirements
Specimen
Cerebrospinal fluid (CSF), vitreous fluid, whole blood, or swab
Volume
0.5 mL CSF, vitreous fluid, whole blood, or one swab
Minimum Volume
0.2 mL CSF, vitreous fluid, whole blood, or one swab
Container
Sterile container (CSF or vitreous fluid), lavender-top (EDTA) tube, yellow-top (ACD) tube, or universal transport medium (swab)
Collection
To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.
Storage Instructions
CSF or vitreous fluid: freeze; refrigerate swab.
Stability: CSF or vitreous fluid: Room temperature or refrigerated for 14 days or frozen for 90 days. Swab: Room temperature or refrigerated for 14 days. Whole blood: Room temperature or refrigerated for 14 days.
Causes for Rejection
Quantity not sufficient for analysis; gross specimen contamination; specimen too old; leaking or broken tube
Test Details
Use
This test is intended to be used as an aid in the diagnosis of infections caused by varicella zoster virus (VZV).
Methodology
Real-time polymerase chain reaction (PCR)
Velvet Grass
Expected Turnaround Time
3 - 4 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Information
Related Documents
Specimen Requirements
Specimen
Serum
Volume
0.2 mL
Container
Red-top tube or gel-barrier tube
Storage Instructions
Room temperature
Stability Requirements
| Temperature | Period |
|---|---|
| Room temperature | 14 days |
| Refrigerated | 14 days |
| Frozen | 3 months |
| Freeze/thaw cycles | Stable x3 |
Test Details
Methodology
Thermo Fisher ImmunoCAP®
Viral Culture, General
Synonyms
- Culture, Viral, General
- General Viral Culture
- Mumps Viral Culture
- Routine Viral Culture
- Virus Culture/Isolation
Test Includes
Based on specimen source, viruses to be detected by cytopathic effect and/or antibody staining include adenovirus, CMV, enteroviruses, HSV, influenza, mumps, parainfluenza, RSV, and V-Z cell culture; identification (additional charges/CPT code[s] may apply) by fluorescent antibody or other methods if culture results warrant. CPT coding for microbiology and virology procedures often cannot be determined before the culture is performed.
Special Instructions
Submit one specimen per test requested. Specify the exact specimen source/origin (eg, genital lesion). Indicate a specific test number on the request form. Age of patient, relevant vaccinations, and pertinent clinical history are helpful. Whenever a viral etiology is suspected and whenever appropriate, acute and convalescent serum should be collected for viral serology tests.
Expected Turnaround Time
9 - 12 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Information
- Respiratory Syncytial Virus (RSV), Immunoassay
- Viral Culture, Rapid, Cytomegalovirus (CMV)
- Viral Culture, Rapid, Influenza A and Influenza B Virus
- Viral Culture, Rapid, Lesion (Herpes Simplex Virus and Varicella Zoster Virus)
- Viral Culture, Rapid, Respiratory
- Virology
- Virus Culture, Rapid, Varicella Zoster Virus (VZV)
Related Documents
Specimen Requirements
Specimen
Blood, cerebrospinal fluid (CSF), dermal, ocular, genital, mucosal, oral, rectal, respiratory, stool, tissue, urine, or biopsy
| Specimen | Virus* |
|---|---|
| *Abbreviations: | |
| HSV − herpes simplex virus | |
| CMV − cytomegalovirus | |
| VZV − varicella-zoster virus | |
| RSV − respiratory syncytial virus | |
| †Enteroviruses: coxsackie virus, poliovirus, echovirus, and enterovirus. | |
| ‡Rarely isolated. | |
| §Usually in immunocompromised hosts. | |
| Blood | CMV, enteroviruses†,‡, HSV‡, VZV‡ |
| CSF and CNS tissues | Enteroviruses, mumps virus, HSV‡, CMV |
| Dermal lesions | HSV, VZV, adenovirus, enteroviruses |
| Eye | HSV, VZV, adenovirus, enteroviruses, CMV |
| Genital | HSV, CMV |
| Mucosal | HSV, VZV |
| Oral | HSV, VZV |
| Rectal | HSV, VZV, enterovirus |
| Respiratory tract | |
| upper | Adenovirus, rhinovirus, influenza, parainfluenza, enteroviruses, RSV, reovirus, HSV |
| lower | Adenovirus, influenza, parainfluenza, RSV, CMV§ |
| Stool | Enteroviruses, adenoviruses |
| Tissues | CMV, HSV, enteroviruses |
| Urine | CMV, adenovirus, enteroviruses, mumps |
Volume
1 mL fluid or one swab in viral transport
Container
Viral, Chlamydia, or Mycoplasma culture transport provided by LabCorp, or other appropriate transport medium; sterile screw-cap tube or container for fluids, feces, nasal washings, urine, or biopsy (no preservative); green-top (heparin) tube for blood, bone marrow, and buffy coat
Collection
Specimen should be collected during the acute phase of the disease as follows:
Blood: Collect 5 mL whole blood into a heparinized tube; sodium heparin preferred. Send at room temperature.
Cerebrospinal fluid: Collect 1 mL CSF aseptically in a sterile dry screw-cap vial. Refrigerate immediately.
Skin lesions: Open the vesicle and absorb exudate into a dry swab and/or vigorously scrape base of freshly exposed lesion with a swab to obtain cells that contain viruses. If enough vesicle fluid is available, aspirate the fluid with a fine gauge needle and tuberculin syringe, and place the fluid into cold viral transport medium. Use viral swabs for specimen collection. Refrigerate immediately.
Eye swab or scraping: Use a viral swab to collect conjunctival material. Take conjunctival scrapings with a fine sterile spatula and transfer the scraping to a viral transport medium. Refrigerate immediately.
Genital swab: See skin. Refrigerate immediately.
Rectal swab: Insert a sterile swab 2” to 4” into the rectum and rub the mucosa. Swab may be placed into cold virus transport medium. Refrigerate immediately.
Throat swab: Carefully rub the posterior wall of the nasopharynx with a dry, sterile swab. Avoid touching the tongue or buccal mucosa. Place swab in viral transport tube.
Feces: Collect 4 to 8 g of feces (about the size of a thumbnail) and place in a clean, screw-cap container. Do not dilute the specimen or use preservatives. Viral swab is acceptable. Refrigerate immediately.
Tissue: Use a fresh set of sterile instruments to collect each tissue. Place each specimen in its own dry, sterile nontoxic screw-cap container. To prevent the tissue from drying out, add a small amount of viral transport medium to the container. Identify each tissue with the patient's name, type of tissue, and date collected. Refrigerate immediately.
Urine: Collect clean-catch, midstream urine in a screw-cap, sterile, plastic container. Refrigerate immediately.
Storage Instructions
All specimen types except blood must be kept cold and moist (refrigerated). Blood: Stored and transported at room temperature.
Causes for Rejection
Bacterial swab specimen; specimen received in grossly leaking transport container; dry specimen; specimen submitted in fixative or additive; specimen received in expired transport media or incorrect transport device; inappropriate specimen transport conditions; specimen received after prolonged delay in transport (usually more than 72 hours); specimen types other than blood stored or transported at room temperature; wooden shaft swab in transport device; unlabeled specimen or name discrepancy between specimen and request label; hemolyzed blood sample
Test Details
Use
Aid in the diagnosis of viral diseases (eg, conjunctivitis, congenital viral infections, keratitis, chickenpox, shingles, viral pneumonia, and diseases characterized by skin vesicles and rashes)
Limitations
For all practical purposes, many common viruses are not culturable: Coxsackie A viruses, hepatitis viruses, arboviruses, parvoviruses, human papillomaviruses, reoviruses, measles virus, and gastrointestinal viruses (rota, corona, calici, astro, and Norwalk). Isolation of virus may not be related to the patient's disease. Some positive cultures are sent to State Health Laboratory for specific virus identification. Infectious HSV is rarely present in CSF during encephalitis, resulting in a poor recovery by culture (<5% in adults, <50% in children). Studies have shown a >98% detection of HSV DNA in CSF by polymerase chain reaction (PCR), and this method is now considered the standard for diagnosis of HSV encephalitis. For HSV PCR testing, please order test 138651.
Methodology
Inoculation of specimen into cell cultures, incubation of cultures, observation for characteristic cytopathic effect, and identification by DFA or other methods
Reference Interval
No virus isolated
Additional Information
Give date of onset of illness, date of collection, and brief clinical description or the provisional diagnosis. For example, does the patient have a rash, a respiratory illness, or neurological symptoms?
Viral cultures: Specimens should be collected in the acute stage of the illness, kept moist, and refrigerated immediately. Stool specimens should not be placed into viral transport medium or frozen. Spinal fluid and throat washings must be kept cold and must not be frozen. Swabs of lesions or of throat should be rinsed immediately into 1 or 2 mL of viral transport medium; preferably, the swab should be broken off into the medium and sent in the medium to the laboratory. Autopsy material should be collected in sterile containers. Urine specimens for CMV culture must not be frozen; they should be packed with an ice pack or snow gel, but not with dry ice.
Viral Culture, Rapid, Influenza A and Influenza B Virus
Synonyms
- Culture, Viral, Influenza Virus
- Flu Culture
- Influenza Virus Culture
Test Includes
Shell vials or equivalent multiwell plate cell culture; identification (additional CPT codes/charges will apply) if culture results warrant. This culture is for the isolation of influenza A and influenza B, other viral agents will not routinely be detected. CPT coding for microbiology and virology procedures often cannot be determined before the culture is performed. If a virus other than those specified for this virus-specific culture are recovered, identification will be made, and an additional charge will apply. The client will not be telephoned to approve this charge.
Special Instructions
If reflex testing is performed, concomitant CPT codes/charges will apply.
Submit one specimen per test requested. Specify the exact specimen source/origin (eg, nasopharynx). Indicate a specific test number on the test request form. Do not use transport devices beyond their expiration date.
Expected Turnaround Time
2 - 4 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Information
Related Documents
For more information, please view the literature below.
Comprehensive Influenza Testing
Specimen Requirements
Specimen
Throat or nasopharyngeal (NP) swab or wash, sputum, bronchial washings, bronchoalveolar lavage (BAL)
Container
Viral transport medium for swabs
Collection
Storage Instructions
Specimens should be placed into viral transport medium and kept cold at all times. Do not freeze specimens.
Causes for Rejection
Bacterial swab specimen; specimen received in grossly leaking transport container; dry specimen; specimen submitted in fixative or additive; specimen received in expired transport medium or incorrect transport device; inappropriate specimen transport conditions; specimen received after prolonged delay in transport (usually more than 72 hours); wooden shaft swab in transport device; unlabeled specimen or name discrepancy between specimen and test request label
Test Details
Use
Isolate and identify influenza virus as an etiologic agent in cases of influenza and viral pneumonia
Methodology
Shell vials or equivalent multiwell plate culture with fluorescent antibody staining
Reference Interval
No virus isolated
Viral Culture, Rapid, Respiratory
Synonyms
- Culture, Viral, General
- General Viral Culture
- Routine Viral Culture
- Viral Respiratory Culture
- Virus Culture/Isolation
Test Includes
Shell vials or equivalent multiwell plate cell culture; identification (additional charges/CPT code[s] may apply) by fluorescent antibody or other methods if culture results warrant. CPT coding for microbiology and virology procedures often cannot be determined before the culture is performed. The culture is for the isolation of common respiratory viruses that include adenovirus; influenza A; influenza B; parainfluenza 1, 2, and 3; and respiratory syncytial virus. Other viruses will not be routinely detected; however, if a virus other than those specified for this culture is recovered, identification will be made and an additional charge will apply. The client will not be contacted to approve this charge.
Special Instructions
Submit one specimen per test requested. Specify the exact specimen source/origin (eg, nasopharynx). Indicate a specific test number on the request form. Age of patient, relevant vaccinations, and pertinent clinical history are helpful. Whenever a viral etiology is suspected and whenever appropriate, acute and convalescent serum should be collected for viral serology tests.
Expected Turnaround Time
3 - 5 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Information
Related Documents
For more information, please view the literature below.
Comprehensive Influenza Testing
Specimen Requirements
Specimen
Nasopharyngeal (NP) aspirate or wash, NP swab
Volume
1 mL fluid or one swab in transport
Container
Viral, Chlamydia, or Mycoplasma culture transport provided by LabCorp, or other appropriate transport medium; sterile screw-cap tube or container for nasal washings or bronchoalveolar lavage
Collection
Specimen should be collected during acute phase of disease.
Throat swab: Carefully rub the posterior wall of the nasopharynx with a dry, sterile swab. Avoid touching the tongue or buccal mucosa. Place swab in viral transport tube.
Storage Instructions
Specimen must be kept cold and moist.
Causes for Rejection
Bacterial swab specimen; specimen received in grossly leaking transport container; dry specimen; specimen submitted in fixative or additives; specimen received in expired transport media or incorrect transport device; inappropriate specimen transport conditions; specimen received after prolonged delay in transport (usually more than 72 hours); specimen stored or transported at room temperature; wooden shaft swab in transport device; unlabeled specimen or name discrepancy between specimen and request label
Test Details
Use
Aid in the diagnosis of viral respiratory disease
Methodology
Inoculation of specimen into shell vials or equivalent multiwell plate cell cultures, and identification by DFA or other methods
Reference Interval
No virus isolated
Additional Information
Give date of onset of illness, date of collection, and brief clinical description or the provisional diagnosis.
Virus, Direct Detection DFA, Respiratory Profile With Reflex to Rapid Respiratory Culture
Test Includes
Direct microscopic examination (nonculture) of virus-infected cells for the following viruses: influenza A; influenza B; respiratory syncytial virus (RSV); parainfluenza virus types 1, 2, and 3; adenovirus; and human metapneumovirus (hMPV). Quality of specimen may be evaluated. Negative specimens reflex to rapid respiratory culture.
Special Instructions
This is the same profile as Virus, Direct Detection DFA, Respiratory Profile [186296], except 186304 contains a reflex to Viral Culture, Rapid, Respiratory [186015] when all of the DFA results are negative.
Expected Turnaround Time
5 - 6 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Documents
Specimen Requirements
Specimen
Nasopharyngeal (NP) aspirate or wash, NP swab, nasal swab, bronchoalveolar lavage (BAL)
Volume
One viral transport or 1 mL aspirate/wash
Minimum Volume
One viral transport or 1 mL aspirate/wash
Container
Viral, Chlamydia, or Mycoplasma culture transport (provided by LabCorp) or other appropriate transport medium; sterile screw-cap tube or container for nasal washings or bronchoalveolar lavage
Collection
Specimen should be collected during the acute phase of disease.
Storage Instructions
Refrigerate (2°C to -8°C); stable for 72 hours. Stable frozen at -70°C for >72 hours.
Causes for Rejection
Bacterial swab specimen; specimen received in grossly leaking transport container; dry specimen; specimen submitted in fixative or additive; specimen received in expired transport media or incorrect transport device; inappropriate specimen transport conditions; specimen received after prolonged delay in transport (usually more than 72 hours); specimen stored or transported at room temperature; wooden-shafted swab in transport device; unlabeled specimen or name discrepancy between specimen and test request label
Test Details
Use
Aid in the diagnosis of viral respiratory disease
Limitations
Detection of respiratory viruses will vary greatly depending on the specimen quality and subsequent handling. A negative result does not exclude the possibility of viral infection. Results of the test should be interpreted in conjunction with information available from epidemiological studies, clinical evaluation of the patient, and other diagnostic procedures. Culture should be considered to confirm negative results of this test in a symptomatic patient. The viral antigens detected in some direct specimens may be from nonviable virus. This is particularly true for RSV, which is known for its instability and loss of viability.
Methodology
Direct fluorescent antibody (DFA) with reflex to rapid respiratory culture by inoculation of specimen into shell vials or equivalent multiwell plate cell cultures, and identification by DFA or other methods
Virus, Direct Detection DFA, Varicella Zoster Virus (VZV)
Synonyms
- Direct Detection by DFA, Varicella Zoster Virus
Test Includes
Direct microscopic examination (nonculture) of virus-infected cells. Quality of specimen may be evaluated.
Special Instructions
Submit one specimen per test requested. Specify the exact specimen source/origin (eg, skin lesion). Indicate a specific test number on the request form.
Expected Turnaround Time
1 - 3 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Information
Related Documents
Specimen Requirements
Specimen
Impression smears of tissues, lesion scrapings and swabs, upper respiratory tract swabs
Volume
Two slides per virus
Container
Plain glass slide, no fixative
Collection
Submit two thinly made air-dried slides. Do not use spray fixative.
Storage Instructions
Refrigerate or maintain specimen at room temperature.
Causes for Rejection
Specimen received after prolonged delay in transport (usually more than 72 hours); unlabeled specimen or name discrepancy between specimen and request label; broken or badly scratched slides; fixative used on slides; bacterial swab transport
Test Details
Use
Rapid diagnosis of varicella-zoster virus
Methodology
Direct fluorescent antibody (DFA)
Reference Interval
No virus detected
Viscosity
Synonyms
- Serum Viscosity
Expected Turnaround Time
2 - 5 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Documents
Specimen Requirements
Specimen
Serum
Volume
1 mL
Minimum Volume
0.5 mL
Container
Red-top tube or gel-barrier tube
Storage Instructions
Refrigerate
Stability Requirements
| Temperature | Period |
|---|---|
| Refrigerated | 14 days |
Causes for Rejection
Hemolysis; fibrin clots; quantity not sufficient for analysis
Test Details
Use
Evaluate hyperviscosity syndrome associated with monoclonal gammopathy states (myeloma, macroglobulinemia of Waldenström, and other dysproteinemias), including occasional cases of rheumatoid arthritis, SLE, systemic lupus erythematosus, hyperfibrinogenemia
Limitations
This test was developed, and its performance characteristics determined, by LabCorp. It has not been cleared or approved by the Food and Drug Administration.
Methodology
Viscometry
Reference Interval
1.6−1.9 relative to saline (values >2.7 may indicate paraproteinemia is present)
Additional Information
Hyperviscosity most frequent (33% of cases)1 with IgM monoclonal gammopathy (Waldenström macroglobulinemia); next with IgA myeloma. When IgG myeloma leads to hyperviscosity, IgG levels are usually very significantly elevated. A relative viscosity of 6−7 usually results in symptoms of the hyperviscosity syndrome, they have however been described with lower levels of relative viscosity (ie, 4).2 Neonatal hyperviscosity, usually but not always associated with polycythemia, may be accompanied by a fairly typical clinical picture. Plethora, hypoglycemia, lethargy, and jitteriness/seizures (CNS symptoms) occur. There may be symptoms and findings suggesting congenital heart disease (CHD) (ie, respiratory distress, cardiac enlargement, and cyanosis). False diagnoses of CHD have been made in such cases. About 50% of such infants have modest hyperbilirubinemia (bilirubin >12 mg/dL).
Vitamin A
Synonyms
- A, Vitamin
- Retinol, Serum
Expected Turnaround Time
3 - 5 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Documents
Specimen Requirements
Specimen
Serum
Volume
0.8 mL
Minimum Volume
0.4 mL
Container
Red-top tube or gel-barrier tube
Collection
If a red top is used, transfer separated serum to a plastic transport tube.
Storage Instructions
Room temperature
Stability Requirements
| Temperature | Period |
|---|---|
| Room temperature | 7 days |
| Refrigerated | 14 days |
| Frozen | 14 days |
| Freeze/thaw cycles | Stable x6 |
Patient Preparation
Patient should fast for 12 hours and abstain from alcohol for 24 hours prior to collection. For those who are younger than six months, draw prior to next feeding. Blood should be collected before breakfast in the morning and prior to any medication.
Causes for Rejection
Sample type other than serum received
Test Details
Use
Differential diagnosis of hypervitaminosis A. A combination of a low serum carotene level and a low vitamin A suggests inadequate vitamin A nutrition.
Limitations
This test was developed, and its performance characteristics determined, by LabCorp. It has not been cleared or approved by the US Food and Drug Administration (FDA).
Methodology
Liquid chromatography/tandem mass spectrometry (LC/MS-MS)
Reference Interval
See table.
| Age | Range (μg/dL) |
|---|---|
| 0 to 30 d | Not established |
| 1 m to 5 y | 14.4 − 42.6 |
| 6 to 11 y | 18.2 − 45.7 |
| 12 to 19 y | 18.8 − 54.9 |
| 20 to 39 y | 18.9 – 57.3 |
| 40 to 59 y | 20.1− 62.0 |
| >59 y | 22.0 − 69.5 |
Additional Information
Vitamin A is the name given to a group of biologically active, fat-soluble molecules that includes retinol, retinal and retinoic acid.1,2 These retinoid compounds are derived from the plant precursor molecule, β-carotene. β-carotene (also referred to as provitamin A) has a structure that consists of two molecules of retinal linked at their aldehyde ends.1 β-carotene is converted to vitamin A by intestinal absorptive cells and hepatocytes.1,2 Vitamin A is stored in the liver and transported to extrahepatic tissues bound to retinol binding protein and albumin.1 Both retinol and β-carotene levels are measured in plasma for assessing vitamin A inadequacy and/or toxicity.
Vitamin A exists in humans in several forms and is tightly controlled. Naturally occuring forms of vitamin A include retinol, retinol esters, retinal and retinoic acid. The alcohol form, retinol, predominates in the circulation, but it is too toxic for storage. Instead, the liver stores as retinyl esters - principally palmitate. The active form of vitamin A in the visual cycle is the aldehyde form, retinal. Retinoic acid is the form in tissues responsible for the biological actions of vitamin A in cellular division and differentiation.11
The most important measurand for the estimation of vitamin A status is circulating vitamin A as retinol. Serum retinol levels do not accurately reflect liver retinyl ester levels. Despite this limitation, serum retinol is still useful because the levels will diminish once the supply from the liver is diminished. The serum retinol level at which vitamin A deficiency occurs will coincide with the manifestation of night blindness, due to the interruption of the visual cycle by lack of retinal. Other more serious symptoms will occur later when retinoic acid is depleted by even less available hepatic retinyl esters.12
The body must acquire vitamin A from the diet in order to sustain a number of essential physiological processes.3 These include vision, organogenesis, tissue differentiation, immune function, reproduction, embryonic development and maintenance of healthy skin and barrier functions.3-7 More than five hundred genes are thought to be regulated by vitamin A.3
Vitamin A deficiency only manifests when liver stores are depleted by prolonged reduction of dietary intake.1,10 In healthy individuals, serum retinol concentrations are homeostatically controlled and do not begin to decline until liver reserves of vitamin A are dangerously low.2,4,10 The initial symptom of vitamin A deficiency is an inability to adapt vision to darkness (ie, night blindness).1 Vitamin A is an essential component of rhodopsin, a protein that absorbs light in the retinal receptors.2 Vitamin A also supports the normal differentiation and functioning of the conjunctival membranes and cornea.2 Protracted vitamin A deficiency causes degenerative changes in the retina due to progressive keratinization of the cornea, a condition referred to as xerophthalmia.2 In developing countries, vitamin A deficiency is the most common cause of preventable blindness.
Additional symptoms of vitamin A deficiency include follicular hyperkeratinosis, increased susceptibility to infection and an anemia similar to iron deficient anemia.1 β-carotene is an important, but insufficient, source of vitamin A among poor populations due to the inefficiency of the conversion to retinol.5 Vitamin A deficiency in poor countries is also a significant cause of infection and death, particularly from diarrhea and measles.6
Excessive levels of vitamin A can lead to toxicity. Vitamin A intoxication is a concern in normal adults who ingest more than 15 mg per day and children who ingest more than 6 mg per day of vitamin A for a period of several months. The symptoms of acute vitamin A toxicity include dizziness, nausea, vomiting, headaches, blurred vision, vertigo, reduced muscle coordination, skin exfoliaton.13,14 More chronic vitamin A toxicity symptoms include weight loss, fatigue cheilosis, glossitis, alopecia, bone demineralization, hypercalcemia, lymph node enlargement, hyperlipidemia and amenorrhea. Excess accumulation of vitamin A in the liver can also lead to hepatosplenomegaly, liver fibrosis with portal hypertension.1,13 Congenital malformations, including craniofacial abnormalities and valvular heart disease as well as spontaneous abortions have been reported in children born to pregnant women taking vitamin A in excess. A number of studies have reported an increased risk of lung cancer among high-risk individuals (smokers and asbestos workers) who were given high doses of β-carotene alone or in combination with other antioxidants.5
Toxicity generally results from excessive ingestion of vitamin A supplements but regular intake of large amounts of liver, although usually not a problem in vitamin A-deficient areas, may also result in toxicity due to its high content of vitamin A.15
The World Health Organization recommendations supplementation when vitamin A levels fall below 20.0 ug/dL.16 Severe deficiency is indicated at levels <10.0 ug/dL. 2,9,10
Vitamin A and E
Expected Turnaround Time
4 - 6 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Documents
Specimen Requirements
Specimen
Serum
Volume
0.8 mL
Minimum Volume
0.4 mL
Container
Red-top tube or gel-barrier tube
Collection
If red-top tube is used, transfer separated serum to a plastic transport tube.
Storage Instructions
Room temperature
Stability Requirements
| Temperature | Period |
|---|---|
| Room temperature | 7 days |
| Refrigerated | 14 days |
| Frozen | 14 days |
| Freeze/thaw cycles | Stable x6 |
Patient Preparation
Patient should fast for 12 hours and abstain from alcohol for 24 hours prior to collection. For those who are younger than six months, draw prior to next feeding. Blood should be collected before breakfast in the morning and prior to any medication.
Causes for Rejection
Sample type other than serum received
Test Details
Use
Assess hyper-vitaminosis or vitamin deficiency. See individual test descriptions for more information.
Limitations
These tests were developed, and their performance characteristics determined, by LabCorp. They have not been cleared or approved by the US Food and Drug Administration (FDA).
Methodology
Liquid chromatography/tandem mass spectrometry (LC/MS-MS)
Vitamin B1, Whole Blood
Synonyms
- B1 Vitamin, Whole Blood
- Thiamine, Whole Blood
Expected Turnaround Time
4 - 6 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Documents
Specimen Requirements
Specimen
Whole blood, frozen
Volume
1 mL
Minimum Volume
0.5 mL
Container
Lavender-top (EDTA) tube
Collection
Draw blood. Do not separate. Transfer to a plastic transport tube. Freeze. To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.
Storage Instructions
Freeze
Stability Requirements
| Temperature | Period |
|---|---|
| Frozen | 14 days |
| Freeze/thaw cycles | Stable x6 |
Patient Preparation
Blood samples should be collected before breakfast in the morning and prior to any medication.
Causes for Rejection
Use of anticoagulants other than EDTA
Test Details
Use
For the assessment of thiamine deficiency
Limitations
The biologically active form of the vitamin, thiamine pyrophosphate (TPP), is best measured in whole blood and is not found in measurable concentration in plasma. Plasma thiamine concentration reflects recent intake rather than body stores; therefore, whole blood is the preferred specimen for thiamine assessment.
This test was developed and its performance characteristics determined by LabCorp. It has not been cleared or approved by the Food and Drug Administration.
Methodology
Liquid chromatography/tandem mass spectrometry (LC/MS-MS)
Reference Interval
66.5−200.0 nmol/L
Additional Information
Vitamin B1 refers to a group of compounds that include thiamin and its phosphate esters: thiamine monophosphate (TMP), thiamine pyrophosphate (TPP), and thiamine triphosphate.1-5 All living organisms require thiamine, but it is only synthesized by bacteria, fungi, and plants. Thus, thiamine is an essential nutrient for animals that must obtain it from their diets. The principal biologically active form of thiamine is the pyrophosphate, TPP, which serves as a coenzyme for essential decarboxylation reactions by which carbohydrates, fats, and alcohol are metabolized to produce energy. Thiamine serves a role in the biosynthesis of acetylcholine and gamma-aminobutyric acid (GABA). TPP also facilitates the production of reducing substances involved in oxidant stress defenses, as well as for the synthesis of nucleic acid precursors.5 Thiamine triphosphate serves an important role in the regulation of ion channels of the nervous system.2
Primary thiamine deficiency is most common in underdeveloped countries due to poor oral intake or diets consisting of non-enriched grains.1,5-8 The most common causes of thiamine deficiency in more affluent countries are alcoholism or malnutrition in nonalcoholic patients.5 Secondary thiamine deficiency can occur due to impaired gastrointestinal absorption related to disease or bariatric surgery. Consumption of anti-thiamin enzymes found in raw fish, ferns and betel nuts can reduce the absorption of thiamin.6 A relative thiamine deficiency can also occur in patients receiving enteral or parenteral nutrition therapy, in prolonged diarrheas, and in impaired utilization conditions such as in severe liver disease.5 Conditions that increase metabolic requirements for thiamine such as hyperthyroidism, pregnancy, lactation, and systemic infections with or without fever have been associated with thiamin deficiency. Increased gastrointestinal or renal losses, especially for patients on hemodialysis, can be a risk factor as well as advanced age, diabetes mellitus, AIDS, malignancies and any critical illness.5,7
The earliest symptoms of thiamine deficiency are nonspecific and include fatigue, irritation, poor memory, sleep disturbances, anorexia, abdominal discomfort, and constipation.5 Severe thiamin deficiency is rare and can present as congestive heart failure (wet beriberi), peripheral neuropathy (dry beriberi), Wernicke encephalopathy (WE) and/or Korsakoff syndrome.3-5
Dry beriberi is characterized by central and peripheral neuropathy that can be permanent even following thiamin repletion.3,4 Clinical signs of dry beriberi are bilateral and symmetric, predominantly involving the lower extremities and have been well described in the literature.5 The neurological side effects of thiamin deficiency can progress to Wernicke encephalopathy (WE) and Korsakoff psychosis.3,5,7,9 This diagnosis denotes the acute cerebral manifestation of severe thiamine deficiency that can lead to irreversible memory loss and dementia.5,7,9 Patients with WE present with nystagmus, ophthalmoplegia, mental-status changes, and unsteadiness of stance and gait.9,10 Korsakoff psychosis, an irreversible amnestic confabulatory state, can be the initial presentation in some patients, or it may be a sequel to WE.7 These patients present with clinical manifestations that are highly variable that can include oculomotor abnormalities, gait disturbance, and global confusion with retrograde amnesia, cognitive impairment, and confabulation.3
Wet beriberi refers to a thiamine deficiency condition where impaired cardiac performance leads to systemic symptoms.4,5 In the initial stages of wet beriberi, high cardiac output produces peripheral vasodilation with warm extremities and excessive sweating.5 As the heart starts to fail further symptoms including tachycardia, a wide pulse pressure and lactic acidosis develop, leading to salt and water retention in the kidneys.5 The resulting fluid overload leads to edema of the dependent extremities.5 A more rapidly progressing form of wet beriberi has been referred to as acute fulminant cardiovascular beriberi or Shoshin beriberi, in which vasodilation continues, resulting in shock in a patient with heart failure.5
The signs and symptoms of wet beriberi and similar to those associated with heart failure from other causes. Several studies have shown that the prevalence of thiamine deficiency is increased in heart failure patients relative to the general population.4,7,11-15 It has been postulated that thiamin deficiency may actually exacerbate underlying heart failure symptoms.3,6 Research has shown that correction of thiamin deficiency can improve left ventricular ejection fraction, an indicator of long term prognosis in heart failure patients.3,16-18 Malnutrition, advanced age, frequent hospitalization, and use of diuretic medications have all been shown to increase the risk of thiamin deficiency in patients with HF.4,7
The levels of TPP in plasma or serum are very low relative to the erythrocyte. Plasma contains mainly thiamine and TMP, whereas TPP predominates in erythrocytes.20 TPP accounts for 90% of the thiamine content in whole blood.2 The TPP concentration in erythrocytes correlates with that in whole blood, a characteristic that allows the use of whole blood, rather than washed erythrocytes, for thiamine assessment.2,19,20 Thus, whole blood is the preferred sample type for analysis of thiamine concentration.
Vitamin B12
Synonyms
- Cobalamin, True
Special Instructions
This test may exhibit interference when sample is collected from a person who is consuming a supplement with a high dose of biotin (also termed as vitamin B7 or B8, vitamin H, or coenzyme R). It is recommended to ask all patients who may be indicated for this test about biotin supplementation. Patients should be cautioned to stop biotin consumption at least 72 hours prior to the collection of a sample.
Expected Turnaround Time
Within 1 day
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Information
Related Documents
Specimen Requirements
Specimen
Serum
Volume
0.8 mL
Minimum Volume
0.3 mL (Note: This volume does not allow for repeat testing.)
Container
Red-top tube or gel-barrier tube
Collection
If a red-top tube is used, transfer separated serum to a plastic transport tube.
Storage Instructions
Room temperature
Stability Requirements
| Temperature | Period |
|---|---|
| Room temperature | 7 days |
| Refrigerated | 7 days |
| Frozen | 14 days |
| Freeze/thaw cycles | Stable x3 |
Patient Preparation
Fasting specimen preferred; must draw before Schilling test, transfusions or B12 therapy is started.
Causes for Rejection
Citrate plasma specimen; improper labeling
Test Details
Use
Detect B12 deficiency as in pernicious anemia; diagnose folic acid deficiency; evaluate hypersegmentation of granulocyte nuclei; follow up MCV >100; diagnose macrocytic anemia; diagnose megaloblastic anemia; evaluate alcoholism, prenatal care; evaluate malabsorption, neurological disorders, or the elevation of B12 as seen in liver cell damage or myeloid leukemia
Limitations
As with all tests containing monoclonal mouse antibodies, erroneous findings may be obtained from samples taken from patients who have been treated with monoclonal mouse antibodies or have received them for diagnostic purposes.1 In rare cases, interference due to extremely high titers of antibodies to streptavidin and ruthenium can occur.1 The test contains additives, which minimize these effects.
Methodology
Electrochemiluminescence immunoassay (ECLIA)
Reference Interval
232−1245 pg/mL
Additional Information
Vitamin B12, or cyanocobalamin, is a complex corrinoid compound containing four pyrrole rings that surround a single cobalt atom.2 Humans obtain vitamin B12 exclusively from animal dietary sources, such as meat, eggs, and milk. Vitamin B12 requires intrinsic factor, a protein secreted by the parietal cells in the gastric mucosa, for absorption. Vitamin B12 and intrinsic factor form a complex that attaches to receptors in the ileal mucosa, where proteins known as transcobalamins transport the vitamin B12 from the mucosal cells to the blood and tissue.3,4 Most vitamin B12 is stored in the liver as well as in the bone marrow and other tissues.
Vitamin B12 and folate are critical to normal DNA synthesis, which in turn affects erythrocyte maturation.3,5,6 Vitamin B12 is also necessary for myelin sheath formation and maintenance.7 The body uses its B12 stores very economically, reabsorbing vitamin B12 from the ileum and returning it to the liver so that very little is excreted.4,8
Clinical and laboratory findings for B12 deficiency include neurological abnormalities, decreased serum B12 levels, and increased excretion of methylmalonic acid.4,8,9 The impaired synthesis associated with vitamin B12 deficiency causes macrocytic anemias. These anemias are characterized by abnormal maturation of erythrocyte precursors in the bone marrow, which results in the presence of megaloblasts and in decreased erythrocyte survival.3,10
Pernicious anemia is a macrocytic anemia caused by vitamin B12 deficiency that is due to lack of intrinsic factor.5,6 Low vitamin B12 intake, gastrectomy, diseases of the small intestine, malabsorption, and transcobalamin deficiency can also cause vitamin B12 deficiency.3
Pregnant women need increased amounts of folate for proper fetal development.11 If a woman has a folate deficiency prior to pregnancy, it will be intensified during gestation and may lead to premature birth and neural tube birth defects, such as spina bifida, in the child.11
Vitamin B12 and Folates
Test Includes
Folate; vitamin B12
Special Instructions
This test may exhibit interference when sample is collected from a person who is consuming a supplement with a high dose of biotin (also termed as vitamin B7 or B8, vitamin H, or coenzyme R). It is recommended to ask all patients who may be indicated for this test about biotin supplementation. Patients should be cautioned to stop biotin consumption at least 72 hours prior to the collection of a sample.
Expected Turnaround Time
Within 1 day
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Documents
Specimen Requirements
Specimen
Serum
Volume
1.5 mL
Minimum Volume
0.6 mL (Note: This volume does not allow for repeat testing.)
Container
Red-top tube or gel-barrier tube
Collection
If red-top tube is used, transfer separated serum immediately to a plastic transport tube.
Storage Instructions
Refrigerate
Stability Requirements
| Temperature | Period |
|---|---|
| Room temperature | 1 day |
| Refrigerated | 7 days |
| Frozen | 7 days |
| Freeze/thaw cycles | Stable x3 |
Causes for Rejection
Plasma specimen
Test Details
Methodology
Electrochemiluminescence immunoassay (ECLIA)
Vitamin B12 Deficiency Cascade
Synonyms
- Pernicious Anemia Cascade
Test Includes
Vitamin B12 testing is performed on all samples.
If Vitamin B12 is <200 pg/mL: Intrinsic Factor Blocking Antibodies and Antiparietal Cell Antibody (APCA) will be performed at an additional charge.
If Vitamin B12 is between 200 and 400 pg/mL: Methylmalonic Acid (MMA) will be performed at an additional charge.
If Methylmalonic Acid (MMA) is >378 nmol/L: Intrinsic Factor Blocking Antibodies and Antiparietal Cell Antibody (APCA) will be performed at an additional charge.
Related Information
Related Documents
For more information, please view the literature below.
Vitamin B12 Deficiency Cascade: Understanding Nutritional Deficit
Specimen Requirements
Specimen
Serum
Volume
3 mL
Minimum Volume
2 mL (Note: This volume does not allow for repeat testing).
Container
Red-top tube or gel-barrier tube
Collection
If a red-top tube is used, transfer separated serum to a plastic transport tube.
Storage Instructions
Store specimen at room temperature
Stability Requirements
| Temperature | Period |
|---|---|
| Room temperature | 7 days |
| Refrigerated | 7 days |
| Frozen | 14 days |
| Freeze/thaw cycles | Stable x3 |
Test Details
Use
Diagnosis of Vitamin B12 Deficiency. Although often used as the first-line screening test for B12 deficiency, serum B12 measurement used in isolation has a generally poor sensitivity and specificity for detection of B12 deficiency.1,6,19,32 The National Health and Nutrition Examination Survey (NHANES) opted to use the combination of serum total vitamin B12 and methylmalonic acid (MMA) to monitor B12 status in the United States population.35 In the interest of economy, a number of groups have suggested the use of a sequential selection algorithm for the detection of B12 deficiency.5,14,33,34 In this approach, a second-line assay (in this case MMA) is performed only when the outcome of the first-line assay (vitamin B12 level) falls in an "equivocal" range.1,7 It has been suggested that borderline B12 levels (200-400 ng/L) should be followed up with measuring MMA levels.1 MMA levels below the upper limit of the reference interval (0-378 nmol/L) are strongly suggestive of normal B12 status.
Limitations
Ninety per cent of patients with pernicious anemia have gastric parietal cell antibodies, but specificity of this test is poor since they are also found in 15% of elderly subjects.
If IFA results are negative but suspicion for pernicious anemia remains, an elevated serum gastrin level is consistent with the diagnosis.7
Mutations in the gene encoding intrinsic factor, can also lead to an inherited form of B12 malabsorption and deficiency, which resembles pernicious anemia, but without autoantibody involvement.36
In the presence of discordance between laboratory test result and strong clinical features of B12 deficiency, it remains important to proceed with treatment to avoid neurological impairment.14
MMA can increase (300-700 nmol/L) in renal failure and its refractory to B12 administration.1
Some patients with gastric atrophy and diminished parietal cell function are not positive for IFA or PCA. Diminished acid secretion caused by gastric atrophy regardless of the etiology can cause increased secretion of gastrin. Elevated gastrin levels can support the diagnosis of PA in antibody negative patients.24,29 It is important to diagnose hypergastrinaemia arising from loss gastric parietal cells drives development of antral enterochromaffin cell hyperplasia that can further develop into neoplasia and carcinoid syndrome.1,3,24,30,31
Additional Information
B12 is essential for certain enzymatic reactions that are required for numerous physiologic functions including erythropoiesis and myelin synthesis.1,2 Impaired DNA synthesis caused by B12 deficiency impacts nuclear maturation of rapidly dividing cells. This affects hematopoiesis and results in the presence of immature and ineffective red cells that are larger than normal (megaloblasts) in a context of severe anemia and pancytopenia. This megaloblastic anemia is characterized by the hypersegmented neutrophils that can be seen on peripheral smears and giant bands in bone marrow. Other rapidly dividing cells of the small-bowel epithelium can be affected resulting in malabsorption and diarrhea.3 Glossitis is a frequent hallmark of megaloblastic anemia, with the patient experiencing a painful, smooth, red tongue. Ineffective erythropoiesis and associated increased red cell turnover can result in elevation in bilirubin levels, manifesting as jaundice.3
B12 deficiency can also produce neurological manifestations including sensory and motor disturbances (symmetric paresthesias, numbness and gait problems), ataxia, cognitive decline leading to dementia and psychiatric disorders. These neurological symptoms often predominate and can frequently occur in the absence of hematological complications.3,7 In fact, the majority of patients with suspected B12 deficiency do not have anemia.5-8
Emerging evidence indicates that low (though not necessarily deficient) B12 is associated with increased risk of various chronic diseases of ageing including cognitive dysfunction, cardiovascular disease and osteoporosis.5,6 Dietary vitamin B12 is normally bound to proteins in food and requires release by gastric acid and pepsin in the stomach.7 In the small intestine, vitamin B12 binds to intrinsic factor (IF) produced by gastric parietal cells. In the ileum, the B12-IF complex binds to specific receptors, which facilitates absorption into the blood. Large amounts of absorbed vitamin B12 are stored in the liver such that any reduction in vitamin B12 intake/absorption may take many years to manifest clinically.8 Low B12 status, especially in older adults, is rarely attributable to dietary insufficiency9 and is more typically the result of malabsorption related to atrophic gastritis, inflammatory bowel disease or use of proton pump inhibitors or other gastric acid suppressant drugs.2,6,7,10-13
The diagnosis of vitamin B12 deficiency requires consideration of both the clinical state of the patient and the results of laboratory tests. Screening average-risk adults for vitamin B12 deficiency is not recommended.2 However, testing should be considered in patients with risk factors and/or clinical blood count and serum vitamin B12 level.2,5,7,14,15 The World Health Organization16 and the British Committee for Standards in Haematology14 suggested using 200 pg/mL as a cut-off to define B12 deficiency. In practice, detectable disturbances in metabolic networks consistent with possible deficiency occur at B12 levels as high as 400 pg/mL.17
A significant number of B12-deficient patients may be overlooked when serum B12 measurement is used in isolation.5,17 Further investigation using a second-line test can be useful for serum B12 results that fall within the indeterminate range. The enzyme, methylmalonyl-CoA mutase requires vitamin B12 as a cofactor for the conversion of methylmalonyl-CoA to succinyl-CoA.5 In vitamin B12 depletion, reduced activity of this enzyme leads to an accumulation of methylmalonyl-CoA which is, in turn, hydrolyzed to methylmalonic acid. Measurement of serum methylmalonic acid provides biochemical evidence of metabolic abnormalities consistent with B12 insufficiency.2,5,7,10,14,18,19
In the United States and the United Kingdom, the prevalence of vitamin B12 deficiency has been estimated to be approximately 6% of persons younger than 60 years, and nearly 20% in those older than 60 years.10 B12 status in the United States has been assessed in the National Health and Nutrition Examination Survey (NHANES).20 Using NHANES data from 1999 to 2004, the prevalence of B12 status defined as low was estimated to be 2.9%, 10.6% or 25.7% based on serum B12 cut-off values of 200, 300 and 400 pg/mL, respectively.20 Using these cut-off values, the prevalence of low B12 status increased with age from young adults (19-39 years of age) to older adults (greater than or equal to 60 years of age), and was generally higher in women than than in men (prevalence of 3.3% versus 2.4% with a serum B12 level of <200 pg/mL, respectively).20 Using increased levels of MMA as a functional indicator of B12 status, the prevalence of low B12 status was 2.3% or 5.8% based on cut-off values of >376 and >271 nmol/L, respectively.20 The prevalence of increased levels of MMA increased with age and was not different between men and women.20 Notably, only 50-75% of participants in NHANES with low levels of serum B12 had increased levels of MMA.20 It should also be noted that modest increases occur with renal failure.7
Pernicious Anemia (PA) caused by autoimmune destruction of gastric parietal cells and atrophy of the gastric mucosa is the most common cause of vitamin B12 deficiency.3,6,7,21 Asymptomatic autoimmune gastritis, a chronic inflammatory disease of the gastric mucosa, precedes the onset of mucosal atrophy by 10-20 years.22
With disease progression, an increasing number of the parietal cells that produce hydrochloric acid and intrinisic factor are destroyed.22 This may present initially as iron deficiency anemia due to loss of gastric acid, which is required for iron absorption.1,23 Ultimately, diminished production of intrinsic factor together with development of neutralizing antibody against intrinsic factor itself leads to B12 malabsorption.2,3,10,24 The autoimmune nature of PA is reflected by the presence of autoantibodies against the parietal cell proton pump protein (H/K ATPase) and to intrinsic factor.3,20,24,25 This condition frequently coexists with other autoimmune disorders including Hashimoto's thyroiditis and type 1 diabetes mellitus.3,24,29
Parietal Cell Antibodies (PCA) are present at a high frequency in PA (80%-90%), especially in early stages of the disease and are considered a predictive marker of subsequent gastric mucosa atrophy and its hematologic manifestations.3,24 In the later stages of the disease, the incidence of PCA decreases due to the progression of autoimmune gastritis and a loss of gastric parietal cell mass, as a result of the decrease in antigenic rate.26 PCA can precede the clinical symptoms of the gastric disease by several years.3 PCA are found in 90% of patients with PA, but have low specificity and are seen in various autoimmune disorders.1 Intrinsic Factor Antibodies (IFA) are less sensitive, but are considered highly specific for PA.3 Studies have reported positivity for IFA in 40%-60% of patients with PA, which rises to 60%-80% with increasing duration of disease.3,27 The combined assessment of both PCA and IFA increases diagnostic performance, with 73% sensitivity and 100% specificity.28
Diminished acid secretion caused by gastric atrophy resulting from autoimmune disease or some other etiology elevates secretion of gastrin. Elevated gastrin levels can support the diagnosis of PA.24,29 Hypergastrinaemia arising from loss gastric parietal cells drives development of antral enterochromaffin cell hyperplasia that can further develop into neoplasia and carcinoid syndrome.1,3,24,30,31
Vitamin B6, Plasma
Synonyms
- B6
- B6, Vitamin
- PLP
- Pyridoxal-5-Phosphate
- Pyridoxine
Expected Turnaround Time
4 - 6 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Information
Related Documents
Specimen Requirements
Specimen
Plasma (EDTA), protected from light
Volume
0.5 mL
Minimum Volume
0.25 mL
Container
Lavender-top (EDTA) tube; amber plastic transport tube with amber-top. (If amber tubes are unavailable, cover standard transport tube completely, top and bottom, with aluminum foil. Identify specimen with patient's name directly on the container and on the outside of the aluminum foil. Secure with tape.) For amber plastic transport tube and amber-top, order LabCorp item No. 23594.
Collection
Collect blood by venipuncture into a lavender-top tube containing EDTA and mixed immediately by gentle inversion at least six times to ensure adequate mixing. The specimen must be separated and protected from light in an amber transport tube with amber stopper. Specimens should be stored refrigerated or frozen immediately and maintained at temperature during shipping and at the testing facility. To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.
Storage Instructions
Refrigerate or freeze and protect from light.
Stability Requirements
| Temperature | Period |
|---|---|
| Room temperature | 3 days |
| Refrigerated | 15 days |
| Frozen | 15 days |
| Freeze/thaw cycles | Stable x6 |
Causes for Rejection
Anticoagulants other than EDTA; specimen not protected from light
Test Details
Use
Detect vitamin B6 deficiency
Limitations
This test was developed and its performance characteristics determined by LabCorp. It has not been cleared or approved by the Food and Drug Administration.
Methodology
Liquid chromatography-tandem mass spectrometry (LC/MS-MS)
Reference Interval
Male: 5.3−46.7 μg/L; female: 2.0−32.8 μg/L
Additional Information
Vitamin B6 occurs as an alcohol (pyridoxine), an aldehyde (pyridoxal), and an amine (pyridoxamine). These forms are phosphorylated in the 5'-position to produce the physiologically active coenzymes that are critical to their biological function. Eukaryotes cannot synthesize vitamin B6 molecules from smaller compounds and as a result require dietary B6 for the synthesis of 5'-phosphate vitamins. Pyridoxal 5'Phosphate (PLP), the most clinically significant coenzyme form of vitamin B6, is the form most commonly measured in plasma.1-3
PLP serves as a coenzyme for more than 100 enzymes that catalyze key steps in the metabolism of amino acids, neurotransmitters, nucleic acids, heme, and lipids.1,4,5 Vitamin B6 is a critical cofactor for enzymes involved in energy homeostasis through glycogen degradation and gluconeogenesis.5 Inverse associations have been shown between plasma PLP and chronic or acute disease, including rheumatoid arthritis, cardiovascular disease, deep vein thrombosis, and cancer.4-16 A number of epidemiologic studies have shown reduced concentrations of circulating PLP in association the acute phase marker C-reaction protein13-17 and with inflammatory markers.18-19 Diminished vitamin B6 levels are frequently observed without any indication of a lower dietary intake or excessive catabolism of the vitamin, or congenital defects in its metabolism.4 Research is ongoing to determine if these lower vitamin B6 levels are caused by the mobilization of this coenzyme to the site of inflammation for use by the PLP-dependent enzymes4 or due increased catabolism of vitamin B6 during inflammation.5
PLP serves as a coenzyme for δ-aminolevulinate synthase, which catalyzes the first step in heme biosynthesis.1,5 B6 deficiency can produce a hypochromic form of anemia characterized by the presence of ring sideroblasts (iron positive granules deposited about the nucleus of red cell precursors). Occasionally the anemia may have megaloblastic characteristics. Inherited abnormalities of apoenzymes that bind with pyridoxal phosphate are responsible for newborn conditions characterized by mental retardation, skeletal deformities, thrombotic conditions, osteoporosis, and visual defects. Some inherited abnormalities of vitamin B6 metabolism and transport are associated with aminoacidurias including homocystinuria, hypermethioninemia, cystathioninuria.21 A number of studies have demonstration an inverse association between plasma PLP levels and the risk of developing colorectal cancer.20 A recent meta- analysis indicated that the risk of developing this type of cancer decreased by 49% for every 100-pmol/mL increase in blood PLP level.20
Vitamin B6 deficiency can occur in individuals with a variety of genetic conditions including antiquitin deficiency,21 pyridox(am)ine-5'-phosphate oxidase (PNPO) deficiency22 and hyperprolinemia type II (pyrroline-5- carboxylate dehydrogenase deficiency.23 Vitamin B6 levels can be decreased in malabsorption conditions including inflammatory disease of the small bowel and as a consequence of jejunoileal bypass.4,5 Several drugs, including oral contraceptive agents, levodopa, isoniazid, cycloserine, and pyrazinoic acid may cause B6 depletion.1 B6 levels may be decreased with pregnancy, lactation and alcoholism.1 Infants can develop deficiency when fed formula rendered B6 depleted by excessive heating.
Markedly elevated plasma PLP levels are observed in cases of hypophosphatasia (HPP), an inborn error of metabolism caused by a loss-of-function mutation(s) within the gene for the cell surface enzyme, tissue nonspecific isoenzyme of alkaline phosphatase (TNSALP).24-28 This disorder is characterized by low serum alkaline phosphatase activity and increased plasma levels of TNSALP substrates including inorganic pyrophosphate, phosphatidylethanolamine and PLP. Clinical features can include childhood rickets, adult osteomalacia and dental abnormalities. These symptoms are thought to occur as a result of the accumulation of inorganic pyrophosphate which inhibits hydroxyapatite crystal formation and growth, leading to defective skeletal and dental mineralization. PLP, carried in the plasma on albumin, must be de-phosphorylated by TNSALP for pyridoxal to cross cell membranes. Once inside the cell, the pyridoxal is regenerated as PLP to allow it to function as a coenzyme. The diminished TNSALP of individuals with HPP leads to an accumulation of the PLP substrate in plasma. HPP patients do not typically experience B6 related symptoms. However, the extent of PLP elevation has been related to the disease severity.28
Vitamin C
Synonyms
- Ascorbic Acid
- C, Vitamin
Special Instructions
Order Vitamin C (With Dilution) [123253] if sending specimens from patients on high-dose vitamin C (eg, cancer therapy) in which results are expected to be significantly above the reference interval.
Expected Turnaround Time
3 - 5 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Documents
Specimen Requirements
Specimen
Serum, frozen and protected from light
Volume
1 mL
Minimum Volume
0.5 mL
Container
Red-top tube or gel-barrier tube; amber plastic transport tube with amber top. (If amber tubes are unavailable, cover standard transport tube completely, top and bottom, with aluminum foil. Identify specimen with patient name directly on the container and on the outside of the aluminum foil. Secure with tape.) For amber plastic transport tube and amber-top, order LabCorp N° 23598.
Collection
Draw in chilled tube. Separate serum from cells as soon as possible following collection. Keep specimen on ice. Transfer specimen to a plastic transport tube before freezing. Protect specimen from light. To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.
Storage Instructions
Freeze immediately and protect from light. Stable for five days at -30°C and one month at -70°C. There is a 61% decrease in levels in the first 24 hours following collection if the sample is allowed to remain at room temperature.
Patient Preparation
Overnight fasting is preferred. Refrain from taking vitamin C supplements or fruits 24 hours prior to sample collection.
Causes for Rejection
Specimen not received frozen; specimen not protected from light
Test Details
Use
Evaluation of vitamin C deficiency
Methodology
High-pressure liquid chromatography (HPLC) with electrochemical (EC) detection
Reference Interval
• 0 to 11 months: Not established
• 1 to 12 years: 0.2−2.3 mg/dL
• 13+ years: 0.2−2.0 mg/dL
Additional Information
Serum levels of vitamin C are an adequate measurement of clinical status. Vitamin C is a cofactor for protocollagen hydroxylase; it promotes the conversion of tropocollagen to collagen.1 Low values occur in scurvy, malabsorption, alcoholism, pregnancy, hyperthyroidism, and renal failure. Smokers have lower levels than nonsmokers. Patients with scurvy have values <0.2 mg/dL. Principal clinical findings in scurvy include bleeding gums, petechiae, follicular hyperkeratosis, perifollicular hemorrhages beginning on the lower thighs, muscle aches, easy fatiguability, and emotional changes.
Vitamin D, 25-Hydroxy
Synonyms
- 25-Hydroxycalciferol
- 25-OH-D
- Cholecalciferol Metabolite
- Vitamin D3 Metabolite
Special Instructions
This test is not the same as Calcitriol (1,25 di-OH Vitamin D) [081091] (vitamin D3), which must be ordered separately.
Expected Turnaround Time
Within 1 day
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Documents
For more information, please view the literature below.
Assessing Vitamin D Sufficiency in Your Patients
Vitamin D: What You Need to Know
Specimen Requirements
Specimen
Serum
Volume
0.5 mL
Minimum Volume
0.3 mL (Note: This volume does not allow for repeat testing.)
Container
Red-top tube or gel-barrier tube
Collection
If tube other than a gel-barrier tube is used, transfer separated serum to a plastic transport tube.
Storage Instructions
Refrigerate.
Stability Requirements
| Temperature | Period |
|---|---|
| Room temperature | 7 days |
| Refrigerated | 14 days |
| Frozen | 14 days |
| Freeze/thaw cycles | Stable x3 |
Causes for Rejection
Plasma specimen; gross hemolysis; gross lipemia
Test Details
Use
Rule out vitamin D deficiency
Limitations
Values of vitamin D vary with exposure to sunlight. The assay measures other vitamin D metabolites, including dihydroxylated metabolites such as 24,25, 25,26, and 1,25 dihydroxy vitamin D; however, since the physiological concentrations of these metabolites are insignificant compared to those of 25-hydroxy vitamin D, the accuracy in assessing vitamin D levels is not compromised.
Methodology
Immunochemiluminometric assay (ICMA). This assay is performed on the DiaSorin LIAISON® instrument in multiple laboratories throughout LabCorp. This highly automated test measures both D2 and D3 together and reports a total 25-hydroxy vitamin D. Major clinical studies, including (but not limited to) the Centers for Disease Control (CDC) National Health and Nutrition Examination Survey (NHANES) data base, the Women's Health Initiative (WHI) Studies, and the Harvard-Based Health Professionals Studies, employed DiaSorin reagents.
Reference Interval
30−100 ng/mL
Additional Information
The majority of 25-OH vitamin D (25-D) in the circulation is derived from the conversion of 7-dehydrocholesterol in the skin that is irradiated with ultraviolet radiation in the UVB range (wavelength 290 nm to 315 nm).1-5 The extent of vitamin D formation is not tightly controlled and depends primarily on the duration and intensity of the UV irradiation. Levels produced typically reach a plateau within 30 minutes of exposure. Unfortunately, use of a sunscreen with SPF as low as 15 reduces the rate of vitamin D production by 99.9%. Overproduction of vitamin D in the skin is prevented by the photosensitive conversion of vitamin D to tachysterol or lumisterol. Vitamin D is not very water-soluble, so it must be delivered to and carried in the blood as a complex with vitamin D-binding protein. Once in the circulation, vitamin D is metabolized to 25-hydroxy vitamin D (25-D) by the liver. The 25-D form of the hormone is the principle circulating reservoir in plasma and is generally the best indicator of overall vitamin D status. 25-D is further metabolized by the kidney to produce the biologically active form of vitamin D, 1,25-dihydroxy vitamin D (1,25-D). Renal production of 1,25-D is tightly controlled by parathyroid hormone and is important in the regulation of serum calcium homeostasis.
The hormonally active form of vitamin D,1,25-D plays an integral role in calcium homeostasis and the maintenance of healthy bone.1-4 1,25-D stimulates the absorption of calcium at the level of the intestine and may also serve to increase calcium and phosphate resorption at the kidney level. Vitamin D deficiency leads to the mobilization of calcium from bone. Individuals with more severe vitamin D deficiency can develop osteomalacia and/or osteoporosis. Osteomalacia in children, also referred to as rickets, results in well-described skeletal malformations, since children's bones are actively growing. Recent clinical and epidemiological studies suggest that vitamin D deficiency may play a role in several conditions unrelated to bone, including prostate cancer, breast cancer, colon cancer, heart disease, hypertension, multiple sclerosis, and type 1 diabetes.
A number of studies have shown that vitamin D deficiency is very common, especially in certain high-risk populations.1,2 This situation has occurred, in part, because the foods in the typical American diet are very low in vitamin D. Fatty fish, such as mackerel and salmon, and fish liver oils are some of the few natural dietary sources of vitamin D. Most people do not eat enough of these foods to maintain adequate vitamin D levels. In the United States, vitamin D is added to milk in order to prevent the occurrence of rickets in the pediatric population. Unfortunately, too many children do not drink enough milk to raise their vitamin D levels to the optimum range. Also, recent studies have shown that the level of vitamin D in fortified milk is frequently much lower than that recommended by the FDA. Human milk contains very little vitamin D because many mothers are deficient, so children of mothers who choose to breast-feed are at risk of developing rickets if they are not given supplemental vitamin D. The American Academy of Pediatrics recommends that infants who are exclusively breast-feeding should be given a supplement of vitamin D.
Several factors are associated with an increased risk of developing vitamin D deficiency. At risk populations include:1-5
• Individuals with low dietary vitamin D levels. Infants fed only mother's milk and children who do not drink fortified milk are at risk.
• Individuals with malabsorption syndromes. Patients with pancreatic enzyme deficiency, Crohn's disease, cystic fibrosis, celiac disease, and surgical resection of stomach or intestines are at risk.
• Individuals with severe liver disease. Hepatic disease can reduce the conversion of vitamin D to 25-D and can lead to malabsorption of vitamin D.
• Individuals with kidney disease. Nephrotic syndrome can increase the urinary loss of vitamin D.
• Individuals taking certain drugs. Several medications, including phenytoin, phenobarbital, and rifampin accelerate the breakdown of vitamin D by the liver.
• Individuals who live at higher latitudes. Individuals who live in northern climates are at increased risk of deficiency, especially in winter months due to diminished exposure to UVB radiation.
• Individuals who spend little time outside. Individuals who are homebound or simply choose to remain inside are at increased risk.
• Older adults. The skin becomes less efficient at producing vitamin D as one ages because of diminished levels of vitamin D precursors in the skin.
• Individuals with decreased sun exposure for cultural reasons. Women in some societies are required to cover themselves with heavy clothing, reducing exposure to the sun's rays.
• Races with high melanin levels. Increased skin pigmentation can reduce the efficiency of vitamin D conversion in the skin as much as 50-fold. Individuals with dark complexions living at higher latitudes are at increased risk.
Serum concentrations of 25-D are known to vary with age, sex, race, season, and geographic location. This has led to the establishment of seasonal expected ranges for geographic locations and local populations. This approach provides a “reference interval” but does not adequately determine health status with regard to vitamin D levels if a significant portion of the reference population is, in fact, deficient. A more useful parameter in clinical practice would be a nutritional threshold below which an individual could be characterized as vitamin D-deficient. Vitamin D deficiency has been defined by the Institute of Medicine and an Endocrine Society practice guideline as a level of serum 25-hydroxy vitamin D <20 ng/mL.1,3 The Endocrine Society went on to define vitamin D insufficiency as levels between 21 and 29 ng/mL.3
Vitamin D plays an integral role in calcium homeostasis and the maintenance of healthy bone. Vitamin D stimulates the absorption of calcium at the level of the intestine and may also serve to increase calcium and phosphate resorption at the kidney level. Deficiency of vitamin D leads to the mobilization of calcium from bone, which can lead to osteoporosis, osteomalacia, and rickets.1-3 Numerous recent studies have shown a strong association between diminished vitamin D levels and risk for falls6 and for both vertebral and nonvertebral fractures.7
The World Health Organization's International Agency for Research on Cancer (IARC) has concluded that there is a strong link between an individual's vitamin D levels and the risk of developing colorectal cancer.5 Studies have also revealed that low vitamin D levels are associated with an increased incidence of other malignancies, including breast cancer.8
Many tissues and cells in the body have vitamin D receptors.1-3 It has been estimated that the expression of as much as one third of the human genome is influenced by 1,25-(OH)2 vitamin D. Many studies have demonstrated an association of vitamin D deficiency with increased risk for:
• Autoimmune diseases, including both type 1 and type 2 diabetes, rheumatoid arthritis, Crohn's disease, and multiple sclerosis.
• Infectious diseases and asthma
• Cardiovascular disease and hypertension
There are, however, few randomized, controlled trials with a dosing range adequate to provide strong evidence of the benefit of vitamin D in reducing the risk of these chronic diseases.3
Vitamin E (α and γ Tocopherol)
Synonyms
- Alpha Tocopherol
- Gamma Tocopherol
Expected Turnaround Time
3 - 6 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Documents
Specimen Requirements
Specimen
Serum
Volume
0.8 mL
Minimum Volume
0.4 mL
Container
Red-top tube or gel-barrier tube
Collection
If a red-top tube is used, transfer separated serum to a plastic transport tube.
Storage Instructions
Room temperature
Stability Requirements
| Temperature | Period |
|---|---|
| Room temperature | 14 days |
| Refrigerated | 14 days |
| Frozen | 14 days |
| Freeze/thaw cycles | Stable x6 |
Causes for Rejection
Sample type other than serum received
Test Details
Use
Evaluate vitamin E deficiency in hemolytic disease in premature infants, and neuromuscular disease in infants (and adults) with chronic cholestasis; evaluate patients on long-term parenteral nutrition; patients with malignancy or malabsorption (eg, patients with cystic fibrosis, cases of intestinal bypass surgery); investigate brown-bowel syndrome
Limitations
This test was developed and its performance characteristics determined by LabCorp. It has not been cleared or approved by the Food and Drug Administration.
Methodology
Liquid chromatography/tandem mass spectrometry (LC/MS-MS)
Reference Interval
See table.
| Age | Range (mg/L) |
|---|---|
| Alpha Tocopherol | |
| <6 y | Not established |
| 6 to 11 y | 5.5−13.6 |
| 12 to 19 y | 5.0−13.2 |
| 20 to 39 y | 5.9–19.4 |
| 40 to 59 y | 7.0–25.1 |
| >59 y | 9.0–29.0 |
| Gamma Tocopherol | |
| <6 y | Not established |
| 6 to11 y | 0.7−3.9 |
| 12 to 19 y | 0.8−3.8 |
| 20 to 39 y | 0.7−4.9 |
| 40 to 59 y | 0.5–5.5 |
| >59 y | 0.5–4.9 |
Additional Information
The term vitamin E refers to a class of plant-derived, lipid-soluble compounds which possess a substituted chromanol ring attached to a long phytyl side chain.1-3,12,13 The ring structure is necessary to confer vitamin E activity. The human diet includes eight vitamin E compounds: the α-, β-, γ-, and δ-tocopherals and the α-, β-, γ-, and δ-tocotrienols.1-3,13 Mammals do not interconvert the tocopherol(TC) isoforms.13 γ-TC is found in corn and soybean oil as well as walnuts, pecans, pistachios, and sesame seeds.20 The main sources of β-TC and δ-TC are corn, corn oil, and rapeseed oil. Other good sources of δ-TC are tomato seeds, rice germ, and soybean oil.14 α-TC is found predominantly in peanuts, almonds, and sunflower seeds.
α-TC is the only form of vitamin E that is actively retained by the body.1 The TCs are extremely hydrophobic molecules.3 Consequently, the delivery of α-TC into target tissues and cells requires the presence of a specific enzyme, α-TC transfer protein (α-TTP).3-5 α-TTP also facilitates the intracellular trafficking of α-TC from lysosomes to the plasma membrane and from hepatocytes to circulating lipoproteins.4,13 The critical role of this protein and its ligand are revealed by the debilitating pathologies that characterize individuals with mutations in the α-TTP gene.3,4 Heritable mutations in this protein lead to severe vitamin E deficiency characterized by progressive neurodegeneration, ataxia and eventually death if vitamin E is not provided in large quantities to overcome the lack of α-TTP.2 Due to lack of specific transfer mechanisms, other tocopherols and tocotrienols are not efficiently retained by the liver, and are instead metabolized, and predominantly eliminated.21 As a result, tissue levels of α-TCs are 10-fold higher than the levels of other TCs.4,13
α-TC acts as a lipid-soluble peroxyl radical scavenger that disrupts the chain reaction by which lipid peroxidation propagates.3,6 During lipid oxidation, oxidized tocopheroxyl radicals are produced that can be recycled back to the active, reduced form through reduction by vitamin C.13 This process prevents oxidative damage to long-chain polyunsaturated fatty acids in cell membranes during times of oxidative stress.1,2,3,6 Consequently, vitamin E adequacy is critical for numerous physiologic functions that rely on bilayer integrity such as cell permeability and adhesion.6 α-TC is also thought to play a role in controlling the expression of several genes.7
Symptomatic dietary vitamin E deficiency is rare.3 The main manifestation of deficiency is peripheral neuropathy associated with the degeneration of the large-caliber axons of sensory neurons.10 Clinical features include dysarthria, clumsiness of the hands, loss of proprioception, areflexia, dysdiadochokinesia, decreased visual acuity, and positive Babinski sign. Primary deficiency is seen in cases of the autosomal recessive disorder ataxia due to heritable mutations in α-TTP.3 Primary deficiency is associated by very low plasma vitamin E levels.3 Secondary deficiency occurs in disorders of lipid absorption or lipoprotein metabolism and transport.3 Compromised intestinal fat absorption diseases including cholestatic liver disease, short bowl syndrome, Crohn's disease, and abetalipoproteinemia can cause secondary vitamin E deficiency.3 Cystic fibrosis associated fat malabsorption can also cause deficiency in fat-soluble vitamins, including vitamin E. Diseases caused by molecular defects that affect lipid transport and trafficking, including Niemann-Pick disease-type C and Tangier disease are also associated with vitamin E deficiency. Vitamin E deficiency is also seen in some hematological disorders including, beta-thalassemia major, sickle-cell anemia, and glucose-6-phosphate dehydrogenase deficiency.1
A number of animal studies, observational human studies, and clinical trials have investigated the possibility that vitamin E may have a cardioprotective effect.8 α-TC has been shown to increase oxidative resistance in vitro and to reduce atherosclerotic plaque formation in mouse models. In addition, α-TC inhibits oxidation of low- density lipoprotein cholesterol and modulates expression of proteins involved in the uptake, transport, and degradation of atherogenic lipids.14 Consumption of foods rich in α-TC has been associated with decreased risk of coronary heart disease in middle-aged to older men and women. While some reports have been encouraging, the majority of clinical studies have not demonstrated a benefit of vitamin E supplementation in the primary and secondary prevention of cardiovascular disease.8,14
Animal studies have reported preventive effects of vitamin E on Alzheimer's disease neuropathology.26 A recent study found that α-TC was effective in slowing the functional decline of mild to moderate Alzheimer disease and was also effective in reducing caregiver time in assisting patients.15 However, the therapeutic effect seen was modest and related to disease symptoms and not to the reversal of the disease process.16 Vitamin E isoforms may also have a role in the production and clearance of amyloid beta.23
Until recently, most research on vitamin E has focused on α-TC, because it is the predominant form of vitamin E in tissues and low intake of α-TC is associated with clinical manifestations including peripheral neuropathy and ataxia.14 However, there is accumulating evidence for a role for another member of the vitamin E family, γ-TC in health and disease.14,20 γ-TC is the major form of vitamin E in the corn and soybean oils that are a major staple of the American diet.14 γ-TC is low in other oils such as sunflower and olive oil that are more prevalent in European diets.13,17 The average serum concentrations of α-TC are similar among these populations while serum γ-TC levels in United States are 2- to 6-fold higher than levels in Europeans.13,18 It has been suggested that the conflicting outcomes of a number of vitamin E studies performed in different countries may, in part, reflect differences in the serum levels of γ-TC in foods and supplements administered.14,18
Reactive oxygen species (ROS) are produced as byproducts of the aerobic cellular metabolism and lipid oxidation.14 α- and γ-TC have similar capacity to scavenge these ROS.13,19,20 This process produces oxidized TC radicals that are recycled back to their active, reduced forms via reduction by vitamin C.13 ROS accumulation beyond the body's ability to scavenge them results in "oxidative stress," which has been implicated in the pathophysiology of numerous diseases.14,19,22 Unlike α-TC, γ-TC also reacts with reactive nitrogen species (RNS) that are produced by neutrophilic inflammation.13,18,20 It has been suggested that the γ-TC's ability to scavenge RNS may reduce inflammation.18,19
Recent studies reveal disparate effects from supplementation with α- γ- and TC in clinical studies of asthma and atherosclerosis.13,17,18,20 It has been suggested that excess α-TC taken in supplements causes a reduction of γ-TC concentration in plasma due to more rapid metabolism of γ-TC.24 Reports indicate that allergic inflammation is inhibited by supplementation with α-TC but elevated by supplementation with γ-TC.13 Studies suggest that γ-TC elevates inflammation in experimental asthma and ablates the anti-inflammatory benefit of α-TC treatment.17 A recent clinical study found that α-TC supplementation produced improved spirometric parameters while γ-tocopherol produced a negative effect on spirometric parameters.18 Another recent study revealed a positive association between dietary vitamin E intake and lung function, and evidence of an inverse relationship between serum levels of γ-tocopherol and lung function.25
Volatiles, Urine
Test Includes
Acetone; ethanol; isopropanol; methanol
Expected Turnaround Time
2 - 3 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Specimen Requirements
Specimen
Urine (random)
Volume
5 mL
Minimum Volume
1.1 mL
Container
Plastic transport tube (preferred) or plastic urine container
Storage Instructions
Room temperature
Stability Requirements
| Temperature | Period |
|---|---|
| Room temperature | 14 days |
| Refrigerated | 14 days |
| Frozen | 14 days |
Test Details
Methodology
Gas chromatography (GC)
von Hippel-Lindau Disease (VHL): VHL (NEP) (Known Mutation)
Test Includes
All coding nucleotides of the specified gene(s), plus at least two and typically 20 nucleotides flanking each coding region.
Special Instructions
This option is available when the mutation is known and can be documented by the ordering physician. If the mutation cannot be documented, please order test 252546.
Expected Turnaround Time
28 - 35 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Documents
For more information, please view the literature below.
Consent for Genetic Testing (Consentimiento para análisis genético)
Von Hippel-Lindau Syndrome Genetic Testing
Test Details
Methodology
DNA sequencing
von Hippel-Lindau Disease (VHL): VHL (OPT) (Full Gene Sequencing)
Test Includes
This test covers all coding nucleotides of gene VHL, plus at least two and typically 20 flanking intronic nucleotides upstream and downstream of each coding exon, covering the conserved donor and acceptor splice sites, as well as typically 20 flanking nucleotides in the 5′ and 3′ UTR.
Special Instructions
In cases in which a known mutation can be documented, the physician may prefer to order test 252562.
Expected Turnaround Time
21 - 35 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Documents
For more information, please view the literature below.
Consent for Genetic Testing (Consentimiento para análisis genético)
Von Hippel-Lindau Syndrome Genetic Testing
Specimen Requirements
Specimen
Whole blood; DNA is accepted (Call 800-345-4363 for DNA collection information.)
Volume
2 mL
Container
Lavender-top (EDTA) tube
Collection
Samples may be stored for brief periods at 4°C. Ship overnight at room temperature.
Storage Instructions
Maintain specimen at room temperature.
Causes for Rejection
Container broken or leaking; container not labeled or label not legible; improper anticoagulant
Test Details
Use
Confirm a clinical diagnosis of VHL; identify presymptomatic family members
Limitations
This method does not reliably detect mosaic variants; large deletions; large duplications, inversions, or other rearrangements; or deep intronic variants. It may be affected by allele-dropout, it may not allow determination of the exact numbers of T/A or microsatellite repeats, and it does not allow any conclusion as to whether two heterozygous variants are present on the same or on different chromosome copies.
Results of this test are for investigational purposes only. The performance characteristics of this assay have been determined by LabCorp. The result should not be used as a diagnostic procedure without confirmation of the diagnosis by another medically established diagnostic product or procedure.
Methodology
DNA sequencing
Reference Interval
Normal equals reference sequence or variants that are known or predicted to be benign; abnormal equals all other variants.
Additional Information
von Hippel-Lindau (VHL) disease is a dominantly inherited familial cancer syndrome characterized by multifocal occurrence of retinal, cerebellar, and/or spinal hemangioblastomas, pheochromocytomas, and renal cell carcinomas. In addition, numerous other visceral neoplasms have been observed. VHL is associated with mutations in the gene VHL, and almost all mutation carriers are symptomatic by 65 years of age. Risk of renal cell carcinoma, the major cause of mortality in VHL, is correlated to the type of VHL mutation, with large deletions or truncations conferring a high risk. Genetic testing can confirm a clinical diagnosis of VHL and detect mutation carriers within affected families.
Voriconazole, Serum or Plasma
Synonyms
- UK-109,496
- Vfend®
Expected Turnaround Time
3 - 7 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Documents
Specimen Requirements
Specimen
Serum (preferred) or plasma
Volume
1 mL
Minimum Volume
0.5 mL
Container
Red-top tube or lavender-top (EDTA) tube
Collection
Transfer separated serum or plasma to a plastic transport tube. Do not use a gel barrier tube. The use of gel-barrier tubes is not recommended due to slow absorption of the drug by the gel. Depending on the specimen volume and storage times, the decrease in drug level due to absorption may be clinically significant.
Storage Instructions
Refrigerate. Stable for 14 days at room temperature, refrigerated, or frozen.
Causes for Rejection
Gel-barrier tube
Test Details
Use
Treatment of invasive aspergillosis; treatment of esophageal candidiasis; treatment of candidemia; treatment of candida deep tissue infections; treatment of serious fungal infections caused by Scedosporium apiospermum and fusarium spp in patients intolerant or refractory to other therapy.
Limitations
This test was developed, and its performance characteristics determined, by LabCorp. It has not been cleared or approved by the US Food and Drug Administration (FDA). The FDA has determined that such clearance or approval is not necessary.
Methodology
Liquid chromatography/tandem mass spectrometry (LC/MS-MS)
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COMMON LAB TESTS
Complete Blood Count
This test, also known as a CBC, is the most common blood test performed. It measures the types and numbers of cells in the blood, including red and white blood cells and platelets. This test is used to determine general health status, screen for disorders and evaluate nutritional status. It can help evaluate symptoms such as weakness, fatigue and bruising, and can help diagnose conditions such as anemia, leukemia, malaria and infection.
Prothrombin Time
Also known as PT and Pro Time, this test measures how long it takes blood to clot. This coagulation test measures the presence and activity of five different blood clotting factors. This test can screen for bleeding abnormalities, and may also be used to monitor medication treatments that prevent the formation of blood clots.
Basic Metabolic Panel
This test measures glucose, sodium, potassium, calcium, chloride, carbon dioxide, blood urea nitrogen and creatinine which can help determine blood sugar level, electrolyte and fluid balance as well as kidney function. The Basic Metabolic Panel can help your doctor monitor the effects of medications you are taking, such as high blood pressure medicines, can help diagnose certain conditions, or can be part of a routine health screening. You may need to fast for up to 12 hours before this test.
Comprehensive Metabolic Panel
This test combines the Basic Metabolic Panel with six more tests for a more comprehensive evaluation of metabolic functions, with a focus on organ systems.
Lipid Panel
The lipid panel is a group of tests used to evaluate cardiac risk. It includes cholesterol and triglyceride levels.
Liver Panel
The liver panel is a combination of tests used to assess liver function and establish the possible presence of liver tumors.
Thyroid Stimulating Hormone
This test screens and monitors the function of the thyroid.
Hemoglobin A1C
This test is used to diagnose and monitor diabetes.
Urinalysis
Often the first lab test performed, this is a general screening test used to check for early signs of disease. It may also be used to monitor diabetes or kidney disease.
Cultures
Cultures are used to test for diagnosis and treatment of infections. Illnesses such as urinary tract infections, pneumonia, strep throat, MRSA and meningitis can be detected and tested for appropriate antibiotic treatment.