Test Details
Methodology
The FVIII chromogenic substrate assay measures the FVIII-dependent activation of FX using purified bovine coagulation factors.1,2 This test consists of two steps. In the first step, patient plasma is added to a reaction mixture containing FIXa, FX, calcium ions, phospholipids and trace amounts of thrombin. Thrombin triggers the activation of FVIII and the subsequent FIXa-mediated activation of FX. FXa production is proportional to the concentration of FVIII in the plasma samples. In the second step, the amount of FXa produced is quantified using a chromogenic peptide substrate that binds selectively to FXa.3
Result 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.
Use
This test is used in the measurement of factor VIII activity in hemophilia patients.1,4-8 The chromogenic assay can be used in place of the more commonly used one-stage assay (OSA) for a number of clinical indications where limitations of OSA require a secondary option for FVIII testing.8,9
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.
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 inhibitor therapy may cause factitiously low results.
This test was developed and its performance characteristics determined by Labcorp. It has not been cleared or approved by the Food and Drug Administration.
Custom Additional Information
The factor VIII (FVIII) is an essential cofactor for factor IX (FIX) and plays a key role in the intrinsic pathway of the coagulation cascade.10,11 Upon tissue injury, FVIII potentiates activated FIX (FIXa) activity to form the intrinsic FXase (tenase) complex, which is responsible for the activation of factor X (FXa) generated by the coagulation cascade. FXa then combines with activated factor V (FVa) to form the FXa/FVa prothrombinase complex, which converts prothrombin to thrombin. Thrombin cleaves fibrinogen, to form fibrin monomers, and activates factor XIII (FXIIIa), which catalyzes the formation of covalent bonds between fibrin monomers and a stabilized fibrin clot. 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.17,18 Factor VIII circulates in the plasma bound to von Willebrand factor (vWF) at a concentration of approximately 0.1 mg/mL.5 The plasma half-life of factor VIII is short at about eight to 10 hours.5 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).
Factor VIII is an acute phase reactant with levels that rise during periods of acute stress, following surgery and in inflammatory conditions.6 Factor VIII levels are elevated at birth and increase during pregnancy.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.5,12 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.13 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.5 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.12
Hemophilia A, or classic hemophilia, occurs as the result of congenital deficiency of factor VIII.1,4,6,7,11 Clinical features of hemophilia A are the same as for hemophilia B, which is caused by factor IX deficiency. Hemophilia A is the second most common inherited bleeding abnormality (second only to von Willebrand disease), occurring in approximately one of every 5,000 live male births.4,6,14 Hemophilia A accounts for approximately 85% of all hemophilia cases.6 This condition is transmitted as an X chromosome-linked hereditary disorder.4,6 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.4,6 The prevalence of hemophilia A is equal in all ethnic groups.4,6 Female carriers of hemophilia A may rarely present with excessive bleeding.4 Hemophilia symptoms can also occur in female carriers who have a high degree of lyonization of the factor VIII allele.6 Females with Turner syndrome karyotype XO also can be symptomatic.6
The severity of hemophilia A can be defined by the level of factor VIII activity.6,7 The lower the measurable factor VIII (FVIII:C) or factor IX (FIX:C) functional “coagulant” activity, the more significant the bleeding diathesis. HA is classified into severe (FVIII <1 dL), moderate (FVIII 1–5 IU/dL) and mild (FVIII >5 to <40 IU/dL) disorders based on the level of clotting factor activity.15 Patients with mild HA have fewer bleeding problems than those with moderate or severe forms, often only requiring replacement factor therapy following significant trauma or postoperatively. Patients with moderate hemophilia may bleed following minor trauma, whereas severely affected patients may exhibit spontaneous bleeding, which can occur into joint spaces (hemarthroses).
Either one‐stage activated partial thromboplastin time (aPTT)‐based clotting or two‐stage chromogenic factor activity assays can be used in the diagnosis of hemophilia A or B, to classify disease severity, for potency labelling of FVIII and FIX concentrates by manufacturers, to monitor post‐infusion activity levels of FVIII and FIX during treatment and to test for FVIII and FIX antibodies (inhibitors).4,8,9,11,16 The coagulation factor activity assay used by the majority of clinical laboratories, the one-stage assay (OSA), may underestimate or overestimate the true FVIII activity in up to 30% of patients with mild or moderate (nonsevere) hemophilia A.1,4,8,9,17-25 Approximately 16% of patients with mild hemophilia A have a normal FVIII OSA, and the correct diagnosis relies on the chromogenic factor VIII assay.17,18 Differences in factor activity measurements between the OSA and chromogenic substrate assay (CSA) in nonsevere hemophilia is called discrepant hemophilia. This occurs in 30% of patients with nonsevere hemophilia A.17,18,26 Such discrepancies may also occur in hemophilia carriers. Either OSA results can be greater than CSA or vice versa, depending on the underlying FVIII gene mutation.8,16-19,26 Both possibilities can misclassify hemophilia severity, but the former may result in a missed diagnosis.
Discrepant hemophilia A has a genetic basis, generally due to missense mutations that affect the stability of the activated form of FVIII (FVIIIa) or the ability of FVIII to successfully bind the activated form of FIX (FIXa), von Willebrand factor or thrombin.8,17,19 Missense mutations clustered in the A1-A2-A3 domain interfaces of the FVIII protein cause reduced stability of FVIIIa, which is more apparent in FVIII activity assays where the FVIIIa is generated during a relatively long (for example, two-to-10-minute) incubation such as the CSA or the infrequently performed two-stage assay.18,19 In the OSA, FVIII is in the activated form for only a brief period. Missense mutations clustered around thrombin cleavage sites or FIXa binding sites are more readily identified in OSA since the factors are present at physiological concentrations, unlike the CSA, where factor concentrations are optimized. Also, long incubation times in the CSA may help to overcome mutations that interfere with binding. The underlying mutations and discrepancies between OSA and CSA are consistent within and between discrepant hemophilia A families.
Certain modified recombinant FVIII replacement products demonstrate variable and clinically significant differences in post-infusion recovery (that is, the amount of factor measured vs. the actual concentration present), based on the activated partial thromboplastin time (APTT) reagent used in the OSA assay methodology.4,8,9,16,27,28 Overestimation of post-infusion plasma factor activity can lead to underdosing of the replacement factor and an increased risk of bleeding. Conversely, underestimation of factor activity in the post-infusion sample may lead to overdosing of the replacement factor, which not only has cost implications but also may place the patient at risk for thrombosis. Most recombinant FVIII products may be accurately measured using a chromogenic assay, even when this is performed with a plasma calibrator rather than a product-specific calibrator.29,30,31 The United Kingdom Haemophilia Centre Doctors’ Organization (UKHDCO) has published guidance for the laboratory monitoring of FVIII and FIX concentrates.32
Emicizumab (Hemlibra ™) is a humanized bispecific antibody directed to activated human FIX (FIXa) and FX, which activates FX in the absence of activated factor VIII (FVIIIa).33 Unlike FVIII, emicizumab does not require preactivation to be functional resulting in a more rapid activation of FX,34 impacting on some hemostasis tests.8,35 Several organizations have published guidance for the monitoring of patients receiving emicizumab therapy.36,37 Quantitative measurement of the emicizumab drug concentration can be accomplished employing the standard OSA using an emicizumab-specific calibrator and high plasma dilutions. However, the standard OSA for FVIII produces artificially increased values, often far above the top of the reference range. Consequently, the presence of emicizumab interferes with clotting‐based assays that rely on FVIII activity, such as the aPTT and one‐stage FVIII assays.8,11,37 Chromogenic FVIII assays employing bovine factors are insensitive to emicizumab at therapeutic concentrations.38-40 Levels of FVIII inhibitors in patients treated with emicizumab can be accomplished using a Bethesda method based on a CSA employing bovine factors.8,11,37,41,42
The chromogenic assay uses a high dilution of plasma making it insensitive to lupus anticoagulants, heparin, low-molecular-weight heparins [LMWHs] and lepirudin, all of which may result in major interference with the one-stage clot-based assay.8,16,43,44 A chromogenic factor activity assay does not demonstrate lupus anticoagulant interference due to the high initial dilution used in the assay and the decreased phospholipid dependence of the assay.8
Specimen Requirements
Specimen
Plasma, frozen
Volume
1 mL
Container
Blue stopper 3.2% sodium citrate plasma evacuated tube
Collection Instructions
Blood should be collected in a blue-top tube containing 3.2% buffered sodium citrate.45 Evacuated collection tubes must be filled to completion to ensure a proper blood to anticoagulant ratio.46,47 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.48,49 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 and carefully remove the plasma using a plastic transfer pipette, being careful not to disturb the cells. Transfer the plasma into a Labcorp PP transpak frozen purple tube with screw cap (Labcorp No. 49482). Freeze immediately and maintain frozen until tested. To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.
Please print and use the Volume Guide for Coagulation Testing to ensure proper draw volume.
Reference Range
49–126%
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.
Footnotes
1. Müller J, Miesbach W, Prüller F, et al. An Update on Laboratory Diagnostics in Haemophilia A and B. Hamostaseologie. 2022 Aug;42(4):248-260. PubMed 35104901
2. Amiral J, Seghatchian J. Usefulness of chromogenic assays for potency assignment and recovery of plasma-derived FVIII and FIX concentrates or their recombinant long acting therapeutic equivalents with potential application in treated pediatric hemophiliac patients. Transfus Apher Sci. 2018 Jun;57(3):363-369. PubMed 29895509
3. Rodgers S, Duncan E. Chromogenic Factor VIII Assays for Improved Diagnosis of Hemophilia A. Methods Mol Biol. 2017;1646:265-276. PubMed 28804835
4. Mehta P, Reddivari AKR. Hemophilia. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan. 2023 Jun 5. PubMed 31869071
5. Chandler WL, Rodgers GM, Sprouse JT, Thompson AR. Elevated hemostatic factor levels as potential risk factors for thrombosis. Arch Pathol Lab Med. 2002 Nov;126(11):1405-1414. PubMed 12421150
6. Cohen AJ, Kessler CM. Hemophilia A and B. In: Kitchens CS, Alving BM, Kessler CM, eds. Consultative Hemostasis and Thrombosis. Philadelphia, Pa: WB Saunders Co. 2002; 43-56.
7. Triplett DA. Coagulation abnormalities. In: McClatchey KD, ed. Clinical Laboratory Medicine. 2nd ed. Philadelphia, Pa: Lippincott Williams and Wilkins. 2002, 1033-1049.
8. Bowyer AE, Gosselin RC. Factor VIII and Factor IX Activity Measurements for Hemophilia Diagnosis and Related Treatments. Semin Thromb Hemost. 2023 Sep;49(6):609-620. PubMed 36473488
9. Peyvandi F, Oldenburg J, Friedman KD. A critical appraisal of one-stage and chromogenic assays of factor VIII activity. J Thromb Haemost. 2016 Feb;14(2):248-261. PubMed 26663865
10. Lee C, Berntorp E, Hoots W. Textbook of Hemophilia. 2nd ed. Chichester, UK: Blackwell Publishing Ltd; 2010.
11. Marlar RA, Strandberg K, Shima M, Adcock DM. Clinical utility and impact of the use of the chromogenic vs one-stage factor activity assays in haemophilia A and B. Eur J Haematol. 2020 Jan;104(1):3-14. PubMed 31606899
12. Kamphuisen PW, Eikenboom JC, Rosendaal FR, et al. High factor VIII antigen levels increase the risk of venous thrombosis but are not associated with polymorphisms in the von Willebrand factor and factor VIII gene. Br J Haematol. 2001 Oct;115(1):156-158. PubMed 11722428
13. Cristina L, Benilde C, Michela C, Mirella F, Giuliana G, Gualtiero P. High plasma levels of factor VIII and risk of recurrence of venous thromboembolism. Br J Haematol. 2004 Feb;124(4):504-510. PubMed 14984502
14. Srivastava A, Santagostino E, Dougall A, et al. WFH guidelines for the management of hemophilia, 3rd edition. Haemophilia. 2020;26 Suppl 6:1-158. PubMed 32744769
15. White GC 2nd, Rosendaal F, Aledort LM, et al. Definitions in hemophilia. Recommendation of the scientific subcommittee on factor VIII and factor IX of the scientific and standardization committee of the International Society on Thrombosis and Haemostasis. Thromb Haemost. 2001 Mar;85(3):560. PubMed 11307831
16. Moser KA, Adcock Funk DM. Chromogenic factor VIII activity assay. Am J Hematol. 2014 Jul;89(7):781‐784. PubMed 24676945
17. Oldenburg J, Pavlova A. Discrepancy between one-stage and chromogenic factor VIII activity assay results can lead to misdiagnosis of haemophilia A phenotype. Hemostaseologie. 2010 Nov;30(4):207-211. PubMed 21057709
18. Kamphuisen PW, Eikenboom JC, Rosendaal FR, et al. High factor VIII antigen levels increase the risk of venous thrombosis but are not associated with polymorphisms in the von Willebrand factor and factor VIII gene. Br J Haematol. 2001 Oct;115(1):156-158. PubMed 11722428
19. Pavlova A, Delev D, Pezeshkpoor B, Müller J, Oldenburg J. Haemophilia A mutations in patients with nonsevere phenotype associated with a discrepancy between one-stage and chromogenic factor VIII activity assays. Thromb Haemost. 2014 May 5;111(5):851-861. PubMed 24452774
20. Duncan EM, Rodgers SE, McRae SJ. Diagnostic testing for mild hemophilia a in patients with discrepant one-stage, two-stage, and chromogenic factor VIII:C assays. Semin Thromb Hemost. 2013 Apr;39(3):272-282. PubMed 23460037
21. Schwaab R, Oldenburg J, Kemball-Cook G, et al. Assay discrepancy in mild haemophilia A due to a factor VIII missense mutation (Asn694Ile) in a large Danish family. Br J Haematol. 2000 Jun;109(3):523-528. PubMed 10886198
22. Bowyer AE, Van Veen JJ, Goodeve AC, Kitchen S, Makris M. Specific and global coagulation assays in the diagnosis of discrepant mild hemophilia A. Haematologica. 2013 Dec;98(12):1980-1987. PubMed 23812942
23. Poulsen AL, Pedersen LH, Hvas AM, Poulsen LH, Thykjaer H, Ingerslev J. Assay discrepancy in mild haemophilia A: entire population study in a National Haemophilia Centre. Haemophilia. 2009 Jan;15(1):285-289. PubMed 19149854
24. Michnick DA, Pittman DD, Wise RJ, Kaufman RJ. Identification of individual tyrosine sulfation sites within factor VIII required for optimal activity and efficient thrombin cleavage. J Biol Chem. 1994 Aug 5;269(31):20095-20102. PubMed 8051097
25. Bowyer AE, Goodeve A, Liesner R, Mumford AD, Kitchen S, Makris M. p.Tyr365Cys change in factor VIII: haemophilia A, but not as we know it. Br J Haematol. 2011 Sep;154(5):618-625. PubMed 21751985
26. Peyvandi F, Oldenburg J, Friedman KD. A critical appraisal of one-stage and chromogenic assays of factor VIII activity. J Thromb Haemost. 2016 Feb;14(2):248-261. PubMed 26663865
27. Kitchen S, Tiefenbacher S, Gosselin R. Factor activity assays for monitoring extended half-life factor VIII and factor IX replacement therapies. Semin Thromb Hemost. 2017 Apr;43(3):331-337. PubMed 28264199
28. Dodt J, Hubbard AR, Wicks SJ, et al. Potency determination of factor VIII and factor IX for new product labeling and postinfusion testing: challenges for caregivers and regulators. Haemophilia. 2015 Jul;21(4):543-549. PubMed 25623631
29. Tiefenbacher S, Robinson MM, Ross EL, et al. Comparison of FVIII activity of select novel recombinant FVIII replacement products in commonly used FDA approved one-stage clot assay systems. J Thromb Haemost. 2015;13(Suppl 2):566 (abstract).
30. Kitchen S, Kershaw G, Tiefenbacher S. Recombinant to modified factor VIII and factor IX - chromogenic and one-stage assays issues. Haemophilia. 2016 Jul;22(Suppl 5):72-77. PubMed 27405680
31. Jacquemin M, Vodolazkaia A, Toelen J, et al. Measurement of B-domain-deleted ReFacto AF activity with a product-specific standard is affected by choice of reagent and patient-specific factors. Haemophilia. 2018 Jul;24(4):675-682. PubMed 28124445
32. Gray E, Kitchen S, Bowyer A, et al. Laboratory measurement of factor replacement therapies in the treatment of congenital haemophilia: A United Kingdom Haemophilia Centre Doctors' Organisation guideline. Haemophilia. 2020 Jan;26(1):6-16. PubMed 31846168
33. Kitazawa T, Igawa T, Sampei Z, et al. A bispecific antibody to factors IXa and X restores factor VIII hemostatic activity in a hemophilia A model. Nat Med. 2012 Oct;18(10):1570-1574. PubMed 23023498
34. Lenting PJ, Denis CV, Christophe OD. Emicizumab, a bispecific antibody recognizing coagulation factors IX and X: how does it actually compare to factor VIII? Blood. 2017 Dec 7;130(23):2463-2468. PubMed 29042366
35. Adamkewicz JI, Chen DC, Paz-Priel I. Effects and Interferences of Emicizumab, a Humanised Bispecific Antibody Mimicking Activated Factor VIII Cofactor Function, on Coagulation Assays. Thromb Haemost. 2019 Jul;119(7):1084-1093. PubMed 31064025
36. Jenkins PV, Bowyer A, Burgess C, et al. Laboratory coagulation tests and emicizumab treatment A United Kingdom Haemophilia Centre Doctors' Organisation guideline. Haemophilia. 2020 Jan;26(1):151-155. PubMed 31859415
37. National Bleeding Disorders Foundation NBDF). MASAC Document 268 - Recommendation on the Use and Management of Emicizumab-kxwh (Hemlibra®) for Hemophilia A with and without Inhibitors. NBDF website: https://www.bleeding.org/healthcare-professionals/guidelines-on-care/masac-documents/masac-document-268-recommendation-on-the-use-and-management-of-emicizumab-kxwh-hemlibrar-for-hemophilia-a-with-and-without-inhibitors. Updated April 27, 2022. Accessed October 6, 2025.
38. Tripodi A, Chantarangkul V, Novembrino C, et al. Emicizumab, the factor VIII mimetic bi-specific monoclonal antibody and its measurement in plasma. Clin Chem Lab Med. 2020 Sep 4;59(2):365-371. PubMed 32892172
39. Oldenburg J, Mahlangu JN, Kim B, et al. Emicizumab prophylaxis in hemophilia A with inhibitors. N Engl J Med. 2017 Aug 31;377(9):809-818. PubMed 28691557
40. Mahlangu J, Oldenburg J, Paz-Priel I, et al. Emicizumab prophylaxis in patients who have hemophilia A without inhibitors. N Engl J Med. 2018 Aug 30;379(9):811-822. PubMed 30157389
41. Bowyer A, Kitchen S, Maclean R. Measurement of antifactor VIII antibody titre in the presence of emicizumab; Use of chromogenic Bethesda assays. Int J Lab Hematol. 2021 Aug;43(4):O204-O206. PubMed 33764652
42. Miller CH, Boylan B, Payne AB, Driggers J, Bean CJ. Validation of the chromogenic Bethesda assay for factor VIII inhibitors in hemophilia a patients receiving Emicizumab. Int J Lab Hematol. 2021 Apr;43(2):e84-e86. PubMed 33174329
43. de Maistre E, Wahl D, Perret-Guillaume C et al. A chromogenic assay allows reliable measurement of factor VIII levels in the presence of strong lupus anticoagulants. Thromb Haemost. 1998 Jan;79(1):237-238. PubMed 9459356
44. Blanco AN, Peirano AA, Grosso SH, Gennari LC, Bianco RP, Lazzari MA. A chromogenic substrate method for detecting and titrating anti-factor VIII antibodies in the presence of lupus anticoagulant. Haematologica. 2002 Mar;87(3):271-278. PubMed 11869939
45. Adcock DM, Kressin DC, Marlar RA. Effect of 3.2% vs 3.8% sodium citrate concentration on routine coagulation testing. Am J Clin Pathol. 1997 Jan;107(1):105-110. PubMed 8980376
46. Reneke J, Etzell J, Leslie S, Ng VL, Gottfried EL. Prolonged prothrombin time and activated partial thromboplastin time due to underfilled specimen tubes with 109 mmol/L (3.2%) citrate anticoagulant. Am J Clin Pathol. 1998 Jun;109(6):754-757. PubMed 9620035
47. National Committee for Clinical Laboratory Standardization. Collection, Transport, and Processing of Blood Specimens for Coagulation Testing and General Performance of Coagulation Assays; Approved Guideline. 5th ed. Villanova, Pa: NCCLS; 2008. Document H21-A5:28(5).
48. Gottfried EL, Adachi MM. Prothrombin time and activated partial thromboplastin time can be performed on the first tube. Am J Clin Pathol. 1997 Jun;107(6):681-683. PubMed 9169665
49. McGlasson DL, More L, Best HA, Norris WL, Doe RH, Ray H. Drawing specimens for coagulation testing: Is a second tube necessary? Clin Lab Sci. 1999 May-Jun;12(3):137-139. PubMed 10539100
LOINC® Map
| Order Code | Order Code Name | Order Loinc | Result Code | Result Code Name | UofM | Result LOINC |
|---|---|---|---|---|---|---|
| 086295 | Factor VIII Act, Chromogenic | 3211-0 | 086296 | Factor VIII Act, Chromogenic | % | 3211-0 |
| Order Code | 086295 | |||||
| Order Code Name | Factor VIII Act, Chromogenic | |||||
| Order Loinc | 3211-0 | |||||
| Result Code | 086296 | |||||
| Result Code Name | Factor VIII Act, Chromogenic | |||||
| UofM | % | |||||
| Result LOINC | 3211-0 |