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There are currently 27 names in this directory beginning with the letter F.
Factor V Activity
Synonyms Proaccelerin Special Instructions If the patient's hematocrit exceeds 55%, the volume of citrate in the collection tube must be adjusted. Refer to Coagulation Collection Procedures for directions. 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. Related Information Abnormal Screening Results Related Documents For more information, please view the literature below. Procedures for Hemostasis and Thrombosis: A Clinical Test Compendium Sample Report Specimen Requirements Specimen Plasma, frozen Volume 1 mL Container Blue-top (sodium citrate) tube Collection Blood should be collected in a blue-top tube containing 3.2% buffered sodium citrate.1 Evacuated collection tubes must be filled to completion to ensure a proper blood-to-anticoagulant ratio.2,3 The sample should be mixed immediately by gentle inversion at least six times to ensure adequate mixing of the anticoagulant with the blood. A discard tube is not required prior to collection of coagulation samples unless the sample is collected using a winged (butterfly) collection system. With a winged blood collection set a discard tube should be drawn first to account for the dead space of the tubing and prevent under-filling of the evacuated tube.4,5 When noncitrate tubes are collected for other tests, collect sterile and nonadditive (red-top) tubes prior to citrate (blue-top) tubes. Any tube containing an alternative anticoagulant should be collected after the blue-top tube. Gel-barrier tubes and serum tubes with clot initiators should also be collected after the citrate tubes. Please print and use the Volume Guide for Coagulation Testing to ensure proper draw volume. Storage Instructions Freeze. Patient Preparation Ideally the patient should not be on anticoagulant therapy. Avoid warfarin (Coumadin®) therapy for two weeks prior to the test and heparin, direct Xa, and thrombin inhibitor therapies for about three days prior to testing. Do not draw from an arm with a heparin lock or heparinized catheter. Causes for Rejection Severe hemolysis; improper labeling; clotted specimen; specimen diluted with IV fluids; samples thawed in transit; improper sample type; sample out of stability Test Details Use Evaluate an isolated prolonged PT or for evaluation when both the aPTT and PT are prolonged and to assess factor V activity level.6-8 Limitations This test is not used for the diagnosis of factor V Leiden mutation. Direct Xa or thrombin inhibitor therapy may cause factitiously low results. Methodology Factor V activity is determined utilizing a prothrombin time (PT)-based one-stage clotting time assay. Factor V-depleted plasma is used as the substrate, and the clotting time with the patient plasma is compared to the clotting time of normal pooled plasma. Additional Information Factor V is a large (330 kilodalton) single-chain nonenzymatic cofactor that is synthesized in hepatocytes, megakaryocytes, and endothelial cells.6,7,9 Approximately 20% of the total factor V is carried in the α granules of platelets and is released when platelets are activated.6 The structure of factor V is similar to that of factor VIII.9 Factor V's plasma concentration is 7 mg/mL and half-life is about 15 to 36 hours. Factor V activation occurs by both the extrinsic and intrinsic pathways. Factor V deficiency should be considered when a patient with bleeding history has both extended protime (PT) and activated partial thromboplastin time (aPTT). Congenital factor V deficiency, sometimes referred to as parahemophilia, is rare (less than one case per million individuals) and is inherited as an autosomal recessive trait.6,7,9 This condition affects both males and females and the prevalence of inherited factor V deficiency is equal in all ethnic groups.9 Factor V levels are decreased both in plasma and platelets.6 A syndrome of combined factor V and VIII deficiencies has been described in over 60 families in and around the Mediterranean basin.8 Symptoms (homozygotes) can include hematoma formation, postsurgical and postpartum hemorrhage, menorrhagia, hematuria, and umbilical cord hemorrhage.6,9 Factor V plasma activity <30% may result in excessive bleeding following a traumatic event.9 Unlike individuals with severe hemophilia, patients with factor V levels <1% do not typically develop spontaneous joint hemarthroses.6 Diminished factor V levels can be seen in liver disease, disseminated intravascular coagulation (DIC) syndromes, and in other consumption coagulopathies.9,10 Specific factor V inhibitors can occur, especially after surgical procedures that involve multiple exposures to bovine topical thrombin.9 Postoperative treatment with aminoglycosides and penicillin has also been associated with development of factor V inhibitors.6,7 Inhibitors do not typically develop in individuals with factor V deficiency.6 One study found that elevated factor V activity may be associated with increased risk for myocardial infarction;11 however, a recent consensus conference of the College of American Pathologists on diagnostic issues in thrombophilia did not recommend measurement of factor V levels for the assessment of thrombotic risk.10
Factor V Leiden Mutation Analysis
Synonyms Factor V Leiden DNA Test Expected Turnaround Time 5 - 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 Information Activated Protein C Resistance (APCR) Factor II (Prothrombin), DNA Analysis Methylenetetrahydrofolate Reductase (MTHFR) Thermolabile Variant, DNA Analysis Thrombotic Risk Profile, DNA Analysis Related Documents For more information, please view the literature below. Procedures for Hemostasis and Thrombosis: A Clinical Test Compendium Sample Report Specimen Requirements Specimen Whole blood or LabCorp buccal swab kit (buccal swab collection kit contains instructions for use of a buccal swab) Volume 7 mL whole blood or LabCorp buccal swab kit Minimum Volume 3 mL whole blood or two buccal swabs Container Lavender-top (EDTA) tube, yellow-top (ACD) tube, or LabCorp buccal swab kit Storage Instructions Maintain specimen at room temperature. Causes for Rejection Frozen specimen; hemolysis; quantity not sufficient for analysis; improper container; one buccal swab; wet buccal swab Test Details Use Detection of Leiden (R506Q) mutation in factor V gene (OMIM 227400) associated with increased risk of thrombosis Limitations This test detects the factor V R506Q (Leiden) mutation and will help identify those individuals who are at increased risk of thrombosis; however, increased risk of thrombosis can be caused by a variety of genetic and nongenetic factors not screened for by this assay. 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 Allele-specific polymerase chain reaction (PCR) Additional Information Details of how the blood coagulation system is regulated have become well understood in recent years. Many of the abnormalities that cause some patients to have an increased risk for thrombosis have been defined at the molecular level. The poor anticoagulant response to activated protein C (APC), or APC resistance, that is found in up to 50% of patients with a family history of thrombosis, and in 3% to 8% of apparently normal individuals, was shown to correlate with the inheritance of a single-point mutation in the factor V gene. This mutation has been reported in patients with deep vein thrombosis, pulmonary embolus, central retinal vein occlusion, cerebral sinus thrombosis, and hepatic vein thrombosis. Ten percent to 20% of people with a first-time venous clot have this mutation. Strikingly, 40% of people younger than 50 with a first-time venous clot, and 60% of pregnant women with venous thrombosis have this mutation as well. Beyond the risk for thrombophilia, this mutation has also been associated with an increased risk for recurrent pregnancy loss, severe preëclampsia, fetal growth retardation, stillbirth, and placental problems (infarction and abruption). The mutation is characterized by a guanine to adenine substitution at nucleotide 1691 in exon 10 of the factor V gene that replaces an arginine at codon 506 with a glutamine. It is designated as FV R506Q (Leiden), and confers resistance to inactivation by activated protein C. As a result, factor V persists in the circulation, leading to a mild hypercoagulable state. The Leiden mutation accounts for 90% to 95% of APC resistance. Heterozygous carriers of this mutation have a four- to eightfold increased risk of thrombosis. Individuals homozygous for the mutation (ie, they have a copy of the mutation on each chromosome) carry an 80- to 100-fold risk of thrombosis. All offspring of a factor V Leiden homozygote will inherit at least a single copy of the mutation. Genetic counseling is recommended for these patients. The risk of venous thrombosis increases exponentially in patients with more than one risk factor, including age, surgery, oral contraceptive use, pregnancy, elevated homocysteine levels, or malignancy. A 2005 study reports malignancy carries a sevenfold increased risk for thrombosis, and that this effect is most pronounced for hematological malignancies, for recently diagnosed cancers, and/or for patients with distant metastases. Malignancy and genetic predisposition together may compound risk, as carriers of the factor V Leiden mutation who have cancer are more likely to develop thrombosis than mutation carriers without cancer. Other risk factors to be considered in the work-up for venous thrombosis include the G20210A mutation in the factor II (prothrombin) gene, mutations in the MTHFR gene, protein S and C deficiency, and antithrombin deficiencies. Anticardiolipin antibody and lupus anticoagulant analysis may be appropriate for certain patients, as well as homocysteine levels. Genetic counselors are available for health care providers to discuss results, and for information on how to order additional testing, if desired, at 800-345-4363.
Factor VIII Activity
Synonyms Antihemophilic Factor (AHF) Special Instructions If the patient's hematocrit exceeds 55%, the volume of citrate in the collection tube must be adjusted. Refer to Coagulation Collection Procedures for directions. 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. Related Information Abnormal Screening Results Collagen-binding Activity (CBA) Profile von Willebrand Factor (vWF) Profile Related Documents For more information, please view the literature below. Procedures for Hemostasis and Thrombosis: A Clinical Test Compendium Sample Report Specimen Requirements Specimen Plasma, frozen Volume 1 mL Container Blue-top (sodium citrate) tube Collection Blood should be collected in a blue-top tube containing 3.2% buffered sodium citrate.1 Evacuated collection tubes must be filled to completion to ensure a proper blood-to-anticoagulant ratio.2,3 The sample should be mixed immediately by gentle inversion at least six times to ensure adequate mixing of the anticoagulant with the blood. A discard tube is not required prior to collection of coagulation samples unless the sample is collected using a winged (butterfly) collection system. With a winged blood collection set a discard tube should be drawn first to account for the dead space of the tubing and prevent under-filling of the evacuated tube.4,5 When noncitrate tubes are collected for other tests, collect sterile and nonadditive (red-top) tubes prior to citrate (blue-top) tubes. Any tube containing an alternative anticoagulant should be collected after the blue-top tube. Gel-barrier tubes and serum tubes with clot initiators should also be collected after the citrate tubes. Please print and use the Volume Guide for Coagulation Testing to ensure proper draw volume. Storage Instructions Freeze. Patient Preparation Ideally the patient should not be on anticoagulant therapy. Avoid warfarin (Coumadin®) therapy for two weeks prior to the test and heparin, direct Xa, and thrombin inhibitor therapies for about three days prior to testing. Do not draw from an arm with a heparin lock or heparinized catheter. Causes for Rejection Severe hemolysis; improper labeling; clotted specimen; specimen diluted with IV fluids; samples thawed in transit; improper sample type; sample out of stability. Test Details Use Used in the evaluation of an isolated prolonged aPTT. Diagnosis of hemophilia A and as an aid in the diagnosis of von Willebrand factor (vWF) deficiency6-9 Limitations Factor VIII is an acute phase reactant and can be elevated in a number of clinical conditions. This can affect the accuracy of the test in diagnosing hemophilia. Factor VIII levels should not be used to determine the carrier status of females. Genetic testing should be used for this purpose. Factor VIII inhibitors (both autoantibodies that develop after replacement therapy and autoantibodies that develop spontaneously) can result in low factor VIII levels. A lupus anticoagulant may cause factor VIII activity to appear spuriously low and a chromogenic factor VIII activity is recommended in this circumstance. Direct Xa or thrombin inhibitor therapy may cause factitiously low results. Methodology Factor VIII activity is determined utilizing an aPTT-based one-stage clotting time assay. Factor VIII-depleted plasma is used as the substrate and the clotting time with the patient plasma is compared to the clotting time of normal pooled plasma. Reference Interval 56% to 140% Additional Information Factor VIII is a large glycoprotein cofactor (320 kilodaltons) that is produced mainly in hepatocytes, but also to some extent by liver macrophages, megakaryocytes, and endothelial cells.6,10 Factor VIII circulates in the plasma bound to von Willebrand factor (vWF) at a concentration of approximately 0.1 mg/mL.10 The plasma half-life of factor VIII is short at about 8 to 10 hours.10 Factor VIII deficiency should be suspected when a patient with excessive bleeding has a normal protime (PT) and an extended activated partial thromboplastin time (aPTT). Hemophilia A, or classic hemophilia, occurs as the result of congenital deficiency of factor VIII.6,11 Clinical features of hemophilia A are the same as for hemophilia B which is caused by factor IX deficiency (see Factor IX Activity [086298]). Hemophilia A is the second most common inherited bleeding abnormality (second only to von Willebrand disease), occurring in approximately 1 of every 5000 live male births.6,11 Hemophilia A accounts for approximately 85% of all hemophilia cases.11 This condition is transmitted as an X chromosome-linked hereditary disorder.11 The majority of cases occur in men whose mothers are carriers of the genetic defect. About 30% of factor VIII deficiencies arise in men as spontaneous mutations.6,11 The prevalence of hemophilia A is equal in all ethnic groups.6,11 Female carriers of hemophilia A may rarely present with excessive bleeding.6 Hemophilia symptoms can also occur in female carriers who have a high degree of lyonization of the factor VIII alleles.11 Females with Turner syndrome karyotype XO, can also be symptomatic.11 The severity of hemophilia A can be defined by the level of factor VIII activity.7,11 Severe hemophilia, which represents approximately half the cases, is associated with a factor VIII level 5%. Approximately 45% of cases of severe hemophilia A occur as the result of a genetic inversion of intron 22 of the factor VIII gene locus.7,11,12 This genetic mutation results in the production of a protein that has no functional or immunologic factor VIII activity.11 Numerous deletions, point mutations, and missense mutations have also been implicated in hemophilia A.7,11 Family studies combined with genetic testing can determine if at-risk women are carriers for a hemophilia A mutation.11 Factor VIII activity levels should not be used as the method of determining carrier status because a number of clinical conditions including pregnancy, infection, or inflammation can affect activity levels.11 Patients with hemophilia A can present with any number of bleeding manifestations.6,11 Often, infants with severe hemophilia are first diagnosed during the neonatal period because of excessive bleeding after circumcision or due to cord necrosis.11 Hemophilic infants also frequently suffer from intracranial hemorrhage or scalp hematomas. Spontaneous hemarthroses, a common symptom of hemophilias, typically do not occur until the child starts walking.7,11 Hematomas can often be observed at the sites of intramuscular injections for vaccination or medication. The most common sites of spontaneous bleeding in patients with severe hemophilia involve the joints and muscles. Recurrent bleeding leads to chronic muscle injury and degeneration of the joint tissue.6,11 Gastrointestinal bleeding can occur in approximately 10% of hemophiliacs.11 Males with mild-to-moderate hemophilia and female carries may have an increased bleeding tendency, especially following surgery or trauma.7 Most individuals with von Willebrand disease will have decreased factor VIII levels because the von Willebrand factor (vWF) is the carrier protein for factor VIII in plasma.6,11 Individuals with von Willebrand disease type 2 Normandy will have normal to slightly low vWF ristocetin cofactor activity and von Willebrand factor antigen and low factor VIII levels due to defective binding of factor VIII to the variant vWF molecule.11 Factor VIII levels are elevated at birth and increase during pregnancy.6 Factor VIII is an acute phase reactant with levels that rise during periods of acute stress, following surgery, and in inflammatory conditions.6 Levels can also increase as the result of strenuous exercise or the administration of several drugs including epinephrine, DDAVP, or estrogen (for birth control or hormone replacement therapy). Factor VIII levels can be elevated in a number of clinical conditions including carcinoma, leukemia, liver disease, renal disease, hemolytic anemia, diabetes mellitus, deep vein thrombosis, and myocardial infarction.6 Persistent elevation of factor VIII above 150% is associated with an increased risk for venous thrombosis of more than fivefold.10,13 Elevated factor VIII is also associated with an increased risk for recurrence of venous thromboembolism. Risk is graded such that the higher the factor VIII activity, the higher the risk.14 The basis for this increased risk is not well understood as genetic studies of the factor VIII and von Willebrand factor genes failed to identify a genetic basis for this increased risk.10 Values >150% are observed in 20% to 25% of individuals with venous thrombosis or thromboembolism in the absence of other known causes of factor VIII elevation.13 A syndrome of combined factor VIII and V deficiencies has been described in over 60 families in and around the Mediterranean basin.15 Hemophilia A patients receiving replacement products can develop inhibitors to factor VIII due to the production of alloantibodies.6,8 Acquired hemophilia caused by the development of autoantibodies to factor VIII can also occur.9 This rare condition (1 in 1,000,000 individuals) can following pregnancy and in elderly individual with autoimmune disorders. In this life-threatening condition, patients have bleeding symptoms similar to those seen in severe congenital hemophilia A.
Factor X Activity
Synonyms Stuart Prower Factor Special Instructions If the patient's hematocrit exceeds 55%, the volume of citrate in the collection tube must be adjusted. Refer to Coagulation Collection Procedures for directions. 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. Related Information Abnormal Screening Results Factor X, Chromogenic Related Documents For more information, please view the literature below. Procedures for Hemostasis and Thrombosis: A Clinical Test Compendium Sample Report Specimen Requirements Specimen Plasma, frozen Volume 1 mL Container Blue-top (sodium citrate) tube Collection Blood should be collected in a blue-top tube containing 3.2% buffered sodium citrate.1 Evacuated collection tubes must be filled to completion to ensure a proper blood-to-anticoagulant ratio.2,3 The sample should be mixed immediately by gentle inversion at least six times to ensure adequate mixing of the anticoagulant with the blood. A discard tube is not required prior to collection of coagulation samples unless the sample is collected using a winged (butterfly) collection system. With a winged blood collection set a discard tube should be drawn first to account for the dead space of the tubing and prevent under-filling of the evacuated tube.4,5 When noncitrate tubes are collected for other tests, collect sterile and nonadditive (red-top) tubes prior to citrate (blue-top) tubes. Any tube containing an alternative anticoagulant should be collected after the blue-top tube. Gel-barrier tubes and serum tubes with clot initiators should also be collected after the citrate tubes. Please print and use the Volume Guide for Coagulation Testing to ensure proper draw volume. Storage Instructions Freeze. Patient Preparation Ideally, the patient should not be on anticoagulant therapy. Avoid warfarin (Coumadin®) therapy for two weeks prior to the test and heparin, direct Xa, and thrombin inhibitor therapies for about three days prior to testing. Causes for Rejection Severe hemolysis; improper labeling; clotted specimen; specimen diluted with IV fluids; samples thawed in transit; improper sample type; sample out of stability Test Details Use Evaluate an isolated, prolonged PT, evaluate prolongation of both the aPTT and PT, and to document factor X deficiency6-8 Limitations Direct Xa or thrombin inhibitor therapy may cause factitiously low results. Methodology Factor X activity is determined using an aPTT-based one-stage clotting time assay. Factor X-depleted plasma is used as the substrate, and the clotting time with the patient plasma is compared to the clotting time of normal pooled plasma. Additional Information To evaluate an isolated prolonged PT or to evaluate prolongation of both the APTT and PT and to document factor X deficiency.6-8 Factor X is a 54.8 kilodalton vitamin K-dependent glycoprotein coagulation factor that is produced by the liver.6 Normal factor X's plasma concentration is approximately 10 mg/mL and half-life is about 40 hours.6 Factor X activation occurs by both the extrinsic and intrinsic pathways. Factor X deficiency should be considered when a patient with bleeding history has both extended protime (PT) and activated partial thromboplastin time (aPTT). The dilute Russell viper venom (dRVVT) measures the activation of factor X and will be prolonged in patients with deficiency.7,8 Congenital factor X deficiency is rare and is inherited as an autosomal recessive trait.6 This condition affects both males and females.6 A few cases of combined congenital factor II, VII, IX, and X factor deficiencies have been reported.6 Acquired deficiencies occur with significant hepatic dysfunction, with vitamin K antagonist (warfarin) therapy, and in individuals with vitamin K deficiency.6,7 Factor X deficiency may be associated with primary systemic amyloidosis.6,8 Isolated factor X deficiency may also occur in patients with respiratory infections, acute myeloid leukemia, amyloidosis, and with other malignancies.7 Acquired specific factor X inhibitors are rare in patients without congenital deficiency.6,7 Symptoms (homozygotes) include hematoma formation, postsurgical hemorrhage, menorrhagia, hematuria, and umbilical cord hemorrhage.6,7 Factor X plasma activity <30% may result in excessive bleeding following a traumatic event.6 Spontaneous bleeding similar to that observed in severe hemophilia may occur when the activity is <1%.6,7
Factor X Antigen
Expected Turnaround Time 4 - 8 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. Procedures for Hemostasis and Thrombosis: A Clinical Test Compendium Sample Report Specimen Requirements Specimen Plasma, frozen Volume 2 mL Minimum Volume 1 mL Container Blue-top (sodium citrate) tube Collection Citrated plasma samples should be collected by double centrifugation. Blood should be collected in a blue-top tube containing 3.2% buffered sodium citrate.1 Evacuated collection tubes must be filled to completion to ensure a proper blood to anticoagulant ratio.2,3 The sample should be mixed immediately by gentle inversion at least six times to ensure adequate mixing of the anticoagulant with the blood. A discard tube is not required prior to collection of coagulation samples, except when using a winged blood collection device (ie, "butterfly"), in which case a discard tube should be used.4,5 When noncitrate tubes are collected for other tests, collect sterile and nonadditive (red-top) tubes prior to citrate (blue-top) tubes. Any tube containing an alternate anticoagulant should be collected after the blue-top tube. Gel-barrier tubes and serum tubes with clot initiators should also be collected after the citrate tubes. Centrifuge for 10 minutes and carefully remove 2/3 of the plasma using a plastic transfer pipette, being careful not to disturb the cells. Deliver to a plastic transport tube, cap, and recentrifuge for 10 minutes. Use a second plastic pipette to remove the plasma, staying clear of the platelets at the bottom of the tube. Transfer the plasma into a LabCorp PP transpak frozen purple tube with screw cap (LabCorp No. 49482). Freeze immediately and maintain frozen until tested. Please print and use the Volume Guide for Coagulation Testing to ensure proper draw volume. Storage Instructions Freeze. Stable at room temperature for eight hours. Test Details Use Measurement of factor X antigen concentration Limitations This procedure may be considered by Medicare and other carriers as investigational and, therefore, may not be payable as a covered benefit for patients. Methodology Enzyme-linked immunosorbent assay (ELISA)
Familial Hypercholesterolemia (FH) Screen
Synonyms FH Screen LDL and Non-HDLC FH Screen Test Includes Cholesterol, total; high-density lipoprotein (HDL) cholesterol; non-HDL cholesterol (calculation); LDL cholesterol direct 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. Spanning the Continuum of Cardiovascular Care Familial Hypercholesterolemia LABupdate Sample Report Specimen Requirements Specimen Serum Volume 2 mL Minimum Volume 1 mL (Note: This volume does not allow for repeat testing.) Container Red-top tube or gel-barrier tube Collection Separate serum from cells within 45 minutes of venipuncture. Lipid profiles are best avoided following acute myocardial infarction, for up to three months, although cholesterol can be in the first 24 hours. Storage Instructions Maintain specimen at room temperature. Patient Preparation Patient should be on a stable diet, ideally for two to three weeks prior to collection of blood, and should fast for 12 to 14 hours prior to the blood draw. Causes for Rejection Improperly labeled specimen Test Details Use The 2011 clinical guidance from the National Lipid Association Expert Panel1 recommends universal screening of children age 9 to 11 years and adults with a fasting lipid profile that include LDL cholesterol and/or non-HDL cholesterol for identification of patients at risk of familial hypercholesterolemia (FH). Cholesterol screening should be considered beginning at age two for children with a family history of premature cardiovascular disease or elevated cholesterol. All individuals should be screened by age 20. For all patients with LDL-C and/or non-HDL-C levels listed in the table above, a family history of high cholesterol and heart disease in first-degree relatives should be collected. The likelihood of FH is higher in individuals with a positive family history of hypercholesterolemia or of premature CHD (onset in men before age 55 years and women before age 65 years). Cascade screening of all first-degree relatives for lipid levels is considered the most cost-effective lifesaving procedure. Genetic screening for FH-associated mutations in LDL receptor, Apo B, and proprotein convertase subtilisin/kexin type 9 (PCSK9) genes may be useful when the diagnosis is uncertain. The prevalence of FH in general population is reported to be 1 in 300 to 500 making FH among one of the most common serious genetic disorders. Some populations, such as French Canadian and Dutch Afrikaner, have a prevalence as high as 1 in 100. Methodology See individual tests. Reference Interval See table. Interpretation Age (y) LDL-C (mg/dL) Non-HDL-C (mg/dL) FH should be suspected if at age: >19 >189 >219 159 >189 FH should be strongly suspected (with approximate probability of 80%) if at age: >29 >249 NA 20−29 >219 NA 189 NA
Fecal Fat, Qualitative
Synonyms Fatty Acid, Stool Neutral Fat, Stool Qualitative Fat Test Includes Neutral and total fats Expected Turnaround Time 2 - 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 Special Chemistry Related Documents Sample Report Specimen Requirements Specimen Stool (fresh random) Volume Approximately 3 g Minimum Volume 0.5 g Container Plastic screw-cap vial Collection Do not contaminate outside of container; do not overfill container. Storage Instructions Refrigerate at 2°C to 8°C. Stability Requirements Temperature Period Room temperature 14 days Refrigerated 14 days Frozen 14 days Freeze/thaw cycles Stable x3 Patient Preparation Patient should be on a diet containing at least 60 g of fat. The patient should not use suppositories or mineral oil before the specimen is collected. Oily material (eg, creams, lubricants, etc) should be avoided prior to collection of the specimen. Causes for Rejection Specimen contaminated with urine and/or water; specimen on outside of container; specimen containing interfering substances (eg, castor oil, bismuth, Metamucil®, barium) Test Details Use Detect the presence of fecal fatty acids and neutral fat. Increases in neutral fat are commonly associated with pancreatic exocrine insufficiency. Increase in stool total fats (neutral fats, soaps, and fatty acids) is likely to be associated with small bowel disease. 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 Microscopic examination following staining with Oil Red O Contraindications Administration of barium, bismuth, Metamucil®, castor oil, mineral oil, or ingestion of oily salad dressing within one week prior to collection of the specimen Reference Interval • Total fats (neutral fats, soaps, and fatty acids): Normal (<100 droplets/hpf) • Neutral fats: Normal (<60 droplets/hpf)
Fentanyl and Analogues, Urine
Synonyms China White Test Includes Acetyl fentanyl; acetyl norfentanyl; alfentanil; fentanyl; norfentanyl; sufentanil; norsufentanil Expected Turnaround Time 7 - 10 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 2 mL Container Plastic urine container without preservative Storage Instructions Submission/transport (<3 days): Room temperature. For storage beyond three days, specimen should be refrigerated or frozen. Causes for Rejection Urine from preservative tube Test Details Use Detect presence of fentanyl and analogues, potent synthetic Methodology Liquid chromatography/tandem mass spectrometry (LC/MS-MS)
Fentanyl and Metabolite
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 Sample Report Specimen Requirements Specimen Serum, plasma, or whole blood Volume 0.25 mL Minimum Volume 0.05 mL Container Red-top tube, lavender-top (EDTA) 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 Separate serum or plasma within two hours of collection and transfer to a plastic transport tube. Storage Instructions Maintain specimen at room temperature. Stability Requirements Temperature Period Room temperature 14 days Refrigerated 14 days Frozen 14 days Causes for Rejection Gel-barrier tube Test Details Use Relief of pain adjunct to general or regional anesthesia moderate to moderately-severe pain. Indications for monitoring include the following: to confirm or identify suspected drug toxicity in chronic use, therapeutic misadventure, or accidental or intentional acute overdose; to aid in the identification of an unknown drug ingested in unknown quantities, drug identification and/or quantitation may be performed as an adjunct for patient management; to monitor selected patient groups at greater risk for analgesic drug toxicity or drug-to-drug interaction; to confirm complete drug absorption and adequate drug elimination as an adjunct to overdose management. 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) References Drug Information Handbook. 24th ed. Hudson, OH: Wolters Kluwer Clinical Drug Information, Inc; 2015; 857-868. White S, Wong SH. Standards of laboratory practice: Analgesic drug monitoring. National Academy of Clinical Biochemistry. Clin Chem. 1998 May; 44(5):1110-1123. PubMed 9590395
Fentanyl/Norfentanyl, Screen and Confirmation, Urine
Test Includes Immunoassay 1; reflex to confirmation Special Instructions This assay is intended for pain management. It is not intended for workplace testing and does not comply with state regulatory workplace testing programs. Expected Turnaround Time 1 - 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. Specimen Requirements Specimen Urine Volume 20 mL Container Plastic urine container Storage Instructions Maintain specimen at room temperature. If arrival at lab will extend beyond seven days, refrigerate. Test Details Use Detect and confirm the presence of fentanyl or norfentanyl 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 Initial testing by immunoassay (IA); confirmation of positives by mass spectrometry (MS)
Ferritin
Special Instructions Values obtained with different assay methods should not be used interchangeably in serial testing. It is recommended that only one assay method be used consistently to monitor each patient's course of therapy. This procedure does not provide serial monitoring; it is intended for one-time use only. If serial monitoring is required, please order the serial monitoring test 480111. 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 For more information, please view the literature below. Hereditary Hemochromatosis Sample Report 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 Refrigerate. Stability Requirements Temperature Period Room temperature 3 days Refrigerated 5 days Frozen 14 days Freeze/thaw cycles Stable x3 Causes for Rejection Citrate plasma specimen; improper labeling Test Details Use Diagnose hypochromic, microcytic anemias. Decreased in iron deficiency anemia and increased in iron overload. Ferritin levels correlate with and are useful in evaluation of total body storage iron. In hemochromatosis, both ferritin and iron saturation are increased. Ferritin levels in hemochromatosis may be >1000 ng/mL. Limitations Ferritin is an acute-phase reactant and thus may be increased in people with inflammation, liver disease, chronic infection, autoimmune disorders, and some types of cancer. Ferritin measurement is of limited usefulness during pregnancy because it diminishes late in pregnancy, even when bone marrow iron is present. 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 Methodology Electrochemiluminescence immunoassay (ECLIA) Reference Interval See table. Age Male (ng/mL) Female (ng/mL) 0 to 5 m 13−273 12−219 6 to 12 m 12−95 12−110 1 to 5 y 12−64 12−71 6 to 11 y 16−77 15−79 12 to 19 y 16−124 15−77 Adult 30−400 15−150 Additional Information Ferritin is found in virtually all cells of the body and serves as the cellular storage repository for iron.2,3 Ferritin is a macromolecule with an average molecular weight of near 440 kD that varies depending on the iron content. Ferritin consists of a protein shell (apoferritin) of 24 subunits surrounding an iron core consisting of up to 4000 ferric iron ions. The majority of ferritin iron stores are found in the liver, spleen, and bone marrow. Ferritin is present in small concentration correlates with total-body iron stores, making its measurement valuable for the assessment of disorders of iron metabolism. Low levels of ferritin can be found when iron stores are exhausted, well before the serum iron level has become affected. In the setting of anemia, low serum ferritin is a very specific biomarker for iron deficiency anemia. In fact, there is no clinical situation other than iron deficiency in which extremely low values of serum ferritin are seen; however, some clinical states involving infection or inflammation can cause the ferritin level in the serum of patients with iron deficiency to increase into the normal range. Ferritin is an acute-phase reactant that is thought to play a role in the body's defense against oxidative stress and inflammation. Increased ferritin values can also be observed in malignant disease, including acute leukemia; Hodgkin's disease; and carcinoma of the lung, colon, liver, and prostate. Consequently, serum ferritin in the normal range reflects iron sufficiency only in the absence of these conditions. Patients with a serum ferritin concentration below the lower limit of the reference interval have a very high probability of being iron deficient; however, given the low sensitivity of a low ferritin level (below the lower limit of normal), a higher ferritin cutoff may be more appropriate for screening for potential iron deficiency in some populations.4-7 It is exceedingly uncommon for ferritin levels to exceed 100 ng/mL in patients with iron deficiency.6,7 An elevated ferritin level can result from iron overload due, in part, to increased hepatic ferritin synthesis.8 Iron overload can occur in hemochromatosis, other excess iron storage disorders, and in individuals who have received multiple blood transfusions. Ferritin can also become markedly elevated secondary to obesity, chronic alcohol consumption, steatohepatitis, chronic inflammation, viral hepatitis, and malignancy. The increased prevalence of obesity has likely resulted in the increased incidence of ferritin elevations, as fatty liver may be the most common cause of an elevated serum ferritin.8 Clinical assessment is required to determine whether the serum ferritin elevation is related to hemochromatosis or another underlying liver disease.9 To confirm the diagnosis of hemochromatosis, other iron tests (iron, TIBC), and genetic testing may be performed.
Fibrinogen Activity
Synonyms Clottable Fibrinogen Factor I Activity Special Instructions If the patient's hematocrit exceeds 55%, the volume of citrate in the collection tube must be adjusted. Refer to Coagulation Collection Procedures for directions. 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 Fibrinogen Antigen Genetic Thrombophilia Two Phases of Coagulation Related Documents For more information, please view the literature below. Spanning the Continuum of Cardiovascular Care Procedures for Hemostasis and Thrombosis: A Clinical Test Compendium Sample Report Specimen Requirements Specimen Whole blood or plasma Volume 4.5 mL, 2.7 mL, 1.8 mL Minimum Volume 90% of full draw Container Blue-top (sodium citrate) tube; do not open tube. Collection Blood should be collected in a blue-top tube containing 3.2% buffered sodium citrate.1 Evacuated collection tubes must be filled to completion to ensure a proper blood to anticoagulant ratio.2,3 The sample should be mixed immediately by gentle inversion at least six times to ensure adequate mixing of the anticoagulant with the blood. A discard tube is not required prior to collection of coagulation samples.4,5 When noncitrate tubes are collected for other tests, collect sterile and nonadditive (red-top) tubes prior to citrate (blue-top) tubes. Any tube containing an alternate anticoagulant should be collected after the blue-top tube. Gel-barrier tubes and serum tubes with clot initiators should also be collected after the citrate tubes. If testing cannot be completed within 24 hours, specimens should be centrifuged for at least 10 minutes at 1500xg. Plasma should then be transferred to a LabCorp PP transpak frozen purple tube with screw cap (LabCorp No. 49482). Freeze immediately and maintained frozen until tested. Refer to Coagulation Collection Procedures for directions. Please print and use the Volume Guide for Coagulation Testing to ensure proper draw volume. Storage Instructions Specimens are stable at room temperature for 24 hours. If testing cannot be completed within 24 hours, specimens should be centrifuged for at least 10 minutes at 1500xg. Plasma should then be transferred to a LabCorp PP transpak frozen purple tube with screw cap (LabCorp N° 49482). Freeze immediately and maintain frozen until tested. Refer to Coagulation Collection Procedures for directions. Stability Requirements Temperature Period Room temperature 1 day Frozen Plasma: 14 days Causes for Rejection Clotted specimen; gross lipemia or hemolysis; tubes <90% full; improper labeling; specimen collected in tube other than 3.2% citrate Test Details Use Diagnosis of homozygous and heterozygous fibrinogen deficiency as well as dysfibrinogenemia; diagnosis of disseminated intravascular coagulation;6-8 fibrinogen levels can be used to assess the effectiveness of thrombolytic therapy.9 Limitations Fibrinogen is an acute-phase reactant and can often become significantly increased in conditions involving tissue damage, infection, or inflammation.6 Increased levels may be seen in smokers, during pregnancy, and in women taking oral contraceptives.6 Fibrinogen levels can be diminished in advanced liver disease.9 Very high levels of heparin, presence of direct thrombin inhibitors, or fibrin breakdown products may falsely reduce fibrinogen levels because they interfere with the rate of clot formation.6 Lipemia or hemolysis may interfere with this assay. Methodology The measurement of fibrinogen activity is based on determination of fibrin polymerization function by the Clauss method.10 This method measures the rate of clot formation after adding a high concentration of thrombin to citrated plasma. The fibrinogen activity is then derived from a standard curve relating the clotting time to plasma standards of known fibrinogen activity. Reference Interval • <6 months: Not established • 7 months to 16 years: 180−383 mg/dL • ≥17 years: 193−507 mg/dL Additional Information Fibrinogen, also referred to as factor I, is a 340-kilodalton glycoprotein that is produced by the liver.6 Fibrinogen has a plasma half-life of about four days. Proteolytic conversion of fibrinogen to fibrin occurs through both the extrinsic and intrinsic pathways.6 Severe fibrinogen deficiency should be considered when a patient with bleeding history has both extended protime (PT) and activated partial thromboplastin time (aPTT).7,8 Mild deficiency may not produce prolongation of either the aPTT or PT and, therefore, fibrinogen activity should be measured in individuals with a bleeding tendency even when the aPTT and PT are in the normal reference interval. Congenital afibrinogenemia, a condition associated with the complete absence of fibrinogen, is rare with only about 150 cases reported in the literature.6,7 Fibrinogen deficiency is inherited as an autosomal recessive trait.7,8 Afibrinogenemia occurs in individuals who are homozygous or doubly heterozygous for mutations. These individuals have infinite protime and aPTT results due to the inability to produce fibrin. Approximately 25% of patients with afibrinogenemia have mild thrombocytopenia.7 Individuals who are heterozygous for congenital fibrinogen deficiency are usually asymptomatic unless their fibrinogen levels fall to <50 mg/dL.7 Both functional (activity) and antigenic levels are diminished in these individuals.7 Fibrinogen deficiency affects both males and females with a prevalence that is equal in all ethnic groups.7 Acquired deficiencies occur in individuals with significant hepatic dysfunction, renal disease, and after L-asparaginase therapy.6 Diminished levels can also be seen in patients with disseminated intravascular coagulation (DIC) or who are undergoing thrombolytic therapy.6 Fibrinogen is one of the major determinants of the erythrocyte sedimentation rate and individuals with afibrinogenemia typically have greatly extended sedimentation rates.7 Individuals with dysfibrinogenemia have fibrinogen that is qualitatively defective with low functional fibrinogen levels (activity) and normal or decreased antigenic levels.6 Congenital dysfibrinogenemia is inherited as an autosomal dominant mutation.6 A number of disfibrinogenemic defects have been identified with a variety of manifestations including abnormal fibrin polymerization, impaired fibrinopeptide release, abnormal fibrin stabilization, and abnormal fibrin clot lysis.6,7 Fibrinogen activity and antigen levels are useful in the diagnosis of dysfibrinogenemia since these individuals often have diminished activity relative to antigen levels.8 Typically, dysfibrinogenemia is associated with an elevated thrombin time and greatly elevated reptilase time. Individuals with afibrinogenemia have a bleeding tendency of varying severity.7 Symptoms often start in early infancy with umbilical cord bleeding, intracerebral hemorrhage, or bleeding at circumcision.6-8 Individuals with afibrinogenemia also suffer from deep muscle and joint bleeding and other mucous membrane bleeding throughout life.6 Women with afibrinogenemia typically do not experience menorrhagia.8 Patients with heterozygous hypofibrinogenemia usually have a minimal history of bleeding with symptoms only observed after major surgery or trauma.6,7 Approximately 50% of individuals with dysfibrinogenemia are asymptomatic suffering neither bleeding nor thrombosis.6,7 These individuals are usually detected when prolonged clotting times are discovered as a result of routine laboratory testing. About one in four will suffer prolonged bleeding after surgery and approximately 20% will have an increased tendency toward thrombosis.6 A number of clinical and epidemiological studies have revealed a consistent association between elevated fibrinogen levels and increased risk for atherosclerotic vascular disease;11 however, it remains to be determined whether increased fibrinogen acts as a mediator of arterial thrombosis or simply reflects the inflammation associated with atherosclerosis.11
Fibrinogen Antigen
Synonyms Factor I Antigen Fibrinogen Level 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 Fibrinogen Degradation Products (FDP), Plasma Genetic Thrombophilia Thrombin Time Related Documents For more information, please view the literature below. Procedures for Hemostasis and Thrombosis: A Clinical Test Compendium Spanning the Continuum of Cardiovascular Care Sample Report Specimen Requirements Specimen Plasma, frozen Volume 1 mL Minimum Volume 0.5 mL Container Lavender-top (EDTA) tube or blue-top (sodium citrate) tube Collection Separate plasma from cells. Transfer specimen to a plastic transport tube and transport frozen. 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. Stable frozen (-20°C) for one year if frozen within 24 hours after collection. Repeated freeze/thaw cycles are to be avoided. Alternatively, refrigerate at 2°C to 8°C for no more than eight days. Causes for Rejection Microbially contaminated samples; hemolysis; gross lipemia that cannot be cleared by ultracentrifugation; serum sample Test Details Use Diagnosis of homozygous and heterozygous fibrinogen deficiency as well as dysfibrinogenemia; diagnosis of disseminated intravascular coagulation;1-3 fibrinogen levels can be used to assess the effectiveness of thrombolytic therapy.4 Limitations Fibrinogen is an acute-phase reactant and can often become significantly increased in conditions involving tissue damage, infection, or inflammation.1 Increased levels may be seen in smokers, during pregnancy, and in women taking oral contraceptives.1 Fibrinogen levels can be diminished in advanced liver disease.4 Very high levels of heparin, direct thrombin inhibitors, or fibrin breakdown products may falsely reduce fibrinogen levels because they interfere with the rate of clot formation.1 Lipemia or hemolysis may interfere with this assay. Methodology Immunonephelometry Additional Information Fibrinogen, also referred to as factor I, is a 340 kilodalton glycoprotein that is produced by the liver.1 Fibrinogen has a plasma half-life of about four days. Proteolytic conversion of fibrinogen to fibrin occurs through both the extrinsic and intrinsic pathways.1 Fibrinogen deficiency should be considered when a patient with bleeding history has both extended protime (PT) and activated partial thromboplastin time (aPTT).2,3 Fibrinogen activity should be measured when a patient has a history of bleeding and the PT and aPTT are normal, as these assays are generally insensitive to fibrinogen deficiency unless levels drop to <100 mg/dL. Congenital afibrinogenemia, a condition associated with the complete absence of fibrinogen, is rare with only about 150 cases reported in the literature.1,2 Fibrinogen deficiency is inherited as an autosomal recessive trait.2,3 Afibrinogenemia occurs in individuals who are homozygous or doubly heterozygous for mutations. These individuals have infinite protime and aPTT results due to the inability to produce fibrin. Approximately 25% of patients with afibrinogenemia have mild thrombocytopenia.2 Individuals who are heterozygous for congenital fibrinogen deficiency are usually asymptomatic unless their fibrinogen levels fall to <50 mg/dL.2 Both functional (activity) and antigenic levels are diminished in these individuals.2 Fibrinogen deficiency affects both males and females with a prevalence that is equal in all ethnic groups.2 Acquired deficiencies occur in individuals with significant hepatic dysfunction, renal disease, and after L-asparaginase therapy.1 Diminished levels can also be seen in patients with disseminated intravascular coagulation (DIC) or who are undergoing thrombolytic therapy.1 Fibrinogen is one of the major determinants of the erythrocyte sedimentation rate and individuals with afibrinogenemia typically have greatly extended sedimentation rates.2 Individuals with dysfibrinogenemia have fibrinogen that is qualitatively defective with low functional fibrinogen levels (activity) and normal or decreased antigenic levels.1 Congenital dysfibrinogenemia is inherited as an autosomal dominant mutation.1 A number of disfibrinogenemic defects have been identified with a variety of manifestations including abnormal fibrin polymerization, impaired fibrinopeptide release, abnormal fibrin stabilization, and abnormal fibrin clot lysis.1,2 Fibrinogen activity and antigen levels are useful in the diagnosis of dysfibrinogenemia since these individuals often have diminished activity relative to antigen levels.3 Reptilase time is generally greatly prolonged, to a greater degree than prolongation of the thrombin time. Individuals with afibrinogenemia have bleeding tendencies of varying severity.2 Symptoms often start in early infancy with umbilical cord bleeding, intracerebral hemorrhage, or bleeding at circumcision.1-3 Individuals with afibrinogenemia also suffer from deep muscle and joint bleeding and other mucous membrane bleeding throughout life.1 Women with afibrinogenemia typically do not experience menorrhagia.3 Patients with heterozygous hypofibrinogenemia usually have a minimal history of bleeding with symptoms only observed after major surgery or trauma.1,2 Approximately 50% of individuals with dysfibrinogenemia are asymptomatic.1,2 These individuals are usually detected when prolonged clotting times are discovered as a result of routine laboratory testing; however, about one in four will suffer prolonged bleeding after surgery and approximately 20% will have an increased tendency toward thrombosis.1 A number of clinical and epidemiological studies have revealed a consistent association between elevated fibrinogen levels and increased risk for atherosclerotic vascular disease;5 however, it remains to be determined whether increased fibrinogen acts as a mediator of arterial thrombosis or simply reflects the inflammation associated with atherosclerosis.5
Ficus
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 Individual Allergens Related Documents Sample Report Specimen Requirements Specimen Serum Volume 1 mL Container One 8.5-mL red-top tube or one 8.5-mL 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®
Finch Feathers
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 Individual Allergens Related Documents Sample Report Specimen Requirements Specimen Serum Volume 0.2 mL Container 10 mL red-top tube or 10 mL 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®
Fir, Douglas
Synonyms Douglas Fir 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 Individual Allergens Related Documents Sample Report 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®
First Trimester Screen With Nuchal Translucency
Synonyms First Trimester Screening, Combined Test Test Includes Dimeric inhibin A (DIA); hCG; pregnancy-associated plasma protein A (PAPP-A) Special Instructions For test inquiries, call CMBP genetic services at 800-345-4363. Client must provide a fetal nuchal translucency (NT) measurement and crown rump length measurement. The NT measurement must be performed by a sonographer credentialed by the Fetal Medicine Foundation or other equivalent entity. The sonographer's credential/certification number must be provided. The following information must also be provided: patient's weight, patient's date of birth, and the number of fetuses. Also indicate relevant patient history (i.e. prior Down syndrome pregnancy, ultrasound anomalies). Complete information is necessary to interpret the test. Patient information may be provided to the laboratory using the Maternal Prenatal Screening request form (0900). Serum testing is provided from 10.0 to 14.0 weeks' gestation. NT can be assessed when the CRL is 45 to 84 mm. 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 For more information, please view the literature below. First Trimester Serum Screening: Early Screening for Down Syndrome Sample Report Specimen Requirements Specimen Serum Volume 3 mL Minimum Volume 1 mL Container Gel-barrier tube Collection Collect in serum separator tube with gel barrier. Allow blood to clot, avoiding hemolysis. Separate serum from cells by centrifugation. Transport spun tube to testing laboratory. Pour-off is not advised. Maternal serum specimens must be drawn prior to amniocentesis to avoid contamination with fetal blood. Storage Instructions Room temperature Stability Requirements Temperature Period Room temperature 7 days Refrigerated 14 days Frozen 14 days Freeze/thaw cycles Stable x3 Causes for Rejection Gross hemolysis; gross lipemia; quantity not sufficient for analysis; improper specimen type Test Details Use Screening test in the first trimester of pregnancy for fetal Down syndrome and trisomy 18 Limitations Screening test for Down syndrome and trisomy 18. A positive result means that diagnostic testing may be offered to the pregnant woman to determine if a chromosome abnormality is present. This test does not screen for open neural tube defects. Methodology Chemiluminescent immunoassay
FLT3 Mutation Analysis
Synonyms FLT3 D835 mutation FLT3 Internal Tandem Duplication and Tyrosine Kinase Domain mutation FLT3 ITD and D835 mutations FLT3 ITD and TKD mutations FLT3 ITD mutation FLT3 TKD mutation Special Instructions Please direct any questions regarding this test to customer service at 800-345-4363. Related Information c-KIT Mutation Analysis in Tumors of Hematopoietic Tissue CEBPA Mutation Analysis Chromosome Analysis, Leukemia/Lymphoma IntelliGEN® Myeloid NPM1 Mutation Analysis Specimen Requirements Specimen Whole blood, bone marrow or cell pellet Volume 3-5 mL whole blood or 1-2 mL bone marrow Minimum Volume 3 mL whole blood or 1 mL bone marrow Container Lavender-top (EDTA) tube or green-top (sodium heparin) tube Collection Ship specimen at room temperature. Specimen should arrive in the laboratory within 48 hours of collection. Indicate date and time of collection on the request form. Storage Instructions Refrigerate. If specimen is to be stored prior to shipment, store at 2°C to 8°C. Causes for Rejection Specimen does not meet collection criteria; frozen whole blood, marrow, or cell pellet; leaking tube; clotted blood or marrow; grossly hemolyzed specimen or otherwise visibly degraded; contamination by another specimen; specimens containing suspicious foreign material Test Details Use Mutations in the FLT3 gene are common mutations in acute myeloid leukemia (AML). This assay detects internal tandem duplication (ITD) mutations and mutations in the tyrosine kinase domain (TKD) of FLT3. Presence of these mutations in AML provide prognostic information and can aid in the determination of therapeutic regimen. Limitations This PCR assay is capable of detecting a mutant cell population with a sensitivity of 5 mutant cells per 100. 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 Polymerase chain reaction (PCR); restriction enzyme digest; capillary electrophoresis Additional Information FLT3 is a receptor tyrosine kinase (RTK) that dimerizes on binding its ligand, the cytokine FLT3 ligand (FL), which then undergoes autophosphorylation, and transduces signals downstream (STAT, AKT, ERK) that promote proliferation and survival. Activating mutations of FLT3 are common mutations found in AML. A particular form of FLT3 is mutated by duplicating coding sequence derived from the juxtamenbrane domain inserted in tandem (internal tandem duplication (ITD). These FLT3-ITD mutations result in the constitutive activation of the tyrosine kinase function. Patients with FLT3-ITD mutations have increased relapse rates and reduced overall survival. Point mutations in the activation loop of the kinase domain, most commonly at the residue Asp 835 (D835), also known as tyrosine kinase domain (TKD) mutations, also result in the constitutive activation of the FLT3 kinase. Signaling from FLT3-TKD mutations does not appear as abnormal, and the prognostic impact appears to be less severe when compared with ITD mutations (FLT3-ITD mutations are found in ~23% of AML cases, whereas TKD mutations are found in 7%). Recently the FDA approved a new combination treatment of AML that is FLT3 mutation positive. The kinase inhibitor RYDAPT® (midostaurin), in combination with chemotherapy was approved as the first targeted therapy for AML.
Fluoride, Urine
Synonyms F, Urine Sodium Fluoride Test Includes Creatinine, urine; fluoride, urine; fluoride:creatinine ratio Special Instructions Do not use preservative. Preservatives used for routine analysis may contain mercuric oxide (ie, Stabilur), which interferes with all metal testing. If both urinalysis and metal testing are ordered, please submit a separate urine specimen (containing no additive) for the metal testing. 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 Fluoride Specimen Requirements Specimen Urine (random) Volume 5 mL Minimum Volume 2.2 mL Container Plastic urine container, no preservative. Do not use glass container. Collection Sampling time is prior to shift or end of shift for industrial monitoring. Inorganic analytes with timing “end of shift” (meaning the last two hours of exposure) or “prior to next shift” are eliminated rapidly with a half-life less than five hours. Such analytes do not accumulate in the body and, therefore, their timing is critical only in relation to the exposure and postexposure periods. Storage Instructions Maintain specimen at room temperature. Causes for Rejection Specimen received in a glass container. Test Details Use Monitor chronic exposure to fluoride Methodology Ion-selective electrode (ISE) potentiometry Reference Interval • Environmental exposure: 0.2−3.2 mg/L • Occupational exposure: BEI® (sampling time is prior to shift): 3.00 mg/g creatinine;1 BEI® (sampling time is end of the shift): 10.00 mg/g creatinine1 Additional Information BEI® are reference values intended as guidelines for evaluation of occupational exposure. BEI® represent biological levels of chemicals that correspond to workers with inhalation exposure equivalent to the threshold limit value (TLV®) of the chemicals. TLVs refer to the airborne concentrations of substances and represent conditions under which it is believed that nearly all workers may be repeatedly exposed, day after day, without adverse health effects.1
Fluoxetine, Serum or Plasma
Synonyms Prozac® Prozac® Weekly Sarafem® Selfemra™ Test Includes Norfluoxetine 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 Sample Report Specimen Requirements Specimen Serum or plasma Volume 2 mL Minimum Volume 0.6 mL Container Red-top tube, lavender-top (EDTA) 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. Storage Instructions Room temperature Stability Requirements Temperature Period Room temperature 14 days Refrigerated 14 days Frozen 14 days Causes for Rejection Gel-barrier tube Test Details Use The efficacy of fluoxetine in the treatment of nondelusional, moderately depressed patients is comparable to that of the tricyclic agents; its efficacy in severely depressed hospitalized patients has not been established. In limited studies, fluoxetine was useful in treating patients with atypical depression, panic disorder, and the depressed component of bipolar disorder. Fluoxetine may be indicated as initial therapy in patients with concurrent obsessive-compulsive disorder. Its efficacy in obesity and bulimia is being explored. The selection of fluoxetine appears to be most appropriate for patients who are at special risk from sedative, hypotensive, and anticholinergic side effects caused by other antidepressants. In addition, it appears to be relatively safe for use in the elderly, although its very long elimination half-life may pose special problems for these individuals. 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 Therapeutic: fluoxetine: 91−302 ng/mL, norfluoxetine: 72−258 ng/mL. After dosing at 40 mg/day for 30 days, plasma concentration of fluoxetine in the range of 91−302 ng/mL and norfluoxetine in the range of 72−258 ng/mL were observed. In a well-designed pharmacokinetic study, with patients (N = 38) taking fluoxetine for five weeks of fixed doses between 20 mg and 80 mg per day, the majority of plasma concentrations were between 100−800 ng/mL for fluoxetine and between 100−600 ng/mL for norfluoxetine. Additional Information Fluoxetine is well absorbed after oral administration, whether or not food is present, and peak plasma concentrations are attained six to eight hours after a dose. Steady-state plasma concentrations are reached after two to four weeks. Fluoxetine is widely distributed throughout the body, and about 94% of a dose is bound to plasma protein. The drug is metabolized in the liver to norfluoxetine, which also selectively inhibits serotonin reuptake, and other unidentified metabolites. Fluoxetine is excreted in the urine primarily as inactive metabolites. Renal impairment does not appear to alter the pharmacokinetics, although alcohol-induced cirrhosis does prolong the half-life. The elimination half-life is long: one to four days for fluoxetine and 7 to 10 days for norfluoxetine. Because of the long half-life, the drug can be administered once daily, efficacy is unaffected by an occasional missed dose, and abrupt termination of therapy results in gradual cessation of effects. This drug's pharmacokinetic profile is similar in elderly and younger patients.
Folate (Folic Acid)
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 Vitamin B12 Vitamin B6, Plasma Related Documents Sample Report 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 immediately to a plastic transport tube. Avoid hemolysis. 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; hemolysis; improper labeling Test Details Use Detect folate deficiency; monitor therapy with folate; evaluate megaloblastic and macrocytic anemia; evaluate alcoholic patients and those with prior jejunoileal bypass for morbid obesity or those with intestinal blind-loop syndrome Limitations Folate assays of samples from patients receiving therapy with certain pharmaceuticals (eg, methotrexate or leucovorin), are contraindicated because of the cross-reactivity of folate-binding protein with these compounds.1 Serum samples should not be altered with additives (biocides, antioxidants, or substances possibly changing the pH of the sample) in order to avoid erroneous folate recovery. Hemolysis may significantly increase folate values due to high concentrations of folate in red blood cells; therefore, hemolyzed samples are not suitable for this assay.1 Samples with extremely high total protein concentrations (eg, patients suffering from Waldenström macroglobulinemia) are not suitable for use in this assay, since they may lead to the formation of protein gel in the assay cup.1 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 that minimize these effects. Methodology Electrochemiluminescence immunoassay (ECLIA) Reference Interval >3.0 ng/mL Additional Information Folates are compounds of pteroylglutamic acid (PGA) that function as coenzymes in metabolic reactions involving the transfer of single-carbon units from a donor to a recipient compound. Folate, with vitamin B12, is essential for DNA synthesis, which is required for normal red blood cell maturation.2 Humans obtain folate from dietary sources including fruits, green and leafy vegetables, yeast, and organ meats.3 Folate is absorbed through the small intestine and stored in the liver. Low folate intake, malabsorption as a result of gastrointestinal diseases, pregnancy, and drugs such as phenytoin are causes of folate deficiency.4 Folate deficiency is also associated with chronic alcoholism.5 Folate and vitamin B12 deficiency impair DNA synthesis, causing macrocytic anemias. These anemias are characterized by abnormal maturation of red blood cell precursors in the bone marrow, the presence of megaloblasts, and decreased red blood cell survival.2 Since both folate and vitamin B12 deficiency can cause macrocytic anemia, appropriate treatment depends on the differential diagnosis of the deficiency. A serum folate concentration <3 ng/mL is considered to represent clinical deficiency by the World Health Organization and numerous subsequent clinical studies.6,7 Serum folate measurement provides an early index of folate status3; however, folate is much more concentrated in red blood cells than in serum so the red blood cell folate measurement more closely reflects tissue stores.5,8 Erythrocytes incorporate folate as they are formed, and levels remain constant throughout the life span of the cell. RBC folate levels are less sensitive to short-term dietary effects than are serum folate levels. Red blood cell folate concentration is considered the most reliable indicator of folate status.3 Low serum folate during pregnancy has been associated with neural tube defects in the fetus.9,10 In the 1990s mandatory increased fortification of enriched cereal-grain products along with the requirement of folate-related health and nutrient content claims on food and dietary supplement products significantly increased the folic acid content of the US food supply.11-13 Several reports have shown that serum folate concentrations have increased in the general US population since these measures were implemented.11-13
Folate, RBC
Synonyms Folates RBC (With Hct) Test Includes RBC folate; hematocrit 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 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 Sample Report Specimen Requirements Specimen Whole blood (two tubes) Container Two full lavender-top (EDTA) tubes Collection Transfer 4 mL from one whole blood tube into a plastic transport tube and freeze. Second whole blood tube should be at room temperature. 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 whole blood transport tube; store whole blood specimen at room temperature. Stability Requirements Temperature Period Room temperature Folate: Unstable; Hematocrit: 1 day Refrigerated Folate: 1 day; Hematocrit: 3 days Frozen Folate: 14 days; Hematocrit: Unstable Freeze/thaw cycles Folate: Stable x3; Hematocrit: Unstable Patient Preparation Verify that the patient has not had vitamins containing folic acid during the previous three to five days; if so, consult physician. Causes for Rejection No frozen whole blood; transport tubes with whole blood for the hematocrit portion Test Details Use Detect folate deficiency; monitor therapy with folate; evaluate megaloblastic and macrocytic anemia Limitations Folate assays of samples from patients receiving therapy with certain pharmaceuticals (eg, methotrexate or leucovorin), are contraindicated because of the cross-reactivity of folate binding protein with these compounds.1 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 that minimize these effects. Methodology Electrochemiluminescence Immunoassay (ECLIA) Reference Interval >498 ng/mL Additional Information Folates are compounds of pteroylglutamic acid (PGA) that function as coenzymes in metabolic reactions involving the transfer of single-carbon units from a donor to a recipient compound. Folate, with vitamin B12, is essential for DNA synthesis, which is required for normal red blood cell maturation.2 Humans obtain folate from dietary sources including fruits, green and leafy vegetables, yeast, and organ meats.3 Folate is absorbed through the small intestine and stored in the liver. Low folate intake, malabsorption as a result of gastrointestinal diseases, pregnancy, and drugs such as phenytoin are causes of folate deficiency.4 Folate deficiency is also associated with chronic alcoholism.5 Folate and vitamin B12 deficiency impair DNA synthesis, causing macrocytic anemias. These anemias are characterized by abnormal maturation of red blood cell precursors in the bone marrow, the presence of megaloblasts, and decreased red blood cell survival.2 Since both folate and vitamin B12 deficiency can cause macrocytic anemia, appropriate treatment depends on the differential diagnosis of the deficiency. Serum folate measurement provides an early index of folate status3; however, folate is much more concentrated in red blood cells than in serum so the red blood cell folate measurement more closely reflects tissue stores.5,6 Erythrocytes incorporate folate as they are formed, and levels remain constant throughout the life span of the cell. RBC folate levels are less sensitive to short-term dietary effects than are serum folate levels. Red blood cell folate concentration is considered the most reliable indicator of folate status.3 Low serum folate during pregnancy has been associated with neural tube defects in the fetus.7,8
Follicle-stimulating Hormone (FSH)
Synonyms Pituitary Gonadotropin 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 Inhibin A, Ultrasensitive Inhibin B Luteinizing Hormone (LH) Related Documents Sample Report 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. Avoid hemolysis. Storage Instructions Room temperature Stability Requirements Temperature Period Room temperature 14 days Refrigerated 14 days Frozen 14 days Freeze/thaw cycles Stable x3 Test Details Use Excessive FSH and LH are found in hypogonadism, anorchia, gonadal failure,1 complete testicular feminization syndrome, menopause, Klinefelter syndrome, alcoholism, and castration. FSH and LH are pituitary products, useful to distinguish primary gonadal failure from secondary (hypothalamic/pituitary) causes of gonadal failure, menstrual disturbances, and amenorrhea. Useful in defining menstrual cycle phases in infertility evaluation of women and testicular dysfunction in men. FSH is commonly used with LH, which also is a gonadotropin. Both are low in pituitary or hypothalamic failure. FSH and LH levels are high following menopause. Limitations Secretion of both LH and FSH are pulsatile, in response to the normal intermittent release of gonadotropin-releasing hormone (GnRH). In addition, in females, both FSH and LH vary over the course of the menstrual cycle, with peaks at time of ovulation. Thus, interpretation of a single determination may be difficult. It has been suggested that samples be obtained at 15- to 30-minute intervals and equal volumes of serum be pooled to decrease the effect of pulsatile secretion. 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 who have received them for diagnostic purposes.2 In rare cases, interference due to extremely high titers of antibodies to streptavidin and ruthenium can occur.2 The test contains additives, which minimize these effects. Methodology Electrochemiluminescence immunoassay (ECLIA) Reference Interval See table. Children (Male and Female) (mIU/mL) <24 h <0.2−0.8 1 d <0.2−0.8 2 d <0.2−0.8 3 d <0.2−2.4 4 d <0.2−2.3 5 d <0.2−3.4 6 d <0.2−4.5 7 d <0.2−21.4 8 to 30 d <0.2−22.2 Age Children (Male) Children (Female) 1 to 12 m Not established Not established 1 to 4 y 0.2−2.8 0.2−11.1 5 to 9 y 0.4−3.8 0.3−11.1 10 to 12 y 0.4−4.6 2.1−11.1 13 to 16 y 1.5−12.9 1.6−17.0 Adult Male (mIU/mL): 1.5−12.4 Adult Female (mIU/mL) follicular 3.5−12.5 ovulatory 4.7−21.5 luteal 1.7−7.7 postmenopausal 25.8−134.8 Additional Information FSH is a glycoprotein consisting of two subunits (α- and β-chains). Its molecular weight is approximately 32,000 daltons. FSH together with LH (luteinizing hormone), belongs to the gonadotropin family. FSH and LH regulate and stimulate the growth and function of the gonads (ovaries and testes) synergistically.3 FSH and LH are released in pulses from the gonadotropic cells of the anterior pituitary. The levels of the circulating hormones are controlled by steroid hormones via negative feedback to the hypothalamus. In the ovaries, FSH, together with LH, stimulates the growth and maturation of the follicle and hence also the biosynthesis of estrogens in the follicles. In women, the gonadotropins act within the hypothalamus-pituitary-ovary regulating circuit to control the menstrual cycle.1,4 The FSH level shows a peak at midcycle, although this is less marked than with LH. Due to changes in ovarian function and reduced estrogen secretion, high FSH concentrations occur during menopause.1 The determination of FSH in conjunction with LH is utilized for the following indications: congenital diseases with chromosome aberrations, polycystic ovaries (PCO), amenorrhea (causes), and menopausal syndrome. In men, FSH serves to induce spermatogonium development. Determination of the FSH concentration is used in the elucidation of dysfunctions within the hypothalamus-pituitary-gonads system. Depressed gonadotropin levels in men occur in azoospermia.1,3,5,6 Footnotes 1. Runnebaum B, Rabe T. Gynäkologische Endokrinologie und Fortpflanzungsmedizin. Berlin, Germany: Springer Verlag;1994. Band 1:17, 253-255; Band 2: 152-154, 360, 348. ISBN 3-540-57345-3, ISBN 3-540-57347-X. 2. FSH on Elecsys 1010/2010 and Modular Analytics E170, package insert 2007-10, V 14, Indianapolis, Ind: Roche Diagnostics; 2007. 3. Johnson MR, Carter G, Grint C, Lightman SL. Relationship between ovarian steroids, gonadotropins and relaxin during the menstrual cycle. Acta Endocrinol (Copenh). 1993 Aug; 129(2):121-125. PubMed 8372595 4. Beastall GH, Ferguson KM, O'Reilly DS, Seth J, Sheridan B. Assays for follicle stimulating hormone and luteinizing hormone: Guidelines for the provision of a clinical biochemistry service. Ann Clin Biochem. 1987 May; 24(Pt 3):246-262. PubMed 3111341 5. Schmidt-Mathiesen H. Gynäkologie und Geburtshilfe. Schattauer Verlag; 1992. 6. Scott MG, Ladenson JH, Green ED, Gast MJ. Hormonal evaluation of female infertility and reproductive disorders. Clin Chem. 1989 Apr; 35(4):620-630. PubMed 2522836
Follicle-stimulating Hormone (FSH), Eight Specimens
Special Instructions Please refer to the directions for Sequential Sampling. 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 Sample Report LOINC® Map Order Code Order Code Name Order Loinc Result Code Result Code Name UofM Result LOINC 208819 FSH, Serum (8 Specimens) 019696 FSH#1 (Follicle Stim.Hormone) mIU/mL 32317-0 208819 FSH, Serum (8 Specimens) 019703 FSH#2 (Follicle Stim.Hormone) mIU/mL 55611-8 208819 FSH, Serum (8 Specimens) 019711 FSH#3 (Follicle Stim.Hormone) mIU/mL 55610-0 208819 FSH, Serum (8 Specimens) 019729 FSH#4 (Follicle Stim.Hormone) mIU/mL 27865-5 208819 FSH, Serum (8 Specimens) 019737 FSH#5 (Follicle Stim.Hormone) mIU/mL 27870-5 208819 FSH, Serum (8 Specimens) 100370 FSH#6 (Follicle Stim.Hormone) mIU/mL 27868-9 208819 FSH, Serum (8 Specimens) 141176 FSH#7 (Follicle Stim.Hormone) mIU/mL 27880-4 208819 FSH, Serum (8 Specimens) 141184 FSH#8 (Follicle Stim.Hormone) mIU/mL 55612-6
Foxtail, Meadow
Synonyms Meadow Foxtail 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 Individual Allergens Related Documents Sample Report 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®
Free Androgen Index (FAI)
Synonyms Testosterone:SHBG Ratio Test Includes Testosterone; sex hormone-binding globulin (SHBG) Special Instructions State the patient's age and sex on the test request form. 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 Testosterone, Free and Weakly Bound Testosterone, Free, Direct Related Documents Sample Report Specimen Requirements Specimen Serum Volume 1 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 a red-top tube is used, transfer separated serum to a plastic transport tube. Storage Instructions Room temperature Causes for Rejection Plasma specimen Test Details Use The free androgen index can be used to estimate physiologically active testosterone. Methodology Electrochemiluminescence immunoassay (ECLIA) Reference Interval • Male: − 20 to 29 years: 30.0−128.0 − 30 to 39 years: 24.0−122.0 − 40 to 49 years: 14.0−126.0 − Older than 49 years: 18.0−82.0 • Female: − 20 to 49 years: 0.4−8.4 − Older than 49 years: 0.4−6.6 Additional Information In most men and women, >50% of total circulating testosterone is bound to sex hormone-binding globulin, SHBG, and most of the rest is bound to albumin.1-3 SHBG-bound testosterone is not readily available for intracellular complex formation because of SHBG's high binding affinity for testosterone.2 Thus, testosterone-bound SHBG is considered to be biologically inactive. Albumin has a much lower binding affinity for testosterone but binds a significant portion of the total testosterone because albumin is present at much higher plasma concentrations than SHBG.2,4 The rapid dissociation of “weakly bound” testosterone from albumin, together with a relatively long transit time of albumin through target tissue capillary beds, result in the availability of essentially all albumin-bound testosterone for steroid-receptor interaction.4 The sum of the free- and albumin-bound testosterone is often referred to as bioavailable testosterone. The concentration of testosterone in the various free and bound forms is essentially a function of total testosterone concentration and the relative concentrations of SHBG and albumin. It can be predicted that increased SHBG will decrease the concentration of both free and bioavailable testosterone for a given total testosterone concentration. The free androgen index can be used to estimate physiologically active testosterone.2,3 This index is calculated as the ratio of total testosterone divided by SHBG (both expressed in the same units) and multiplied by 100 to yield numerical results comparable in free testosterone concentration.2,5-7
Fungus (Mycology) Culture
Synonyms Blood Culture, Fungus Culture, Fungus (Mycology) Fungus Blood Culture Fungus Culture, Blood Mold Culture Yeast Culture Test Includes Culture for fungi. Isolation and identification (additional charges/CPT code[s] may apply) if culture results warrant. CPT coding for microbiology and virology procedures often cannot be determined before the culture is performed. Expected Turnaround Time 24 - 42 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 Dermatophyte Culture Fungus Culture With Stain Mycology, Mycobacteriology, and Other Reference Microbiology Testing Organism Identification, Mold Organism Identification, Yeast Related Documents Sample Report Specimen Requirements Specimen Biopsy, blood, body fluid, aspirates, bronchoalveolar lavage (BAL), swab of conjunctiva, skin, nails, hair, sputum, stool, throat, tissue, urine, or vaginal Volume 2 mL or 1 cm³ tissue, 10 mL blood, whole nails, 50 mL body fluid (5 mL CSF), 5 mL aspirates or sputum; skin scrapings may be submitted on Mycosel® medium (not supplied by LabCorp) Container Sterile container for fluid or tissue or green-top (sodium heparin) tube, blood culture bottle Collection Biopsy: Surgical specimen in sterile container. A small amount of sterile nonbacteriostatic water should be added to prevent drying. Body fluid, aspirates: Aspirated material in sterile container. Eye: For keratitis, scrapings with a Kimura spatula directly inoculated using “C” streaks are best. Skin: Cleanse the area with 70% alcohol and collect a portion from the active border of the lesion. Nails: For all types of onychomycosis, clean the nail area well with 70% alcohol, then, depending on type of nail disease, collect the following: • Distal subungual: Clip the abnormal nail as close to the proximal edge as possible. Scrape the nail bed and underside of nail plate with a curet. Discard the outermost debris, which likely contains contaminants. Nail clippings are less desirable for culture. • Proximal subungual: Pare down the normal surface of nail plate in the area of the lunula. Collect white material from the deeper portion of plate. • White superficial: Scrape the white spots, discarding the outermost surface, which likely contains contaminants. Collect the white areas directly underneath. • Candida infection: Collect material closest to the proximal and lateral nail edges. Hair: Epilate 10 to 12 hairs and place them in a sterile container. Stool: Random sample in sterile container. Swabs: Throat, nose, nasopharynx, and ear swabs are acceptable; material from the ear is better than a swab. Urine: Clean catch midstream sample in sterile container. Wound: Aspirate of purulent material or fluid, scraping of lesion border, or swab (least preferred) in sterile container. Swabs cannot be split for other tests. Avoid contamination of the specimen with commensal organisms as much as possible. Specify the source of the specimen and include any pertinent clinical information. Cultures are incubated one to four weeks (depending on source) before a final negative report is issued. Storage Instructions Refrigerate nonsterile respiratory specimens; all others should be maintained at room temperature. Patient Preparation Usual sterile preparation (see Blood Culture, Routine [008300]). Causes for Rejection Unlabeled specimen or name discrepancy between specimen and request label; specimen received after prolonged transport (usually more than 72 hours); lithium heparin tube; swab without evidence of specimen present; specimen received after leaking transport container into specimen bag; inappropriate transport device, including syringe with needle. (Trach-suction devices will often leak if the cap with tubing is not removed and replaced by a solid cap. This may need to be done by personnel collecting the specimen as the solid cap is usually in with the device. If there is not solid cap, the specimen should be transferred to a leakproof sterile cup with metal cap.) Test Details Use Isolate and identify fungi. Blood: establish the diagnosis of fungal infections including fungemia, fungal endocarditis, and disseminated mycosis in patients at risk for fungal infections. Limitations Blood: A single (or even multiple) negative fungal blood culture does not exclude disseminated fungal infection. If disseminated or deep fungal infection is strongly suspected despite repeatedly negative blood cultures, biopsy of the appropriate tissue and/or bone marrow aspiration for sections and fungus culture should be considered. Stool: Use of this test is generally limited to detection of Candida. Stool cultures have a low yield and are not recommended for the isolation of systemic fungi; however, Histoplasma capsulatum is recovered from the stool of AIDS patients with disseminated infection. Methodology Culture Additional Information Blood: Fungemia can be a complication of venous or arterial catheterization, hyperalimentation, the acquired immunodeficiency syndrome (AIDS), and therapy with steroids, antineoplastic drugs, radiation, or broad spectrum antimicrobial agents. Intravenous drug abusers are prone to Candida endocarditis. Although many fungal species, including Histoplasma capsulatum, Coccidioides immitis, and Cryptococcus neoformans are recoverable from blood cultures, the most common cause of fungemia is Candida albicans followed by other Candida sp, including Candida glabrata. Fungemia represents a failure of the host defense system. Fungemia may be precipitated by contamination of an indwelling catheter or, in the critically ill and immunocompromised patient, contamination of the gastrointestinal and less frequently the urinary tract.1 In a review of 356 patients with neoplastic disease, Candida sp was recovered in 7% of neutropenic patients. In the potentially immunocompromised host, a temperature of 38.5°C (101°F) for more than two hours, which is not associated with the administration of a pyrogenic drug (chemotherapy), indicates the presence of infection until proven otherwise. In these patients, characteristic signs and symptoms are frequently absent. A careful physical examination, including mouth, anus, and genitalia, may reveal the site of infection. Therapy must be instituted as soon as appropriate specimens are collected. Most infections in these patients are caused by gram-negative organisms (eg, E coli, Pseudomonas sp, Klebsiella sp) and by S aureus; however, fungi and other usually nonpathogenic organisms must be considered significant.2 Rarely, blastospores (budding yeast structures) and pseudohyphae can be seen by examination of Wright-stained venous peripheral blood smears. This technique may allow early diagnosis and therapy before culture results are available.3 Eye: The more common causes of keratomycosis include Fusarium solani, Candida albicans, Aspergillus fumigatus, Curvularia sp, Aspergillus flavus, other species of Aspergillus, Penicillium, Paecilomyces, Fusarium, and many other species.4 A keratomycosis-like clinical presentation may also be encountered caused by Nocardia asteroides and Mycobacterium fortuitum. Keratomycosis is a rare complication of contact lens use.5 Sinus: Fungal sinusitis has been increasingly recognized in otherwise healthy teenagers who often present with a history of recurrent sinusitis, asthma, and/or polyps. At surgery, material is consistently described as thick peanut butter-like or pistachio pudding-like. Dematiaceous fungi are the most common cause. Skin: Candida sp may colonize skin. Clinical diagnosis of Candida infection involves consideration of predisposing factors such as occlusion, maceration altered cutaneous barrier function. Signs of Candida infection include bright erythema, fragile papulopustules, and satellite lesions.6 Patients with defects in T-lymphocyte responses, such as AIDS patients or individuals being treated with antineoplastic drugs, are especially susceptible to many fungal infections including superficial mycoses.7,8 See tables. Selection of Specimens for the Diagnosis of Superficial Mycosis and Dermatomycosis Diagnosis Specimen of Choice Superficial Mycoses Piedra Hair Tinea nigra Skin scraping Pityriasis versicolor Skin scraping Dermatomycoses (Cutaneous Mycoses) Onychomycosis Nail scraping Tinea capitis Hair (black dot) Tinea corporis Skin scraping Tinea pedis Skin scraping Tinea cruris Skin scraping Candidiasis Thrush Scraping of oral white patches Diaper dermatitis Scraping of pustules at margin Paronychia Scraping skin around nail Cutaneous candidiasis Scraping of pustules at margin Erosio interdigitalis blastomycetia (coinfection with gram-negative rods) Scrapings of interdigital space (routine culture also) Congenital candidiasis Scraping of scales, pustules and cutaneous debris, cultures of umbilical stump, mouth, urine, and stool Mucocutaneous candidiasis Scraping of affected area Selection of Specimens for the Diagnosis of Systemic and Subcutaneous Mycosis Diagnosis Specimen of Choice in Order of Usefulness Systemic Mycoses Aspergillosis Sputum Bronchial aspirate Biopsy (lung) Blastomycosis Skin scrapings Abscess drainage (pus) Urine Sputum Bronchial aspirate Candidiasis Sputum Bronchial aspirate Blood Cerebrospinal fluid Urine Stool Coccidioidomycosis Sputum Bronchial aspirate Cerebrospinal fluid Urine Skin scrapings Abscess drainage (pus) Cryptococcosis Cerebrospinal fluid Sputum Abscess drainage (pus) Skin scraping Urine Mycormycosis / phycomycosis / zygomycosis Sputum Bronchial aspirate Biopsy (lung) Paracoccidioidomycosis (South American blastomycosis) Skin scrapings Mucosal scrapings Biopsy (lymph nodes) Sputum Bronchial aspirate Subcutaneous Mycoses Chromomycosis Skin scrapings Biopsy (skin) Drainage (pus) Maduromycosis (mycetoma) Abscess drainage Biopsy (lesion) Granules Sporotrichosis Drainage (pus) Abscess drainage Biopsy (skin, lymph node) Hair: The leading agent of tinea capitis in the United States is Trichophyton tonsurans. Other dermatophytes such as T violaceum, T mentagrophytes, and Microsporum canis are also recovered routinely. Unlike at the beginning of the 20th century, M audouinii is rarely seen. Nails: Nail disease can be caused by dermatophytes and nondermatophytes. The leading cause of nail infection is Trichophyton rubrum, but it is not unusual to find T mentagrophytes and T tonsurans. Recovery of dermatophytes from nail can be difficult and careful cleansing, scraping of the diseased nail, and collecting debris under the nail is required. Attributing nail disease to nondermatophytes is more problematic. Fungi such as Fusarium, Scopulariopsis, and some aspergilli are routinely associated with disease, however, Chrysosporium, Paecilomyces, Trichoderma and others may likely represent environmental contamination unless repeatedly isolated in the absence of other pathogens. Sputum: Deeply coughed sputum, transtracheal aspirate, bronchial washing or brushing, or deep tracheal aspirate are preferred specimens. Oncology patients, transplant patients, and patients with the acquired immunodeficiency syndrome (AIDS) are particularly prone to infection with fungi.8 Primary fungal pulmonary infections include Histoplasma capsulatum, Coccidioides immitis, Cryptococcus neoformans, and Blastomyces dermatitidis. The incidence is largely related to geographic exposure and cases can occur in seemingly normal hosts. Numbers of reports of opportunistic fungal pulmonary infections due to a variety of etiologic agents that are ubiquitous in the environment are being published. Definitive diagnosis depends upon the presence of clinical signs of pulmonary infection, a chest x-ray revealing abnormality such as granuloma; laboratory isolation of a potentially significant organism from a suitable specimen; histologic documentation of tissue invasion by the isolated organism. A list of etiologic agents of pulmonary fungal disease has been compiled.9 In practice a diagnosis sufficient for therapy can frequently be established by observation of hyphae, pseudohyphae, spherules, or yeast cells in tissue sections; recovery of the organism from a normally sterile site; repeated isolation of the same suspect organism from the same or different sites; seroconversion (ie, the development of an immune response to the suspected organism).10 Candida and Aspergillus sp are the most frequently isolated fungal organisms; however, they are frequently present as the result of contamination from the patient's normal flora or airborne sources. Their presence may represent colonization rather than invasion. Recovery of Candida from blood is a major adjunct to definitive diagnosis. Even without invasion Aspergillus may cause IgE mediated asthma, allergic alveolitis cell mediated hypersensitivity, mucoid impaction, and bronchocentric granulomatosis.11 Fungal tracheobronchitis has recently been recognized as a pseudomembranous form involving the circumference of the bronchial wall or as multiple or discrete plaques. The plaques or pseudomembranes are composed of necrotic tissue exudate and fungal hyphae.12 Stool: Candida can be isolated in up to 30% of oropharyngeal cultures and 65% of stool cultures; thus, it is a common saprophyte.13 Neonates and adults may develop watery diarrhea due to intestinal overgrowth by yeast that readily responds to specific therapy. Candida may become disseminated in patients with leukopenia, immunosuppressive therapy, AIDS, corticosteroid therapy, phagocytic defects, hyperalimentation, use of broad spectrum antibiotics, and oral contraceptives. Travelers in endemic areas with poor sanitation have also experienced intestinal overgrowth with Candida, although the specific mechanism causing diarrhea is unknown.14 Candida-associated diarrhea is predominantly of the secretory type, characterized by frequent watery stools, usually without blood, mucus, tenesmus, or abdominal pain.15 Overgrowth of Candida sp should be considered when evaluating Clostridium difficile negative cases of antibiotic-associated colitis.16 Urine: Asymptomatic funguria often clears spontaneously; however, candiduria with >15,000 colony forming units/mL of urine and with such evidence of dissemination as elevated serum precipitin antibody titers, is associated with increased mortality.17 Patients with candiduria may or may not have candidemia; positive urine culture for fungi often may be followed by positive blood culture for fungi. Ascending infections occur in patients with diabetes, prolonged antimicrobial therapy, or following instrumentation. Urinary obstruction due to “fungus balls” may occur in diabetes and following renal transplantation. Candiduria associated with hematogenous infections is observed in patients with granulocytopenia, corticosteroid therapy, and with immunosuppression. The source is frequently the gastrointestinal tract or indwelling catheters particular with hyperalimentation.18 A blood fungus culture is useful to define invasive disease; however, proof of invasive Candida infection requires direct cystoscopic or operative visualization, fungus balls, pyelonephritis, or histological evidence of mucosa invasion. Urine is a useful specimen for culture in cryptococcosis, blastomycosis, and candidiasis. The incidence of genitourinary fungal infections is increasing. They are usually associated with broad spectrum antibiotic therapy, corticosteroid therapy, underlying general debility, and AIDS. In addition to Candida, opportunistic pathogens in the genitourinary tract include Aspergillus and Cryptococcus. Endemic pathogens such as Histoplasma, Blastomyces, and Coccidioides are also encountered.19 Mold spores are common in the environment and it is not uncommon for saprophytic environmental fungi to be recovered from respiratory and skin specimens.

Common Lab Tests

Complete Blood Count

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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

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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

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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.

Lipid

Panel

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The lipid panel is a group of tests used to evaluate cardiac risk. It includes cholesterol and triglyceride levels.

Liver Panel

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The liver panel is a combination of tests used to assess liver function and establish the possible presence of liver tumors.

Hemoglobin A1C

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This test is used to diagnose and monitor diabetes.

Urinalysis

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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

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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.

APG Labs offers fast & accurate results for a wide range of specialty tests!

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