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Antipancreatic Islet Cells

Performing Lab:

LabCorp

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Antipancreatic Islet Cells (C611)

Performing Lab:

Access Medical Labs

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Antiparietal Cell Antibody (APCA)

Performing Lab:

LabCorp

Description:

Detection of gastric parietal cell antibodies of the IgG class in human sera. Autoantibodies to gastric parietal cells are found in approximately 90% of patients with pernicious anemia and in about 30% of first degree relatives of patients with pernicious anemia. Increased levels of gastric parietal cells have been found in patients with thyroid disease, iron deficiency anemia, alopecia areata, and vitiligo.

The presence of immune complexes in a patient's sample may cause an elevated level of nonspecific binding and produce false-positive results. Assay performance has not been established for pediatric patients.

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Antiphosphatidylserine, IgA, IgG, IgM

Performing Lab:

LabCorp

Description:

An adjunct to β₂-glycoprotein and anticardiolipins in diagnosing aPS (antiphospholipid syndrome) for assessing thrombotic risk and other obstetric complications such as miscarriage or fetal growth restrictionAntiphospholipid antibodies are a heterogeneous group of immunoglobulins that bind to several anionic phospholipids, including cardiolipin and phosphatidylserine. High serum levels of antiphospholipid antibodies are frequently detected in patients with autoimmune (ie, SLE) and nonautoimmune diseases, as well as in apparently healthy individuals. These antibodies have been associated with an increased risk for recurrent arterial and venous thrombotic events, thrombocytopenia, and fetal loss. These manifestations are the main features of the antiphospholipid syndrome. Antiphospholipid antibodies are detected either by ELISAs using cardiolipin or other negatively-charged phospholipids as the antigen (anticardiolipin antibodies) or coagulation assays (lupus anticoagulants). Unlike cardiolipin, phosphatidylserine is a more physiologically relevant phospholipid due to its presence in cell membranes of endothelial cells and platelets and its role in the coagulation cascade. The detection of antiphosphatidylserine (aPS) antibodies by ELISA has been recommended for the serological diagnosis of antiphospholipid syndrome. Patients with positive reactions to both cardiolipin and phosphatidylserine are more likely to have clinical complications than those positive for only one. Higher prevalence and mean serum levels of antiphosphatidylserine antibodies have been reported in autoimmune patients. In addition, antiphosphatidylserine antibodies in SLE patients correlated with clinical manifestations of antiphospholipid syndrome and their pathogenic role has been demonstrated in a murine model.

Barna LK, Triplett DA, Foster WM, et al. A study of relationships among antiphosphatidylserine and anticardiolipin antibodies, the lupus anticoagulant and clinical implications. Lupus. 1994; 3:357.

Corgenix Inc. The significance of IgA antiphosphatidylserine (aPS) antibodies. The Reader. 2000; 10(2). Antiphosphatidylserine Semiquantitative Test Kits [package insert ]. Keedy KJ, Buckner TR, Taylor DO, et al. Antiphospholipid syndrome: Detection and clinical significance of antiphosphatidylserine antibodies by ELISA. 49th Annual AACC Clinical Laboratory Meeting, July 22nd-24th, 1997.

Keedy KJ, Santos M, Lopez L. Antiphosphatidylserine antibodies require beta 2-glycoprotein 1 as cofactor in ELISA. Lupus. 1994: 3:327.

Keedy KJ, Santos M, Lopez L. Prevalence and clinical significance of antiphosphatidylserine antibodies. Arthritis Rheum. 1994; 37:S392.

Miyakis S, Lockshin MD, Atsumi T, et al. International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS). J Thromb Haemost. 2006 Feb; 4(2):295-306. PubMed 16420554

Yodfat O, Blank M, Krause I, Schoenfeld Y. The pathogenic role of antiphosphatidylserine antibodies: Active immunization with the antibodies leads to the induction of antiphospholipid syndrome. Clin Immunol Immunopathol. 1996 Jan; 78(1):14-20. PubMed 8599879

Zuazu-Jausoro I, Oliver A, Monserrat I, et al. Importance of antiphosphatidylserine antibodies in patients with lupus anticoagulant. Analysis of 30 cases. Med Clin (Barc). 1990 Jul 7; 95(6):210-213. PubMed 2123507

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Antiphosphatidylserine/Prothrombin Complex, IgG and IgM

Performing Lab:

LabCorp

Description:

As an aid in the diagnosis of certain autoimmune thrombotic disorders, such as antiphospholipid syndrome (aPS). Antibodies to PS/PT correlate with the presence of lupus anticoagulants (LA) and this test may be useful in cases with difficult LA test interpretation. This assay may also assist in the determination of risk for thrombosis as well as obstetric complications in patients with antiphospholipid antibodies.

The clinical significance of aPS/PT antibodies in diseases other than aPS or SLE is under investigation. Diagnosis cannot be made on the basis of aPS/PT antibody results alone and results must be interpreted with the patient's clinical condition. Treatment must not be initiated on the basis of aPS/PT antibody results alone and should also rely on supportive clinical indications. Patients with aPS and be a PS/PT positive yet lupus anticoagulant, anticardiolipin or anti-B2Gp1 negative.

Antiphospholipid antibodies (aPL) are a family of immunoglobulins of considerable clinical significance due to their association with arterial and/or venous thrombosis, recurrent pregnancy loss, neurological disorders, pulmonary hypertension and thrombocytopenia. These antibodies are directed against phospholipid binding proteins or their complex with phospholipid. The best-studied phospholipid-binding proteins include B2 glycoprotein 1 and prothrombin.

Current laboratory assays recommended in the diagnosis of antiphospholipid syndrome (aPS), based on an international consensus guidelines, include anticardiolipin antibodies (aCL), B2 glycoprotein 1 antibodies (aB2Gp1) and detection of a lupus anticoagulant (LA) using clot-based assays. In regard to correlation with clinical manifestations of aPS, lupus anticoagulants are the most important laboratory finding followed by B2Gp1 IgG, then B2Gp1 IgM with isolated aCL, antiprothrombin and antiphosphatidylserine antibodies demonstrating significantly less correlation with aPS clinical manifestations. It has more recently been demonstrated that the antibodies most closely associated with aPS and LA are actually directed to a complex of anionic phospholipids such as phosphatidylserine/prothrombin (PS/PT) rather than to prothrombin alone. Also, thrombosis and pregnancy-related complications are more common in those with positivity in all three assays (LA, aCL and B2GpI of the same isotype) when the ELISA assays at positive at significant titer and this constellation is called triple positivity.

A very high degree of concordance has been demonstrated between the concentration of aPS/PT and lupus anticoagulant (LA) activity, and thus aPS/PT may play a useful role in confirming LA activity in those patients on anticoagulant therapy where LA testing may be spuriously positive due to the anticoagulant interference or when there is difficult LA test interpretation.¹ Furthermore, in APS patients, aPS/PT antibodies have been found to be highly associated with venous thrombosis and obstetric abnormalities.¹

aPS/PT testing may help identify APS in patients with thrombosis or pregnancy loss in whom APS is strongly suspected but conventional antiphospholipid testing is repeatedly negative. In a cohort of patients with SLE, triple positivity for LA, antiB2GP1 and aPS/PT was more strongly associated with thrombosis and/or pregnancy loss (OR 23.2) than any other combination of LA and antiphospholipid antibodies, including triple positivity for LA, anticardiolipin and antiB2Gp1 (OR 14.9).² Inclusion of aPT/PS testing into the standard aPL battery of assays may allow better quantitation of thrombotic risk and risk for pregnancy loss. Antiprothrombin IgG, IgM and antiphosphatidylserine IgG, IgM and IgA assays demonstrate little specificity for the clinical manifestations of aPS.³

1. Fabris M, Giacomello R, Poz A, et al. The introduction of antiphosphatidylserine/prothrombin autoantibodies in the laboratory diagnostic process of antiphospholipid syndrome: six month observation. Autoimmune Highlights. 2014 Aug;5:63. PubMed 26000157

2. Sciascia S, Sanna G, Murru V, et al. antiprothrombin (aPT) and antiphosphatidylserine/prothrombin (aPS/PT) antibodies and the risk of thrombosis in the antiphospholipid syndrome. A systematic review. Thromb Haemost. 2014 Feb;111:354. PubMed 24172938

3. Sciascia S, Murru V, Sanna G, et al. Clinical accuracy for diagnosis of antiphospholipid syndrome in systemic lupus erythematosus: evaluation of 23 possible combinations of antiphospholipid antibody specificities. J Thromb Haemost. 2012 Dec;10:2512. PubMed 23025466

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Antiphospholipid Syndrome (APS) Profile *

Performing Lab:

LabCorp

Description:

Use: Qualitative detection of lupus anticoagulants (LA) in plasma;6 semiquantitative detection of anticardiolipin and β2-glycoprotein 1 (β2GP1) antibodies in serum

Limitations: Anticoagulant therapies may result in false-positive LA results but will not interfere with aCL and β2GP1 testing.

Methodology: Clot; enzyme-linked immunosorbent assay (ELISA). A written assessment of the APS profile results is also provided as an aid in interpretation.

Additional Information: Antiphospholipid antibodies are a heterogeneous population of immunoglobulins directed against phospholipid-binding proteins that fall into one or two groups: lupus anticoagulants (which are identified using plasma-based clotting assays) and solid phase antibodies (which are identified using enzyme immunoassays and include anticardiolipin antibodies, antibodies to β2-glycoprotein 1 (β2GP1), antibodies to prothrombin, and others). Antiphospholipid antibodies, if present persistently during at least a 12-week period, may be associated with venous thrombosis, pulmonary embolism, arterial thrombosis, and pregnancy morbidity including recurrent fetal loss.7,8 In order to determine the presence of APS, both lupus anticoagulants (LA) and immunoassays for anticardiolipin and β2GP1 antibodies should be performed. Lupus anticoagulants are nonspecific inhibitors that extend the clotting time of phospholipid-dependent clotting assays, such as the activated partial thromboplastin time (aPTT).6,7 Unlike specific factor inhibitors, LA are not associated with an increased bleeding risk, unless the patient also suffers from thrombocytopenia or hypoprothrombinemia as a manifestation of the antibody. LA do not specifically inhibit individual coagulation factors; rather they neutralize anionic phospholipid-protein complexes that are involved in the coagulation process. Prolongation of clot-based assays is highly dependent on the sensitivity of the reagent employed to the presence of LA. Reagents with reduced amounts of phospholipid, such as the hexagonal phospholipid neutralization assay (aPTT LA) and dilute Russell viper venom time (dRVVT), have enhanced sensitivity for LA.6 Due to the heterogeneity of LA antibodies, no single assay will identify all cases.8 The International Society of Thrombosis and Haemostasis (ISTH) has established criteria for the diagnosis of lupus anticoagulants; there is also an international consensus statement describing criteria for antiphospholipid syndrome diagnosis.6-8 The laboratory criteria for definitive APS include one or more of the following; positive anticardiolipin IgG or IgM antibody at significant titer (>40 GPL or MPL units), positive β2GP1 IgG or IgM antibody, positive LA, and at least one result must demonstrate persistence of positivity at an interval of at least 12 weeks. Testing for lupus anticoagulant, anticardiolipin and β2GP1, and the antiphospholipid syndrome that is associated with these antibodies is described in more detail in the online coagulation appendices: Lupus Anticoagulants and Antiphospholipid Syndrome.

Footnotes: 1. 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; 107(1):105-110. PubMed 8980376
2.Reneke J, Etzell J, Leslie S, et al. 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; 109(6):754-757. PubMed 9620035
3. 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.
4. Gottfried EL, Adachi MM. Prothrombin time and activated partial thromboplastin time can be performed on the first tube. Am J Clin Pathol. 1997; 107(6):681-683. PubMed 9169665
5. McGlasson DL, More L, Best HA, et al. Drawing specimens for coagulation testing: Is a second tube necessary? Clin Lab Sci. 1999; 12(3):137-139. PubMed 10539100
6. Pengo V, Tripodi A, Reber G, et al. Update of the guidelines for lupus anticoagulant detection. Subcommittee on Lupus Anticoagulant/Antiphospholipid Antibody of the Scientific and Standardisation Committee of the International Society on Thrombosis and Haemostasis. J Thromb Haemost. 2009 Oct; 7(10):1737-1740. PubMed 8560433
7. Keeling D, Mackie I, Moore GW, Greer IA, Greaves M; British Committee for Standards in Haematology. Guidelines on the investigation and management of antiphospholipid syndrome. Br J Haematol. 2012 Apr; 157(1):47-58. PubMed 22313321
8. Miyakis S, Losckshin MD, Atsumi T, et al. International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS). J Thromb Haemost. 2006 Feb; 4(2):295-306. PubMed 16420554

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Antiproteinase 3 (PR3) Antibodies

Performing Lab:

LabCorp

Description:

For diagnosis and monitoring inflammatory activity in primary systemic small vessel vasculitides. Antineutrophil antibodies are best demonstrated in these diseases by using a combination of IFA and EIAs that detect ANCA specific for PR3-ANCA or MPO-ANCA. Presence of anti-MPO antibodies are highly specific for idiopathic and vasculitis associated crescentic glomerulonephritis, classic polyarteritis nodosa, Churg-Strauss syndrome, and polyangiitis overlap syndrome without renal involvement.

Presence of anti-PR3 antibodies are highly specific for Wegener granulomatous (WG) disease, for which the sensitivity is reported to be 98%. Some patients with WG have pANCA with MPO specificity. About 60% of patients with microscopic polyangiitis or pauci-immune segmental necrotizing glomerulonephritis have pANCA with MPO specificity but 30% have cANCA with PR3 specificity. Levels of anti-PR3 or anti-MPO are elevated during active phases of disease and lower during remission and can be monitored for management of disease.

Results of this assay are not diagnostic proof of the presence or absence of disease and should be used in conjunction with clinical findings and other serological tests.

De'Oliviera J, Gaskin G, Dash A, Rees AJ, Pusey CD. Relationship between disease activity and anti-neutrophil cytoplasmic antibody concentration in long-term management of systemic vasculitis. Am J Kidney Dis. 1995 Mar; 25(3):380-389. PubMed 7872315

Gross W, Csernok E. Immunodiagnostic and pathophysiologic aspects of antineutrophil cytoplasmic antibodies in vasculitis. Curr Opin Rheumatol. 1995 Jan; 7(1):11-19 (review). PubMed 7718417

Jennette JC, Falk RJ. Antineutrophil cytoplasmic antibodies: Discovery, specificity, disease associations and pathogenic potential. Adv Pathol Lab Med. 1995; 8:363-378.

Savige J, Gillis D, Benson E, et al. International Consensus Statement on Testing and Reporting of Antineutrophil Cytoplasmic Antibodies (ANCA). Am J Clin Pathol. 1999 Apr; 111(4):507-513. PubMed 10191771

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Antiribosomal P Antibodies

Performing Lab:

LabCorp

Description:

Ribosomal P antibodies are found in 10% to 20% of patients with systemic lupus erythematosus (SLE) and are purported to be associated with lupus psychosis.

Astion ML, Wener MH, Hutchinson K. Autoantibody testing: The use of immunofluorescence and other assays. Clin Lab News. 2000; (7):30-34.

Berner ES, Webster GD, Shugerman AA, et al. Performance of four computer-based diagnostic systems. N Engl J Med. 1994 Jun 23; 330(25):1792-1796. PubMed 8190157 Centers for Disease Control and Prevention. Manual Guide—Safety Management N° CDC-22 Decontamination of Laboratory Sink Drains to Remove Azide Salts. Atlanta, Ga: CDC; April 30, 1976.

Eriksson C, Engstrand S, Sundqvist KG, Rantapää-Dahlqvist S. Autoantibody formation in patients with rheumatoid arthritis treated with anti-TNF alpha. Ann Rheum Dis. 2005 Mar; 64(3):403-407. PubMed 15297281

Fulton RJ, McDade RL, Smith PL, Kienker LJ, Kettman JR Jr. Advanced multiplexed analysis with the FlowMetrix system. Clin Chem. 1997 Sep; 43(9):1749-1756. PubMed 9299971 Golightly M,

Golightly C. Laboratory diagnosis of autoimmune diseases. MLO Med Lab Obs. 2002 Jul; 34(7):12-16, 20. PubMed 12134551

Homburger HA, Cahen YD, Griffiths J, Jacob GL. Detection of antinuclear antibodies: Comparative evaluation of enzyme immunoassay and indirect immunofluorescence methods. Arch Pathol Lab Med. 1998 Nov; 122(11):993-999. PubMed 9822128

Isenberg DA. Systemic lupus erythematosus and Sjögren's syndrome: Historical perspective and ongoing concerns. Arthritis Rheum. 2004 Mar; 50(3):681-683. PubMed 15022304

Kallenberg CG, Wouda AA, Hoet MH, van Venrooij WJ. Development of connective tissue disease in patients presenting with Raynaud's phenomenon: A six year follow-up with emphasis on the predictive value of antinuclear antibodies as detected by immunoblotting. Ann Rheum Dis. 1988 Aug; 47(8):634-641. PubMed 3261966

Kavanaugh A, Tomar R, Reveille J, Solomon DH, Homburger HA. Guidelines for clinical use of the antinuclear antibody test and tests for specific autoantibodies to nuclear antigens. American College of Pathologists. Arch Pathol Lab Med. 2000 Jan; 124(1):71-81. PubMed 10629135

Narain S, Richards HB, Satoh M, et al. Diagnostic accuracy for lupus and other systemic autoimmune diseases in the primary care setting. Arch Intern Med. 2004 Dec 13-27; 164(22):2435-2441. PubMed 15596633

Phan TG, Wong RC, Adelstein S. Autoantibodies to extractable nuclear antigens: Making detection and interpretation more meaningful. Clin Diagn Lab Immunol. 2002 Jan; 9:(1):1-7. PubMed 11777822

Reeves WH, Satoh M. Autoantibodies in systemic lupus erythematosus. In: Koopman WJ, ed, Arthritis and Allied Conditions: A Textbook of Rheumatology. 14th ed. Philadelphia, Pa: Lippincott, Williams and Wilkins; 2001:1483.

Reichlin M, Harley JB. Antinuclear antibodies: An overview. In: Wallace DJ, Hahn BH, eds. Dubois Lupus Erythematosus. 5th ed. Baltimore, Md: Williams and Wilkins;1997:403.

Reisner BS, DiBlasi J, Goel N. Comparison of an enzyme immunoassay to an indirect fluorescent immunoassay for the detection of antinuclear antibodies. Am J Clin Pathol. 1999 Apr; 111(4):503-506. PubMed 10191770

Rekvig OP, Kalaaji M, Nossent H. Anti-DNA antibody subpopulations and lupus nephritis. Autoimmun Rev. 2004 Feb; 3(2):1-6. PubMed 15003181

Simón JA, Cabiedes J, Ortiz E, Alcocer-Varela J, Sánchez-Guerrero J. Anti-nucleosome antibodies in patients with systemic lupus erythematosus of recent onset. Potential utility as a diagnostic tool and disease activity marker. Rheumatology (Oxford). 2004 Feb; 43(2):220-224. PubMed 13130152

Sturgess A, Edmonds J. Improving the effectiveness of autoantibody testing in the clinic. Autoimmun Rev. 2002 Oct; 1(5):273-278. PubMed 12848980

Tan EM. Autoantibodies in diagnosis and in identifying antigens. Immunologist. 1999; 7(3):85-92.

Tan EM, Smolen JS, McDougal JS, et al. A critical evaluation of enzyme immunoassays for detection of antinuclear autoantibodies of defined specificities. I. Precision, sensitivity, and specificity. Arthritis Rheum. 1999 Mar; 42(3):455-464. PubMed 10088768

Tozzoli R, Bizzaro N, Tonutti E, et al. Guidelines for the laboratory use of autoantibody tests in the diagnosis and monitoring of autoimmune rheumatic diseases. Am J Clin Pathol. 2002 Feb; 117(2):316-334. PubMed 11863229

Zlatkis A, Lee KY, Poole CF, Holzer G. Capillary column gas chromatographic profile analysis of volatile compounds in sera of normal and virus-infected patients. J Chromatogr. 1979 Jun 11; 163(2):125-133. PubMed 541363

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Antiscleroderma - 70 Antibodies

Performing Lab:

LabCorp

Description:

Differential diagnosis of scleroderma (progressive systemic sclerosis).

Scl-70 antibody is seen in 20% of patients with scleroderma, and in some patients with CREST syndrome (calcinosis, Raynaud, esophageal dysfunction, sclerodactyly, telangiectasia). These syndromes are also associated with a high frequency of speckled pattern immunofluorescent antinuclear antibody tests. Scl-70 may identify a subset of scleroderma patients with severe skin, joint, and lung disease. In addition, the presence of Scl-70 in Raynaud phenomenon may indicate a poor prognosis.

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Antistreptolysin O (ASO) Antibodies

Performing Lab:

LabCorp

Description:

Document exposure to streptococcal streptolysin O. A marked rise in titer or a persistently elevated titer indicates that a Streptococcus infection or poststreptococcal sequelae are present.

False-positive ASO titers can be caused by increased levels of serum ß-lipoprotein produced in liver disease and by contamination of the serum with Bacillus cereus and Pseudomonas sp ASO titers are elevated in 85% of patients with rheumatic fever but may not be elevated in cases involving skin or renal sequelae. For patients suffering from skin or renal involvement, anti-DNase B test (096289) may be a better choice.

Streptolysin is a hemolysin produced by group A streptococci. In an infected individual streptolysin O acts as a protein antigen, and the patient mounts an antibody response. A rise in antibody level begins about one week after infection and peaks two to three weeks later. In the absence of complications or reinfection, the ASO titer will usually fall to preinfection levels within 6 to 12 months. Both clinical and laboratory findings should be correlated in reaching a diagnosis.

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Antistreptolysin O (ASO) Antibodies (P200)

Performing Lab:

Access Medical Labs

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Antithrombin (AT) Deficiency Profile

Performing Lab:

LabCorp

Description:

Confirmation and characterization of congenital AT deficiency.

AT testing should not be performed on patients on heparin therapy because heparin decreases plasma AT levels.^6,7 AT results for individuals on warfarin therapy should be interpreted with caution because warfarin can increase levels of AT of patients with heterozygous deficiency into the normal range.⁷ Thrombin inhibitors, such as dabigatran, hirudin, and argatroban, interfere with the AT activity assay when it is based on thrombin inhibition. Direct Xa anticoagulant will interfere with the assay when it is based on inhibition of Xa causing it to be falsely, elevated possibly masking a deficiency.⁶

Antithrombin (AT), often referred to as antithrombin III, is a glycoprotein produced in the liver.^7-9 AT is a serine protease inhibitor, or SERPIN, that irreversibly inhibits several of the enzymes involved in hemostasis. In this way, AT serves an important role in controlling coagulation by limiting the extent of thrombus formation. AT inhibits several steps of the coagulation cascade by binding to the catalytic sites of thrombin (factor IIa) and factors IXa, Xa, XIa, and XIIa. The complexes of AT with these thrombogenic serine proteinases are then rapidly cleared from the plasma. The binding of AT to these coagulation factors is slow in the absence of heparin. Heparin sulfate from endothelial cells or exogenously administered heparin binds to a specific site on the AT molecule. This produces a conformational change in the structure of AT, enhancing its binding to the activated coagulation factors by 1000-fold.⁸ Congenital defects in both the heparin binding site and the proteinase binding site of AT can cause functional deficiencies in AT activity.

Congenital AT deficiency: Congenital AT deficiency has been estimated to occur in approximately 3 out of 1000 individuals.⁸ Heterozygous AT deficiency is responsible for approximately 4% of families with inherited thrombophilia.⁷ Approximately 1% of cases of initial episodes of venous thrombosis are associated with congenital AT deficiency.⁷ Approximately 85% of individuals with congenital AT deficiency will experience at least one thrombotic episode by age 55 and recurrent thrombotic events are common.^8,9 Initial thrombotic events frequently occur between 20 and 30 years of age.⁸ Thrombosis can sometimes occur at unusual sites such as the mesenteric and axillary veins. In the majority of cases, thrombosis can be linked to trauma, surgery, pregnancy, oral contraceptive use, or other risk factors; however, thrombosis occurs spontaneously with no precipitating events or other known risk factors in about 33% of cases.⁸

Congenital AT deficiency can be classified as either type I or type II.^7-9 Type I deficiency results from a quantitative reduction in AT production, leading to a simultaneous decrease of both the functional and antigenic levels of AT. In type II deficiency, AT antigen concentration is normal but its activity is diminished because a fraction of the AT is dysfunctional due to genetic defect. This is reflected by a diminished AT activity in the context of normal AT antigen levels. Type II deficiency is more common than type I.

Acquired AT deficiency: Acquired AT deficiency is more common than congenital deficiency.^7-9 AT levels can be diminished in women receiving oral contraception or estrogen replacement therapy.⁷ Levels can also be diminished during pregnancy. Oral anticoagulant therapy with warfarin will lower AT levels. AT levels are usually diminished in patients with disseminated intravascular coagulation (DIC) and sepsis. AT levels can be transiently diminished after a thrombotic event or surgery. AT deficiency can be found in patients with severe hepatic disorders (hepatitis, cirrhosis, etc) due to diminished synthesis and nephrotic syndrome due to urinary protein loss. Malignancy and inflammatory bowel disease can also produce diminished AT levels.⁹ Drug therapy with L-asparaginase or fluorouracil can also reduce AT levels.

1. 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; 107(1):105-110. PubMed 8980376

2. Reneke J, Etzell J, Leslie S, et al. 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; 109(6):754-757. PubMed 9620035

3. 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).

4. Gottfried EL, Adachi MM. Prothrombin time and activated partial thromboplastin time can be performed on the first tube. Am J Clin Pathol. 1997; 107(6):681-683. PubMed 9169665

5. McGlasson DL, More L, Best HA, et al. Drawing specimens for coagulation testing: Is a second tube necessary? Clin Lab Sci. 1999; 12(3):137-139. PubMed 10539100

6. Van Cott EM, Laposata M. Coagulation. In Jacobs DS, DeMott WR, Oxley DK eds. Laboratory Test Handbook With Key Word Index. Hudson, Ohio: Lexi-Comp; 2001: 327-358.

7. Zwicker J, Bauer KA. Thrombophilia. In Kitchens CS, Alving BM, Kessler CM, eds. Consultative Hemostasis and Thrombosis. Philadelphia, Pa: WB Saunders Co; 2002:181-196.

8. Adcock DM, Bethel MA, Macy PA. Coagulation Handbook. Aurora, Colo: Esoterix-Colorado Coagulation; 2006.

9. Triplett DA, Thrombophilia. In: McClatchey KD, ed. Clinical Laboratory Medicine. 2nd ed. Philadelphia, Pa: Lippincott Williams and Wilkins; 2002:1050-1056.

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Apo E Genotyping: Cardiovascular Risk

Performing Lab:

LabCorp

Description:

Evaluate individuals with elevated cholesterol and triglycerides for the E2/E2 genotype associated with type III hyperlipoproteinemia. Aids in the diagnosis of hyperlipoproteinemia.

Type III hyperlipoproteinemia (broad β disease) is a familial dyslipidemia characterized by the combination of elevated serum cholesterol and triglycerides and the presence of the apolipoprotein E (Apo E) genotype E2/E2. Type III hyperlipoproteinemia has an incidence of 1/2,000−1/10,000. This lipid disorder is associated with a high risk of coronary heart disease and peripheral vascular disease. Onset of type III hyperlipoproteinemia is generally in adulthood but varies from late teens to old age. Before vascular disease develops there are usually no symptoms, and most patients with type III hyperlipoproteinemia are identified only from elevated serum cholesterol and triglycerides discovered during a routine screen. Symptoms include angina, heart attack, claudication, and leg pain. In untreated patients, xanthomas (fat deposits) are occasionally seen (flat in palmar creases or tuberous in joints).

The E2 variant of apolipoprotein E is defective in binding to receptors that normally clear harmful lipid particles called B-VLDL from the circulation. One percent of the general population has the E2/E2 genotype, and development of the frank lipid disorder occurs in 1% to 5% of these predisposed individuals, triggered by secondary genetic, hormonal or environmental factors. Ninety-five percent of patients with type III hyperlipoproteinemia are homozygous for E2. Demonstration of the E2/E2 genotype is essential for diagnosis of type III hyperlipoproteinemia.

Distinguishing this disorder from other causes of elevated cholesterol is important because effective treatment of type III hyperlipoproteinemia to prevent atherosclerosis often requires a different approach than treatment of other dyslipidemias.

Also known as APOE

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Apolipoprotein A-1

Performing Lab:

LabCorp

Description:

Apo A-1 comprises 60% to 70% of the protein content of HDL. Apo A-1 serves as an activator of LCAT which is involved in the transport of cholesterol from peripheral tissues to the liver where it is degraded. Decreased serum HDL cholesterol levels have been reported to correlate with increased risk of coronary artery disease (CAD); however, Apo A-1 has been suggested as a better discrimination of CAD than HDL.1 Apo A-1 levels also correlate with survival rates or risk factors for patients with myocardial infarction and peripheral vascular disease. Measurement of Apo A-1 may also aid in the diagnosis of Tangier disease (absence of alpha-lipoprotein).

1. Maciejko JJ, Holmes DR, Kottke BA, et al. Apolipoprotein A-1 as a marker of angiographically assessed coronary-artery disease. N Engl J Med. 1983; 309(7):385-389. PubMed 6410239

Colantonio DA, Kyriakopoulou L, Chan MK, et al. Closing the gaps in pediatric laboratory reference intervals: A CALIPER database of 40 biochemical markers in a healthy and multiethnic population of children. Clin Chem. 2012 May; 58(5):854-868. PubMed 22371482

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Apolipoprotein A-1 (00175)

Performing Lab:

Access Medical Labs

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Apolipoprotein A-I (ApoA-I) (301)

Performing Lab:

Boston Heart Diagnostics

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Apolipoprotein Assessment

Performing Lab:

LabCorp

Description:

Studies have shown that the ratio of apolipoprotein A-1:apolipoprotein B may correlate better with increased risk of coronary artery disease (CAD) than total cholesterol, and LDL:HDL ratio.

In 1971, Alaupovic suggested that apolipoproteins should be measured when assessing the relation of lipids and lipoproteins to CHD.2 Many patients with CHD were found to have normal serum and cholesterol levels. It was postulated that the chemical composition of the lipoproteins was more important for understanding the process of CHD than their blood levels. Subsequent studies have demonstrated that apolipoproteins are better discriminators than lipids and lipoproteins in patients with CHD and their relatives.

A number of studies have shown that apo A-1 and apo B correlate better with evidence of CHD than do lipoprotein measurements alone. In an investigation of first-degree relatives of patients with CHD, serum apo A-1 levels were significantly lower and apo B levels were significantly higher than those of healthy controls. Apo B was a better discriminator between male relatives, and apo A-1 was a better discriminator between female relatives and CHD patients. Furthermore, the percentage of correctly classified subjects increased by 12% when apo A-1 and apo B measurements were added as variables.

Avogaro et al found that serum apo A-1 and apo B levels, as well as various ratios using apolipoprotein measurements, were the variables that best discriminated male myocardial infarction survivors from age- and sex-matched controls.3

In 1983, Maciejko et al compared apo A-1 and HDL cholesterol measurements for their ability to identify male patients with angiographically assessed CHD.4 Analysis of their results indicated that apo A-1 alone misclassified 12.9% of the individuals compared to a misclassification error of 21.3% for HDL cholesterol alone. When apo A-1 and HDL cholesterol were used in combination, a misclassification error of 10.6% resulted. More recent studies have drawn similar conclusions.

When apo A-1, apo B, lipids, and lipoprotein cholesterol were measured in school-aged children (mean age of 10 years), apo A-1 and apo B levels were associated with a history of myocardial infarction in their parents. In striking contrast, the levels of serum lipids and lipoprotein-cholesterol values in these children were not related to myocardial infarction in either parent. Although no definite relationship between childhood apolipoprotein levels and adult CHD can be drawn, the results indicate that apolipoprotein measurements are more related to clinical disease than are conventional lipid measurements.5

Although the relationship of triglyceride measurements and CHD remains controversial, apolipoprotein measurements may be of benefit in identifying patients with hypertriglyceridemia who are at risk for CHD. Maciejko has suggested that apo B levels are helpful in differentiating primary causes of hypertriglyceridemia, provided that secondary causes (diabetes, alcohol ingestion, uremia, acromegaly, emotional stress or stress from acute illness, and certain drugs such as estrogen or beta blockers) have been ruled out. In familial endogenous hypertriglyceridemia, the apo B concentrations will be low while the patient with hypertriglyceridemia from familial combined hyperlipidemia will have a high apo B level.

Apolipoprotein measurements are also useful in the differentiation of familial hyper- or hypolipidemias. As mentioned, apo B may be used to differentiate familial combined hyperlipidemia from familial hypertriglyceridemia. Apo B measurements will also provide laboratory evidence of hyperapobetalipoproteinemia with excess apo B, whereas apo B deficiency states are found in abetalipoproteinemia, hypobetalipoproteinemia, familial hypobetalipoproteinemia with chylomicronemia, and abetalipoproteinemia with normotriglyceridemia. Apo A-1 deficiency states include Tangier disease, hypoalphalipoproteinemia, and HDL deficiency.

These studies indicated that apolipoprotein measurements can provide clarification in a variety of clinical states involving dyslipidemias. The Maciejko, Kottke, and Naito studies have concluded that apolipoprotein concentrations have greater discrimination in classifying patients who have or are predisposed to CHD and are more stable parameters than are lipids and lipoproteins.6 Lipids and lipoproteins are dynamic molecules whose concentration and composition are continually changing due to normal biologic variation, whereas apo A-1 and apo B levels are less affected, with change reflecting disease rather than biologic variability. In summary, apo A-1 and apo B measurements may be useful in the presence of the following conditions:

• Borderline elevations of cholesterol

• High cholesterol:HDL ratio with normal cholesterol

• Borderline elevations of LDL

• Normolipidemic children with a positive family history

• Normolipidemic adults with a positive family history

• Primary dyslipoproteinemias

1. Contois JH, McConnell JP, Sethi AA, et al. Apolipoprotein B and cardiovascular disease risk: Position statement from the AACC Lipoproteins and Vascular Diseases Division Working Group on Best Practices. Clin Chem. 2009; 55(3):407-419. PubMed 19168552

2. Alaupovic P. Apolipoproteins and lipoproteins. Atherosclerosis. 1971; 13(2):141-146. PubMed 5560875

3. Avogaro P, Bon GB, Cazzolato G, et al. Relationship between apolipoproteins and chemical components of lipoproteins in survivors of myocardial infarction. Atherosclerosis. 1980; 37(1):69-76. PubMed 7426089

4. Maciejko JJ, Holmes DR, Kottke BA, et al. Apolipoprotein A-1 as a marker of angiographically assessed coronary-artery disease. N Engl J Med. 1983; 309(7):385-389. PubMed 6410239

5. Kottke BA, Zinsmeister AR, Holmes DR Jr, et al. Apolipoproteins and coronary artery disease. Mayo Clin Proc. 1986; 61(5):313-320. PubMed 3702492

6. Naito HK. The association of serum lipids, lipoproteins, and apolipoproteins with coronary artery disease assessed by coronary arteriography. Ann N Y Acad Sci. 1985; 454:230-238. PubMed 3865610

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Apolipoprotein B

Performing Lab:

LabCorp

Description:

LDL and its major protein, apolipoprotein B, play an essential role in lipid transport and metabolism. Apo B may regulate cholesterol synthesis through its interaction with specific cell membrane receptors and by inhibition of HMG Co A reductase. This enzyme has been identified as the rate controlling enzyme in cholesterol biosynthesis. Apo B may be important in the genesis of atherosclerosis and its quantitation useful in the evaluation of patients at risk for or having coronary atherosclerosis (CAD). High levels indicate increased risk for CAD.

Colantonio DA, Kyriakopoulou L, Chan MK, et al. Closing the gaps in pediatric laboratory reference intervals: A CALIPER database of 40 biochemical markers in a healthy and multiethnic population of children. Clin Chem. 2012 May; 58(5):854-868. PubMed 22371482

Contois JH, McConnell JP, Sethi AA, et al. Apolipoprotein B and cardiovascular disease risk: position statement from the AACC Lipoproteins and Vascular Diseases Division Working Group on Best Practices. Clin Chem. 2009 Mar;55(3):407-419. PubMed 19168552

Jacobson TA, Ito MK, Maki KC, et al. National lipid association recommendations for patient-centered management of dyslipidemia: part 1–full report. J Clin Lipidol. 2015 Mar-Apr;9(2):129-169. PubMed 25911072

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Apolipoprotein B (00176)

Performing Lab:

Access Medical Labs

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Apolipoprotein B (ApoB) (302)

Performing Lab:

Boston Heart Diagnostics

Description:

ApoB is a protein produced in the liver and intestine that provides structure to triglyceride (TG) carrying atherogenic lipoprotein particles. Each particle carries only one apoB protein. Thus, apoB is a direct measure of the number of atherogenic particles in the bloodstream. ApoB is also a surrogate marker for LDL particle concentration or LDL particle number since LDL comprises about 90% of the atherogenic lipoprotein particles.

Very low-density lipoproteins (VLDL)
Intermediate-density lipoproteins (IDL)
Low-density lipoproteins (LDL)
Lp(a)
Chylomicrons

Methodology

Immunoturbidimetric

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Apolipoprotein E (apoE) Genotype Test (806)

Performing Lab:

Boston Heart Diagnostics

Description:

ApoE is a critical protein component of very low-density lipoprotein (VLDL) and chylomicrons. ApoE is important for:

Cholesterol absorption from the intestine

Uptake of triglyceride-rich lipoproteins by the liver

The intended use of apoE genetic testing is as an aid in the selection of optimal cholesterol-lowering protocols by the healthcare provider. The genetic test identifies individuals with altered lipid transport. Depending on the apoE genotype, cholesterol-lowering dietary interventions are very effective in these individuals, so the determination of the genotype allows the physician to select the most efficacious treatment regimen for the patient for lowering low-density lipoprotein cholesterol and reducing heart disease risk.

The APOE gene has three common alleles (E2, E3, E4) that encode for three protein isoforms (E2, E3, E4). ApoE3 is the most common form of apoE. Population frequencies for these apoE alleles are: E2 (15%) E3 (65%) E4 (20%)

E3/E3
Most common genotype; associated with:1-2
- Decreased uptake of cholesterol by the liver
- Lower total cholesterol and LDL-C
E2/E2, E2/E3
Associated with:1-2
- Lower LDL-C levels than the common E3/E3 genotype
- Lower total cholesterol and LDL-CV
E4/E4, E3/E4
Associated with higher LDL-C levels than the common E3/E3 genotype. Also associated with increased:1-2
- Cholesterol absorption in the intestine
- Uptake of intestinal cholesterol by the liver
- Total cholesterol and LDL-C
References:
1. Wilson PWF, Myers RH, Larson MG, Ordovas JM, Wolf PA, Schaefer EJ. Apolipoprotein E alleles, dyslipidemia, and coronary heart disease: the Framingham Off spring Study. JAMA. 1994;272(21):1666-1671.
2. Bennet AM, Di Angelantonio E, Ye Z, et al. Association of apolipoprotein E genotypes with lipid levels and coronary risk. JAMA. 2007;298(11):1300-1311.

Methodology - Real-time polymerase chain reaction (PCR)

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Apolipoprotein E (apoE) Genotype Test (Buccal Swab) (806)

Performing Lab:

Boston Heart Diagnostics

Description:

ApoE is a critical protein component of very low-density lipoprotein (VLDL) and chylomicrons. ApoE is important for:

Cholesterol absorption from the intestine

Uptake of triglyceride-rich lipoproteins by the liver

E3/E3
Most common genotype; associated with:1-2
- Decreased uptake of cholesterol by the liver
- Lower total cholesterol and LDL-C
E2/E2, E2/E3
Associated with:1-2
- Lower LDL-C levels than the common E3/E3 genotype
- Lower total cholesterol and LDL-CV
E4/E4, E3/E4
Associated with higher LDL-C levels than the common E3/E3 genotype. Also associated with increased:1-2
- Cholesterol absorption in the intestine
- Uptake of intestinal cholesterol by the liver
- Total cholesterol and LDL-C
References:
1. Wilson PWF, Myers RH, Larson MG, Ordovas JM, Wolf PA, Schaefer EJ. Apolipoprotein E alleles, dyslipidemia, and coronary heart disease: the Framingham Off spring Study. JAMA. 1994;272(21):1666-1671.
2. Bennet AM, Di Angelantonio E, Ye Z, et al. Association of apolipoprotein E genotypes with lipid levels and coronary risk. JAMA. 2007;298(11):1300-1311.

Methodology - Real-time polymerase chain reaction (PCR)

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Apple IgE

Performing Lab:

LabCorp

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Aromatic Solvents, Blood (790530)

Performing Lab:

LabCorp

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Arsenic (98416)

Performing Lab:

Boston Heart Diagnostics

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